Xalatan

Quoting Wikipedia, "The amount of glucokinase can be increased by synthesis of new protein. Insulin is the principal signal for increased transcription, operating mainly by way of a transcription factor called sterol regulatory element binding protein-1c (SREBP1c) except in the liver. This occurs within an hour after a rise in insulin levels, as after a carbohydrate meal". Insulin indeed increases G6P concentration by both increasing GLUT4 expression and glucokinase transcription.

Clostridium and bacillus both belong to the bacterial phylum Firmicute, in which some of the members uniquely possess sporulation genes that enable endospore formation. Phylogenetically firmicutes are believed to have diverged from other phyla fairly early, which may contribute to their unique sporulation capabilities.

Wellbutrin is interesting because while it is used as an antidepressant, it's atypical in its dopaminergic action. Which is why it is also indicated for smoke cessation, to try and maintain a higher level of DA at the reward centre after the cigarettes are gone. It's still meant to alleviate depressive conditions but it's interesting you describe a qualitatively different feel to buproprion than more conventional serotonergic agents.

As far as I know glucokinase and hexokinase are not regulated by insulin per se. The main regulation of hexokinase is G6P, to inhibit overuse of the glycolytic pathway. GLUT4 on muscle and adipose surface is increased by insulin to take up the blood glucose, so this may be the means to increase glucose consumption and G6P production.

Buproprion is a norepinephrine-dopamine reuptake inhibitor, where as St. John's Wort may be a general monoamine reuptake inhibitor, so St. John's Wort raises the synaptic concentration of serotonin as well as NE and DA. The pharmacological difference may be serotonin hit, which may be the source of the deeper content happiness you are describing. St. John's wort works comparably to tricyclic antidepressants and SSRIs. Tricyclics are serotonin-norepinephrine reuptake inhibitors so there is the serotonergic component, SSRIs are more selective to serotonin Reuptake. With buproprion I think the manic happiness you describe may more cocaine like in terms of the dopamine buzz.

She is the donor source of HeLa cells, an immortalised cervical cancer cell line.

As far as I know no genes have been proven to relate to Asperger's, but is there a hereditary component to the syndrome? Around 70% is related to comorbid MR and it makes one wonder about organic and genetic (and perinatal) causes.

The problem with rabies virus is that in reality it travels so slowly that after being bitten, you could still give the rabies vaccine as a treatment as there is enough time for adaptive immunity to develop. The lytic viral cycle requires entering host cell, viral genomic replication, transcription, translation, and post translational modification and assembly. This is not a biochemical process that could occur in 10-20 seconds, because viral proteins need to be mass-produced from a few strands of genetic material. A more plausible mode of infection may be something like an ultrafast prion disease that only requires protein modification and aggregation. maybe if there was a mutant prion agent that had ultrahigh affinity and potency Butthe reality is cjd is also really slow. Kakwok, good point you makes regarding the infection agent relying on host metabolism as a limiting factor. This is why a highly pathogenic prion agent may be interesting. I don't think proteins are considered living.

People differ in the amounts of daily exercise and basal metabolism too. Unless experimental subjects are matched in terms of age, gender, race, BMI, etc, and keep strict diaries about caloric inputs and outputs, it is difficult to compare what is really going on. Also good point about mental health conditions - in particular drugs like antipsychotics can affect appetite and lead to weight changes.

Yeah I find this arrangement interesting. There may be an embryological explanation for this pattern of development, perhaps some sort of somite or notochord signalling mechanism.

I find the term disorder slightly confusing as per dsm and would appreciate someone giving clear medically accurate definitions. Disease: a medical condition with clear cut aetiology, pathology, treatment response and prognosis. Syndrome: a set of clinical signs and symptoms. No implications of aetiology. Disorder: a syndrome that causes present distress or disability, or increases the risk of suffering death, pain, loss of freedom. Is this accurate?

In children, the brain is relatively plastic, so it learns to switch off vision processing from one eye as adaptation to diplopia. This is why if strabismus is not corrected in children it leads to amblyopia. In adults a squint will cause double vision. There are specially designed prism glasses that correct the angle of incident light hitting the affected eye as means for correction. Hilary Clinton wears them. http://www.theblaze.com/wp-content/uploads/2013/01/clinton-fresnel-prism-glasses-620x446.jpg Surgery can also correct strabismus.

