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Biomedical subjects

A Sahu

Publications and source records attributed to A Sahu.

At least 19 recordsLinked to original sources
PubMed2006

Attitudes and behaviour of ophthalmologists to smoking cessation.

AIMS: Growing evidence suggests a causal association between smoking and eye disease. This study explores the current beliefs and practice among UK consultant ophthalmologists towards delivering smoking cessation advice to eye clinic attenders. METHODS: A cross-sectional survey using a postal questionnaire of all UK NHS hospital based consultant ophthalmologists was conducted. The questionnaire explored whether: ophthalmologists identify the smoking status of their patients, advise about the increased risk of eye diseases among smokers, and deliver smoking cessation advice. The availability of departmental smoking cessation resources was also ascertained. RESULTS: The response rate was 55% (485/886). Of the responders 79% were males. Only 35% of responders asked about smoking status every time or most times for new patients and 5% for follow-up patients. In all, 40% claimed to always or usually advise patients to quit smoking and 61% claimed to always or usually mention eye disease as a reason to quit. Only 14% assessed motivation to quit and 22% provided advice and assistance about how to stop smoking to smokers who wished to quit. Female ophthalmologists were more likely to undertake most aspects of smoking assessment and intervention. Only 18% of responders stated that their departments provide information about smoking for patients and 6% stated that support is available for patients wanting to quit smoking. CONCLUSION: The assessment of smoking status and provision of targeted support for smokers to quit could be substantially improved in UK ophthalmology departments. There is a need to introduce smoking cessation support into routine ophthalmic practice and provide the resources to support this.

Attitude of Health Personnel↗
PubMed2006

Alteration in hypothalamic neuropeptide Y (NPY) secretion may underlie female reproductive ageing: induction of steroid-induced luteinising hormone surge by NPY in ovariectomised aged rats.

A large body of evidence suggests that a defect in the hypothalamic function may be the primary cause of reproductive ageing in female rats. We have previously shown that luteinising hormone (LH)-surge associated changes in hypothalamic neuropeptide Y (NPY) gene expression and median eminence (ME) NPY levels seen in young rats do not occur in middle-aged (MA) rats. The present study examined whether hypothalamic NPY release is altered during the steroid-induced LH surge in ovariectomised (OVX) MA rats, and whether exogenous NPY initiates steroid-induced LH surge in OVX old rats. In the first study, NPY release from the ME-arcuate nucleus, as assessed by the push-pull cannula technique, was significantly increased before and during the progesterone-induced LH surge in oestrogen (E(2))-primed ovariectomised young rats (2-3 months old). This antecedent increase in NPY release seen in young rats was not apparent in MA rats (11-13 months old) in association with a delayed and attenuated LH surge. In the second study, whereas progesterone failed to induce LH surges in E(2)-primed ovariectomised old rats (23-25 months old), intracerebroventricular NPY (0.1-0.5 microg) injections at 1100, 1200 and 13.00 h resulted in LH surge induction in E(2) + progesterone-primed ovariectomised old rats. Because increased hypothalamic NPY synthesis and release is obligatory for the preovulatory LH discharge in young rats, the present findings suggest that alteration in NPY release from the ME-arcuate nucleus contributes to the delayed and reduced LH surges in MA rats and may be involved in the subsequent loss of the LH surges in old rats.

Aging↗
PubMed2005

Perceptions of blindness related to smoking: a hospital-based cross-sectional study.

