Conflicting results have been reported regarding the role of carbohydrate on human immunodeficiency virus (HIV) envelope glycoprotein gpl20 in CD4 receptor binding. Glycosylated, deglycosylated, and nonglycosylated forms of HIV type 1 (HIV-1) and HIV-2 gpl20s were used to examine CD4 receptor-binding activity. Nonglycosylated forms of gpl20 generated either by deletion of the signal sequence of HIV-1 gpl20 or by synthesis in the presence of tunicamycin failed to bind to CD4. In contrast, highly mannosylated gpl20 bound to soluble CD4 molecules well. Enzymatic removal of carbohydrate chains from glycosylated gpl20 by endoglycosidase H or an endoglycosidase F/N glycanase mixture had no effect on the ability of gpl20 to bind CD4. An experiment which measured the ability of gpl20 to bind to CD4 as an assay of the proper conformation of gpl20 showed that carbohydrate chains on gpl20 are not required for the interaction between gpl20 and CD4 but that N-linked glycosylation is essential for generation of the proper conformation of gpl20 to provide a CD4-binding site.

The effects of intravenous ketamine (1 mg/kg) on cerebral cortical blood flow and O 2 uptake were evaluated in 13 anesthetized, ventilated rabbits. Blood flow was measured either directly (Group 1) or by the H 2 clearance method (Group 2). In those animals of Groups 1 and 2 with normal control arterial pH (pHa), ketamine produced a significant increase in cerebral cortical blood flow of 18 and 34%, respectively, but had no effect on cerebral cortical O 3 uptake. However, in rabbits with low control pHa, ketamine caused an increase in blood flow (30%) accompanied by a significant increase in O 3 uptake (22%). Ketamine produced nonsignificant changes in mean arterial blood pressure and arterial blood gases, except for a significant reduction in pressure in animals with low pHa. It is concluded that ketamine is a cerebral vasodilator without cerebral metabolic effect when mean arterial blood pressure and arterial Pcoj, Poj, and pH are held constant at physiologic levels. The vasodilator effect of ketamine is probably due to direct dilating action or activation of a cholinergic cerebral vasodilator system. (Stroke 1987;18:441-444)A FTER the introduction of ketamine as an anes-/ \ thetic agent in 1966, many studies were con-A. X . ducted on experimental animals and humans to characterize the effect of this agent on cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMROj The wide difference in results reported in those publications, previously discussed by Schwedler et al,4 prompted the present study. We were interested in evaluating the possible cerebral metabolic effect of ketamine in a rabbit preparation to elucidate the role of a cholinergic cerebral vasodilator mechanism activated by ketamine recently proposed by Reicher et al 9 to explain their findings. Materials and MethodsThirteen male New Zealand rabbits weighing 2.7-3.5 kg were anesthetized with 6% halothane added to O 2 and room air. After tracheostomy, anesthesia was maintained via a tracheal tube with 0.5% halothane in Received May 29, 1985; accepted October 20, 1986. O 2 and room air until all surgical procedures were finished. Halothane was then discontinued, and the animals were maintained under 50% N 2 O-50% O 2 for at least 1 hour before the beginning of CBF and O 2 consumption measurements. Pancuronium bromide (Pavulon, Organon) at 0.2 mg/kg/hr was given to ensure muscle paralysis. Mechanical ventilation with a T-system was adjusted to maintain end-tidal CO 2 (ETCOj) at 3.5-4% monitored with a Beckman LB-2 analyzer. The femoral artery and vein were cannulated for blood pressure measurement, blood sampling, and drug administration. Two screw electrodes were placed in the left parietal region for continuous recording of the electroencephalogram (EEG). Rectal temperature was continuously monitored and maintained at 38.5-39.0° C by radiant heating or ice-water cooling of the animal. Arterial pressure, ETCO 2 , EEG, and hydrogen (HJ clearance were recorded on a Grass Model 7 polygraph. Arterial blood samples (0.5-0.8 ml) were collecte...

