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Biomedical subjects

M Ashraf

Publications and source records attributed to M Ashraf.

At least 145 records · Page 8Linked to original sources
PubMed1984

Ectopic decidual cell reaction in para-aortic and pelvic lymph nodes in the presence of cervical squamous cell carcinoma during pregnancy.

Bilateral para-aortic lymphadenectomy is routine prior to radical surgery in cancer of the cervix. A pregnant patient with invasive cancer of the cervix and ectopic decidual cell reaction in para-aortic and pelvic nodes is presented. A decidual cell reaction in frozen sections of para-aortic lymph nodes could be confused with metastatic disease. Pathogenesis of ectopic decidual cell reaction is discussed.

Adult↗
PubMed1984

Heterogeneity of cell response to early anoxia and reoxygenation in rat heart.

Heterogeneous cell injury and increased tissue calcium levels were observed in the isolated rat hearts perfused with anoxic medium for 5, 10, 15, 20, 25 and 30 min. These changes were intensified after reoxygenation of the anoxic hearts. The cell injury was quantitated using a score of 0, 1, 2 or 3 (0 being normal and 3 being severe injury). All four classes of cells were present even after 5 min of anoxia. The injury and calcium content increased with increase in duration of anoxia. Reduction in the percentage of injured cells was observed on reoxygenation of hearts perfused with anoxic medium for 5 to 20 min. However, reoxygenation of hearts initially perfused with anoxic medium for 25 to 30 min resulted in a higher percentage of injured myocytes. Beneficial effects of reoxygenation were observed in the anoxic hearts when the percentage of cells with an injury score of 1 and glycogen deposit were high, coupled with low calcium levels.

Animals↗
PubMed1984

Cardiac injury in short duration anoxia and modification by diltiazem, a calcium channel blocking agent.

The protective effects of diltiazem were studied in isolated perfused rat hearts after 10, 20 and 30 minutes of anoxia and 10 minutes of reoxygenation. The hearts were treated with diltiazem, 4 mg/liter, during anoxia and reoxygenation. The myocardial tissue was processed for electron microscopy and tissue calcium was measured. Four types of cell injury ranging from normal to severe were observed. The prominent morphologic changes in the nondiltiazem-treated tissue were contraction bands, distortion and calcification of mitochondria and loss of glycogen. In the treated group, a partial reduction of cell injury was noted. The mitochondria were usually well preserved, but contraction bands were present. The tissue calcium decreased after treatment with diltiazem. The observations suggest that diltiazem decreases tissue calcium and protects mitochondria more than other cellular components against calcium overload, and this protection may be responsible for the beneficial action of this drug.

Animals↗
PubMed1984

Effects of diltiazem, a calcium channel inhibitor, in retarding cellular damage produced during early myocardial ischemia in pigs: a morphometric and ultrastructural analysis.

A protective effect of intravenous diltiazem pretreatment on transmural histologic damage in ischemic hearts of 30 pigs was determined morphometrically. The pig hearts were rendered ischemic by ligation of the distal left anterior descending coronary artery for 20, 40 and 120 minutes in separate experiments. Heart rate, left ventricular systolic pressure and systemic diastolic pressure decreased slightly during 40 minutes of occlusion, and then recovered to control levels. However, there were no significant differences between control and diltiazem-treated groups. Blood flow, measured by the microsphere technique, was uniformly absent in the ischemic areas in both control and diltiazem-treated hearts. In the few cell layers immediately beneath the endocardium and epicardium, little cellular damage was observed in either group regardless of the duration of ischemia. In the subendocardial, mid-myocardial and subepicardial layers, less cellular damage was detected after all periods of ischemia in hearts exposed to diltiazem in comparison with that observed in control hearts. However, even in the drug-treated hearts, after 2 hours of occlusion, the cells remained severely injured. The protective effect of diltiazem on the cellular integrity in the ischemic myocardial regions appears to be independent of blood flow and may be a reflection of a direct effect of diltiazem on myocytes. The precise mechanism is unresolved. Nevertheless, in the ischemic heart without a significant collateral circulation, pretreatment with the calcium channel blocking drug, diltiazem, results in a delayed onset of cellular damage after acute coronary artery ligation and less cellular damage at ischemic periods up to 40 minutes' duration.

