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Mycobacterium tuberculosis (MTB)-induced T cell responses are depressed in peripheral blood mononuclear cells of persons with newly diagnosed pulmonary tuberculosis (TB), and levels of interferon (IFN)-gamma remain low even after completion of antituberculous therapy. Loss of MTB-reactive T cells through apoptotic mechanisms could account for this prolonged T cell hyporesponsiveness. T cell apoptosis was studied in TB patients and healthy control subjects. Both spontaneous and MTB-induced apoptosis (in CD4 and non-CD4 T cells) from TB patients was increased when compared with healthy control subjects, whereas coculture with control antigen (candida) had no effect on T cell apoptosis in either group of study subjects. An inverse correlation existed between increased MTB-induced T cell apoptosis and IFN-gamma and interleukin (IL)-2 immunoreactivities. Successful antituberculous chemotherapy resulted in a 50% reduction in both spontaneous and MTB-induced apoptosis, which coincided with 3- and 8-fold increases in levels of MTB-stimulated IL-2 and IFN-gamma, respectively. These data indicate that apoptotic pathways are operant during active MTB infection and may contribute to deletion of MTB-reactive T cells and the immunopathogenesis of this disease.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10068591&dopt=Abstract

J Neurovirol. 1998 Dec;4(6):619-26.
Cocaine opens the blood-brain barrier to HIV-1 invasion.

Zhang L, Looney D, Taub D, Chang SL, Way D, Witte MH, Graves MC, Fiala M.

Department of Neurology, UCLA School of Medicine, Los Angeles, California 90095-1769, USA.

Cocaine abuse has been associated with vasculitis and stroke, and is suspected to influence the progression of AIDS dementia. Cocaine may enhance HIV-1 neuroinvasion by actions directed at the blood-brain barrier. HIV-1 appears to penetrate the human brain microvascular endothelial cell barrier by a paracellular route breached by tumor necrosis factor-alpha (TNF-alpha). Cocaine's effects on the blood-brain barrier were investigated using human brain microvascular endothelial cells and peripheral blood monocytes. Cocaine (10(-5) M and 10(-6) M) increased molecular permeability of the barrier and viral invasion by the macrophage-tropic HIV-1(JR-FL) into the brain chamber. Cocaine also augmented apoptosis of brain endothelial cells and monocytes, increased secretion of four chemokines (interleukin-8, interferon-inducible protein-10, macrophage inflammatory protein-1alpha, and monocyte chemoattractant protein-1) and the cytokine, TNF-alpha, by human monocytes. TNF-alpha enhanced invasion of the brain compartment by macrophage-tropic, lymphotropic, and bitropic HIV-1 strains. These data indicate that HIV-1 neuroinvasion can be increased by (a) cocaine's direct effects on brain microvascular endothelial cells and (b) paracrine effects of cocaine-induced pro-inflammatory cytokines and chemokines on the blood-brain barrier.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10065903&dopt=Abstract

Neurol Med Chir (Tokyo). 1998 Dec;38(12):865-70.
Secondary glioblastoma remarkably reduced by steroid administration after anaplastic transformation from gliomatosis cerebri--case report.

Hirose Y, Hayashi T, Sagoh M, Murakami H.

Department of Neurosurgery, Ashikaga Red Cross Hospital, Tochigi.

A 45-year-old female presented with gliomatosis cerebri manifesting as hemiballismus-like involuntary movement in the arm, motor weakness in the leg, and hypesthesia in her left side. Computed tomography showed only diffuse swelling of the right cerebral hemisphere, but T2-weighted magnetic resonance imaging revealed a diffuse lesion spreading from the right thalamus to the temporal, parietal, and occipital lobes on the same side. No abnormal enhancement was recognized. Cerebral angiography showed no specific finding. A right occipital lobectomy was performed to confirm the diagnosis of gliomatosis cerebri. Anaplastic transformation was recognized 5 months later. The disease did not resolve with radiation or interferon administration, but steroid therapy achieved remarkably effective tumor regression. The patient died due to pneumonia. Autopsy showed the features of diffuse glioblastoma. Steroid therapy may be an effective treatment for gliomatosis cerebri before the terminal stage.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10063361&dopt=Abstract

Blood. 1999 Mar 15;93(6):1843-50.
Human immunodeficiency virus-1-infected macrophages induce inducible nitric oxide synthase and nitric oxide (NO) production in astrocytes: astrocytic NO as a possible mediator of neural damage in acquired immunodeficiency syndrome.

Hori K, Burd PR, Furuke K, Kutza J, Weih KA, Clouse KA.

