the tiffinian journal of general medicine - issue 1 - january 2015

TheTiffinian Journalof GeneralMedicine

Issue Number 1 - January 2015

Featured in this issue:

How HIV Works

Bee Venom & HIV

Xenotransplantation

LVADs & Drivline Associated Infections

MRSA & Antibiotic Resistance

Antibiotics and New Alternatives

Affiliate Of

Photo: istockphoto.com

Contents

PAGE

A Message From The Founder...................................................4

The Publishing Team..................................................................5

MRSA And Antibiotic Resistance.............................................6-7

HIV - An Introduction ..................................................................8

Dengue Fever.............................................................................9

Marfan Syndrome......................................................................10

A Mental Health Crisis..............................................................11

Left Ventricular Assist Device Associated Infection................12

Antibiotics and New Alternatives...............................................13

Xenotransplantation..........................................................14-15

Mycoplasmia Pneumonia..........................................................16

Insulin Growth Like Factor.........................................................17

ALS and Animal Testing............................................................18

Bees' Venom and HIV..............................................................19

DRESS Syndrome....................................................................20

Allergies - How They Work and How They're Deadly ..............21

Hyperthyroidism .......................................................................22

An Ending Note From The Co-Editor-in-Chief......................23

About us

A Message from The FounderThe Tiffinian Journal of General Medicine is a quarterly medicine6orientated publishing, targeted ataspiring medical and natural science students, hoping to inform and pass on interesting knowledgerelated toall areasof clinical and researchmedicine. Since themagazinewas founded inNovember2014,the publishing team have been focused on conveying university6level knowledge to pre6universitystudents in well6written, coherent and easily understood articles. All of our journalists only write abouttopics they find intriguing and thought provoking. I believe that this freedom of writing allows for themto maintain their interests in their chosen topics whilst writing their articles, which is important as tomeet the high standards of the editing team, a lot of time and dedication is needed.To maintain the high quality of our published material, our journalists are advised to utilise and quotedata fromreliable sources such as researchpapers andothermedical journals such as theLancet and theNew England Journal of Medicine.I hope that you enjoy reading our articles and browsing through our other material. I believe that ourmagazine provides an easily accessible discussion forum for fellow students reading our publishing, soall are welcome to send us some feedback and questions. The Publishing Team and I are extremelygrateful for you support by reading our journal and I hope you enjoy reading our other upcoming issues.

Thank you,Senthooran Kathiravelupillai,Founder and Co6Editor In Chief

About Us

The Publishing Team

David CohenCo-FounderAn aspiring orthopaedicsurgeon with current interestsin Preventattive Medicine,Virology (Zoonotic Diseases)and Geriatrics. Also hasinterests in the efficacy ofantibiotics and their link toCrohn's Disease.

Zakaria AchercoukAn aspiring neurosurgeon withcurrent interests in Embryologyand Biological Developmentand Maturation.

Hassan HussainWishes to specialise intoOncology. Has specificinterests in haemato-oncology.

Vamsi ThammandraWishes to specialise intoTrauma and EmergencyMedicine. Has current intereststhe 3D printing of organs andmind controlled limbs usingneuron-bypassed surgery.

SenthooranKathiravelupillaiFounder and Co-Editor-in-ChiefAn aspiring neurosurgeon withcurrent interests inImmunotherapy, Barrett'sOesophagus and the HumanImmunodeficiency Virus.

Saamir MirzaCo-Editor-in-ChiefAn aspiring neurosurgeon withcurrent interests in the releaseof neurotransmitters from cellbodies and dendrites.

Huw ChildInterested in the application ofrevoltionary technology intoMedicine and Surgery.

The invention of antibiotics could be cited as one of the mostimportant breakthroughs in medicine to this day. Antibioticsare so effective because they directly combat bacteria byaltering a specific function, causing them todie.However if allof the bacteria do not die, the surviving bacteria sometimesmultiply into resistant colonies, which will then require adifferent treatment. Thus many of the bacterial infectionsantibioticshad initiallybeendeveloped tocombatnowrequirenew and different antibiotics. As a result, we must search formore newantibiotics to supersede those that have lost efficacydue to resistance. Also, many antibiotics are being used on awide scale for all sorts of infections. Such universality of theantibiotics has led to their overuse, increasing the demand fornewer antibiotics. Studies have led to the discoveryof possiblealternatives to antibiotics, by combining natural products andcomparing their effectiveness with antibiotics with knownactivity against Methicillin-resistant Staphylococcus aureus(MRSA).Methicillin-resistant Staphylococcus aureus, morecommonly known as MRSA, is the term used to describestrains of Staphylococcus aureus (SA) bacteria, that areresistant to a number of antibiotics, including methicillin. Ingeneral, one in four people carry Staphylococcus aureus. Itcan be found primarily near the nose and all over the skin’ssurface. Although Staphylococcus aureus is usually quiteharmless, once it enters the body through a cut, wound, oreven a hair follicle, it can multiply and form colonies whicheventually form an infection. In the past, many SA infectionscould be treatedwith Beta-lactam antibiotics, which includedmethicillin and penicillin. As time progressed, many Staphinfections became resistant to the Beta-lactams. This could beattributed to the fact that patients had failed to finish theirentire course of antibiotics, allowing a few bacteria to remain.The remaining bacteria would’ve only experienced a portionof the antibiotic course, and became tolerant to some of themost common antibiotics. Today, two in every one hundredpeople carry a strain of Staph bacteria that is resistant to Beta-lactams (MRSA). In Turkey, Onlen et al. found a significantbenefit from Propolis in their 2007 study, AntibacterialActivity of Propolis against MRSA and Synergism withTopical Mupirocin.

By Saamir Mirza

MRSA And Antibiotic Resistance

Conclusion

1. Dugdale III, David C., Jatin M. Vyas, and David Zieve. "MRSA - PubMedHealth."Public Medical Health. U.S. National Library of Medicine, 09 June 2011. Web. 18 Jan. 2012.

2. "Fact Sheet: The Safe Use of Antibiotics - PubMed Health."Public Medical Health. U.S. National Library of Medicine, 18 Jan. 2011. Web. 18 Jan. 2012.

3. Nordqvist, Christian. "What Is MRSA? Why Is MRSA a Concern? How Is MRSATreated?" Medical News Today: Health News. Medical News Today, 12 June 2004. Web. 17Jan. 2012. Onlen, Yusef, Nizami Duran, Esin Atik, Lutfu Savas, Enes Altug, SalvinazYakan, and Ozkan Aslantas."Antibacterial Activity of Propolis against MRSA and Synergism with Topical Mupirocin."Diss. Mustafa Kemal University Faculty of Veterinary, Hatay, Turkey, 2007.

4. Abstract. Antibacterial Activity of Propolis against MRSA and Synergism withTopical Mupirocin.Mary Ann Liebert, Inc, 11 Oct. 2007. Web. 3 Feb. 2012.

5. "WHO | Antimicrobial Resistance."WHO Fact Sheets. World Health Organization, Feb. 2011. Web. 18 Jan. 2012.

Sources

They infectedNewZealandRabbitswith strainsofMRSA,andfound that the addition of Propolis was able to reduce thebacterial cell count as well as the inflammatory responsemuchmore effectively when compared to the original medication.

Wang et al. looked past thematter of efficacy and attempted topinpoint the mechanism of how honey affects Pseudomonasaeruginosa. This could be attributed to the factthat patients had failed to finish their entire course ofantibiotics, allowing a few bacteria to remain.

The remaining bacteriawould’ve only experienced a portionofthe antibiotic course, and became tolerant to some of the mostcommon antibiotics. Today, two in every one hundred peoplecarry a strain of Staph bacteria that is resistant to Beta-lactams(MRSA).In Turkey, Onlen et al. found a significant benefitfrom Propolis in their 2007 study, Antibacterial Activity ofPropolis against MRSA and Synergism with TopicalMupirocin. They infectedNewZealandRabbitswith strains ofMRSA, and found that the addition of Propolis was able toreduce the bacterial cell count as well as the inflammatoryresponsemuchmore effectivelywhen compared to the originalmedication.Wang et al. looked past the matter of efficacy andattempted to pinpoint the mechanism of how honey affectsPseudomonas aeruginosa. Through a broth testing method,they were able to conclude two things: honey disrupts thequorum sensing (QS), and this ability has a relationship withthe sugar content of the honey.The importance of synergycomes into play when looking to the relationship betweenantimicrobials and bacteria. Each antimicrobial combats thebacteria in different ways, for example: inhibiting the quorumsensing (QS) functionof thebacteria, penetrating thewall of thebacteria, or even disrupting the energy supply for the bacteria.If just one antibiotic was being used individually, a probabilityexists such that over time, resistance will develop in thebacteria.However, if two antimicrobial agents are present, inthe case that one fails, the other agent will be able to use itsdifferent mechanism to defeat the bacteria, significantlydecreasing the probability for resistance.In this article is an account of a study done by Adeel Ahmad,a university student in Minnesota, USA, which facilitated adirect side-by-side comparison of antibiotics and naturalproducts. This was done by running culture sensitivity testsagainst a strain of MRSA (Methicillin-resistantStaphylococcus aureus) aswell asMSSA(Methicillin-sensitiveStaphylococcus aureus). Each natural product was tested byitself, and in combination with the other natural products. Thecombination of propolis and garlic was thought to be the mosteffective against the Staph bacteria, for two reasons.First, theproposed activity of propolis is different than that of an

antibiotic. Antibiotics directly combat bacteria’s functions,while propolis inhibits bacterial growth by strengthening one’simmune system.The initial uses of propolis could also be datedback to the ancient Greeks and even to the ancient Egyptianeras. Similar claimshave also beenmade for garlic,whichdatesback to the ancient Egyptian era. This evidence suggests thatbacteria have yet to become tolerant to propolis and garlic.Because MRSA is resistant, the experiment had to becompleted at a Bio-Safety Level 2 lab.

