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Biomedical subjects

A S Dhillon

Publications and source records attributed to A S Dhillon.

At least 19 recordsLinked to original sources
PubMed2004

High mortality in egg layers as a result of necrotic enteritis.

A new facility was designed to hold 1.8 million birds in 10 houses; chickens were placed in five of the houses, and the remaining five houses were under construction when this outbreak occurred. An increase in mortality was reported in five houses; however, mortality in house 7 was quite high. Well-fleshed birds were suddenly found dead without a significant drop in egg production. The middle and distal intestines were distended with gas, congested, thin walled, atonic, and bluish or pale in color with sloughed mucosa in some places. Necrotic enteritis was diagnosed as the cause of increased mortality. The ingesta in the crop occasionally contained flies. The 4-wk mortality in house 7 was 6.55% with a loss of 10,898 chickens. The 4-wk mortality rate in the other houses ranged from 0.54% to 1.98%. The houses affected with necrotic enteritis were treated for coccidiosis with amprolium because low numbers of the oocysts were present in the intestinal specimens of some of the chickens. Household bleach was added to the water at a dilution of one part bleach to 1040 parts water to control bacterial contamination. The fly (Musca domestica) population was out of control. Clostridium perfringens was isolated from the alcohol-washed macerated flies caught from houses 4 and 7. Dead flies were often seen in the feed troughs. The chickens may possibly have had C. perfringens infection as a result of consumption of dead flies or their secretions/excretions. The alcohol-washed, macerated, clarified fly extract from the affected houses caused death in 11 inoculated mice and paralysis in one mouse. Similarly, illness and mortality were present in four mice inoculated with clarified intestinal contents. The bacterium isolated on anaerobic culture was identified as C. perfringens by polymerase chain reaction. The disease was brought under control after straw was added and mixed in with the litter. As a result, the litter temperature increased, causing a decrease in the fly population. This study suggests that flies in the poultry houses acted as mechanical transmitters of C. perfringens and that the development of necrotic enteritis was by ingestion of bacteria present in the flies and their secretions/excretions.

Animals↗
PubMed2004

Diagnosis and management of gastro-oesophageal reflux in preterm infants in neonatal intensive care units.

AIM: There is relatively little published information regarding gastro-oesophageal reflux (GOR) in preterm infants, therefore the aim of this study was to elucidate the incidence of GOR and management regimes employed for this condition in major neonatal intensive care units (NICUs). METHODS: A standard questionnaire was sent to consultants in 77 level II (or secondary) and III (or tertiary) NICUs. RESULTS: Seventy-eight percent of consultants responded. Of babies born in these units, 40% were less than 34 wk gestational age and the estimated incidence of GOR in this group was 22%. GOR was diagnosed on a clinical basis alone in 42% of units, 8% used clinical features and/or investigations, and 50% used clinical features plus investigations and/or therapeutic trials. Intra-oesophageal pH monitoring was available in 93% of units but used regularly in only 32% of suspected cases. Common treatment strategies for diagnosed GOR included non-drug options--body positioning (98%) and placement on a slope (96%); and drugs--H2-receptor antagonists (100%), feed thickeners (98%), antacids (96%), prokinetic agents (79%), proton-pump inhibitors (65%) and dopamine-receptor antagonists (53%). However, the frequency with which all of these treatments were used varied widely between units. Surgery was required in only 1% of cases. CONCLUSIONS: GOR is perceived to be a common condition in preterm infants but the lack of published evidence relating to the management of GOR in preterm infants is reflected in the wide variation in diagnostic and treatment strategies used in major NICUs. It is clear that randomized, controlled trials to evaluate appropriate and effective treatments are needed.

Antacids↗
PubMed2003

Massive acute haemolysis in neonates with glucose-6-phosphate dehydrogenase deficiency.

Three neonates with glucose-6-phosphate dehydrogenase (G6PD) deficiency are described. All three patients suffered an episode of massive acute haemolysis, in the absence of blood group incompatibilities, infection, or ingestion of oxidising agents known to trigger haemolysis. One patient died, but the other two survived after an exchange transfusion. This highlights that G6PD deficiency in the neonatal period may present with severe anaemia in association with hyperbilirubinaemia.

