Biomedical subjects

I Chaudhry

Publications and source records attributed to I Chaudhry.

11 recordsLinked to original sources

PubMed2005

Towards consensus in the long-term management of relapse prevention in schizophrenia.

APPROACH TO DEVELOPING GUIDANCE: When developing guidance for the long-term management of schizophrenia, one approach is to adopt a proactive strategy that sets out clear treatment goals and strategies. This should involve a broad view being taken, embracing overall mental and physical well-being rather than simply the absence of illness. Although relapse prevention is an important goal of any long-term management strategy, there are other aspects that need to be considered, such as reintegration into society, regaining independence and quality of life. CURRENT TREATMENT: To help achieve these goals, a range of interventions can be incorporated into long-term management strategies for schizophrenia, including pharmacological interventions, psychosocial therapies and alliance-building initiatives. The current UK National Institute for Clinical Excellence guidelines already recommend that continuous therapy should be practised using an atypical (second-generation) antipsychotic drug, whenever possible, in preference to older typical drugs. The launch of the first long-acting atypical antipsychotic is an interesting new advance that may benefit many patients with schizophrenia. Psychosocial interventions, particularly family-based therapies, as well as cognitive behavioural and compliance therapies, when used alongside antipsychotics, have been shown to reduce relapse rates dramatically and to assist in social reintegration. In addition, forging collaborative alliances with patients and their carers can help to demystify schizophrenia and empower patients to take responsibility for their illness. CONSENSUS STATEMENT: This article outlines a consensus reached by a panel of leading UK healthcare professionals working with schizophrenia brought together to discuss long-term management strategies.

Antipsychotic Agents↗

PubMed2003

Chronic O2 exposure in the newborn rat results in decreased pulmonary arterial nitric oxide release and altered smooth muscle response to isoprostane.

Chronic oxygen exposure in the newborn rat results in lung isoprostane formation, which may contribute to the pulmonary hypertension evident in this animal model. The purpose of this study was to investigate the pulmonary arterial smooth muscle responses to 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2a)) in newborn rats exposed to 60% O2 for 14 days. Because, in the adult rat, 8-iso-PGF(2alpha) may have a relaxant effect, mediated by nitric oxide (NO), we also sought to evaluate the pulmonary arterial NO synthase (NOS) protein content and NO release in the newborn exposed to chronic hyperoxia. Compared with air-exposed control animals, 8-iso-PGF(2a) induced a significantly greater force (P < 0.01) and reduced (P < 0.01) relaxation of precontracted pulmonary arteries in the 60% O2-treated animals. These changes were reproduced in control pulmonary arteries by NOS blockade by using NG-nitro-L-arginine methyl ester. Pulmonary arterial endothelial NOS was unaltered, but the inducible NOS protein content was significantly decreased (P < 0.01) in the experimental group. Pulmonary (P < 0.05) and aortic (P < 0.01) tissue ex vivo NO accumulation was significantly reduced in the 60% O2-treated animals. We speculate that impaired pulmonary vascular tissue NO metabolism after chronic O2 exposure potentiates 8-iso-PGF(2alpha)-induced vasoconstriction in the newborn rat, thus contributing to pulmonary hypertension.

Animals↗

PubMed1998

Uric acid, a natural scavenger of peroxynitrite, in experimental allergic encephalomyelitis and multiple sclerosis.

Uric acid, the naturally occurring product of purine metabolism, is a strong peroxynitrite scavenger, as demonstrated by the capacity to bind peroxynitrite but not nitric oxide (NO) produced by lipopolysaccharide-stimulated cells of a mouse monocyte line. In this study, we used uric acid to treat experimental allergic encephalomyelitis (EAE) in the PLSJL strain of mice, which develop a chronic form of the disease with remissions and exacerbations. Uric acid administration was found to have strong therapeutic effects in a dose-dependent fashion. A regimen of four daily doses of 500 mg/kg uric acid was required to promote long-term survival regardless of whether treatment was initiated before or after the clinical symptoms of EAE had appeared. The requirement for multiple doses is likely to be caused by the rapid clearance of uric acid in mice which, unlike humans, metabolize uric acid a step further to allantoin. Uric acid treatment also was found to diminish clinical signs of a disease resembling EAE in interferon-gamma receptor knockout mice. A possible association between multiple sclerosis (MS), the disease on which EAE is modeled, and uric acid is supported by the finding that patients with MS have significantly lower levels of serum uric acid than controls. In addition, statistical evaluation of more than 20 million patient records for the incidence of MS and gout (hyperuricemic) revealed that the two diseases are almost mutually exclusive, raising the possibility that hyperuricemia may protect against MS.