Towards the end of the 1960’s, Staphylococcus Aureus beganresisting the four main antibiotics that were initially made totreat them: Penicillin, Methicillin, Tetracycline, andErythromycin, leaving Vancromycine as the only effectiveantibiotic known. However in 2001, cases of VRSA(Vancromycine-Resistant Staphylococcus Aureus) beganappearing in the United States, furthering the need to researchmore alternatives.The six reagents that hadbeen chosen for theproject had been confirmed to express some microbial traitsfrom either cultural significance, or parallel studies. After theculture sensitivity tests, it was clear that honey, ginger, andonion displayed no clearance zone at all. However, this doesnot allow us to conclude that these reagents aren’t effective incuring MRSA. We can only see that these reagents do notcombat the bacteria directly. On the other hand, garlic,Propolis, and olive-leaf extract proved to be effective againstboth strains of MRSA and MSSA. Different densities of thebacteria had to be tried, because the clearance zones weren’tperfectly round. Also, garlic showed a “shaded” zone, in allfour plates with a higher density of bacteria. To fix this, thedensity of the bacteriawas reduced fifty-fold, and clearer zonesthat were circular were exhibited. The new plates clearly gavethe significant data to conclude thatGarlic, Propolis and olive-leaf extract are all natural products that can be used to treatcases of both MRSA and MSSA.

Garlic'Crushed Garlic'Extract Ginger'Extract Olive'Leaf'Extract Onion'Crushed Propolis Cefoxitin Trimetho'Sulfisoxazole VancomycinGarlic'Crushed 1.6 0 0 0 0 0.8Garlic'Extract 0 0 0 0 0 1.2Ginger'Extract 0 0 0 0 0 1Olive'Leaf'Extract 0 0 0 0 0 0.93Onion'Crushed 0 0 0 0 0 1Propolis 0.8 1.2 1 0.93 1 1.1Cefoxitin 1.14Trimetho'Sulfisoxazole 1.82Vancomycin 1.74

Practical Results

MRSA Trial 1

MSSA Trial 1

Garlic'Crushed Garlic'Extract Ginger'Extract Olive'Leaf'Extract Onion'Crushed Propolis Cefoxitin Trimetho'Sulfisoxazole VancomycinGarlic'Crushed 0 0 0 0 0 0.73Garlic'Extract 0 0 0 0 0 0.86Ginger'Extract 0 0 0 0 0 0.96Olive'Leaf'Extract 0 0 0 0 0 0.95Onion'Crushed 0 0 0 0 0 0.65Propolis 0.73 0.86 0.96 0.95 0.65 0.92Cefoxitin 2.89Trimetho'Sulfisoxazole 1Vancomycin 1.68

MRSA Trial 2

Garlic'Disc Garlic'Extract Ginger'Extract Olive'Leaf'Extract Onion'Disc Propolis Cefoxitin Trimetho'Sulfisoxazole VancomycinGarlic'Disc 0 1.43 0.75 0.91 0 1.82Garlic'Extract 1.43 0 0 0 0 1.12Ginger'Extract 0.75 0 0 0 0.68 1.1Olive'Leaf'Extract 0.91 0 0 1.86 0.74 1.08Onion'Disc 0 0 0.68 0.74 0 1.1Propolis 1.82 1.12 1.12 1.08 1.1 1.14Cefoxitin 1.13Trimetho'Sulfisoxazole 1.81Vancomycin 1.76

MSSA Trial 2

Garlic'Disc Garlic'Extract Ginger'Extract Olive'Leaf'Extract Onion'Disc Propolis Cefoxitin Trimetho'Sulfisoxazole VancomycinGarlic'Disc 2.41 2.3 0.9 0 0 1.08Garlic'Extract 2.3 0 0 0.81 0 1.02Ginger'Extract 0.9 0 0 0 0 1.07Olive'Leaf'Extract 0 0.81 0 0.72 0 0.94Onion'Disc 0 0 0 0 1.03Propolis 1.08 1.02 1.07 0.94 1.03 0.98Cefoxitin 2.91Trimetho'Sulfisoxazole 1Vancomycin 1.64

Medic&AID UK Photography

HIV - An Introduction - Part I of III

By SenthooranKathiravelupillai

The Human Immunodeficiency Virus (HIV) is theetiological agent of the Acquired ImmunodeficiencySyndrome (AIDS) epidemic which was responsiblefor approximately 1.5 million deaths worldwide in2013. HIV weakens the immune system bymultiplying within T-helper lymphocytes, thusdestroying them. HIV was first isolated in 1983 at thePasteur Institute in Paris, from the lymph node of apatientwith lymphadenopathy, a conditionwhere thelymph nodes have swollen due to an infection.Following electron microscopy as well as sequenceanalysis, HIV was considered to be a lentivirus, agenus of the Orthoretrovirinae sub-family and thewider Retroviridae family.

A distinct feature of the Retroviridae family is thatthey are enveloped viruses which are able to replicatewithin a host cell through the process of reversetranscription. Reverse transcription makes use of anenzyme called reverse transcriptase which creates aDNA intermediate from the viral RNA. This allowsthe genetic information to be produced by theribosomes of the host cell from theDNA intermediatefor viral replication. Viruses in the genus Lentivirus,to which HIV belongs, are characterized by theirassociation to diseases of immunosuppression and bytheir long incubation periods after infection beforesigns and symptoms of illness become obvious.Lentiviruses have also been found in many primatespecies. As well as the variants of HIV, HIV-1 andHIV-2, another example is the SimianImmunodeficiency Virus (SIV), which is found tocause Simian AIDS, a disease which develops mostcommonly if the Asian or Indian Rhesus Macaque isinfected.Notably, SIVs are able to infect up to 45 of allAfrican non-human primates [1], however, in manycases SIV infections seem to be non-pathogenic.

The two types of human retroviruses are HIV-1 andHIV-2. Amongst HIV-1, there are four subtypes,groups M, N, O and P. Group M has been identifiedas the group responsible for the HIV pandemic whichcurrently affects approximately 35 million peopleworldwide [2]. The other groups of HIV-1 are lesscommon, with Group O, identified in 1990,

representing less than 1% of global HIV-1 infections,groupN, identified in1998,with13documentedcasesand group P, discovered in 2009, with only 2documented cases.

Before studying the replication mechanism of HIV-1within cells, it is important to analyse the virus’sstructure, and how its components make it suited forentering cells such as theCD4+T-helper lymphocyte.The mature virus has a diameter of 100-120nanometres with a spherical morphology. The viralcore is a bar-shaped, electron dense core, containingtwo short strands of genomic ribonucleic acid (RNA),around 9200 nucleotide bases long, as well as theenzymes reverse transcriptase, protease, ribonucleaseand integrase. All of this is encased in an outer lipidmatrix, also referred to as anenvelope,which containskey surface antigens and glycoproteins. The envelope,which is derived from a host cell, has 72 surfaceprojections and contains the antigen gp120, which isimportant in thebindingof thevirus to target cellswithCD4 receptors as well as a co-receptor (e.g CCR5 orCXCR4). Also, there is a second glycoprotein, gp41that helps the gp120 to bind to the lipid envelope oftarget cells.

The genetic makeup of the HIV virion, also known asits genome, consists of threemajor genes, gag, pol andenv. The genes code for the production of polypeptidecomponents that will serve structural and functionalroles. For example, the enzyme reverse transcriptaseserves a crucial role in the copying of theHIV genomeinto DNA during the life cycle of the HIV virus.Amongst the genome, regulatory or accessory genessuch as tat, rev and nef are present. Regulatory genesoften code for repressor proteins, which in turnprevent RNA polymerase from transcribing RNA.Thegaggene codes for the viral capsidproteins,whichis important as it codes for the important proteinswhich will make up the viral core in which all thegenetic material of the virus is located. The pol genecodes for the production of four extremely importantenzymes, reverse transcriptase, protease, RNAse Hand integrase. Protease is the enzyme responsible forpreparing proteins made from the HIV genome, sothat they can be incorporated into newly produced,functioningHIV daughter particles. Integrase is a keyenzyme involved in a process in which the DNAreplica of the HIV’s genome is incorporated into theDNA of the host cell. The Env gene codes for theproduction of the surface glycoprotein 160 alsoreferred to as gp160. Glycoproteins are originallyproteins however; they aremodified in organelle such

as the Golgi apparatus, where carbohydrates or lipidsare added. The synthesis of gp160 is extremelyimportant since it eventually splits apart into the twotypes of surface receptor proteins or ‘spikes’ found onmature HIV virions gp120 and gp41 which actuallylies embedded in the viral membrane. The gp41protein acts as an anchor of the gp120 glycoprotein. Itshould be noted that the gag and pol gene can often beexpressed together as one, in a long strand called ‘gag-pol’. Having gained a preliminary understanding ofthe structure of the HIV virus, the pathogenesis of theHuman Immunodeficiency Virus will be explainedand discussed in the second part to ‘HIV – AnIntroduction’ in the upcoming issue.

Dengue Fever

By David Cohen

In wake of the recent Ebola Haemorrhagic diseaseoutbreak inWestAfrica, Itwould seemappropriate toexplore a similar disease. Dengue fever is a mosquitoborne virus responsible for 22,000 deaths a year(CDC), where approximately 50 million people areinfected with the disease and 500,000 cases developinto the haemorrhagic disease.

The responsibility for transmission of the disease lieswith one specific type of mosquito, the Female AedesMosquito. The female Aedes requires proteins in theblood to help aid the development of mosquito eggs,where up to 100 eggs can be laid in a single cycle.According to the SingaporeanNational EnvironmentAgency “eggs can lie dormant for up to nine months,and hatch when conditions are suitable for sustainedlife”. This means that in areas especially prone tomosquito infestations, stagnant water must beremoved. It is believed that approximately 800 to1000years ago the dengue virus originated from severalmonkey species in South East Asia, and mutated tobecome Zoonotic; meaning that the disease could betransmitted from species to species. Today there arefour strains of dengue fever virus, DEN-1, DEN-2,DEN-3 and DEN-4, all of which are infectious.

Common symptoms of dengue fever often do notappear immediately after transmission, it can takeanywhere from 3 to 10 days to appear. The fever itselfis also aptly nicknamed “BreakboneFever” accordingto the discomfort dengue patients feel. A temperatureof 40 Degrees Celsius or above would be consistentwith dengue fever, as well as nausea, vomiting andmigraines. In the more developed form of denguefever (Dengue Haemorrhagic fever), patients willexperience a state similar to shock. Patients sufferingfromDHFwill also have red, blotchy rashes related tothe increased tendency to bruise and or haemorrhage.

