3 results
A comparison of GABAC and ρ subunit receptors from the white perch retina
- Aohua Qian, George Hyatt, Andres Schanzer, Rohan Hazra, Abigail S. Hackam, Garry R. Cutting, John E. Dowling
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- Journal:
- Visual Neuroscience / Volume 14 / Issue 5 / September 1997
- Published online by Cambridge University Press:
- 02 June 2009, pp. 843-851
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There is increasing evidence that GABAC receptors are composed of GABA ρ subunits. In this study, we compared the properties of native GABAC receptors with those of receptors composed of a GABA ρ subunit. A homologue of the GABA ρ gene was cloned from a white perch (Roccus americana) retinal cDNA library. The clone (perch-s) has an open reading frame of 1422 nucleotide base pairs and encodes a predicted protein of 473 amino acids. It is highly homologous to GABA ρ subunits cloned from human and rat retinas. The receptors (perch-s receptor) expressed by this gene in Xenopus oocytes show properties similar to those of the GABAC receptors present on white perch retinal neurons. GABA induced a sustained response that had a reversal potential of –27.1 +minus; 3.6 mV. The EC50 for the response was 1.74 +− 1.25 μM, a value similar to that reported for GABAC receptors. Pharmacologically, the responses were bicuculline insensitive and not modulated by either diazepam or pentobarbital as is the case for GABAc receptors. There were, however, some distinct differences between native GABAc and perch-s receptors. I4AA acts as a partial agonist on perch-s receptors whereas it is strictly an antagonist on native GABAC receptors. Picrotoxin inhibition is noncompetitive on perch-s receptors, but both competitive and noncompetitive on GABAC receptors. We conclude that GABAC receptors are formed by GABA p subunits but that native GABAc receptors probably consist of a mixture of GABA ρ subunits.
31 - Tuberculosis
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- By Rohan Hazra, HIV and AIDS Malignancy Branch, NIH, Bethesda, MD
- Edited by Steven L. Zeichner, National Cancer Institute, Bethesda, Maryland, Jennifer S. Read
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- Book:
- Handbook of Pediatric HIV Care
- Published online:
- 23 December 2009
- Print publication:
- 04 May 2006, pp 674-684
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Summary
The HIV/AIDS epidemic has led to a resurgence in the rates of tuberculosis in the developed world. In the developing world, co-infection with HIV and tuberculosis is extremely common and a major cause of morbidity and mortality. Tuberculosis in HIV-infected children can be more severe than disease in HIV-uninfected children, and treatment is complicated by drug–drug interactions between antiretrovirals and tuberculosis medications. Nevertheless, effective treatment of tuberculosis in the HIV-infected child is critically important for prolonged survival, even in the absence of antiretroviral therapy.
Epidemiology
Mycobacterium tuberculosis is the etiologic agent of tuberculosis. Humans are the only reservoir for the organism. In the USA the number of cases of tuberculosis has been declining, but the global burden of disease is staggering. World Health Organization (WHO) data for 1997 estimated almost 8 million new cases that year, 16.2 million existing cases, 1.87 million deaths attributable to tuberculosis, and global prevalence of infection of 32% [1]. WHO estimates that the worldwide prevalence of tuberculosis and HIV co-infection is 0.18%, with 8% of new cases of tuberculosis occurring in patients who are HIV seropositive. This rate of HIV seropositivity among incident tuberculosis cases is as high as 65% in some African nations.
In an adult, a case of tuberculosis can result from either reactivation of endogenous latent infection or exogenous primary infection or reinfection [2].
38 - Tuberculosis
- from Part V - Infectious problems in pediatric HIV disease
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- By Rohan Hazra, HIV and AIDS Malignancy Branch, National Cancer Institute, NIH, Bethesda, MD
- Edited by Steven L. Zeichner, National Cancer Institute, Bethesda, Maryland, Jennifer S. Read, National Cancer Institute, Bethesda, Maryland
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- Book:
- Textbook of Pediatric HIV Care
- Published online:
- 03 February 2010
- Print publication:
- 28 April 2005, pp 569-579
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Summary
The HIV/AIDS epidemic has led to a resurgence in the rates of tuberculosis in the developed world. In the developing world, co-infection with HIV and tuberculosis is extremely common and a major cause of morbidity and mortality. Tuberculosis in HIV-infected children can be more severe than disease in HIV-uninfected children, and treatment is complicated by drug—drug interactions between antiretrovirals and tuberculosis medications. Nevertheless, effective treatment of tuberculosis in the HIV-infected child is critically important for prolonged survival, even in the absence of antiretroviral therapy.
Epidemiology
Mycobacterium tuberculosis, the etiologic agent of tuberculosis, is the major species of the M. tuberculosis complex, which also includes M. bovis, M. ulcerans, M. microti, a rodent pathogen, and M. africanum, a rare cause of tuberculosis in Africa. Humans are the only reservoir for M. tuberculosis. In the USA the number of cases of tuberculosis in 2001 reached an all-time low of 15 991 cases [1]. The incidence rate had risen from the mid-1980s until 1992, secondary to the HIV epidemic and decreased attention to public health. Since 1992 there has been a steady decline in the number of cases per year. Pediatric surveillance data, which began in 1953, demonstrates a similar pattern of decline in the incidence until 1988, increase until 1992, and subsequent decline [2].
Internationally, the global burden of disease is staggering.