Animals↗

PubMed1996

Recognizing glaucoma. A guide for the primary care physician. .

Glaucoma is a group of diseases leading to characteristic cupping and damage of the optic nerve head associated with progressive visual loss. The exact mechanism of damage is unknown, but current research is pointing toward a multifactorial disease process, in which elevated intraocular pressure is just one of the factors. Early detection and proper management are imperative because of the disease's prevalence, progressive and often insidious nature, and significant associated morbidity.

Acute Disease↗

PubMed1996

The management of stab wounds to the chest: sixteen years' experience.

In a retrospective review of 16 years of admissions to a regional cardiothoracic unit, 76 patients were admitted with stab wounds to the chest. Of these wounds, 75% were managed conservatively with tube drainage and observation and 25% required surgical intervention. 5.2% were managed as emergency room thoracotomies, 15.8% as urgent procedures in the operating theatre and 4% as late procedures. The total mortality was 1.3% and was seen in the emergency room thoracotomy group (mortality 25%). The risk if sub-diaphragmatic injury in the presence of chest injury is highlighted.

Adolescent↗

PubMed1995

Results of pneumonectomy for cancer in patients with limited ventilatory function.

It is well established that patients with compromised pulmonary function have a greater incidence of morbidity and mortality following lung resection. The prognosis of 36 (9.7%) patients with poor respiratory function (forced expiratory volume in ls (FEV1) and FEV1/FVC (forced vital capacity) ratio were equal to or less than 50% of the predicted value) of a total of 369 patients who underwent pneumonectomy due to non-small cell lung carcinoma over 10 years were reviewed. All but three patients were male with a median age of 62.5 years. Right pneumonectomy was carried out in 12 (33%) and left in 24 (67%) patients. Median FEV1 and FEV1/FVC were 1.51 (46%) and 46.5% respectively. Three (8%) patients died within 30 days of surgery. The postoperative complication rate in patients with poor respiratory function was 44%. Nine (27%) of the hospital survivors died due to non-malignant causes (recurrent chest infection/respiratory failure) and 12 (36%) due to recurrent tumour. The cause of death in one patient was second primary lung tumour and it was unknown in three (9%) patients. Eight (24%) long-term surviving patients did not have severe respiratory symptoms; their FEV1 and FEV1/FVC were remeasured and revealed a median 1.05 l (38%) and 50%, respectively of the predicted value. Actuarial 5-year survival was 29%. Poor respiratory function is associated with postoperative complications and non-malignant deaths arising secondary to respiratory failure. The survival profile demonstrates that patients were successfully treated with pneumonectomy and suggests that surgery should not be withheld from those with limited lung function if detailed investigations predict adequate residual lung function.

Aged↗

PubMed1990

Temperature dependence of rat diaphragm muscle contractility and fatigue.

The diaphragm is a skeletal muscle of mixed fiber type that is unique in its requirement to maintain contractile function and fatigue resistance across a wide range of temperatures to sustain alveolar ventilation under conditions of hypo- or hyperthermia. The direct effect of temperature (15-41 degrees C) on rat diaphragm isometric contractility and fatigue was determined in vitro. As temperature decreased from 37 to 15 degrees C, contraction and relaxation times increased, and there was a left shift of the diaphragm's force-frequency curve, with decreased contractility at 41 and 15 degrees C. Fatigue was induced by 10 min of stimulation with 30 trains/min of 5 Hz at a train duration of 900 ms. Compared with 37 degrees C, fatigue resistance was enhanced at 25 degrees C, but no difference in fatigue indexes was evident at extreme hypothermia (15 degrees C) or hyperthermia (41 degrees C). Only when the fatigue program was adjusted to account for hypothermia-induced increases in tension-time indexes was fatigue resistance evident at 15 degrees C. These findings indicate that despite the diaphragm's unique location as a core structure, necessitating exposure to in vivo temperatures higher than found in limb muscle, the temperature dependence of rat diaphragm muscle contractility and fatigue is similar to that reported for limb muscle of mixed fiber type.

Animals↗

PubMed1988

The effect of digoxin on contractility and fatigue of isolated guinea pig and rat hemidiaphragms.

