Medical Study Notes For PG Preparation: Biology

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HIV - Pneumocystis carinii

Toxoplasma gondii was first described by Nicolle in 1909 in a North African rodent, Ctenodactylus gondii. The pathogen derives its species name from this. It is a unicellular parasite that is very widespread in nature and can infect many animal species. It is localised and replicates in practically all nucleated cells. The parasite has 3 principal forms: (1) banana-shaped trophozoites (hence the generic name “toxon” = bow) which reproduce asexually in nucleated cells, (2) intracellular dormant cysts with bradyzoites. In the cells the parasite forms cysts that are held in check by the immune system. The parasite thus remains present in the body, especially in muscle cells and in the brain, throughout the animal’s life. (3) oocysts that are the result of the parasite’s sexual cycle in the intestine of the cat. These oocysts can survive in the outside world for several months. If tissue cysts are present the parasite can become active again due to diminished activity of the immune system.

People are infected primarily via cat faeces or by eating contaminated and insufficiently cooked meat. In adults with an intact immune system Toxoplasma usually causes few problems, apart from occasional lymph node swelling and/or hepatitis. Reactivated parasites can attack the brain and retina in immunodepressed persons. Headache, neurological problems, blindness and focal cerebral lesions can occur. Such focal lesions can lead to epileptic fits. A favourable clinical response to anti-toxoplasmosis therapy is suggestive of cerebral toxoplasmosis (a good clinical response usually occurs within 2 weeks). Cerebral biopsy and PCR (Polymerase chain reaction) can be performed if there is doubt about the diagnosis. Toxoplamosis is an infection that can be prevented by prophylactic therapy. Cerebral localisations of lymphomas as well as tuberculomas can resemble cerebral toxoplasmosis.

Posted in Biology , Conditions and Diseases , Health , Immune system , Infection , Lymph node , Medical Subject Notes , Muscle , Toxoplasmosis | |By Vishaal ViewPost

HIV - What can we analyse in cerebrospinal fluid?

Posted in Bacteria , Biochemistry and Molecular Biology , Biology , Fungus , Health , Medical Subject Notes , Meningitis , Polymerase chain reaction , Protein | |By Vishaal ViewPost

Genetic Disorders of the HL System

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-Hematopoesis is known to be guided by more than 20 genes. There are a bunch of mutations that create impairment because of this. Certain mutations will arrest differentiation in different stages and you won’t have an effective population of certain cells to carry out a specific function. This commonly leads to lethality of the cell line since critical cells are not produced.

-Significant subset of genes relative to hematopoesis and to functioning of the differentiated cells are a set of growth factors and their receptors. They function to regulate replication of the hematopoetic cells and transcription of these genes. There are two broad categories of these receptors/growth factors

-tyrosine kinase activity receptors- membrane bound, the cytoplasmic domain has tyrosine kinase activity, which will phosphorylate other molecules, this will trigger an intracellular cascade of phosphorylations. The external domain includes a series of immunoglobulin like domains (100 amino-acids in length, two cysteines in each domain, there is sulfur-sulfur reduction between the two domains to bring about a certain confirmation.)

-cytokine super family: example erythropoietin it is a grow factor that stimulates the differentiations of erythopoietic cells. There can be certain mutations in the receptor for erythropoietin. These mutations represent, Intra Locus Genetic Heterogeneity, and phenotype heterogeneity.

There are a couple of mutations in the locus that make for impairment of erythropoiesis and some that stimulate it. 4 examples of these mutations are:
-extracellular motif in the receptor that is highly conserved sequence. Mutations in it have the consequence that they bring about sequestration of the receptor when it is taken into the cell. So, that it cannot function as a transmission signal

-mutation in the cytoplasmic domain of the receptor called a truncating mutation, a segment is blocked off by the mutation. There will be no transmission of signal when erythropoietin binds.

-there is a arginine at position 129 in the receptor, if you substitute for the arginine, with cysteine this will bring a dimerization between two receptors and this will make the receptor independent. It will keep signaling in the absence of erythopoetin

-there is a truncating mutation in the cytoplasmic domain of the receptor which will bring an abnormal signaling so that you have an excessive erythrocytosis (increased numbers of RBC). 70 amino acids are truncated