HepB foundation defines HepB vaccine non-responders as not developing Anti-HbsAg after two full courses, and for whom acute or chronic HepB infection has been ruled out. 5-15% of people may be HepB vaccine non-responders. http://www.hepb.org/professionals/vaccine_non-responders.htm Non-responders to vaccination who are HBsAg-negative should be considered susceptible to HBV infection and should be counseled regarding precautions to prevent HBV infection and the need to obtain HBIG prophylaxis for any known or probable percutaneous or permucosal exposure to HBsAg-positive blood. Not sure if it would affect your ability to work though, since you may be working with needles.

CTLA-4 provides the regulatory mechanism that counteracts B7 and CD28 interaction. CD-4 cells express both CTLA-4 and CD28. B7-CD28 provides the co-stimulatory second signal for T cell activation, but B7-CTLA4 leads to anergy and tolerance in the Th cells. Mutations in CTLA4 causes autoimmune diseases such as IDDM, Grave's, Hashimoto's, Coeliac's, SLE.

If you are talking about mitosis and meiosis specifically, then vinca alkaloids and taxanes can inhibit microtubule assembly and disassembly, respectively. Eg. Vincristine, vinblastine, paclitaxel, docitaxel. They are used for chemotherapy. The antifungal equivalent of microtubule inhibitor is griseofulvin. If you are talking about slowing down the cell cycle, then most cell-cycle specific chemotherapeutic agents can disrupt cell cycle turnover at various stages.

The first eukaryotic chromosome has in fact been synthesised. http://science.sciencemag.org/content/344/6179/55

There is a range of immune disorders that results in immunodeficiency. For example, adenine deaminase deficiency, scid, digeorge athymia. These may impair t or b cell function to the point of not being able to produce immmunoglobulins. Acquired immunodeficiency may be due to HIV, high dose glucocorticoids, cyclosporine etc. Also some vaccines are not antigenic enough to induce antibody production, for example hib needs conjugation for eliciting a proper response.

Is this light microscopic photo or SEM? Kinda looks like sem from this view. Anatomically you may be looking at the innermost layer of the retina, which would be the ganglionic fibre layer.

Liver Mets are still colon cancer, but the cancer cells may be a more clonally invasive subgroup of the primary. They may have acquired mutations in enzymes that can breakdown tissue matrix like MMP, or lost polarity or cell adhesion molecules like cadherin. Once in the liver the Mets will disrupt the function of the heptocytes, you will see enzymes like ALT and GGT go up in biochemistry so eventually it may cause the organ to fail, to scar. Any chemo or radiotherapy to the liver mets may also induce necrosis and increase scarring.

Conjugation reactions in the liver typically refers to processes like glucuronidation that attaches charged or ionic functional groups to metabolites for ease of renal excretion.

A syndromic classification doesn't explain he underlying causes for the observation though. I don't know if general visceral afferent stimulation from bladder bowel is enough to cause global confusion but it may be enough in the elderly? There may be an infective or secondary component to the retention, eg. Severe faecal impaction, urosepsis, also exacerbations of comorbid conditions or medications need to be considered too.

There are different models of memory formation. The long term potentiation model describes the hippocampal neurons using excitatory NMDA based signalling to strengthen synaptic connections, perhaps even forming new axons and synapses as the anatomical basis for short term memory. Long term memory may be then transported and stored elsewhere in the cortex.

Cutaneous filariasis like loaiasis can give skin ulcers. They are caused by a different species of filaria to lymphatic filariasis, such as W. bancrofti.

http://www.telegraph.co.uk/news/science/science-news/12112051/First-head-transplant-successfully-carried-out-on-monkey-claims-surgeon.html Just saw this in the news - the first head transplant successfully carried out on a monkey. Brain was kept alive at -15 degrees c. "The plan for the first human head transplant is on schedule, towards its expected date of realisation, Christmas 2017".

If the 17p micro deletion is not inherited, then it is a sporadic mutation. It sounds like the micro deletion may be acquired during fertilisation in the sperm or the ovum, or at the zygote stage? All ESCs in the blastocyst are still pluripotent so sporadic mutations here may still affect all three embryonic layers.