Once the dengue virus has been transmitted, the viruswill launch a direct attack onto the leukocytes,essentially infecting the cells. The infected cells arethen transported to the lymphatic system,where thereis a brief incubationperiod.This iswhere the viruswillreplicate. Once replicated, the virus is thentransported to the blood stream in a process known asviraemea. Later stages of the virus will lead to theblood vessels becoming permeable. This means thatcomponents of the blood can diffuse across intosurrounding tissues to achieve dynamic equilibrium.Blood components include platelets, which areprimarily responsible for blood clotting, helping toblock lacerations in the vessel and thus reduce bloodloss. The lack of platelets will leave DHF patients toincreased probability of haemorrhages occurring. Atthe point at which dengue develops into the latterhaemorrhagic condition, hospitalisation would benecessary.

To date there is no known cure for the Dengue virus,however, once diagnosed patients will need to havefluid intakemonitored. Painkillersmay be taken, suchasParacetamol, however “blood thinning”drugs suchasAspirin andWarfarin shouldbe avoidedas they canexacerbate the probability to bleed. Patients will alsoneed to stay confined to their beds throughout themanifestation of the disease.

With almost 40% of the world’s population at risk ofbeing infected with dengue fever, research facilitiesboth state and privately funded are evaluating theoptimal ways to prevent infections. Preventing adengue outbreak can be expensive and timeconsuming, however, in countries with a high risk ofinfection, such as Singapore, where there is anextremely high population density, investing inpreventative steps is worthwhile. The first call toaction would be to remove any existing and potentialbreeding grounds for the Aedes mosquito; this willinclude low lying areas with stagnant water. Incountries like Singapore, one can be fined forneglecting to remove stagnant water. Otherpreventativemeasures can be taken such as “fogging”where large amounts of pesticides are “fogged” intothe air. This controversial method has been banned ina majority of countries as pesticides such as DDT areused. There is no vaccination for dengue fever, yetthere is reason to believe that one will be available tothe public by 2016. These vaccinations will work byinhibiting synthesis of virus proteins. Moreconventional means of preventing the virus would beimplementing theuseof regular storebrand repellents.

A primary infection will give patients a degree ofimmunityonly to the specific strainofdengue theyhadbeen infected with. However, a primary infection willincrease the probability of an infection of the otherstrains. This is because when a new strain isintroduced, antibodies are produced for the originalstrain, which will fail to neutralise the dengue virus.The antibody will then attach to the virus and returnthem to themonocytes, increasing the efficiencyof theinfection. Thus recovered patients need to take extraprecautions when in areas prone to dengue.

Dengue is the most widely reported mosquito bornevirus in theworld, it effects up to 50million a year anda further 2.5 billion are at risk of being infected. A vastmajority of the countries that are affected by dengue,with the exception of Singapore, are LEDC’s. Thequestion that should truly arise out of this article, iswhether our society, being a MEDC is doing enoughto prevent viruses such as dengue. That if there was amarket for a dengue vaccine, which could only viablyexist in a developed country, would we as a societyhave access to one?

Marfan SyndromeBy VamsiThammandra

Marfan syndrome is a genetic condition that anindividual inherits from a parent who also has thecondition, or a parent who has a faulty gene in theirsperm or egg. The fault is carried by a gene calledFBN1, which encodes a connective protein calledfibrillin-1. This goes on to affect the connective tissueswhich are fibres that help to provide support andstructure toother tissue andorgans.Marfan syndromecan affect different parts of the humanbody, includingthe heart, blood vessels, bones, joints, and eyes.Sometimes, the lungs and skin are also affected,however this is usually only in the most severe cases.

Although it is mainly an inherited condition, in about25% of cases, no close relative with the condition isidentified.ApersonwithMarfan syndromehas a 50%risk of passing it on to each offspring. AlthoughMarfan syndrome is incurable, there are therapieswhich can help improve the patient's quality of life.

Marfan syndrome's effects on a human being canrange frommild, moderate, severe to life-threatening.Themost serious complications includedamage to theheart valves and/or the aorta.According to theNationalHealthService (NHS),UK,about 1 in every 5,000 British people has Marfansyndrome. It affects males and females equally.Individuals with Marfan syndrome tend to have longarms, legs and fingers. Often their arm-span is longerthan their height. Some individualswho are bornwithMarfan syndrome may be completely unaware untillater on in life.

The disease is named after Antoine Marfan(1858-1942), a French paediatrician. Marfanfirstdescribed the syndrome in 1896 after observingdistinctive features in a 5-year-old girl. Later, in 1991,

the identification of the syndrome causing gene wasfurther studied due to developments in genetics.

The disease is named after Antoine Marfan(1858-1942), a French paediatrician. Marfan firstdescribed the syndrome in 1896 after observingdistinctive features in a 5-year-old girl. Later, in 1991,the identification of the syndrome causing gene wasfurther studied due to developments in genetics.

SinceMarfan syndrome can affect varying parts of thebody, it has no unique symptoms, making it verydifficult to diagnose and treat; however, the followingcombination of symptoms are usually sufficient tomake a diagnosis:

•Very long limbs

•Long fingers

•Aortic dilation

Experts say there are several possible signs andsymptoms that involve the skeleton, eyes andcardiovascular system and that the symptoms varyfrom one to the other. Also, patients may be atdifferent stages, making it difficult for doctors todiagnose immediately. However, as stated above,there are several indicationswhich are seen in the eye,skeleton and the heart. These signs are listed below:

Skeleton (bones, teeth):

•Dolichostenomelia - long limbs (wrists may bethin and weak)

•Extremely flexible joints

•Small bottom jaw - can occasionally causespeech disorders

•Overcrowded teeth

Eyes:

•Myopia – nearsightedness

•Exctopia lentis - dislocation of the crystallinelens; can affect just one or both eyes

•Early cataracts

Cardiovascular system:

•Shortness of breath

•Angina pectoris - pain radiates to the back,shoulder or arm

•Dilated aorta

•Pregnancy - women at risk of aortic dissection(a tear in the wall of the aorta).

A fault (mutation) in the FBN1 gene causes Marfansyndrome.Chromosome 15 encodes fibrillin-1, a typeof glycoprotein. The fibrillin-1 protein is vital for theformation of the (extracellular) matrix, including themaintenance of elastic fibres. The extracellularmatrixis the defining feature of connective tissue in animals.The lack of elasticity and strength in connective tissuerestricts movement and the support of organs andvarious body parts. Most healthy individuals have anabundance of fibrillin-1in their eyes, bones and heart.Individuals with Marfan syndrome have a lack offibrillin-1 which causes their bones grow longer thannormal, and other symptoms and complicationsdevelop.

Marfan syndrome is incurable, however, varioustherapies are available to ease symptoms andminimize or prevent possible complications. Thediagnosiswill bemade based onwhich body parts andsystems are affected. Damage in the skeletal systemsuggests that the patient needs to be regularlyevaluated so that any changes in the spine or sternum(breastbone) can be detected, especially when theindividual is a child and is still growing. Mostproblems with ocular damage can be corrected withglasses or lenses. Sometimes the patient may have toundergo corrective surgery.The National MarfanFoundation advises patients with heart problems towear a medical alert bracelet and to go straight tohospital if any chest, back or abdominal pain is felt.Beta-blockers may be prescribed for heart valveproblems. Sometimes surgery is needed to repair theaorta or replace a heart valve. Prompt surgicalintervention is an important preventive measureagainst possible aortic dissection (tearor ruptureof thewall of the aorta).

A Mental Health Crisis

By HassanHussain

When you or someone in your family suffers theanguish of a mental illness, you would expect to becared for with dignity and given the treatment youdeserve. Unfortunately, the NHS has not been able toprovide the service they should have in recent years,and their standard of care is continuing to drop,leading toamentalhealthcarecrisis. Ina recent surveyof 600 GPs, 1 in 5 said that they have seen a patientharmed because they couldn’t receive the help thatthey needed, with half of the GPs saying that thecurrent state of affairs had recently worsened.

Currently the NHS wards are overfilled at 101%intended capacity with adult patients with acuteailments on an average monthly basis, with somewards having to accommodate a load of 120%, eventhough the recommendation is around 85 percent.Mental health nurse numbers have dropped by 3,300and to make matters worse, more and more beds forpatients suffering with mental disorders are being cuteach year, with 468 being cut last year, rising to a totalof 2,100 since April 2011, even with a 30% rise indemand for them.

Beds are being filled up so rapidly due to them beingfilled temporarily, then having patients sent home fora short period of time in order for the psychiatrists toassess whether or not they still need care in the ward.However,when thepatientsareon leave, thebeds theyformerly occupied are given to new patients. Thismeans if they have a relapse, there is no place for themin thewardsand theydon’t get the treatment theyneedand deserve. Some then turn to A&E and this cancause delays there, and patients may still not evenreceive appropriate treatments or even be referred todepartments that can give them the treatment theyneed.

The stress placed on patients with mental disorderswith no treatment can lead to their own suicide, withseven suicides and even a murder due to the lack ofbeds since March 2011. People with mental healthproblems have even been detained in police stationsdue to bed shortages. Between 2012 and 2013, 22,000people over the country were detained in police

stations, with 750 people, including 28 children,having to suffer this fate last year in Devon andCornwall alone. Police themselves are furious, as theyare forced to detain innocent patients that deservetreatment, even children as young as 12,whoare oftenheld for longer than a criminal would be detained.

CAMHS, (Child and Adolescent Mental HealthService), provides mental health services for thoseaged 17 and younger. CAMHS is responsible fordealingwith the first three tiers of cases, but for the toptier case, which is an emergency, the CAMHS’professionals can only respond, while NHS Englandworkers are responsible for finding them beds fortreatments. If there are no beds available, the patientsare unjustly detained in police cells. CAMHS is underincreasing pressure, as it has had to deal with a 20%increase in cases aswell asmoredifficult cases, despiteno increase in its budget.

Patients are disgruntled by the either being prescribedtoomany drugs, evenwhen they don’twork or havingCBT (Cognitive Behavioural therapy, a talkingtherapy that helps patients overcome their problemsby changing the way they think and act), even whentherapists have said it won’t help them. Thismistreatment is costing the NHS and CAMHSmillions, and simply pairing patients with theirnecessary and effective treatment would save time forboth the services and the patients, aswell asmoney forthe servicesandmost importantly savingpatients fromhaving to suffer.