Division of Cytokine Biology and the Division of Cellular and Gene Therapies, Center for Biologics Evaluation and Research, Food and Drug Administration, Rockville, MD, USA.

Nitric oxide (NO) plays an important role in normal neural cell function. Dysregulated or overexpression of NO contributes to neurologic damage associated with various pathologies, including human immunodeficiency virus (HIV)-associated neurological disease. Previous studies suggest that HIV-infected monocyte-derived macrophages (MDM) produce low levels of NO in vitro and that inducible nitric oxide synthase (iNOS) is expressed in the brain of patients with neurologic disease. However, the levels of NO could not account for the degree of neural toxicity observed. In this study, we found that induction of iNOS with concomitant production of NO occurred in primary human astrocytes, but not in MDM, when astrocytes were cocultured with HIV-1-infected MDM. This coincided with decreased HIV replication in infected MDM. Supernatants from cocultures of infected MDM and astrocytes also stimulated iNOS/NO expression in astrocytes, but cytokines known to induce iNOS expression (interferon-gamma, interleukin-1beta, and tumor necrosis factor-alpha) were not detected. In addition, the recombinant HIV-1 envelope protein gp41, but not rgp120, induced iNOS in cocultures of uninfected MDM and astrocytes. This suggests that astrocytes may be an important source of NO production due to dysregulated iNOS expression and may constitute one arm of the host response resulting in suppression of HIV-1 replication in the brain. It also leads us to speculate that neurologic damage observed in HIV disease may ensue from prolonged, high level production of NO.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10068656&dopt=Abstract

Eur J Histochem. 1998;42(4):327-32.
Heterogeneity and susceptibility to apoptosis of human renal carcinoma cells in vitro.

Dell'Antonio G, Rovere P, Mangili F, Manfredi AA.

Divisione di Anatomia Patologica, Istituto Scientifico H S. Raffaele, Milano, Italy.

Tumors are heterogeneous in terms of morphology and susceptibility to drugs or radiation. Among primary and metastatic cells of a human renal carcinoma, a population (type II) of larger cells with prominent nucleoli, eosinophilic globules of intermediate filaments in paranuclear bundles, margination of subcellular organelles and peripheral pools of glycogen was evident. Paranuclear structures were recognized by monoclonal antibodies specific for cytokeratin 8, 18 and 19, but not by vimentin specific antibodies. We propagated a cell line in vitro (referred to as BKR cells), and observed culture in vitro, the almost complete disappearance of the type II cells. Pharmacological agents that influence cell differentiation, such as retinoic acid, rescued the expression of type II cells in vitro. Long-term treatments with insulin or alpha-interferon, but not with the epithelial growth factor (EGF), similarly differentiated BKR cells and abated their susceptibility to spontaneous and actinomycin-D induced apoptosis. These data support the contention that differentiation of tumor cells is actively maintained in vivo and further strengthen the caveat on tumor lines stabilized in vitro, that poorly represent the morphologic and antigenic heterogeneity of neoplasms in vivo.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10068906&dopt=Abstract

The average human scalp is covered by approximatey 100,000 hair follicles. Each hair undergoes hair cycle and normally 50-100 hairs randomly fall out a day, which is unnoticeable because lost hair is replaced by as many new hairs springing up daily. Hair loss results from the fall out of hair from the hair follicle. Alopecia or excessive, premature hair loss is the condition caused by many factors. Loss of hair itself does not pose critical health problems because biological role of human hair is relatively marginal. Hair on our scalp protects the head from mechanical shock, heat loss, and exposure to UV-light. The eyelashes and eyebrowes protect the eyes, and hair in the ear canal or the nasal passages help filter out particles and pathogens, thus protecting our internal organs. However, hair does play important social role: it is one of the major determinants of our appearance and identity in daily life. Fullness of hair also implicates or manifests physical integrity and youthfulness of the person. Losing hair could have more than just emotional impacts on individuals. The hair is a unique organ that goes through a characteristic cycle consisting of an immature phase, a growing phase called anagen, a transitional phase between the growing phase and the resting phase called catagen, and finally a resting phase called telogen in which the hair stops growing, waiting to fall out. 85-90% of hairs on our body are in anagen phase or growing phase, which lasts anywhere from two to five years. This phase is followed by a short regression phase, or catagen, which lasts 2-3 weeks. Approximately 1% of hair follicles are in catagen. Approximately 10-15% of hair follicles are in the resting phase, the telogen, which lasts about 3-5 months. Hair follicles typically goes through 10-20 asynchronous cycles during the lifetime. Persistent loss of more than 150 hairs would consist a state of hair loss, or alopecia, albeit it could be temporary.

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