Acute Disease↗
PubMed2001

Alcoholic myopathy: biochemical mechanisms.

Between one- and two-thirds of all alcohol abusers have impairment of muscle function that may be accompanied by biochemical lesions and/or the presence of a defined myopathy characterised by selective atrophy of Type II fibres. Perturbations in protein metabolism are central to the effects on muscle and account for the reductions in muscle mass and fibre diameter. Ethanol abuse is also associated with abnormalities in carbohydrate (as well as lipid) metabolism in skeletal muscle. Ethanol-mediated insulin resistance is allied with the inhibitory effects of ethanol on insulin-stimulated carbohydrate metabolism. It acutely impairs insulin-stimulated glucose and lipid metabolism, although it is not known whether it has an analogous effect on insulin-stimulated protein synthesis. In alcoholic cirrhosis, insulin resistance occurs with respect to carbohydrate metabolism, although the actions of insulin to suppress protein degradation and stimulate amino acid uptake are unimpaired. In acute alcohol-dosing studies defective rates of protein synthesis occur, particularly in Type II fibre-predominant muscles. The relative amounts of mRNA-encoding contractile proteins do not appear to be adversely affected by chronic alcohol feeding, although subtle changes in muscle protein isoforms may occur. There are also rapid and sustained reductions in total (largely ribosomal) RNA in chronic studies. Loss of RNA appears to be related to increases in the activities of specific muscle RNases in these long-term studies. However, in acute dosing studies (less than 1 day), the reductions in muscle protein synthesis are not due to overt loss of total RNA. These data implicate a role for translational modifications in the initial stages of the myopathy, although changes in transcription and/or protein degradation may also be superimposed. These events have important implications for whole-body metabolism.

Alcoholism↗
PubMed2001

Cerebellar defect associated with Schimke immuno-osseous dysplasia.

UNLABELLED: We report the finding of an absent cerebellar hemisphere and partial absence of the cerebellar vermis in a child with dysmorphic features, spondyloepiphyseal dysplasia, steroid resistant nephrotic syndrome secondary to focal segmental glomerulosclerosis and T-cell lymphopenia (Schimke immuno-osseous dysplasia). These findings have not, to our knowledge, been described before and are likely to represent the consequence of a vascular event either in-utero or in early infancy. CONCLUSION: Cerebral imaging should be performed early in the course of the disease and should be repeated if further neurological events develop.

Cerebellum↗
PubMed2001

Pathogenicity of environmental origin Salmonellas in specific pathogen-free chicks.

Two hundred sixty 1-d-old specific pathogen-free (SPF), Single Comb White Leghorn chicks were used in this study to determine pathology caused by Salmonella enteritidis (SE) isolated from a poultry environment. The chicks were subdivided into 10 equal groups of 26 chicks each. Eight groups of chicks were inoculated individually with 0.5 mL of brain heart infusion broth culture containing 1 x 10(6) cfu of SE phage type (PT) -8 (1, 2, 3), SE PT5 A (1, 2), or SE PT4 (Ch-env-CA, chicken-CA, and human) by crop gavage. One group of 26 chicks were inoculated with 1 x 10(6) cfu of Salmonella pullorum per bird by crop gavage. Another group of 26 chicks were kept as an uninoculated control group. All the chicks were observed daily for clinical signs and mortality. Salmonella was reisolated from different organs at 7, 14, 21, and 28 postinoculation (DPI). All of the chicks were weighed individually at each interval. Two chicks at random from each group were euthanised and necropsied at each DPI for gross pathology. Selected tissues were examined for histopathological changes at 7 and 14 DPI. Dead chicks were examined for gross and histopathological lesions. Mortality rates were 30.7, 15.3, and 7.6% in the groups inoculated with S. pullorum, SE PT5A, and SE PT4 (chicken-CA), respectively. No mortality or clinical sign were observed in other treatment groups or in uninoculated control groups. Cecal pouches were found to be the ideal organ for reisolation of Salmlonella at acute or chronic infection compared with other organs. Mean body weights were reduced to 1.8 to 12.6% in inoculated groups compared with the uninoculated control group. The consistent gross and hispathological lesions were of peritonitis, perihepatitis, yolk sac infection, and enteritis. Subclinical Salmlonella infection identified in this study resulted in reduced body weights of inoculated birds compared with uninoculated controls.