You may ask, what is being done to help stop thiscrisis? TheMentalHealthCrisisConcordant has beensetup to try to improve the standardof care,withmanydifferent agencies signingup, suchas thepolice,healthservices, local councils and voluntary services.Agencies who become part of this organisation haveagreed to increase early prevention formental patientsbefore they reachcrisis point,making sure the separateagencies work well together to help those who havereached crisis point and provide their needs in ahealthcare setting, and to create a plan to help thoseafter a crisis, to help them recover and stop it fromhappening again.

The NHS has said that they have increased theirmental health services and that the number of peoplewithmental illnesses being detained in police cells hasdecreased by 25%. The NHS has also agreed to fundthe Assertive Outreach Team that aims to supportyoung people with mental illnesses at home, wherethey will be in a more comfortable environment andhelping to alleviate beds in hospitals and stoppingyoung people from being detained in police stations.Soalthough theNHShasalmost let this crisis growoutofhand, theyare implementing strategies toattempt torepair the damage before it’s too late.

By Saamir Mirza

Left Ventricular Assist Device Associated Infection

1. Steven Tsui, June Davision.“Focus on: Left ventricular assistdevices.”Heart Matters Magazine, BritishHeart Foundation. Web.

2. Sanjay Maniar, SreekanthKondareddy, Veli K Topkara. “Leftventricular assist deviceCrelatedinfections: past, present and future”PMC, NIH Public Access, US NationalLibrary of Medicine. Web.

3. Simon D, Fischer S,Grossman A, Downer C, Hota B,Heroux A, Trenholme G. “Leftventricular assist deviceIrelatedinfection: treatment and outcome.”Public Medical Health, NIH PublicAccess, US National Library ofMedicine. Web.

Sources

A Left Ventricular Assist Device (LVAD) is a devicewhich bypasses the left ventricle of the heart to theaorta, the large artery leaving the heart, and acts as amechanical pump. Heart failure can, in the moresevere cases, render a heart too weak to pump bloodaround thebodyand this iswhere theLVADcomes in.At first, thiswasonly a temporary solution for patientswho would not survive long enough waiting for adonor for a heart transplant but with new innovationsand technological advances, hospitals can now givethese LVADs to most patients with heart failure as along term solution. The device helps the failing heartand restores normal blood flow. The installation of aLVAD requires open heart surgery and is a bigoperation. Around 80 Britons undergo this operationeach year.

This mechanical pump demands a stable, powerfulbattery since people’s lives are depending on thedevice. The battery is worn around the waist of thepatient. A cord called the driveline connects theLVAD to a controller which is in turn connected tothis externalbatterypackwhichhasa lifeofaround4-6hours. The driveline is composed of two majormaterials, silicone and Dacron fibres (Polyethyleneterephthalate). Dacron fibres are like a netted, wovensheet that areon theoutermost surfaceof the cord.Thenetted structure promotes skin growth through thelayer in order to perfectly seal the incision at thetranscutaneous region.

At the moment there are approximately 100 peopleliving in the UK with a LVAD. The quality of life ofpatients receiving LVADs is very poor prior to theoperation. They are often very weak and unable toleave the house. However, following the LVADimplant, blood flow is quickly restored and theseformerly weak patients are quickly back up on theirfeet and they can return to their normal routines.

However, there are certain problems associated withLVADs. The operation for the implantation of anLVADleaves thepatient vulnerable to infection.Post-implantation sepsis and device related infectionsaccounts for more than twice the number of deaths

than device failure does. LVAD related infections canbe split up into driveline related infections, pumppocket related infections and LVAD associatedendocarditis.Driveline infectionsoccur along the leadconnecting the LVAD to the power source. Althoughthe netted structure of the Dacron fibres are supposedto promote skin growth and facilitate a perfect seal,this is rarely the case. The transcutaneous region isgenerally an open wound, a site for many infections.Many bacteria thrive on the human skin and are oftenfound in LVAD driveline related infections. Thesebacteria can then multiply and spread to the pumppocket, the recesswhich ismadewithin theabdominalcavity in order to house the LVAD device itself. Thiscan lead to many conditions including fever,leukocytosis, abdominal tenderness, as well aspersistent purulent drainage from the driveline site. Ifthe bacteria spread further, it can lead to endocarditis.This is a very rare and potentially fatal infection of theinner lining of the heart (the endocardium).

This is clearly a very major issue and so currentresearch is using biofilms to test and examine effectivetreatment methods. Biofilms are agar platesinoculated with different bacteria. Segments of thesilicone and Dacron fibre driveline were imbeddedinto these biofilms in order to simulate what happens.A recent study used biofilms inoculated withStaphylococcus aureus, Staphylococcus epidermis,Enterobacter aerogenes, Psuedomonas aeruginosa,and Candida albicans. Then they developed aprototype of a driveline which was impregnated withchlorhexidine, triclosan, and silver sulfadiazine inorder to resist bacterial and fungal colonization. Theyrepeated the experiment with this new prototype andthen measured the zones of inhibition around thesample after 24 hours of incubation at 37oC. Aftermeasuring and compiling results, itwas found that theprototype driveline retained around 80% of micro-organismactivity.Fromthis, itwas concluded that theantimicrobial driveline worked to reduce thecolonisation of bacteria and that in this way it mightprevent early infection while still facilitating thegrowth of skin to provide protection against lateinfection.

Antibiotics and New AlternativesBy HussanHussain

Antibiotics: the medicine that signalled the end of theera of folk law treatments and hailed the beginning ofeffective care for the ill. They were first discovered bythe scientist Alexander Fleming in 1928, when heobserved themould Penicillium that had been left in aPetri dish full of bacteria produced a bacteria free haloaround itself. Since then, antibiotics haverevolutionisedhealthcarearound theworld.Howeverour obsessive and careless use has led to the worstscenario feared by doctors and scientists: bacteria arebecoming resistant.

An antibiotic can work in many different ways,depending on its classification. The two mainclassifications of antibiotics are those that arebactericidal; they kill bacteria, and those that arebacteriostatic; they stop bacteria from multiplyinguncontrollably. Bactericidal antibiotics mainly workby inhibiting the biochemical pathway inside thebacterium cell that makes or attaches to one of themain parts of the cell wall. This then makes the cellwall of the bacterium weaker, so after many celldivisions, the cell wall of the daughter cells are veryweak. They cannot strengthen their cell wall as themolecules required are being inhibited. The cell wallcollapses, the cell undergoes lysis and the bacteriadies.

Some bactericidal antibiotics attack the cellmembrane instead of the cell wall, which then allowsthe content of the cells to leakout, suchasmineral ionsand other molecules the bacterium would use forgrowth, repair and general function. Molecules thatareessential for thebacteriumtosurvive, suchasDNAandRNAare also lost, contributing to the bacterium’sdeath. Other types of bactericidal bacteria work byaffecting the important internal processes of the cell.For example somebind to the bacteria’s ribosomes, sothe bacteria are unable to produce vital proteins, andtherefore die.

Bacteriostatic antibiotics work by stopping thebacteria from dividing uncontrollably, allowing thebody’s immune system to fight them off easier. Forexample, by binding to ribosomes, but in this case lessimportant ones, means that the bacteria affected willstill be able to survive, butwill not be able to reproduceand create daughter cell to overwhelm the patient’simmune system.

One of the main worries of medicine currently is theresistance of dangerous bacteria to antibiotics, ourmain method of treatment. Antibiotic resistance inbacteria is simply due to natural selection. If onebacterium mutates, and then becomes resistant to acertain antibiotic, when that antibiotic is used to treatthat bacterium, the bacteria without the mutations

will die, but the mutated bacterium will survive, andthen replicate to produce many other resistantbacteria, that cannot be treatedwith that antibiotic.Tomake matters worse, bacteria can transfer the gene orgenes that makes them resistant to antibiotics to otherbacteria by horizontal gene transfer,which can lead tothe spread of resistance even faster.

The creation of resistant bacteria can be caused bothby too long or too short courses of antibiotics. Tooshort courses can mean the bacteria are in anenvironment of low antibiotic concentration. Notenough to kill them, but enough for them to develop aresistance to the antibiotic, rendering it useless. Toolong a course has also been shown to increase the riskof antibiotic resistance. To make matters worse,bacteria have been becoming immune to antibioticsdue to doctors over-prescribing antibiotics to peoplewho are demanding them to help fight viruses, such asthe common cold, even though antibiotics don’t affectviruses, so the antibiotics have no affect apart fromcausing resistance in the small levels of bacteria thatmay be in the patients body at the time.

Evenour food is contaminatedwith resistant bacteria.Farmers add antibiotics to the food they feed theirlivestock, regardless of the condition of theirlivestock’s health, to prevent an outbreak before itbecomes toomuchof a threat and therefore increasingtheir profit. The farmers therefore unwittingly createmore antibiotic resistant bacteria that will be carriedon by their livestock, and if the meat from theirlivestock is not cooked properly, it could causesickness in humans.

So what do we do now? How can we curb the rate ofresistance? What are our alternatives? The rate ofbacteria resistance can be lowered significantly ifdoctors stop prescribing antibiotics to patientsunnecessarily, and if patients stop taking antibioticswhen they aren’t required. Patients completing theircourse of antibiotics fully even if they feel fine willhelp, as there may be some bacteria still left in theirsystem.

Phage therapy could be a reliable treatment for thosesuffering from bacterial infections. Phage therapyworksby selectingabacteriophage, a virus that attacksbacteria, and administering it to the patient. The viruswill not cause harm to the patient, but will attack thebacteria and use them as hosts to multiply, therebydestroying the bacterial infection. As the viruses onlyaffect bacteria, there are little to no side effects for thepatient, and the virus can be taken orally or applied

straight onto wounds.

New treatments for dangerous bacteria are beingdeveloped all the time. Scientists from the GenevabasedcompanyLasccohavedevelopedsmall particlesthat are made of lipids that are similar to thephospholipids in the cell membranes of the patient’scells. The bacteria’s toxins therefore become attachedto the lipid particles instead of the membranes of theimmunecells; the immunecells canattackanddestroythe bacteria cell with little to no repulsion from thebacterial toxins. This allows the body’s immunesystem to fight off the attack without any extra help.This treatment doesn’t attack the bacteria in the gutflora, which is affected by antibiotics.

