Biomedical subjects
H M Assaf
Publications and source records attributed to H M Assaf.
Coma-induced epidermal necrolysis.
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Intracranial epidural tuberculoma presenting as a scalp swelling.
The first case of an intracranial epidural tuberculoma with the absence of dural and brain involvement in a 27-year-old woman is presented. The possible pathogenesis of this unique lesion is discussed.
Pulmonary alveolar microlithiasis in a Saudi child and two cousins.
Pulmonary alveolar microlithiasis is a rare disease and only 32 cases have been reported in children under 12 years of age. The first report on Saudi children with this disorder and on affected cousins is presented, supporting the possible hypothesis of it being an autosomal recessive disorder. The importance of differentiating it from other conditions, particularly pulmonary tuberculosis, and the current approach to diagnosis and management are discussed.
[Effect of metabolic stress on the release of glutamic acid and GABA in the brain tissue of Mongolian hamsters].
The concentrations of glutamic acid and GABA were determined in the brain tissue in gerbils under conditions simulating "metabolic stress", that is ischaemia, aglycaemia and anoxia. The material for the determinations was taken from fragments of the hippocampus incubated under these conditions in artificial cerebrospinal fluid, and the concentrations of these neurotransmitters were determined by histochemical methods in vitro. The release of glutamic acid and GABA into the extracellular space increased with longer duration of the incubation in a linear fashion in all experimental groups and was most pronounced in ischaemia. In case of calcium absence in the extracellular space inhibition was observed of the release of these neurotransmitters which suggested an important role of bivalent cations in the regulation of the studied process, especially under control conditions. During anoxia and ischaemia a considerable part of the release of glutamic acid and GABA seems to be calcium-independent which may suggest presence of additional sources of release of the amino acid neurotransmitters, apart from their release from the direct pool. It is possible that these sources are activated during metabolic stress involving nerve cells.
Aorticopulmonary paraganglioma. A case report with immunohistochemical studies and literature review.
We present a case of nonfunctioning aorticopulmonary paraganglioma in a 41-year-old man. The mediastinal tumor was accidentally discovered on a chest roentgenogram performed for an unrelated minor chest trauma. Complete resection of the tumor was done and followed by postoperative radiotherapy. Two years after surgery, the patient is well and asymptomatic.
Formation of free choline in brain tissue during in vitro energy deprivation.
Free choline and ATP contents were measured in Mongolian gerbil hippocampal slices (tissue) and incubation media (media) during exposure to 30 min of aglycemia, high potassium, anoxia, or ischemia. Changes in choline levels reflected the degree of energy reduction, lower ATP levels being associated with high choline (4-fold increase during exposure to high potassium and anoxia, and 11-fold increase during ischemia). Media (extracellular) choline was particularly affected and increased about twofold during relatively mild energy depletion (e.g., aglycemia), but tissue choline content was less sensitive to energy reduction. A plot of choline vs. ATP levels indicated a nonlinear correlation, and the sharp increase in choline occurred when ATP values fell to about 2.5 nmol/mg of protein. Inhibition of acetylcholine sterase by 10 microM physostigmine during ischemia did not prevent an increase in choline contents but rather enhanced them, indicating that acetylcholine hydrolysis was not the source of free choline. Formation of free choline was Ca2+ independent. These findings suggest the involvement of phospholipase D and phosphatidylcholine hydrolysis in free choline formation during energy stress. The extent of choline formation may be an indicator of the degree of membranal damage, which in turn reflects damage to the metabolic machinery of the cell.
Lactate compartmentation in hippocampal slices: evidence for a transporter.
Lactic acid accumulation has been implicated in the evolution of brain damage after ischemia. Since compartmentation of lactate may play a role in acid-base balance, lactate release from gerbil hippocampal slices was examined during a number of metabolic stresses including elevated [K+]e, ischemia, anoxia, and aglycemia. Slices were preincubated for 1 hr in artificial cerebrospinal fluid (ACSF) equilibrated with 95% O2/5% CO2 (pH 7.4 at 37 degrees C) and then transferred to tubes containing 300 microliters of test medium. The rate of lactate release in control slices was 9.64 nmol/min/mg protein and increased 2.6- and 3.2-fold in the presence of 60 mM potassium and anoxia, whereas the rate of lactate release was decreased by 50 and 25% during ischemia and aglycemia. Lactate release was temperature dependent and was only minimally influenced by removing Ca2+ or by adding 5 mM d-lactate to the ACSF. In contrast, pyruvate inhibited lactate release with an apparent Ki of 2.4 mM. The results suggest that lactate can be released from cells via a saturable and stereospecific lactate transporter with an apparent Km of 10.7 mM and Vmax of 43.7 nmol/mg protein/min. Such a relatively high-capacity transporter system can rapidly equilibrate brain lactate but is probably not involved in regulating intracellular acid-base balance.
T cell malignancy in Richter's syndrome presenting as hyper IgM. Induction and characterization of a novel CD3+, CD4-, CD8+ T cell subset from phytohemagglutinin-stimulated patient's CD3+, CD4+, CD8+ leukemic T cells.
A patient is described, having Richter's syndrome and immunodeficiency with hyper IgM, who developed suppressor T cell lymphoma (CD3+, CD4-, CD8+) following untreated helper-suppressor T cell chronic lymphocytic leukemia (CD3+, CD4+, CD8+). The neoplastic T cells in both malignancies expressed interleukin (IL) 2 receptors but were deficient in typical CD2+ and CD5+ pan T antigens. Additionally, a large percentage of malignant lymph node T cells expressed HLA-DR+ activation antigens. In vitro immunoglobulin-production experiments demonstrated that the patient's leukemic blood T cells had an excess helper function for IgM synthesis but a suppressor function for IgG and IgA synthesis by normal B and T cells. The leukemic blood T cells demonstrated a poor response to phytohemagglutinin (PHA). A defect in IL 2 receptor expression was evident in PHA-stimulated leukemic blood T cells. Of interest was the observation that PHA stimulated the induction of a novel CD3+, CD4-, CD8+ T cell subset from patient's CD3+, CD4+, CD8+ leukemic blood T cells. These PHA-induced CD3+, CD4-, CD8+ T cell subsets produced an elevated proliferative response to PHA and concanavalin A, had a helper cell function for IgM synthesis and produced highly elevated amounts of IL 2.
A role for gamma-aminobutyric acid (GABA) in the evolution of delayed neuronal death following ischemia.
A series of putative neuroprotective agents was tested to determine their efficacy in preventing the loss of the CA 1 neurons of the hippocampus at 4 days following 5 min of bilateral ischemia in the gerbil. Agents associated with the GABAergic system were determined to be the most effective, but only when given prior to the ischemic episode, suggesting that there was a gamma-aminobutyric acid (GABA)-related event during ischemia which triggers the delayed neuronal death of these cells. In this report, the unidirectional release of GABA and glutamate from gerbil hippocampal slices was determined under conditions mimicking anoxia and/or ischemia. Pentobarbital, the most effective of the GABAergic agents, had little or no effect on the time-dependent release of glutamate. In contrast, pentobarbital reduced in release of GABA in both anoxia and ischemia, but only after 25 to 30 min of incubation.