AIMS: Smoking is associated with several serious eye diseases. Awareness of smoking and blindness, and its potential to act, as a stimulus to assist stopping smoking has not been investigated. METHODS: A cross-sectional survey using a structured interview of adult patients attending district general hospital ophthalmology, general surgery, and orthopaedic clinics. The interview investigated the awareness and fear of blindness for three established smoking-related diseases, and a distractor condition (deafness), and the likelihood that smokers would quit on developing early signs of each condition. RESULTS: Response was 89.1% (358/402). In all, 183 (51.1%) of responders were male and 175 (48.9%) female. Only 9.5% of patients believed that smoking was definitely or probably a cause of blindness, compared with 92.2% for lung cancer, 87.6% for heart disease, and 70.6% for stroke. Patients ranked their fear of each of the five conditions, scoring five for the most feared and one for the least feared. Patients were significantly (P<0.01) less fearful of blindness (mean score 2.80) than lung cancer (3.89), heart disease (3.58), and stroke (3.35). About one-half of smokers stated that they would definitely or probably quit smoking if they developed early signs of blindness or the three established smoking-related conditions, with no significant differences in proportions for these four conditions. CONCLUSION: The findings suggest that awareness of the risk of blindness from smoking is low, but that the fear of blindness is as compelling a motivation to quit as fear of lung cancer, heart disease, and stroke. The link between smoking and eye disease should be publicised to help reduce smoking prevalence.

Adult↗
PubMed2005

Hypothalamic phosphatidylinositol 3-kinase-phosphodiesterase 3B-cyclic AMP pathway of leptin signalling is impaired following chronic central leptin infusion.

Leptin signalling in the hypothalamus is critical for the maintenance of normal body weight. Although hyperleptinaemia in obese people suggests a state of leptin resistance, and diet-induced obesity in rodents is associated with central leptin resistance, the underlying mechanisms remain unclear. Recent evidence suggests that, in addition to the signal transducer and activator of the transcription-3 (STAT3) pathway, leptin action is critical for energy homeostasis through an insulin-like signalling pathway involving an increase in phosphatidylinositol 3-kinase (PI3K) and phosphodiesterase 3B (PDE3B) activities and reduction in cyclic AMP (cAMP) levels in the hypothalamus. Here, we show that chronic central leptin (160 ng/h) infusion, which resulted in the development of resistance to the satiety action of leptin, impaired the PI3K-PDE3B-cAMP pathway of leptin signalling in the hypothalamus in that PI3K and PDE3B activities were increased and cAMP levels were decreased in the hypothalamus on day 2 of leptin infusion but remained unchanged on day 16. Additionally, induction of tyrosyl phosphorylation of insulin receptor substrate-1 observed on day 2 was not evident on day 16 of leptin infusion. By contrast, signalling through the STAT3-pathway remained activated in the hypothalamus throughout 16 days of leptin infusion. These findings show a differential response in PI3K-PDE3B-cAMP (impaired) and STAT3 (up-regulated) pathways to chronic central leptin infusion, and suggest a selective resistance in the PI3K-PDE3B-cAMP pathway of leptin signalling following a chronic increase in hypothalamic leptin tone attained by central infusion of this peptide hormone.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2003

High antigenic cross-reaction among the bacterial species responsible for diseases of cultured freshwater fishes and strategies to overcome it for specific serodiagnosis.

Antigenic sharing among the most commonly bacterial pathogens such as Aeromonas hydrophila, Edwardsiella tarda and Pseudomonas fluorescens of Indian major carps has been studied using immunological reactions such as cross-agglutination, disc diffusion and indirect enzyme linked immunosorbent assay (ELISA). The data were analysed using statistical analysis (SAS), version 6.12. The results showed high antigenic similarities among the bacterial whole cells, whole cell lysates, somatic 'O' antigens, lipopolysaccharides (LPS) and extracellular products (ECP). However, few or no similarities were observed in ECP components of <20kD. The present study indicates a need to develop differential diagnostic methods based on serology by choosing the highly specific less cross-reactive ECP antigen.

Aeromonas hydrophila↗
PubMed2003

Central nervous system receptors involved in mediating the inhibitory action of neuropeptide Y on luteinizing hormone secretion in the male rhesus monkey (Macaca mulatta).