TheDutch biotech companyMicreos has developed anew drug that contains enzymes produced bybacteriophages that are used to cut through the cellwall of the bacteria. In this drug the enzymes tear apartthe cell wall of the bacteria, causing it to die. Theseenzymes are specific to different parts of the cell wall,so in order for the bacteria to become resistant, itwould require manymutations combined for the newdrug to become ineffective.

So although bacteria becoming resistant to antibioticsmay be a terrifying prospect, new and even saferalternatives are coming around the corner to curemore illnesses and save more lives.

XenotransplantationBy Huw Child

Xenotransplantation, the process of transplantingcells, tissuesororgansbetweendifferent species, is oneof the fastest growing areas of medical research andhas significant potential in solving many of thecomplex issues that arise when performing andpreparing transplants. However, this topic of medicalresearch is considered to be very controversial andraises many issues such as whether or not it is ethical.

There are several advantages to xenotransplantationwhen compared to allotransplantation. All animalorgans will be optimal for transplantation, unlikecurrently when it has become normal to accept non-optimal human organs for transplant. This is due tothere being a shortage of available human organs.Furthermore, patients would not have to wait verylong to receive their organs and they would beavailable on demand. In addition, since the time oftransplantation would be able to be prescheduled, thepatient would be able to undergo pre-treatment withimmunosuppressive agents. This greatly reduces thechance of organ rejection.

The first ever xenotransplantation performed on ahumanwas in1982,whereababygirlwithhypoplasticleft heart syndrome (a rare condition where the leftventricle is severely underdeveloped), was therecipient of a baboon heart. This procedure was onlymeant to be a temporary solution to the issue, while areplacement human heart was being found.Unfortunately, no heart could be found and she died21 days later due to graft rejection (mainly due to a

mismatch of blood types).

All types of transplantation, especiallyxenotransplantation, carry a risk of transferringpathogens from the donor to the patient. Whilst thisissue can be solved with pathogens by using animalsthat have been kept in sterile environments, it will notwork with porcine endogenous retroviruses (PERV).All mammalian species carry these viruses as part oftheir genome. This means that PERV could betransmitted by transplantation. Under normalconditions thesevirusesdonot causedisease,howeverit is believed that they could become pathogenicwhentransferred into another species due to the change inenvironment. An example of this was in 1990 whenPERV was seen to be transmitted from pig cells intohuman cells while the cell were being kept in tissueculture. While PERV transmission has never beenobserved in 160 examples of pig to humanxenotransplantation, patients still need to be heavilymonitored for the viruses.

So far, no trials of xenotransplantation have beencompletely successful mainly due to the immuneresponse that xenotransplantation provokes in thereceiving organism. Xenotransplantation normallycauses a more severe response than the responsecaused by allotransplantations (inter-speciestransplantation) due to the significant differencesbetween the tissues. These rejections canoccur almostinstantly and can cause death in the receivingorganism within a few hours. One of the main causesof rejection is due to XNAs (xenoreactive naturalantibodies). These antibodies begin to circulate in theblood and activate the complement system (part of theimmune system that aids antibodies in clearingpathogens from the body). This can lead to celldamage,haemorrhaginganddeath in the transplantedorgan. Whilst this severe response can be overcomeusing a variety of drugs and treatment, there are othermore complex forms of rejection that are not fullyunderstood such as acute vascular rejection. The

body’s natural response means that whole organxenotransplantations are not currently safe or viableoptions and are mostly not used. Instead,xenotransplantations are currently used for muchsmaller procedures such as replacing valveswithin theheart using valves taken from pigs.

Whilst direct whole organ xenotransplantations arenot possible, research has begun on applyingdecellularisation to make pig hearts suitable fortransplantation in humans. Decellularisation is theprocess of taking an organ and stripping it of all itscells, leavingonly theextracellularmatrix.Thiswouldbe particularly useful for xenotransplantation since itwould allow you to take the basic structure of a pig’sheart (orotherorgan/bloodvessel),which is veryeasyto obtain and structured very similarly to a humanheart, and rebuild the heart tissues using cells takenfrom the patient. This would mean that the issues ofrejection would be almost completely negated sinceyou are transplanting the patient’s own tissues.However, due to the complexityofhumanorgans, thisprocess is only currently available for some donortissues such as veins. This means that it will bepotentially several decades before this procedure isavailable for complex transplantations such as theheart.

There are several moral and religious issuessurrounding the topic of xenotransplantation. One ofthese is the way that animals would be treated beforetransplantation; they would have to be kept in acontrolled and sterile environment before organdonation. Many people consider this a cruel andunfair act, especially since animals lack the ability togive permission. Another cause for discussion arepeople’s religious views. Many religions consider theconsumption of certain animals, such as pigs or cows,to go against their religious teachings. Thismeans thatxenotransplantation would not be appropriate inseveral countries and cultures.

To conclude, I believe that xenotransplantation is aparticularly interesting area of medical research anddevelopment, which has been proven to work onseveral occasions. However, as an area of medicine itis still in its infancyandhas several problems includingrejection, ethics and the transfer of pathogens. Due tothese issues, even at the current rate of development,it could be decades before we see xenotransplantationbeing used more widely.

Image source: sciencebuzz.org

Mycoplasma Pneumonia

By David Cohen

Mycoplasma Pneumonia, also known as ‘WalkingPneumonia’, is, like all forms of pneumonia an upperrespiratory infection. It is the smallest known freeliving bacteria, and is very dependent on its hostorganism for ‘life support’ .The mycoplasmapneumoniamicrobe is an atypical bacterium, aswhenit was first discovered it was thought to be a viruspathogen, due to its apathetic response to �-lactamantibiotic treatment. However, with the developmentof modern antibiotics, it has recently been found thatsome antibiotics can treat Mycoplasma pneumoniabased infections. This caused a change inclassification since a virus could not viably be treatedby antibiotics. Understanding the function of BetaLactam antibiotics is key when trying to understandthe structure of mycoplasma pneumonia. BetaLactam antibiotics act as enzyme inhibitors for cellwall synthesis. They have many early variantsincluding Penicillin. Beta Lactam antibiotics at thetimewere revolutionary since they allowed doctors toprescribe adrugwhichwouldnot attack the cells of theperson who was being treated. The antibiotic wouldnot destroy animal cells, since they are notencapsulated by a cell wall. This idea, thatmycoplasma was unresponsive to Beta-lactamantibiotics but was susceptible to alternativeantibiotics, suggested a fundamental deviation fromtypical cell structure. Clearly, mycoplasmapneumonia does not have a cell wall.

The lack of a cell wall means that the state ofmycoplasma pneumonia’s surrounding environmentis imperative, mycoplasma is by no means andextremophile. This limits the bacterium to warm,moist environmentswithminimal changes in osmoticconditions and is only really transmitted through thedroplet medium. To add to that, the fact thatMycoplasma pneumonia is so imperceptible meansthat it can surpass regular immune defences. Thisallows the bacterium to evade the body’s naturaldefences, allowing it to thrive off the conditions. Itssize also contributes to its elevated difficulty ofdetection, as it cannot be seen by standard resolutionlight microscopes.

Two methods of detecting mycoplasma pneumoniaare used today, DNA staining and Lab culture tests.DNA staining is a faster and more common processwhen it comes to narrowing down the possibility of amycoplasma infection. Staining will take up to twodays whereas a lab culture test will take up to 30 days.This is due to the fact that in the space of time thatmycoplasma is in the culture medium, there is apossibility it could remain dormant. This in turnmeans that 3 – 4 weeks are needed to rule out thepossibility that there could be a development of thebacterium.

Symptoms of the infection are not localised to thepulmonary system, however the majority of patientsdiagnosed with mycoplasma tend to have a mild,developing cough or wheeze. To add to that manypatients will feel lethargic, with a headache and fever.According to the Centres for Disease Control andPrevention, “a third of all mycoplasma cases willdevelop into pneumonia”.Mycoplasmapneumonia’srelatively difficult detection, difficulty to treat withconventional antibiotics and seemingly commonmedium of transmission means that it is problematicto contain and avert. Its tendency to stay dormant inmany patients, will lead to chronic outbreaks. Themajority of cases are usually found in the tropics, dueto the suitable conditions.

Mentioned earlier, conventional antibiotics such asBeta-Lactams are unreactive with mycoplasmapneumonia, which means that alternatives have to beused. These alternatives include the sub group ofantibiotics are calledmacrolides and includeKlaricid,better known as Clarithromycin or Erythromycins.

These specific groups of antibioticswork by hinderingthe replication of the mycoplasma’s D.N.A, meaningthat protein synthesis cannot occur. The macrolidesare not bactericidal, rather they are part of thebacteriostatic groups. A common issue withprescription of antibiotics is that bacteria will developa resistance to them, through genetic mutations.Therefore, it is vital that prescribers take into accountboth the event of overmedication andundermedication of patients, especially in this casewith the macrolides group. According to Medscape,“Since 2000, macrolide-resistant M pneumoniacaused by point mutations in domain V of 23Sribosomal RNA has emerged in Asia and has nowbeen reported in Europe and North America. Recentsurveillance conducted primarily in paediatricpopulations has documented resistance rates of46%-93% in Japan, 69%-97% inChina, 12.3%-23% inTaiwan, 61.3% in SouthKorea, 30% in Israel, 9.8% inFrance, and 8.2% in the United States.” These

statistics show that amongst the observed nations, theEast Asian states had the largest proportion of caseswhere Mycoplasma was unresponsive to macrolidetreatment due to adeveloped resistance. Mycoplasmapneumonia’s increasing antibiotic resistance isleading to an increased rate of chronic reinfection, andthere is no evidence to show that an infection ofmycoplasma will lead to any form of immunity.

To conclude, a mycoplasma pneumonia infectiondoes not share the same fatality rate as other relevanttropical diseases however, it can act as a ‘gateway’ tofar more serious conditions such as pneumonia.Although it is important to notwithholdmedications,it is important to be ethical when coming toprescribing antibiotics, as the under and overmedication can lead to serious consequences for boththe patient and society.

Insulin Like Growth Factor

By ZakariaAchercouk

Insulin is a protein hormone that “communicates”with cells in your liver and muscles to absorb excessglucose in the bloodstream and reform it intoglycogen. Also, when your glycogen reserves havebeen filled (in muscles mainly) your bloodstreamstarts to get concentrated with glucose, which isn’tgood for blood pressure. As a response, insulin isproduced todivert asmuchglucoseaspossible toothercells to form fat tissues.