Animals↗
PubMed2001

Raf kinase inhibitor protein interacts with NF-kappaB-inducing kinase and TAK1 and inhibits NF-kappaB activation.

The Raf kinase inhibitor protein (RKIP) acts as a negative regulator of the mitogen-activated protein (MAP) kinase (MAPK) cascade initiated by Raf-1. RKIP inhibits the phosphorylation of MAP/extracellular signal-regulated kinase 1 (MEK1) by Raf-1 by disrupting the interaction between these two kinases. We show here that RKIP also antagonizes the signal transduction pathways that mediate the activation of the transcription factor nuclear factor kappa B (NF-kappaB) in response to stimulation with tumor necrosis factor alpha (TNF-alpha) or interleukin 1 beta. Modulation of RKIP expression levels affected NF-kappaB signaling independent of the MAPK pathway. Genetic epistasis analysis involving the ectopic expression of kinases acting in the NF-kappaB pathway indicated that RKIP acts upstream of the kinase complex that mediates the phosphorylation and inactivation of the inhibitor of NF-kappaB (IkappaB). In vitro kinase assays showed that RKIP antagonizes the activation of the IkappaB kinase (IKK) activity elicited by TNF-alpha. RKIP physically interacted with four kinases of the NF-kappaB activation pathway, NF-kappaB-inducing kinase, transforming growth factor beta-activated kinase 1, IKKalpha, and IKKbeta. This mode of action bears striking similarities to the interactions of RKIP with Raf-1 and MEK1 in the MAPK pathway. Emerging data from diverse organisms suggest that RKIP and RKIP-related proteins represent a new and evolutionarily highly conserved family of protein kinase regulators. Since the MAPK and NF-kappaB pathways have physiologically distinct roles, the function of RKIP may be, in part, to coordinate the regulation of these pathways.

Androgen-Binding Protein↗
PubMed2000

Rehab rounds: overcoming barriers to individualized psychosocial rehabilitation in an acute treatment unit of a state hospital.

Psychiatric rehabilitation begins during the acute stages of a psychiatric disorder and continues throughout the person's lifetime, with the types of services flexibly keyed to the person's phase of illness, needs, and personal goals. During periods of relapse and exacerbation of symptoms, when hospitalization is often required, psychiatric rehabilitation should include the following five objectives: * Clarify how the person's own goals in life, such as a desire for more self-control, freedom of choice, privacy, and time with friends and family, can be served by inpatient treatment and symptom stabilization. * Educate the patient about the nature of his or her illness and how medications work to restore self-control. * Teach the patient about side effects and self-monitoring and negotiating about medication and its effects in a collaborative way with the psychiatrist and other members of the treatment team. * Connect with the family or other natural supports that the person has in the community. * Enable the patient to make appropriate aftercare plans for residential and continuing treatment needs after discharge. When rehabilitation is viewed from the vantage point of these objectives, the inextricable interweaving of "treatment" with "rehabilitation" becomes clear. Treatment and rehabilitation are two sides of the same. It is much easier to integrate psychiatric rehabilitation into more traditional methods of treatment than it is to reorganize a treatment program or facility so that it blends rehabilitation with prevailing treatment imperatives of pharmacotherapy, supervision, and security and safety. In previous Rehab Rounds columns, we have described examples of creative methods for bringing the principles and practices of psychiatric rehabilitation into the treatment milieu (1,2,3). Faced with regulatory criticism from governmental agencies, Dr. Dhillon and his colleagues at Eastern State Hospital in Williamsburg, Virginia, launched a vigorous initiative to bring psychiatric rehabilitation into the forefront of their clinical enterprise. To enable readers to learn from their successful experience and adapt some of the administrative and clinical procedures that worked in Virginia, Dr. Dhillon and Ms. Dollieslager describe the operational details of their odyssey. We believe that their effectiveness in changing a traditional institution can be duplicated in many other places-in units within general hospitals or other community-based settings-as well as in state psychiatric hospitals, where acute treatment has been limited to pharmacotherapy and recreational and diversional activities.

