Biomedical subjects
Publications and source records attributed to M Anwar.
A modification of a popular North American model surgery technique is described, with a brief comparison with the key-spacer planning system of Lockwood. This technique enables bimaxillary movements to be planned with greater accuracy than with the Lockwood system.
This study evaluated the effect of bilateral carotid chemodenervation on the cerebrovascular response to hypoxia in conscious rats. Cerebral blood flow was measured using 4-iodo[N-methyl-14C]antipyrine, and the total and perfused microvasculature was studied by injection of fluorescein isothiocyanate dextran and alkaline phosphatase staining. To maintain constant PCO2, hypoxia was achieved in chemoreceptor-intact rats by the use of 4% CO2-8% O2-88% N2 and in chemodenervated rats by the administration of 8% O2-92% N2. Blood gas and hemodynamic parameters were similar in the two groups of rats. Chemodenervation had no significant effect on either resting blood flow or the perfused microvasculature during normoxia. A significant increase in cerebral blood flow (from 71 +/- 3 to 138 +/- 9 ml/min/100 g in control and from 91 +/- 5 to 127 +/- 7 ml/min/100 g in chemodenervated rats) and in the percent of cerebral arterioles and capillaries perfused occurred in both hypoxic control and chemodenervated rats. In chemoreceptor-intact rats, the greatest increase in blood flow and in perfused microvasculature occurred in caudal structures (medulla and pons) in comparison with rostral structures (cortex, thalamus, and hypothalamus). In chemodenervated rats, a similar increase in blood flow and perfused microvasculature occurred in all brain regions, with no regional differences. Thus, chemodenervation did not affect the overall cerebral blood flow or the microvascular response to hypoxia; however, rostral-to-caudal regional differences in the hypoxic response were lost after chemodenervation.
HLA frequencies on 1231 subjects from within the country, using methods employed by National Institute of Health, USA is reported. Pakistani population appears to be a mixture of an indigenous population with others particularly Orientals and Negroids. Relationship with Caucasians is not convincing.
A simple static model is described to teach students oral surgical procedures and to enable them to practise the design, incision and suturing of muco-periosteal flaps.
Twenty pregnant women with greater than or equal to 36 weeks gestation and Bishop score of less than or equal to 4 were subjected to either intracervical injection of PGE2 (0.25 mg) every 4 h to ripen the cervix and induce labor (study group n = 10) or injection of only the diluent (control group n = 10). PGE2 cases showed significant increase in Bishop score and were successfully induced. The mean induction-establishment and induction-delivery intervals were 4.3 +/- 0.1 min and 6.07 +/- 1.7 h, respectively. The control group showed no response. PGE2 cervical injection is a safe and effective method for cervical ripening and labor induction.
Sera from 13 pregnant women carrying a fetus with a neural tube defect, and from 13 control women with normal pregnancies at the same stage of gestation were used in the culture of postimplantation rat embryos. Serum from women with normal pregnancies had no adverse effect on rat embryo growth and development. Serum from 10 of the women with affected fetuses had a deleterious effect on the rat embryos as abnormalities of neural tube closure were observed in 28% of the conceptuses compared to only 1.3% of the embryos cultured in control serum.
The effects of adenosine on regional cerebral blood flow and indexes of the total and perfused microvascular bed were studied after 1 h of middle cerebral artery occlusion in the anesthetized rat. Iodo[14C]antipyrine was used to determine cerebral blood flow. Fluorescein isothiocyanate-dextran was used to study the perfused microvasculature, and an alkaline phosphatase stain was used to identify the total bed. Mean arterial blood pressure was significantly reduced by adenosine. Cerebral blood flow increased significantly by 75%, except in the flow-restricted cortex where flow averaged 28 +/- 15 (SD) ml.min-1.100 g-1 in control and 34 +/- 33 ml.min-1.100 g-1 in adenosine-treated animals. No significant regional structural differences were observed within the microvascular beds of the two groups. The percentage of the microvascular volume perfused increased significantly in all brain regions in the adenosine-treated rats, including the flow-restricted cortex. The percent perfused arteriolar volume in the flow-restricted cortex was 30 +/- 12% in control and 95 +/- 3% in adenosine-treated animals. Similar values for the capillary bed were 22 +/- 10% in control and 54 +/- 3% in adenosine-treated rats. These results indicate a maintenance of flow with a reduction in diffusion distances in the flow-restricted cortex after treatment with adenosine.