As a result, most cells have receptors for the insulinprotein. This is where the IG Factor comes in. IGFsare proteins similar in structure to insulin and theytend to similar but much less potent ability to insulinso they can bind to all cells, they are mainly involvedin stimulating growth.

The anterior pituitary gland in the brain secretesGrowth Hormone, or Somatropin, which, likeGlucagon, stimulates the release of IGF-1. Thisversion of IGF is a protein of 70 amino acids bondedas a single strandwith 3disulphide bonds in its tertiarystructure. It is primarily used for achieving the finalstages of growth and its concentration in the bloodstream peaks during puberty. It triggers hypertrophy,which is increase in the sizeof the cell andhyperplasia,which is increase in cell division/count through themitosis cell cycle of most tissues.

Because IGF 1 is a protein hormone with paracrineand autocrine effects, it also majorly affectsneurological development. Paracrine effects are thosewhere the chemical involved mainly influencesneighbouring cells and tissues, whereas autocrineeffects are those where the chemical influences thegland/cell/tissue that secretes it. In this case, theBrainis the primary target, so it helps to regulate and cause:

•Neurogenesis: the creation of new neuronsthrough the specialisation of basic neuralstem cells which can replicate indefinitely,orprogenitor cellswhichare limited tohowoften they can divide.

•Neuritic Outgrowth: the branching out ofdendrites of neurons and furthergeneration of synapses to increaseconnections within the brain, especiallyduring embryonic development

•Protection: IGF 1 has been reported to havelinks to neuroprotection in terms of trophicfactors; this is not surprising as IGF hasalso been reported to be able to passthrough the blood-brain barrier, whichprotects the brain from foreign substances.In doing so it can access the brain frommost parts of the brain through theepithelium cells lining the capillaries in thebrain. Trophic factors indicatehyperplasia, which could act to furtherincrease the rigidity of the blood-brainbarrier, preventing access of potentiallyharmful reactive chemical species.

•Myelination: experimentation with mice hasshown that additional serums of IGF 1have triggered a neural overgrowth up to85%,without any problems by hyperplasiaand additional myelination.

Growth Hormone is also largely responsible forstimulating the liver amongst other secretory cells toproduce IGF 2, which is an autocrine, but also amitogenprimarily acting during the gestationphase ofdevelopment. This protein has 2 receptors. It can bindto an IGF 1 receptor, where it then triggers a normalresponse, or to a receptor designated to it and iscomplementary to its structure only. This is a receptorantagonist, which dampens the response of IGF 2.This hormone causes proliferation of most, if not all,tissues at their pre-natal stage, but sometimes they canstill have a further effect in the mature adult bodybecause it still acts as a boosting intermediate tomanyhormonal path ways, particularly with those relativeto sexual organs.

An example of this would be production by ovariantheca cells for the purpose of the proliferation of itssecretory cell as well as granulosa cells in the processof folliculogenesis, leading to the maturation of theovarian follicle which leads to production of FSH(Follicle StimulatingHormone) to develop the oocyte(premature ovum). After ovulation, IGF 2 alsostimulates progesterone secretion, causing theformation of the uterine lining. In addition, it has alsobeen found to improve testosterone levels.

The more remarkable aspect of IGF 2 is its geneticsbecause it is an instance where many processes workcoherently in a sequence. Genomic Imprinting is aphenomenonwhereby1 geneof a pair of alleleswill be“imprinted” and therefore cannot be expressed.Imprinting is the result of themethylation (addition ofa methyl group to a triplet codon) which disables thegene being recognised by DNA polymerase and soanything it codes for is not produced. In the case ofIGF2, the gene (11p15.5) on the alleles are disabledbya genetic insulator located between the gene promoterand gene enhancer, which stops their transcription soto stop theproductionof IGF2,but thepaternal gene’s

insulator has been methylated and so is treated as thedominant allele and so is expressed.

A reversed example of this is that of H19, where itspaternal allele is imprinted. H19 is the neighbouringgene to IGF 2’s gene.

The actual insulator of the IGF2 gene on thematernalchromosome (specifically 11 due to “11”p15.5) iscalled Transcriptional Repressor CTCF. This is aprotein that binds to 3 regions on the stretch of DNAbetween the codons for H19 and IGF 2, which is agenetic enhancer for IGF2. The mechanism for thisbonding actually suppresses the effect of the enhancer,so there is no longer any transcription of the IGF 2maternal allele. This mechanism is still unknown, butis predicted to either be a direct relationship betweenCTCF and the stretch of DNA, or CTCF stimulatesother protein intermediates to interfere/bond.

Insulin Like Growth Factors, one of the manywonders of developmental biology.

By ZakariaAchercouk

ALS And Animal Testing

ALS, or Motor Neurone Disease as it’s known in theUK, has been gaining popularity due to the raisedawareness of the public through the recent culturebomb that has rippled through the internet: The IceBucket Challenge. This involves filling a bucket withice and pouring it over you, with the gist that it is funto do and fun to watch and so spreading the messageof the dangers of ALS and encouraging donations toALS research.

Amyotrophic lateral sclerosis is a neurodegenerativedisease that affects motor neurons stretching from thecentral nervous system to effector muscles. Theindividual neurons start to degenerate losing theirefficiency at transmitting electrical impulses to deliverphysical reactions i.e. muscle movement, to the pointof complete inability. Although this only applies toneurons acting out voluntary movements, so anynatural reflexes (like the heart beat) are not affected byALS. But as most people have noticed, you can holdyour breath; therefore ALS can actually disable yourability to breathe.

As a result, this can cause close to complete paralysis,as can be seen with Stephen Hawking, as well as yourinactive muscles getting atrophy, which is the slowdegeneration of muscle tissue because they haven’tbeen used. This is a visible change, with limbs gettingsmaller and thinner. Yet, the progression of thisdisease is variable and its effects can actually reverse.

ALS can affect anyone and if its progress isn’thindered or reversed, it significantly reduces lifeexpectancy. ALS currently has no cure.

AnimalTesting/Experimentation isamoral issue thathas been raised on numerous cases of drug andmedical developments. Specifically, it is the use ofnon-human animals as the subjects of tests. Manycharities and organisations have been set upcampaigning against it, the main reason being thatanimals, with the ability to feel and experience(especially pain) undergo adrop in standards of living.Consequently, it is a very controversial issue, with themain argument against it being that the animals’quality of life would decrease to levels that would beconsidered “inhumane” if performedonhumans.Themain argument for animal testing is that it helpsproduce potentially life-saving medicines.

ALS has been studied and there have beenexperiments on it in clinical trials, to find drugs andcures for it, but some of these have involved animalmodels, particularly rodents. This is a matter that hasbeen raised by PamelaAnderson. These animals havethe ALS genes (Currently in humans, there are 33known genes that are recognised as a major factor inthe development of the disease) “bred” into them asthey reproduce to form new generations. Thesegenerations are studied for similar behaviouralpatterns to humans with the condition, as well asneuronal development and degeneration.

Whether this is, overall, a “bad” thing is quitedebatable. It has led to the development of the drugriluzole, which does manage to suppress thedevelopment of ALS extending a sufferer’s lifeexpectancy, albeit the effect isn’tmajor. Still, there areother drugs beingdeveloped, partially in the fashionofanimal experimentation, that are showing promise incountering the effects of ALS. This could providerelief andanewlife toover12,000people in theUnitedStates alone. Is the pain of other species worth it?

Obviously, there are people who find this utterlyunacceptable and disagreewith this completely and insome areas of the debate their points are quite valid.ALS varies so much because there are many geneticdysfunctions that cause it or symptoms very similar toits own. Only 5-10% of variations have been studiedfor treatments so far. Current rates of success inclinical trials include a 92% failure rate whenswitching drug patients from animals to humans andof those that are successful inhumans,half are rejecteddue to unexpected/detrimental side effects. Currentstatistics involved with ALS experiments aren’t toodissimilar, leading to a loss of time and money andfaith by people who are in desperate need of this help.So that would lead to amuch lower amount of peoplereceiving effective treatment, with the same level ofharm to animals.

On the other hand, there are other technologies beingdeveloped in the field of aetiology that has helped usobserve ALS in a way that is potentially much lessvague than seeing animal responses and actions underthe effect of the disease. This involves the re-differentiation of skin cells ofALS patients intomotorneurone cells, theprocess ofwhichactually reveals thecell’s genetic mutation to its new shape and purposeand showing how the motor neuron cell actually actsafter these changes.Abetter,moreethical experiment,you could say.

The People for the Ethical Treatment of Animals, orPETA, have labelled their “Top 5 Reasons to StopAnimal Testing”:

1. It’s unethical and unnecessary to cause harmto 100 million undeserving animals

2. The success rate in transferring to humansonce animal trials have succeeded is so lowit’s pointless to engage in animal testing

3. It’swasteful of timeandmoneyand few, if anyare gaining from it

4. Themethod is out-dated andother options areavailable

5. The pros of a new medical developmentdoesn’t level out the cons of needlessanimal suffering

These arguments fit very nicely with the argumentagainst animal testing for ALS, except for the lastreason which is still debatable and is part of anargument that continues to this day. Accordingly, itcan only be assumed that for any substantial changefrom animal testing must be that the majority of casesmust see that it isn’tworth it, but animal suffering isn’tan easily-measured variable. Until an agreed-uponmeasure is foundand is respectedbybothpartiesof theargument, there is no observable end to the argument.

By VamsiThammandra

Bees' Venom And HIV

Figure Above: Nanoparticles (purple) carrying melittin (green)fuse withHIV (small circles with spiked outer ring), destroying thevirus’s protective envelope. Molecular bumpers (small red ovals)prevent the nanoparticles from harming the body’s normal cells,which are much larger in size.

Although bee venom is widely feared, recently,researchershave foundapractical andvery favourableuse for it. It has the ability to destroy the humanimmunodeficiency virus as well as several otherviruses.

Bee venom is a mixture of histamine, pheromones,enzymes, peptides, amino acids and other acids, with63components in total.Themainenzymespresent arephospholipase A, hyaluronidase, and lecithinase;while the main peptides are mellitin and apamin.