An earlier finding that gonadotropin-releasing hormone (GnRH) secretion may be triggered prematurely in the juvenile male monkey by central administration of 1229U91, a Y1 receptor antagonist, contributed to our current hypothesis that neuropeptide Y (NPY) is a major component of the brake that holds pulsatile GnRH release in check during prepubertal development in primates. However, 1229U91 is also a Y4 receptor agonist, and the present study was conducted to further examine the role of the Y1 receptor in mediating the putative inhibitory action of NPY on GnRH release. Agonadal juvenile and postpubertal male monkeys were implanted with i.v. and i.c.v. cannulae to gain continuous access to the venous and cerebroventricular circulations without sedation. Luteinizing hormone (LH) secretion was measured to provide an indirect index of GnRH release. The specific Y1 antagonists, VD-11 (476 microg; n = 4) and isopropyl 3-chloro-5-[1-((6-[2-(5-ethyl-4-methyl-1,3-thiazol-2-yl)ethyl]-4-morpholin-4-ylpyridin-2-yl)amino)ethyl]phenylcarbamate (Compound A, 300 microg; n = 4), did not mimic the stimulatory action of 1229U91 on GnRH secretion in the juvenile male monkey. Additionally, neither NPY (200 microg; n = 2), a general Y receptor agonist, nor rPP (100 microg; n = 4), a Y4 agonist, mimicked the action of 1229U91 in stimulating GnRH release. Moreover, previous exposure of the hypothalamus of juvenile monkeys (n = 5) to NPY (660 microg) failed to block 1229U91-induced (200 microg) GnRH release. However, the action of NPY (364 microg) in inhibiting GnRH release postpubertally was attenuated by 1229U91 (300 microg). We conclude that, although the action of exogenous NPY to suppress GnRH release from the postpubertal hypothalamus appears to be mediated, at least in part, by the Y1 receptor, the existence of a Y1 receptor pathway inhibitory to GnRH release in the prepubertal hypothalamus remains to be substantiated.

Animals↗
PubMed2002

Bath immunisation of spawn, fry and fingerlings of Indian major carps using a particulate bacterial antigen.

Larval mortality in Indian major carps is one of the major problems encountered in the pond culture system. The present investigation was carried out to investigate the proper age, duration of exposure, and optimum bacterin concentration for vaccinating rohu (Labeo rohita) and catla (Catla catla) at their early stages with a formalin killed Edwardsiella tarda bacterin suspension. The development of immunological competence was recorded with spawn of rohu and catla of 3 weeks of age exposed to a bacterin at a concentration 10(9) cfu ml(-1) for 15 min, where it persisted up to 4 weeks post vaccination. They showed significant resistance against challenge with virulent E. tarda bacteria. Significant antibody titre could be recorded in advanced fries and fingerlings exposed to 10(9) cfu/ml(-1) bacterin concentration for 45 and 60 min, respectively.

Age Factors↗
PubMed2002

Resistance to the satiety action of leptin following chronic central leptin infusion is associated with the development of leptin resistance in neuropeptide Y neurones.

Leptin regulates food intake and body weight by acting primarily in the hypothalamus. In humans and rodents, obesity is associated with hyperleptinaemia, suggesting a possible state of leptin resistance. Thus, to begin to examine the mechanisms of leptin resistance, we developed a rat model in which chronic central leptin infusion results in the development of resistance to leptin's satiety action. Adult male rats were infused chronically into the lateral cerebroventricle with leptin (160 ng/h) or phosphate-buffered saline via Alzet pumps for 28 days, followed by artificial cerebrospinal fluid infusion for 3 weeks. After the initial decrease in food intake, rats developed resistance to the satiety action of leptin, and withdrawal of the chronic leptin infusion resulted in hyperphagia. During leptin infusion, body weight was gradually decreased to reach a nadir on day 12, and thereafter, body weight was sustained at a reduced level throughout the entire 28-day infusion, despite normalization in food intake. Body weight was mostly normalized by day 22 postleptin. Since neuropeptide Y (NPY) neurones are one of the targets of leptin signalling in the hypothalamus, we next examined whether the development of resistance to the satiety action of leptin was due to altered NPY gene expression. On day 3-4 of infusion, hypothalamic NPY mRNA levels, as determined by RNAse protection assay (RPA), were significantly decreased in leptin treated rats compared to controls. By contrast, on day 16 of infusion, NPY mRNA levels in the leptin treated group had returned to control levels. In situ hybridization study confirmed the results obtained with RPA and showed further that the effect of chronic leptin infusion on NPY mRNA levels was restricted to the rostral and middle parts of the arcuate nucleus. Overall, the finding that the action of continuous leptin exposure on NPY neurones was not sustained suggests that NPY neurones may be involved in the development of leptin resistance to the satiety action of leptin in the hypothalamus.