Previously, we demonstrated immunocytochemically that certain phenylethanolamine N-methyltransferase neurons in the inner nuclear layer of rat retina contain other catecholamine synthesizing enzymes, including tyrosine hydroxylase and aromatic-L-amino acid decarboxylase but not dopamine beta-hydroxylase (DBH), the norepinephrine biosynthetic enzyme. In the present study by using a sensitive radioenzymatic assay for DBH we demonstrated the presence of DBH enzymatic activity in retinal extracts. Immunocytochemical studies, however, failed to demonstrate DBH-immunoreactive perikarya even in animals pretreated with colchicine, an inhibitor of axonal transport. Probably causes for these discrepant findings are discussed.
Catecholaminergic neurons in the ventrolateral medulla (VLM) and nucleus of the solitary tract (NTS) are important because of their presumed roles in autonomic regulation, including the tonic and reflex control of arterial pressure, neuroendocrine functions, and the chemosensitivity associated with the ventral medullary surface. However, little is known about the connections of these neurons in the human brain. As a first step in analyzing the functional biochemical anatomy of catecholamine neurons in the human, we used antisera against tyrosine hydroxylase (TH) and phenylethanolamine N-methyltransferase (PNMT) to localize medullary catecholamine-containing neurons and processes in the VLM and the NTS. Cells staining for TH were located throughout the VLM. Most cells staining for TH and PNMT, which are therefore adrenergic, occurred in an area of the VLM probably corresponding to the rostroventrolateral reticular nucleus. Axons of TH-immunoreactive neurons in the VLM projected (1) dorsally, in a series of parallel transtegmental trajectories, toward the dorsomedial reticular formation, the NTS, and vagal motor nucleus, (2) longitudinally, through the central tegmental field, as fascicles running parallel to the neuraxis, (3) ventrolaterally toward the ventral surface (VS) of the rostral VLM where they appeared to terminate, and (4) medially into the raphe, where they arborized. Similar systems of fibers were labeled for PNMT; the longitudinal bundles of PNMT-labeled axons were limited to the principal tegmental bundle and concentrated dorsally. Fibers containing PNMT were also identified in the medullary raphe, on the medullary ventral surface, and contacting intraparenchymal blood vessels. In the NTS, neurons exhibited immunoreactivity to both TH and PNMT: Four principal subgroups of TH-immunoreactive neurons were seen: a ventral, an intermediate, a medial, and a dorsal group. Perikarya containing PNMT were restricted to the dorsolateral aspect of the NTS. Processes containing TH and PNMT immunoreactivity were identified in the medial and dorsolateral NTS; others appeared to project between the NTS and the VLM and within the solitary tract. The presence of catecholaminergic fibers of the VLM interconnecting with the NTS, raphe, intraparenchymal microvessels, VS, and possibly the spinal cord suggests that the autonomic and chemoreceptor functions attributed to these neurons also may apply to the human.
SKF 64139, a specific inhibitor of the epinephrine-synthesizing enzyme, phenylethanolamine N-methyltransferase (PNMT), has been widely used as a pharmacological tool for studying the characteristics of epinephrine-containing neurons. However, the mechanism of action of this drug on PNMT in vivo has not been fully elucidated. In the present study, we traced changes of PNMT activity in rat adrenal glands and medulla oblongata between 1 and 48 hr after intraperitoneal injection of SKF 64139 (50 mg/kg body wt). Within 1 hr, enzyme activity in both tissues decreased to 10% of the respective control value. However, starting at 4 hr, activity gradually recovered from the inhibition and completely returned to the respective control level by 48 hr. Removal of the inhibitor by dialysis substantially restored the adrenal enzyme activity in 1, 2 and 4 hr groups and completely returned it to control levels in 18 and 48 hr groups. A similar pattern also seemed to hold with brain extracts. The profiles of immunotitration curves, using dialyzed tissue extracts and specific antibodies to bovine adrenal PNMT, clearly indicate that, even after dialysis, a substantial amount of inactive enzyme was present in tissue extracts from 1, 2 and 4 hr groups. In contrast, by 18 hr a very small amount of inactive enzyme was present. Throughout the experimental periods there was no noticeable differences among the control and the experimental groups in the number or intensity of immunocytochemical stained neurons with PNMT antibodies of the C1 area of ventrolateral medulla. Judging from the data obtained by dialysis, immunochemical titration and immunocytochemical staining, recovery of PNMT activity following its inhibition by SKF 64139 was not due to irreversible inhibition of the enzyme followed by new enzyme synthesis. Instead, reversible binding of inhibitor to PNMT and its release were responsible for recovery. PNMT from the 1, 2 and 4 hr groups resisted further in vitro inhibition by SKF 64139 because the residual inhibitor was probably still bound to the enzyme.