The main substance that was researched was thepeptide,Melittin.Melittin is a powerful toxin found inbeevenom. It is a small protein (consistingof26aminoacids) which makes up 50% of the dry weight of beevenom and acts to destroy blood cells by breaking uptheirmembranes. It also lowers bloodpressure, causeshistamine release, and is the main pain-causingcomponent. The peptide iswater-soluble as a tetramer(oligomer formed from four monomers), but itspontaneously integrates into lipid bilayers with itslytic properties. Another important substance withinthe venom is Phospholipase A, which is an enzymethat hydrolyses phospholipids into fatty acids.

Previous studies have shown that the venom has theability to “poke” holes in the protective viral envelopethat surrounds thehuman immunodeficiencyvirus, aswell as other viruses allowing it to destroy the viruswithout harming surrounding cells. However, oneproblem still remained: Lecithinase (another type ofphospholipase enzyme which constitutes part of thevenom) converts lecithine to lysolecithine (orphospholipaseB),which breaks down themembranesof blood cells. Hence, when the venom came intocontact with the unaffected cells, it had destroyed thecellmembranes, leading to the loss of blood cells in thebody.

To solve this problem, scientists placed the melittintoxin onto nanoparticles which were covered inprotective bumpers, so that when they came intocontact with normal cells (which tend to be muchlarger), the nanoparticles bounced off rather thanattaching themselves. Viruses are much smaller thanthe nanoparticles and fits in between the bumperswhichallows it to come intodirect contactwith thebeetoxin surface. This results in the destruction of thevirus. “Melittin on the nanoparticles fuses with theviral envelope. The melittin forms little pore-likeattack complexes and ruptures the envelope, strippingit off the virus."

Melittin attacks double-layered membranesindiscriminately, which gives it potential for drugtherapies beyond HIV infections. The hepatitis B andC viruses, among several others, rely on the same typeof protective envelope and could be targeted anddestroyed by administering melittin-loadednanoparticles.

Interestingly enough, scientists had found that thebasic substance that they are using in theseexperiments was developed many years ago as anartificial blood product as it has the ability toincorporate non prosthetic groups similar tohaemoglobin. However, it didn't work very well fordelivering oxygen as it couldn’t bind to it stronglyenough, but it circulates safely in the blood andprovides a nice platform that scientists can adapt tofight different kinds of infections.

“In theory, if the nanoparticles are injected into theblood they can securely remove all HIV that resides inthe blood.”

While most anti-HIVmedications work on inhibitingthe virus' ability to replicate, this one attacks a vitalpart of its structure. The problem with attacking apathogen's ability to replicate is that it does not stop itfrom starting an infection. Some HIV strains havefound ways to circumvent replication-inhibitingdrugs, and reproduce regardless. Hence, theproperties of melittin have a better chance oferadicating the virus completely.

The common prescriptions for the reduction of HIV(not complete removal) arenotveryeffectiveand therehave been many side effects that follow theirconsumption.Anexampleof this isATRIPLA,which

only works to decrease the amount of HIV in yourbody so your immune system can function normally.However, the side effects are diarrhoea, nausea,depression and the list continues.

Researchers have developed a gel like substancewhichcanbe localised to theareaofapplication,henceit is much safer and convenient to use than a drugwhich would travel around the entire bloodstream.The gel also has the potential to target sperm, theresearchers explained, making it a possiblecontraceptive medication. The study, however, didnot look at contraception.

Recently, researchers and scientists have opened anew door for fighting a very common virus. Thisallows for the development, further research andimprovement on the possible medication. In thefuture, we can hope to completely destroy HIV andother dangerous viruses.

By David Cohen

DRESS Syndrome

1. George, Helga. "What IsTransaminase?" WiseGEEK. Ed. MichelleArevalo. Conjecture Coorporation, 16 Dec.2014. Web. 19 Dec. 2014. <http://www.wisegeek.org/what-is-transaminase.htm>.

2. Buck, Marcia L., Pharm.D FCCPFPPAG. "Dress Syndrome." Medscape.com.Medscape.com, 18 Nov. 2012. Web. 19 Dec.2014. <http://www.medscape.com/viewarticle/776164>.

3. Promeet, Dutta. "Transaminase |Enzyme." Encyclopedia Britannica Online.Encyclopedia Britannica, 12 Apr. 2009.Web. 19 Dec. 2014. <http://www.britannica.com/EBchecked/topic/602366/transaminase>.

4. "Temporal Lobe - The Brain MadeSimple." Temporal Lobe - The Brain MadeSimple. N.p., n.d. Web. 19 Dec. 2014.<http://brainmadesimple.com/temporal-lobe.html>.

5. Shafer, Patricia O., RN MN, andJoseph I. Sirven, MD. "EpilepsyFoundation." About Epilepsy: The Basics.Epilepsy Foundation, Jan. 2014. Web. 19Dec. 2014. <http://www.epilepsy.com/learn/about-epilepsy-basics>.

6. "Epilepsy and Seizures." JohnHopkins Medicine/ Health Library. JohnHopkins University, n.d. Web. 10 Dec.2014. <http%3A%2F%2Fwww.hopkinsmedicine.org%2Fhealthlibrary%2Fconditions%2Fnervous_system_disorders%2Fepilepsy_and_seizures_85%2CP00779%2F>.

Sources

In September of 2013, a young London basedsolicitor, Amelia Smith, travelled to Peru on a highlyanticipated break from the hustle and bustle ofLondon life. The trip itself included treks at greataltitude up to Machu Picchu along the Inca trail. In amoderately fit state, Amelia felt that it would be amanageable task for bothher partner andherself. Latein theeveningof the first night,Amelia andherpartnerheaded up to their hotel room after frequenting a localbar. Amelia felt content with the night, and wasexcited about the upcoming weeks. However, beforegoing to sleep,Amelia blackedout, fell to the floor andbegan convulsing. Owing to the high irregularity ofthis event, Amelia decided it would be best to visit aspecialist. The next day, upon visiting a neurologist,Amelia was prescribed ‘Phenytoin’, and was advisedto take care throughout the remainderof their holiday.

Phenytoin, also known as ‘Dilantin’ is an anti-epileptic drug usually prescribed to those with severeepilepsy. It works by inhibiting the active transport ofsodium ionswithin the action potentialmechanismofneurone activity. Action Potential describes a processin typical neurone behaviour, in which there is anexchange of sodium ions against a concentrationgradient. This maintains a resting charge potential ofaround -70 mV. When there is an electrochemicalstimulus of the dendrons (the location of synapses),the ion channels open, causing sodium ions to floodacross the axons. This causes a change in overallcharge, and the system exceeds its charge threshold,thus causing a ‘firing’ of an electric pulse. This resultsin more electrochemical messages being transmittedto adjacent neurones; thus causing involuntary chainmisfirings. It is important to take into account thatonly in some sufferers of epilepsy this process isexaggeratedby themalfunctionof sodiumchannels. Itis also important to understand that a diagnosis ofepilepsy can cover a broad spectrum of conditions,some of which are without a definable cause. In thiscasePhenytoinwould act as a sodiumpump inhibitor,hindering the functions of the sodium channelsreducing the patient’s chance of having involuntaryconvulsions.

After completing both the two week holiday and hercourse of prescribed drugs, Amelia returned back toher parents’ home inSurrey.Within twodays,Ameliadeveloped a high fever and severe rash that covered alarge proportion of her body. Again, this was a highlyirregular occurrence since Amelia had no previousmedical history relating to Eczema or any other formofDermatitis. After a period of consideration,Ameliaagain decided it would be best to call an ambulanceservice and to be admitted into Hospital.Upon arrival to Kingston Hospital, vital signs werechecked and blood and urine sampleswere taken. The

urine samples were found to have high levels ofketones, which would suggest the malfunction of thekidneys.After severalmisdiagnoses,dermatologistDrFletcher assumed responsibility for Amelia andenquired about any previously prescribed medicines,Amelia promptly replied ‘Phenytoin’. Afterresearching into ‘Phenytoin’ and its possible sideeffects Dr Fletcher found Amelia’s condition to beconsistent with that of DRESS syndrome.

DRESS syndrome, Drug Reaction with Eosinophiliaand Systemic Symptoms is a form of DrugHypersensitivity.According to ‘www.dermnetz.com’one in every ten thousand patients prescribed withanticonvulsant drugs that share the same category as‘Phenytoin’ will suffer from DRESS syndrome. Thesymptoms that Amelia was suffering was a textbookexample of the adverse effects of DRESS syndrome.

Some of these adverse symptoms include liver failure(which contributes greatly to the condition’sapproximate 20%mortality rate) and haematologicalirregularities including eosinophilia, andleukocytosis. In a study of DRESS syndrome ininfants Marcia L. Buck, Pharm.D, FCCP, FPPAG,found that in a majority of cases in which Phenytoinhad been administered, patients had abnormally hightransaminase levels. Transaminase is an enzymespecific to the liver which, when found in high levels,can cause cirrhosis and other severe forms of liverdamage.

Previous to this Diagnosis, Amelia had been put intoa special isolation bay, as a precaution. Medicalprofessionals were taking caution due to the fact thatthe condition may have been contagious due to thesevere dermatitis, consistent with commoncontagious infections. This had a great psychologicaleffect not only on Amelia, but also on her family. Thenecessity of the isolation was debatable in thissituation because although the condition had beencontagious, the lack of explanation for the reasoningof the isolation raised unnecessary stress. To add tothat, multiple drug administrations advise againstprescribing phenytoin to many patients as it canexacerbate existing psychological conditions and alsosince there are serious side effects including suicidalmotives.

Amelia mentioned that during her prescribed courseofphenytoin,doctorsneglected tokeep incontactwithher, and as a consequence her progress was nottracked. Evidently, throughout the whole episode,medical representatives failed to monitor Amelia’spsychological state which was negligent consideringthe possible side effects. After being able to fullycomprehend the situation at hand, Dr Fletcher wasable to remove Amelia from the isolation ward, andshewas placed into the Coombewing of the KingstonHospital complex. Assessing the situation, DrFletcher had to be weary of Amelia’s dwindlingimmune system, already weakened by the drugreaction. Steroid based creams were administered toareas with the most severe dermatitis, and othermoisturisers where given to ensure skin was notsubject to peeling, which would raise the risk ofinfection.