Acute Disease↗
PubMed1998

Alcohol-related diols cause acute insulin resistance in vivo.

Epidemiological studies suggest that alcohol consumption is an independent risk factor for the development of non-insulin-dependent diabetes mellitus (NIDDM). Alcoholism is known to be associated with increased plasma levels of two novel diols, 2,3-butanediol and 1,2-propanediol, metabolites known to impair insulin action in isolated adipocytes. This study examines whether 2,3-butanediol and 1,2-propanediol have the capacity to impair insulin action acutely in vivo in the rat. Using the euglycemic-hyperinsulinemic clamp, it is shown that the two diols reduce whole-body glucose utilization (by approximately 30%), with the onset of insulin resistance in vivo occurring at plasma concentrations of 2,3-butanediol (33 micromol/L) at least one order of magnitude (P < .001) lower than 1,2-propanediol (432 micromol/L). Tracer methodologies using [U-14C]glucose and 2-deoxy[1-(3)H]glucose indicate that the reduction in whole-body glucose utilization is accompanied by a reduction in glucose uptake and glycogen synthesis in the skeletal muscle and heart. The association between elevated plasma diol levels and insulin resistance demonstrated in this report raises the question of whether there is a link between the high plasma diol levels in alcohol abusers and their increased susceptibility to NIDDM.

Alcoholism↗
PubMed1996

Alcohol and glucose metabolism in skeletal muscles in the rat.

Ethanol is known to cause an acute and profound insulin resistance in man and the rat primarily via effects on glucose utilization. This paper examines the nature of these inhibitory effects on whole-body glucose utilization using the euglycaemic hyperinsulinaemic clamp in the conscious unrestrained rat. We confirm that ethanol infusion causes an acute insulin resistance, the rate of glucose infusion required to maintain euglycaemia (GIR) being decreased markedly by ethanol. To ensure that the GIR is a measure of whole-body glucose disposal, glucose turnover and hepatic glycogen levels were measured. These studies showed that ethanol totally suppressed hepatic glucose production. The reduction in GIR is associated with marked decreases in glucose uptake and glycogen synthesis in most skeletal muscles. In oxidative but not in non-oxidative muscles, the activation of glycogen synthase in response to insulin was decreased by ethanol, suggesting that a defect in glycogen synthase activation may be responsible for the decrease in glycogen synthesis. The basis of the inhibitory effects of ethanol on insulin-stimulated glucose metabolism in muscle is unknown, but may involve membrane-associated impairments in insulin signalling and/or the glucose transport system.

Journal Article↗
PubMed1996

Metabolic effects of alcohol on skeletal muscle.

The purpose of this review is to summarize our current understanding of the acute and chronic interactions between alcohol and nutrient metabolism in skeletal muscle. Insulin is well known to play an important regulatory role in nutrient, especially glucose, uptake and utilization in skeletal muscle. Several studies have shown that alcohol can acutely reduce the normal metabolic responses of skeletal muscle to the action of insulin. The most obvious of these is an acute impairment in glucose metabolism associated with alcohol consumption. While the exact mechanism(s) underlying this acute insulin resistance is presently unclear, several possible factors are discussed in this review. In contrast to these short-term effects, the effects of alcohol on skeletal muscle insulin sensitivity in chronic alcohol abusers are not as well established. Chronic alcohol abuse is known to be associated with skeletal myopathies, believed to result from alcohol induced abnormalities in muscle protein synthesis. Finally, the alcohol-mediated impairments of many aspects of skeletal muscle metabolism are discussed in relation to the insulin resistance associated broad spectrum of common lifestyle-related disorders, including non-insulin dependent diabetes mellitus and obesity, the consequences of which may be important to the pathogenesis of alcohol-related diseases.

Journal Article↗
PubMed1996

Acute ethanol-mediated insulin resistance in the rat: the role of ethanol oxidation.