The normal growth of rat embryos cultured in human serum supplemented with glucose and 10% rat serum is of potential use in the assessment of teratogenic risk in man. Before this technique can be widely applied, it is necessary to know whether the stages of the menstrual cycle at which a serum sample is tested materially affect the results obtained. Moreover, in order to achieve reproducible conditions we have found it necessary to add a minimal amount of rat serum to the human serum used for culture, but unnecessarily high levels of rat serum supplementation could over-compensate for any growth factor deficiency in human serum. Here we report that culture of rat conceptuses gives similar results irrespective of whether human first, second, or third trimester pregnancy serum, postnatal serum, or serum at various stages of the menstrual cycle is used. We also report that addition of 2% rat serum supplement is sufficient to achieve reproducible rat embryonic growth and differentiation in human serum.
The regulatory region of the rat preproglucagon gene targets expression of the SV40 large T oncoprotein to two cell types in transgenic mice, the pancreatic alpha cells and a set of neurons localized in the hindbrain, both of which normally produce preproglucagon. Additional neurons in the forebrain and midbrain stain for T antigen but do not express the endogenous glucagon gene. Synthesis of T antigen in endocrine alpha cells results in the heritable development of pancreatic glucagonomas. In brains of transgenic mice from three independent lineages, expression of the hybrid gene begins at embryonic day 12 in neuroblasts of the hindbrain, where it continues throughout adult life, most notably in the medulla. Remarkably, oncoprotein expression in both proliferating neuroblasts and mature neurons has no apparent consequences, either phenotypic or tumorigenic. Expression of the hybrid glucagon gene in both neurons and islet cells supports a possible interrelationship between these cell types.
The purpose of this study was to evaluate the effects of prazosin, an alpha 1-adrenoceptor antagonist, on morphometric indexes of the total and perfused cerebral microvascular bed 1 hour after middle cerebral artery (MCA) ligation in pentobarbital-anesthetized rats. We hypothesized that this agent would prevent catecholamine-induced vasoconstriction in the ischemic brain. Cerebral blood flow (CBF) was determined with 14C-iodoantipyrine, and the perfused microvascular bed was visualized using fluorescein isothiocyanate-dextran. MCA occlusion did not alter systemic hemodynamic or blood gas parameters. CBF averaged 29 +/- 15 (mean +/- SD) ml/min/100 g in the MCA-ligated cortex and 49 +/- 18 in the other examined brain regions. Prazosin did not significantly alter these CBF values, averaging 26 +/- 14 and 48 +/- 10, respectively. There were no significant regional differences in total capillaries/mm2 in either group. The percent of the capillaries/mm2 perfused (51 +/- 6%) was similar in the two groups in all examined regions except the ischemic cortex. In the MCA-ligated cortex, 22 +/- 8% of the capillary volume was perfused in comparison with 49 +/- 8% in the prazosin-treated group. Prazosin-treated rats had an increased percentage of their microvasculature perfused despite a similarly reduced CBF. Prazosin appeared to reduce diffusion distances in the ischemic cortex. This might be due to its alpha 1-adrenoceptor blocking activity.
To ascertain the regional cerebral blood flow (CBF) responses to hypoglycemia, nine newborn dogs were treated with insulin to blood glucose concentrations ranging from 1 to 35 mg/dl (mean 22 mg/dl). Systemic physiologic monitoring revealed no differences in mean arterial blood pressure, heart rate, paO2, paCO2, pHa, or blood lactate in the hypoglycemis animals and five normoglycemic controls. Significant increases in CBF occurred in 17 of 20 analyzed structures of brain in the hypoglycemic puppies, ranging from 158 to 446% of the normoglyycemic values. The percent increases in CBF were greatest in brainstem structures compared to other major regions of brain. A positive correlation existed between mean arterial blood pressure and cerebral cortical blood flow, suggesting a loss of CBF autoregulation during hypoglycemia. The pathophysiologic mechanism for the elevations in regional CBF might relate to stimulation of beta-adrenergic receptors in brain, as has been shown in adults.