Animals↗
PubMed1984

Characterization of (Ca2+ + Mg2+) adenosine triphosphatase activity and calcium transport in boar sperm plasma membrane vesicles and their relation to phosphorylation of plasma membrane proteins.

Properties of (Ca2+ + Mg2+) adenosine triphosphatase (ATPase) in plasma membranes from boar epididymal spermatozoa are described. Enzyme activity is optimum at high pH and has a high affinity for Ca2+. It is not inhibited by the calmodulin antagonist trifluoperazine (TFP), but it is inhibited by low concentrations of Ca2+. Plasma membrane vesicles obtained by hypotonic lysis of intact sperm [mixed inside-out (IOV) and right side-out (ROV) vesicles] transport 45Ca2+ in the presence of oxalate. Similar to the Ca2+-stimulated Mg ATPase activity, transport is unaffected by TFP, but unlike the ATPase, transport is at an optimum rate near neutral pH and is completely inhibited by p-chloromercurphenylsulfonate (pCMS). When plasma membranes are labeled in the presence and absence of Ca2+ and Mg2+ with [gamma-32P]ATP, differences in the intensity of labeling and lability of bound 32P to alkali and hydroxylamine suggest that two polypeptides between 100-120K may be related to a transport ATPase. The addition of TFP at concentrations which stimulate net Ca2+ uptake in intact cells causes intense labeling of a single neutrally charged protein near 68K. These labeling patterns and the properties of (Ca2+ + Mg2+) ATPase identify particular plasma membrane proteins (PMPs) from the complex surface of these cells that may be involved in Ca2+-dependent functions and support the view that calmodulin is not directly involved in the regulation of ATP-driven Ca2+ efflux from boar spermatozoa.

Animals↗
PubMed1983

Effect of calmodulin antagonists on CA2+ uptake by boar spermatozoa.

Calcium uptake by washed boar sperm suspensions is markedly stimulated by the calmodulin antagonists trifluoperazine and calmidazolium. Both 45Ca2+ uptake and net Ca2+ uptake are increased by these drugs. Drug stimulated Ca2+ uptake is blocked by verapamil (1 mM), by ruthenium red (25 microM) and by carbonyl cyanide p-trifluoromethoxyphenyl hydrazone. Calmodulin antagonists do not slow ATP-dependent Ca2+ extrusion from plasma membrane vesicles, and they do not inhibit plasma membrane Ca2+-ATPase. It is proposed that calmodulin is involved in the control of Ca2+ entry in boar spermatozoa. Most entering Ca2+ in uncapacitated spermatozoa is sequestered by mitochondria or rapidly extruded by plasma membrane pumps. In contrast to the uptake mechanism, ATP-dependent Ca2+ extrusion does not appear to be regulated by calmodulin.

Animals↗
PubMed1983

Mitochondrial function in canine experimental cardiac hypertrophy.

Concentric left ventricular hypertrophy was produced in puppies by coarctation banding of the aorta at age 7 weeks. Hemodynamic, morphologic and biochemical studies were carried out 18 months after the operation. Systolic blood pressure proximal to the aortic constriction was 216 +/- 16 mmHg in experimental dogs compared with 115 +/- 5 mmHg in littermate control dogs. Ejection fraction of control and experimental dogs were 59 +/- 4 and 64 +/- 7, respectively. The left ventricular end-diastolic pressure was 6.0 +/- 0.4 in control and 8.4 +/- 1.1 in experimental dogs. There was no sign of overt heart failure in the experimental dogs. Anatomical analysis of different regions of the heart indicated that LV mass in the experimental dogs was increased by about 60%. Ultrastructure of mitochondria in situ, as observed under electron microscope, was normal both in control and hypertrophic hearts. Mitochondria isolated from epicardial and endocardial regions of the stable hypertrophic hearts showed normal rates of respiration, phosphorylation, citrate synthase, and cytochrome c oxidase activities compared to those isolated from hearts of littermate control dogs. It was, therefore, concluded that mitochondrial function is adequately preserved to meet the increased demand for energy in this model of stable cardiac hypertrophy of long duration.

Animals↗
PubMed1983

Connective tissue changes in early ischemia of porcine myocardium: an ultrastructural study.