The use of high-dose lidocaine for cerebral protection during ischemia has produced varied results. Our study uses a new, single carotid artery preparation in the rabbit to produce incomplete global ischemia by graded carotid occlusion; specific electroencephalographic changes are used as the end point for the extent of blood flow reduction sustained during 20 minutes. We monitored arterial pressure, intracranial pressure, and internal carotid blood flow that were recorded with an electromagnetic flowmeter after surgical ligation of the opposite internal and the two vertebral arteries, and we studied the electroencephalogram and somatosensory-evoked potentials elicited by stimulation of the sciatic nerve. Low-dose lidocaine (0.2 mg/kg/min) infused throughout the experiment significantly accelerated the time course of the return of electroencephalographic and evoked-potential amplitudes toward control. Deep halothane anesthesia alone elicited the slowest recovery, suggesting that the action of lidocaine was independent of its general anesthetic effect There were very small differences among the groups in the measured arterial pressure, intracranial pressure, and cerebral blood flow, suggesting that lidocaine changed recovery rate without markedly modifying any characteristic of the postischemic cerebral perfusion. The protective effect of lidocaine may be the result of a specific blockade of Na + channels or a decrease in excitatory neurotransmitter release, either of which would cause a delay in the onset of the events that lead to neuronal damage during ischemia. (Stroke 1990;21:929-935)

Sharm Obhur is a coastal creek located about 35 km north of Jeddah City and is an attractive recreational area. Urbanization of its coasts is progressively increasing since the eighties. This manuscript aims at the assessment of the impact of human activities on the natural environment of the Sharm through: 1) observation of the morphological changes of its shore using available aerial and satellite images, 2) carrying out an underwater survey to record the present status of the bottom, 3) using geochemical indicators to assess the possible changes in sediment properties. The present study indicates that the Sharm has suffered considerable changes since the eighties. Between 1986 and 2000 the area of the Sharm has been decreased by about 800,000 m 2 , which represents an average annual loss of about 60,000 m 2 due to filling processes. This loss is actually a loss of coral reef ecosystem and its particular habitat. Physical and chemical characteristics of sediments appear to be altered compared with previous observations. Underwater photography showed that the bottom is densely covered with litter composed mainly of plastic bottles, cans and tyres, witnessing the absence of sufficient environmental awareness. To stop or slow the degradation of the area, the following measures are suggested: 1) enforcement of legislation related to management of coastal and marine areas, 2) carrying out studies and programs of coral reefs rehabilitation, 3) enforcement of public awareness activities for coral reef conservation, 4) effective control of dredging and filling, and 5) upgrading of wastewater collection and treatment.

The serological prevalence of coxsackie virus in myocarditis, pericarditis and myopericarditis is largely unknown in our population. The implications of coxsackie virus as causative agent in myopericarditis has not been studied so far in our population. AIMS AND OBJECTIVESThe aims and objectives of this study were to study the serological prevalence of Coxsackie virus in acute pericarditis and myocarditis in a Tertiary Centre and to study the clinical profile of Coxsackie myopericarditis. MATERIAL AND METHODSOur study was a prospective study done from November 2010 -October 2012, the samples were taken from 40 patients with the diagnosed cases of myocarditis, pericarditis and myopericarditis. Myocarditis and pericarditis were diagnosed as per standard guidelines, Enzyme Immunoassay (ELISA) for the determination of IgM antibodies to Coxsackie virus B (CoxB) in human acute and convalescent sera was done. RESULTSOur study comprised of forty patients with mean age of 35.3 years with M:F ratio of 1.35. Among the 40 patients 11 patients were diagnosed with pericarditis (27.50%), 14 with myocarditis (35.00%) and 15 patients with myopericarditis (37.50%). Among the 40 studied patients, 15 were positive for Coxsackie serology. Among the serology positive patients, 6 had diagnosis of myopericarditis (40.00%), 6 had diagnosis of myocarditis (40.00%) and 3 had diagnosis of pericarditis (20.00%). The clinical features of coxsackie positive and negative individuals did not differ significantly; breathlessness (93% vs 76%), chest pain (73% vs 76%), fever (60% vs 60%), cough (46 vs 32%), CCF (53 vs 48%) respectively. Ejection fraction less than 45% was seen in 40% of positive vs 32% of serology negative patients. CONCLUSIONCoxsackie virus as an aetiological factor was found in about one-third of cases of acute myopericarditis. However, the clinical presentation and echocardiographic characteristics did not differ from Coxsackie negative myopericarditis.