After twoweeksof observation,Ameliawas cleared toleave Kingston Hospital. However, the next three

months were to be spent at home, away from work,which resulted in a significant loss of income. To addto the long term implications of the medicalnegligence, Amelia has now developed cold urticaria,and infrequent spouts of dermatitis brought out bystress. Amelia’s case is only one of many cases ofnegligent medical practice and it’s hard to predictwhen drug guidelines across theworldwillmeet somesort of continuity. Although it is not ethical to putanyone through the same ordeal that Amelia wentthrough, arguably she has acted as testimony to boththe stages of DRESS syndrome, how to treat thecondition ethically and effectively and also theimplicationsandconsequencesofmedicalnegligence.

By HassanHussain

Allergies - How They Work and How They're Deadly

Many people these days suffer from one or more typeofallergy,whether it is simplyhay feveroradeadlynutallergy. With the percentage of adults with allergiesincreasing by 5% each year, and 21 millions adultsaffected in theUK alone, allergies are becomingmoreand more prevalent. But what causes allergies andwhy can they be so deadly?

Lymphocytes are the main agents of the immunesystem.When they encounter a certain antigen that isconsidered to be part of a foreign body, they produceantibodies that bind to the said antigen. The 5 types ofantibodies are IgA, IgD, IgE, IgG, IgM, and these areknown as immunoglobulins. The one that causesallergic reactions is IgE. In people who don’t sufferfrom allergic reactions, IgE does not combatsubstances such as food. However in an allergicreaction the opposite occurs. The ability for the bodyto create IgE when it is not needed is inherited, so ifboth parents are allergic to substances, chances aretheir children will have allergies as well.

In order for an allergic reaction to food to occur, firstthe person must be exposed to that food substancefirst. When the food enters the body it starts to bedigested andwill eventually be digested into a protein.The person’s TH2 lymphocyte then detects thisprotein, recognises it as a foreign body and produces acytokine knownas Interleukin-4, or Il-4. The cytokineand the T-lymphocytes interact with B-lymphocytes,which begin making the immunoglobulin IgE. TheIgE binds to mast cells, which are tissue cells, andbasophils, which are a type of white blood cell. Bothare found everywhere in the body, but specifically inparts of the body that generally flare up during anallergic reaction, e.g. lungs, nose, skin, throat andgastrointestinal tract. This process is known assensitizing exposure, and takes around 7-10 days tocomplete.

When a person ingests that food again after thisprocess has been completed, and when that food isdigested into that protein again, the IgE bound to themast cell recognise the protein and binds to it, while

still staying bound to the mast cells and basophils.Proteins called complementary proteins are releasedand attach to the allergen to form a chain. The proteinchain destroys the mast cells and basophils, causingthem to release the contents, which include cytokines,histamines and other chemicals, which then lead tothe symptoms of the allergic reaction. Thesechemicals cause blood vessels to dilate, leading to adrop in bloodpressure. Fluid fills the gaps between thecells near the area affected by the reaction.

So when do allergic reactions become dangerous?Anaphylaxis is the name of a severe allergic reaction,and occurs when the process of an allergic reactiongoes out of control, leading to the body not being ableto function properly, which can cause death in theworst cases. During anaphylaxis, the histamine andother chemicals released from the mast cells and thebasophils means that fluid from the cells is dumped inthe throat, and combined with muscle contractions,results in the throat swelling andclosingup,which canlead to shortness of breath and oxygen starvation,which if not treated quickly could lead to death.Othersymptoms of anaphylaxis include hives, which is araised itchy rash all over the body.Blood pressure may decrease and fluid may be leakedfromthebloodvessels, starvingvitalorgansofoxygen,especially the brain and kidneys, and resulting inconfusion, anxiety and loss of consciousness. Too lowa blood pressure can lead to circulatory collapse,causing death.

So what can we do to counter anaphylaxis? The mainon site treatment is epinephrine,which is the chemicalin EpiPens. Epinephrine reduces the swelling in thethroat and causes vasoconstriction to stop the bloodpressure from dropping too low. Other treatmentsinclude antihistamines, adrenaline and steroids.

Allergies can appear out of nowhere and affect

people who have never been affected before, andcan range from mild to deadly. The most importantthings you can do if you have an allergy is to beprepared: stay away from your known allergens andalways carry an EpiPen if you need it.

HyperthyroidismBy VamsiThammandra

The thyroid gland is a part of the endocrine systemwhichproduces hormones including triiodothyronine(T3), thyroxine (T4), are tyrosine-based hormonesthat are released into the bloodstream to control thebody's growth andmetabolism. The release of thyroidhormones from the thyroid gland is controlled bythyrotrophin, a releasing hormone from thehypothalamus in the brain and by a thyroidstimulating hormone produced by the pituitary gland.

Hyperthyroidism,alsoknownasoveractive thyroid, isa medical condition caused by an abnormally highlevel of thyroid hormone in the bloodstream. Thereare multiple possible causes of hyperthyroidismincluding Graves’ disease, nodular thyroid disease,excessive iodine intake, intake of thyroid hormones,thyroiditis and follicular thyroid cancer.

Graves' disease is an autoimmune condition. Incommoncases, the body's immune systemmistakenlytargets the thyroid gland and causes it to produce toomuch thyroid hormone. It is know that the disease isgenetic, hence it could runwithin the family. Nodularthyroid disease can cause lumps to develop in thethyroid gland. They are known as nodules which areusually non-cancerous. The thyroid is usuallyenlarged, but there is no pain. Nodules may be feltwith the fingertips.Thenodules can contain abnormalthyroid tissue, affecting the regular function of thethyroid. This is known as a toxic form ofhyperthyroidism.After an excessive amount of iodinehas been taken in, the thyroid gland works to removeit from the blood. Iodine commonly comes from foodssuch as seafood, bread, and salt. The thyroid glandthen uses the iodine to produce thyroid hormones.The two most important thyroid hormones arethyroxine (T4) and triiodothyronine (T3). Takingadditional iodine in supplements can cause thethyroid gland to produce an excess of the hormones.Overdosing on thyroidmedication could also result inhyperthyroidism. Thyroiditis is the inflammation ofthe thyroid as a result of a viral infection. Thesymptoms may include fever, sore throat, painfulswallowing, generalized aches and pains in the neck.Finally, follicular thyroid cancer can causehyperthyroidism.Themalignantcellsmay themselvesstart producing thyroxine or triiodothyronine.

The severity of the symptoms of hyperthyroidismvaries from patient to patient. Patients with mildstrains of the disease are often not aware of it becausethey have no symptoms. Usually, the symptoms arerelated to an increased metabolic rate of the body.However the signs are subtly visible to an experienced

specialist.

Signs and symptoms linked to hyperthyroidism mayinclude (patients rarely have all those listed below):

•a swelling in the neck caused by an enlargedthyroid gland (goiter)

•decreased concentration•difficulty breathing• increased appetite• increased bowel movements•menstrual problems in women•muscle weakness• shakiness and muscle weakness• sudden weight loss or gain

In order to diagnose hyperthyroidism, the doctor willfirst ask the patient questions relating to thesymptoms. This is followed by a physicalexamination, and thenablood test.Cases of advancedhyperthyroidism are fairly straightforward todiagnose, however, early on in the condition,symptoms are not so obvious and clear-cut, whichcausesa lotofpatients tobeoverlooked.Theblood testis known as a thyroid function test. This allows thedoctor to understandhow the gland is functioning andto see whether there are any abnormalities such as adifferent hormone content or temperature of theblood.

There are several treatments which can supress themajor symptoms however some medications are alsoaccompanied by complications. As well as thosetreatments, there are others which target theproduction of thyroid hormones directly. A fewpossible treatments are antithyroid drugs, radioactiveiodine or surgery.

Antithyroid drugs stop the thyroid gland fromproducing excess amounts of thyroxine ortriiodothyronine. Radioactive iodine is picked up bythe active cells in the thyroid where it destroys them.The destruction is local, and thus there are nowidespread side effects with this therapy. The dose ofradioactivity contained in the radioiodine is very lowand is not harmful. Surgery in which part of thethyroid gland is removed is often the final resort ifother treatments are not possible. Thismaybe the caseif the patient is pregnant, cannot tolerate othertherapies or has cancer.

Some complications associatedwith hyperthyroidismare thyroid eye disease as well as complications inpregnancy. Thyroid eye diseasemay cause the patientto experience pain within the eye. It can also causelight oversensitivity which leads to other problems in

vision. This links with the symptoms of Graves’disease as the patients’ eyes may start to bulge. Thiscan be supressed with the use of eye drops.Hyperthyroidism may affect a woman's ability tobecome pregnant. Pregnant women with theconditionaremoreat riskofdevelopingcomplicationsduring pregnancy and birth, such as miscarriage andeclampsia (seizures during pregnancy), prematurelabour and low birth weight. In most cases, thepregnancy can be expected to progress normally ifproperly treated with the correct medication and rest.

The severity of hyperthyroidism depends on thebody's capability to react to the changes resulting fromexcess thyroid hormones. Thyroid disease is commonbut with proper care it can be diagnosed and treatedeffectively. Patient loyalty to treatment guidelines(instructions given by the doctor) is crucial foreffective results. This is one of the main reasons whythe treatments are not always successful.

A Closing Note -

The Tiffinian Journal of General Medicine arose as a result of a couple of us, as high achieving, aspiringmedical students, wanting to use our knowledge and ability to create a written publicationwith the aimto intrigueand informotherwith interests in the fieldofmedicineandscience.What startedoff as a smallproject quickly began to grow, as we met new students who were also able to write well about topicswhich they were passionate about. Currently we are a team of seven and are aiming to release issuesquarterly and following our first issue, we hope to produce more high quality material faster and as aresult release new issues more frequently.

I hope that you have enjoyed reading through our publication and that you have learnt something newas a result. Please feel free to send us any questions, comments or suggestions at the email stated on theback cover. In the future, we will be looking to collectively write articles all based around a certain,integral theme. I feel that thiswill help the articles to flowbetter and hopefully allow you, the readers, toenjoy themmore.

Thank you,Saamir MirzaCoEEditorEInEChief

Interested in contacting the Tiffinian Journal of General Medicine's PublishingTeam? Any queries or comments?

Send us an email at: [email protected]

TheTiffinian Journalof GeneralMedicine

Journal Design : Senthooran Kathiravelupillai

the tiffinian journal of general medicine - issue 1 - january 2015

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