Scanning electron microscopy and transmission electron microscopy were used together with tannic acid and ruthenium-red staining to examine connective tissue damage caused by acute myocardial ischemia for 20, 40 and 120 min in pig hearts. The microsphere blood flow technique revealed that blood flow was approximately 0.02 ml/min/g in inner, middle and outer thirds of the ischemic zone. After 20 min of occlusion of the left anterior descending coronary artery, the collagen network and microfilaments became irregularly arranged. After 40 min of occlusion, ruthenium-red positive glycoprotein material around the collagen fibrils and elastin began to disappear. After 2 h occlusion, the collagen fibrils and microfilaments had separated from the basement membrane. Collagen fibrils, elastic fibers, and microfilaments were broken down and were found in decreased quantities. These results have revealed that the connective tissue remains intact during the first 20 min of coronary occlusion despite zero blood flow and mild cellular changes but does undergo prominent alterations after 40 min of occlusion.

Animals↗
PubMed1983

cis-Platinum-induced hypomagnesemia and peripheral neuropathy.

From January 1980 to September 1981, sixty-nine gynecologic oncology patients received cis-platinum at 4-week intervals. Serum magnesium was drawn prior to cis-platinum administration and then at regular intervals thereafter. cis-Platinum toxicity, especially peripheral neuropathy, was monitored closely. Forty-one patients developed hypomagnesemia; thirty-one of these patients developed signs and symptoms of peripheral neuropathy. None of the sixteen patients with normal serum magnesium levels demonstrated any evidence of neurotoxicity. Peripheral neuropathy was the major dose-limiting factor. Variables related to hypomagnesemia and peripheral neuropathy were analyzed in this patient population. It was concluded that cis-platinum-induced hypomagnesemia, as well as peripheral neuropathy, were dependent on the total dose received by a patient.

Cisplatin↗
PubMed1983

Effects of diltiazem on anoxic injury in the isolated rat heart.

The effect of diltiazem, a calcium channel blocking agent, on anoxic injury was studied in isolated perfused rat hearts. Anoxia for 60 minutes caused a considerable release of creatine kinase and significant cell injury. Reoxygenation of these anoxic hearts for 20 minutes accelerated the creatine kinase release and caused severe cell injury. Reoxygenation of anoxic hearts with diltiazem at a rate of either 2 or 4.5 mg/liter did not reduce creatine kinase release significantly (probability [p] greater than 0.05). However, the higher dosage of diltiazem (4.5 mg/liter during both anoxic and reoxygenation phases resulted in significant (p less than or equal to 0.05) preservation of healthy tissue. The data suggest that diltiazem in the higher concentration prevents cell injury and reduces mitochondrial damage in anoxic injury.

Aerobiosis↗
PubMed1983

Ischaemia-induced changes in canine cardiac sarcoplasmic reticulum.

Effects of myocardial ischaemia on sarcoplasmic reticulum (SR) of dog hearts were investigated. Regional ischaemia was produced by occlusion of the left circumflex artery, and a microsomal fraction enriched in vesicles of SR was isolated from subendocardium (Endo) and subepicardium (Epi) of control and ischaemic areas of the heart. No significant changes occurred in ischaemic Epi. A loss of in vitro activities (ie calcium transport and ATPase) was found for SR from ischaemic Endo which paralleled the changes in the histology of the tissue. At 5 min of coronary occlusion, Ca2+ binding and Ca2+-ATPase activities of SR from ischaemic Endo were normal. A decrease in the activities of SR was first evident at 15 min after the occlusion, decreased further at about 30 min and remained at that level at 60 min of ischaemia. The maximal rate of Ca2+ uptake did not parallel the Ca2+-binding and Ca2+-ATPase activities. The degree of cAMP-dependent phosphorylation by endogenous and exogenous protein kinase was not different between SR from control and ischaemic areas. A participatory role of SR in the ischaemic impairment of left ventricular systolic and diastolic performance is discussed.

Animals↗
PubMed1983

Quantitative variability in requirements for opsonization of strains within the Bacteroides fragilis group.