Ethanol causes an acute and profound insulin resistance in humans and in the rat. Recent studies indicate that defects in skeletal muscle glucose uptake and utilization make a major contribution to this insulin resistance. In this study, we used the euglycaemic hyperinsulinaemic clamp to examine the role that hepatic ethanol oxidation via alcohol dehydrogenase (ADH) plays in the acute insulin resistance caused by ethanol in the rat. Treatment with the ADH inhibitor 4-methylpyrazole (4-MP) failed to abolish the insulin resistance as expressed as a decrease in the rate of glucose infusion required to maintain euglycaemia (GIR). A decrease in GIR was also observed in response to tert-butanol, an alcohol that is not a substrate for hepatic ADH. These results indicate that oxidation via ADH is not a prerequisite for the inhibition by ethanol of whole-body glucose utilization. In a separate study, we examined the relationship between blood ethanol concentration and GIR in order to determine the potency of ethanol in causing insulin resistance. These experiments showed that even at low blood concentrations (<2 mM), ethanol caused a profound decrease in GIR, similar in magnitude to that observed at higher blood concentrations (approximately 40 mM)

Journal Article↗
PubMed1991

Research note: effect of electronic treatment of drinking water on growth performance of broiler chickens.

Three electronic devices used to treat drinking water were compared with untreated city well water in a broiler growth performance trial. In each treatment feed conversion and BW were measured in 16 replicate pens of 60 female broilers at 29, 42, and 49 days of age. Two of the devices increased dissolved oxygen content of the water and reduced conductivity and microorganism count. One of these reduced broiler mortality (P = .065), decreased pH (P = .062), and increased Fe and Mn concentration in the water. The other increased water temperature, Ti, and Mn but reduced the concentration of Cl, Al, Ca, Cr, Mg, and Sr in the water. Neither the third device, an electrostatic water treatment, nor the other devices affected BW (P = .586) or feed conversion (P = .564) at 49 days of age. No significant treatment differences (P less than or equal to .05) in hematocrit, bursa of Fabricius weight, or tibial ash weight were observed at 21 days of age.

Animals↗
PubMed1985

Blood sampling from the venous occipital sinus of birds.

Venous occipital sinus blood sampling was demonstrated to be an effective nonlethal method in all species tested including ducks, geese, Chukar partridge, Japanese quail, pea-fowl, pheasants, parakeets, turkeys, and chickens. Maximum blood volume obtained from the occipital sinus of 1-day-old chicks equalled the volume obtained by cardiac puncture and exceeded the volume collected by decapitation. Venous occipital sinus puncture was successfully used to rapidly collect several successive blood samples from individual birds, thus indicating the method's utility for serial blood sampling. Hematocrit values, as well as infectious bronchitis and Newcastle disease virus antibody titers measured in blood samples drawn from the occipital sinus and the brachial vein, were compared. Significant correlation coefficients between the two blood sources for each of the variables measured suggest that occipital sinus blood sampling may be substituted for venipuncture for many routine measurements.

Animals↗
PubMed1984

Pathogenesis of feline gastric chlamydial infection.

Studies were conducted to determine whether the gastric chlamydiae that have been observed recently in cats are of pathologic significance. Chlamydiae were isolated in mouse L cell cultures from the homogenized pooled gastric mucosa of 3 cats that had been identified, by histopathologic examination, to have gastric chlamydiosis. Ten specific-pathogen-free kittens were exposed by aerosol and oral inoculation to the harvested feline gastric chlamydiae cell-culture media. In general, the clinical signs and lesions were conjunctivitis, rhinitis, and mild gastritis. The clinical signs and lesions were most severe in 2 chlamydia-infected kittens that had received methylprednisolone acetate (50 mg/kg of body weight). Chlamydiae were demonstrated in epithelial cells of conjunctival and nasal smears in 10 of 10 infected kittens from postexposure days 7 through 35. In addition, chlamydiae were isolated in L cell cultures from a variety of antemortem and postmortem specimens from infected kittens. The present study provided evidence that feline gastric chlamydiae, under appropriate conditions, were capable of inducing, in cats, clinical signs and lesions similar to those induced by the feline pneumonitis agent.

Animals↗