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We sought to determine whether the insular cortex contributes to the regulation of arterial blood pressure (AP). Responses to electrical and chemical stimulation of the cortex were studied in the anesthetized, paralyzed, and artificially ventilated Sprague-Dawley rat. The insular cortex was initially defined, anatomically, by the distributions of retrogradely labeled perikarya following injections of wheat germ agglutinin-horseradish peroxidase (WGA-HRP) into the nucleus tractus solitarii (NTS). Injections of WGA-HRP into the insular cortex anterogradely labeled terminals in cardiopulmonary and other divisions of the NTS and confirmed projections revealed by retrograde tracing experiments. Electrical stimulation of the insular cortex elicited elevations of AP (less than or equal to 50 mm Hg) and cardioacceleration (less than or equal to 40 bpm). The locations of the most active pressor sites corresponded closely to the locations of retrogradely labeled cells in layer V of granular and posterior agranular areas of the insular cortex (areas 14 and 13) and the extreme capsule. Maximal pressor responses were obtained at a stimulus intensity of three to five times threshold current of 20-30 microA. Responses elicited mostly with higher-threshold currents were also mapped in areas 2a and 5lb and the claustrum and within the corpus callosum. Unilateral injections into the insular pressor area of the excitatory amino acid monosodium glutamate (L-Glu; 0.05 nmol to 10 nmol) or the rigid structural analogue of L-Glu, kainic acid (KA) (0.4 nmol) (which specifically excite perikarya), caused topographically specific elevations in AP and tachycardia. During the course of the anatomical transport studies, new findings were obtained on the organization and characteristics of the cortical innervation of the NTS and the nucleus reticularis parvocellularis. Topographic relationships between the cortex and the NTS were organized in a more complex manner than previously thought. Cells projecting to caudal cardiopulmonary segments of the NTS were fewer and generally located ventrally and caudally and in a more restricted area than cells projecting rostrally or to the parvicellular reticular formation. Anterograde transport data revealed new presumptive terminal fields in dorsolateral, ventral, periventricular, and commissural regions of the NTS, including an area overlapping the terminal field of the aortic baroreceptor nerve. We conclude that neurons within an area of the insular cortex projecting to multiple brainstem autonomic nuclei, including a region of the NTS innervated by baroreceptor afferents, increase arterial blood pressure and heart rate.(ABSTRACT TRUNCATED AT 400 WORDS)
We examined the effect of early phenobarbital therapy on the course of jaundice in 57 infants with birth weight below 1,500 g. The study group of 28 infants was treated with a phenobarbital loading dose of 20 mg/kg at 4.2 (3.6) [mean (SD)] hours of age, followed by a maintenance dose of 5 mg/kg/day for one week; 29 infants served as controls. Seventeen study and 19 control infants suffered from periventricular-intraventricular hemorrhage (IVH). The two groups had comparable risk factors that can potentially affect the course of hyperbilirubinemia. Peak serum bilirubin concentration was 7.9 (1.8) mg/dl in the treated group and 8.6 (2.2) mg/dl in the control group. Three infants in the treated group and seven infants in the control group had peak serum bilirubin concentration above 10 mg/dl. These differences in the peak serum bilirubin concentration or in the number of infants with peak serum bilirubin concentrations above 10 mg/dl are not statistically significant. However, treated infants achieved peak serum bilirubin concentration earlier (mean age 90 hours as compared to 138 hours in control infants), and required phototherapy for a shorter duration of time (5.5 days in the treated group as compared to 7.5 days in the control group). While these differences in the two groups with regard to age of peak serum bilirubin concentration and duration of phototherapy are statistically significant, they do not seem to be clinically important. Thus, in our group of very low birth infants phenobarbital failed to show any clinically important effects on the course of jaundice when used in conjunction with phototherapy.
In this study, the distribution of neurons containing the adrenaline-synthesizing enzyme phenylethanolamine-N-methyltransferase (PNMT) was mapped in the medulla of the cat. Data from recent studies in the rat suggest that the anatomical structure responsible for cardiorespiratory changes that occur following application of neurotransmitters and drugs to Schlaefke's area on the ventral medullary surface is the nucleus reticularis rostroventrolateralis (RVL), which is distinguished from adjacent regions of the reticular formation, in part, by the presence of adrenaline-synthesizing neurons. To determine whether an equivalent adrenergic population is present in the RVL of the cat, we used antibodies raised against bovine adrenal PNMT to map the distribution of adrenaline-synthesizing neurons in the reticular formation. In the ventrolateral medulla, we found that labeled cells extended from the level of the retrofacial nucleus to the calamus scriptorius. The majority of labeled cells were seen in a nucleus designated RVL at the level of the rostral one-third of the inferior olive. In the dorsomedial medulla, cells were labeled in the caudal aspect of the nucleus tractus solitarii (NTS) and were especially dense in the subnucleus gelatinosus and commissural nucleus of the vagus. A few lightly labeled cells were also present in the rostral pole of the area postrema (AP). In contrast to the rat, few or no immunoreactive cells were found in the rostral NTS, medial longitudinal fasciculus, nucleus paragigantocellularis dorsalis, or periventricular gray. Our results are consistent with the notion that an area of the RVL containing adrenergic perikarya is the anatomical structure responsible for cardiovascular changes that occur when chemicals are applied to Schlaefke's area.