Requirements for opsonization of various strains within the species Bacteroides fragilis, Bacteroides thetaiotaomicron, Bacteroides vulgatus, and Bacteroides distasonis were investigated. The minimal concentration of normal human serum that facilitated maximal uptake by human peripheral leukocytes of 14C-labeled strains ranged from 5% to 80%. Heated (56 C at 30 min) serum produced less uptake than untreated serum, suggesting that complement was required for opsonization. Using human serum depleted of C4 by immunoadsorption as the source of opsonins, predominant utilization of the alternative complement pathway during opsonization was established. Acidic polyanionic exopolymer on the strains was also assessed by ruthenium red staining, electron microscopy, and India ink wet mounts. Strains of the species B thetaiotaomicron, B vulgatus, and B fragilis possessed exopolymer, and a unique configuration of this material was observed on two strains that resisted opsonization. Utilization of classical and/or alternative complement pathway activity during opsonization was not related to the presence of exopolymer.

Bacteroides fragilis↗
PubMed1982

Differential cardiovascular effects of calcium channel blocking agents: potential mechanisms.

The three major calcium channel blocking agents, diltiazem, nifedipine and verapamil, inhibit calcium entry into excitable cells. Despite this apparent common action at the cell membrane, these drugs produce quantitative and frequently qualitative differences in cardiovascular variables (for example, heart rate, atrioventricular [A-V] conduction and myocardial inotropic state) when evaluated at equieffective vasodilator doses. All three drugs increase coronary blood flow in a dose-dependent fashion (nifedipine greater than diltiazem = verapamil), and produce a negative inotropic effect in vitro in isolated atria and ventricles, also in a dose-dependent manner (verapamil greater than nifedipine greater than diltiazem). However, in conscious dogs nifedipine increases, verapamil decreases and diltiazem has little effect on the inotropic state. A-V conduction is slowed by diltiazem and verapamil but not by nifedipine in anesthetized dogs and in conscious dogs as judged from the P-R interval in the electrocardiogram. Heart rate is slowed in pentobarbital-anesthetized animals but is accelerated in conscious dogs (nifedipine greater than verapamil greater than diltiazem). Nifedipine also appears to interfere significantly with the arterial baroreceptor reflex by an apparent vagolytic action that is less evident with diltiazem and verapamil. Diltiazem, and possibly verapamil and nifedipine as well, appears to retard myocardial damage that accompanies ischemia. The mechanisms and sites of action of these drugs are presumed to be at the cell membrane; however, intracellular sites may also be involved.

Animals↗
PubMed1982

Interaction of discoidal complexes of dimyristoyl phosphatidylcholine-cholesterol-apolipoprotein A-I with human plasma high density lipoprotein HDL3.

The interaction of human plasma high density lipoproteins (HDL3) with discoidal complexes of apolipoprotein A-I (apo A-I) and dimyristoyl phosphatidylcholine (DMPC) containing 0, 10, 20 or 30 mol % cholesterol was investigated. Discoidal complexes containing various amounts of cholesterol were prepared by incubating apo A-I and DMPC-cholesterol liposomes for 12 hr at 25 C; the protein-lipid complexes were isolated by gel filtration chromatography on Bio-Gel A15m. Increasing the cholesterol content from 0 to 30 mol % caused a decrease in the fluidity of the discoidal complexes as determined by fluorescence polarization with 1,6-diphenyl-1,3,5-hexatriene; a reduced phase-transition amplitude; a decrease in the ratio of apo A-I to DMPC; and an increase in the width of the discoidal complexes as determined by electron microscopy after negative staining. Incubation of the apo A-I-lipid complexes with HDL3 resulted in a complete breakdown of the discoidal structures and a transfer to DMPC and cholesterol to HDL3. As a result of lipid transfer, there was an increase in the size of HDL3. These in vitro results may be of significance as they relate to the interconversion of HDL subfractions during lipoprotein-lipase-induced lipolysis of triglyceride-rich lipoproteins.

Apolipoprotein A-I↗
PubMed1982

Ultrastructural alterations of the mitochondrial ATPase in the calcium paradox as revealed by negative staining.

We have used a simple negative staining technique to study the structural alterations of mitochondria from biopsies of hearts subjected to the calcium paradox and treatment with diltiazem, a calcium channel blocker. A significant (P less than 0.05) decrease in the number of spheres on the mitochondrial membranes occurs during the calcium paradox (58.0 +/0 4.1/micrometer vs. control 80.5 +/- 6.5). Treatment with diltiazem prevented the loss of spheres from mitochondrial membranes during the calcium paradox (75.5 +20 5.0 micrometer). We found that this negative staining technique can be used for quick assessment of the condition of mitochondria in biopsies from normal and pathological organs.

Adenosine Triphosphatases↗