Digoxin could improve diaphragm contractility and fatigability if inhibition of sodium-potassium adenosine triphosphatase enhances calcium influx from extracellular sources, or it could impair contractility and worsen fatigue if it impairs maintenance of the membrane potential. We studied the effects of digoxin on isometric force production, fatigue, and recovery in isolated, directly stimulated, guinea pig and rat diaphragms. Digoxin had no effect on maximal twitch or tetanic tensions compared with control diaphragms in either rat (2 ng/ml to 20 micrograms/ml) or guinea pig (2 ng/ml to 2 micrograms/ml) hemidiaphragms. Digoxin worsened high frequency fatigue and impaired recovery from fatigue in guinea pigs (200 ng/ml to 2 micrograms/ml) but not in rat (2 micrograms/ml) hemidiaphragms. We conclude that digoxin has no effect on diaphragm contractility. Hypopolarization of the membrane potential is the likely cause for the increased fatigability. The difference in responsiveness between species is likely due to insensitivity of rat sodium-potassium adenosine triphosphatase to digoxin.

Aminophylline↗

PubMed1987

Effect of mono- and diaminopyridines on release of [3H]norepinephrine from isolated guinea-pig atrium.

Neurochemical evidence has been obtained that 4-aminopyridine, 3,4-diaminopyridine and 3,3-dimethyl-1-(4-amino-3-pyridyl)urea HBr (LF-14), concentration-dependently enhanced the stimulation-evoked release of [3H]norepinephrine ([3H]NE) from isolated guinea-pig atrium. The effects of aminopyridines, compounds known to inhibit potassium channels, were Ca0-dependent. High pressure liquid chromatography, combined with radiochemical detection, indicated that the increased stimulated release of radioactivity was due to [3H]NE. Since the aminopyridines studied also enhanced the release of [3H]NE from atrium treated with cocaine, a blocker of uptake1, it seems likely that the increased release of NE caused by the aminopyridines is due to the enhanced release of NE from sympathetic axon terminals and not to the inhibition of reuptake. It is probable that the sympathomimetic cardiac effects (positive inotropic and chronotropic effect) of aminopyridines observed in animal experiments is due to the increased release of NE, caused by these compounds.

4-Aminopyridine↗

PubMed1986

Fatigue of isolated rat diaphragm: role of impaired neuromuscular transmission.

We compared the contributions of impaired neuromuscular transmission (transmission fatigue) and impaired muscle contractility (contractile fatigue) to fatigue of the isolated rat diaphragm. To make this comparison, we measured the differences in active tension elicited by direct muscle stimulation and by indirect (phrenic nerve) stimulation before and after fatigue induced by indirect supramaximal stimulation at varying frequencies and durations. Transmission fatigue was observed after all experimental protocols. Although significant contractile fatigue was not demonstrated after brief periods of low-frequency stimulation (6 min, 15 Hz, 25% duty cycle), it was present after longer or higher frequency stimulation. We repeated the direct stimulation in the presence of neuromuscular blockade with 6 microM d-tubocurarine to demonstrate that a reduced response to stimulation of intramuscular branches of the phrenic nerve during direct stimulation was not responsible for the apparent contractile fatigue. Since we found significant decreases in the response to direct stimulation even after neuromuscular blockade, we could verify the presence of contractile fatigue. We conclude that both contractile and transmission fatigue can occur in the isolated rat diaphragm and that transmission fatigue is a much more important factor after brief periods of fatiguing contractions.

Animals↗

PubMed1981

The influence of stimulation parameters on the potency and reversibility of neuromuscular blocking agents.

Voluntary muscle movements in mammalian muscles are initiated by short trains of 16 to 60 Hz impulses (Zierler, 1974). Despite this in most neurophysiological and neuropharmacological studies either single stimuli of 0.1 to 2 Hz or 5 to 10 sec 50 to 500 Hz tetani have been employed. Neither of these two types of stimuli are ideal for the testing of the functional integrity of the motor unit. Stimulation with single impulses, at slow rates, does not reveal incipient pathological or drug induced defects. Recovery of neuromuscular (NM) activity after 5 to 10 sec tetanic stimulation is prolonged and after repeated stimulation of this type the preparations decay rapidly. Stimulation of 0.1 sec trains of 50 Hz impulses applied every 10 to 20 sec eliminate the above disadvantages. This type of stimulation represents adequate challenge for revealing more moderate degrees of functional defects of the myoneural apparatus without causing rapid decay of the in vitro or in vivo preparations. In agreement with this the ED50 of NM blocking agents were found to be significantly lower in both the in vitro phrenic nerve-hemidiaphragm preparation and the in vivo sciatic nervetibialis anterior muscle preparation of rats during stimulation with 0.1 sec trains of 50 Hz impulses, than when single stimuli of 0.1 Hz were used. Recovery of the in vitro preparations after washout or in vivo after discontinuation of the infusion was also slower during stimulation with short trains of tetani. The antagonist potency of anticholinesterases or 4-aminopyridine and maximal recovery after the use of the optimal concentrations of these antagonists was less in the preparations stimulated with short trains of tetani than in those stimulated with single impulses.

Acetylcholine↗