Adipose Tissue↗
PubMed2002

Nutritional regulation of hypothalamic leptin receptor gene expression is defective in diet-induced obesity.

Leptin action in the hypothalamus plays a critical role in maintaining normal food intake and body weight. Hyperleptinaemia is associated with obesity in humans and animal models, suggesting a state of leptin resistance. Although the mechanism of leptin resistance is not clearly understood, alterations in leptin receptor (Ob-R) gene expression have been proposed as a potential mechanism mediating modifications in leptin action in obesity and during changes in nutritional status (fed/fasted). The current study examined the effects of diet-induced obesity (DIO) made by feeding rats a high fat diet for 9 weeks, and nutritional status on levels of long form (Ob-Rb) and total (Ob-Rtot) Ob-R mRNA expression in the hypothalamus. In the fed state, hypothalamic Ob-Rb mRNA and Ob-Rtot mRNA levels were similar in DIO and control standard chow fed rats (SC) despite hyperleptinaemia in DIO rats. However, although an overnight fast moderately increased hypothalamic Ob-Rb mRNA levels in SC rats, fasting did not increase Ob-Rb mRNA levels in DIO rats. To address the possibility that elevated leptin concentration in DIO rats may mediate an alteration in OB-R mRNA levels, we examined the effects of adenovirus-mediated hyperleptinaemia on Ob-R gene expression in SC rats. Despite substantially elevated plasma and cerebrospinal fluid concentrations of leptin, hypothalamic Ob-R mRNA levels were similar in both groups. In conclusion, the current study demonstrates that DIO is associated with a loss of nutritional regulation of hypothalamic Ob-R mRNA levels, and that hyperleptinaemia is not sufficient to alter Ob-R mRNA expression.

Adenoviridae↗
PubMed2002

Elevating circulating leptin in prepubertal male rhesus monkeys (Macaca mulatta) does not elicit precocious gonadotropin-releasing hormone release, assessed indirectly.

The purpose of this study was to examine the hypothesis that the pubertal reaugmentation of pulsatile GnRH release in male primates is triggered by a rise in circulating leptin concentrations. Agonadal juvenile male rhesus monkeys (n = 7) were implanted with indwelling venous catheters and housed in specialized cages that allow continuous access to the venous circulation. GnRH release was monitored indirectly using LH secretion from the in situ pituitary sensitized to the LH releasing action of GnRH as a bioassay for the hypothalamic peptide. Infusion of recombinant human leptin (5 micro g/kg body weight.h for 16 d resulted in a marked square wave increment in circulating leptin concentration from approximately 2-20 ng/ml but did not elicit precocious GnRH release. GH secretion, however, was stimulated confirming that the heterologous leptin preparation was bioactive in the monkey. Parenthetically, recombinant human leptin was found to be immunogenic in the monkey and circulating antileptin IgG was demonstrable 22-35 d after the initial exposure to the human protein. These findings further support the view that circulating leptin is unlikely to provide the signal that triggers the onset of puberty in male primates.

Animals↗
PubMed2001

Kinetic analysis of the interactions of complement receptor 2 (CR2, CD21) with its ligands C3d, iC3b, and the EBV glycoprotein gp350/220.

The molecular mechanisms involved in the interaction of complement receptor 2 (CR2) with its natural ligands iC3b and C3d are still not well understood. In addition, studies regarding the binding site(s) of the receptor on C3 as well as the affinities of the C3 fragments for CR2 have produced contradictory results. In the present study, we have used surface plasmon resonance technology to study the interaction of CR2 with its ligands C3d, iC3b, and the EBV surface glycoprotein gp350/220. We measured the kinetics of binding of the receptor to its ligands, examined the influence of ionic contacts on these interactions, and assessed whether immobilized and soluble iC3b bound with similar kinetics to CR2. Our results indicate that 1) gp350 binding to CR2 follows a simple 1:1 interaction, whereas that of the C3 fragments is more complex and involves more than one intramolecular component; 2) kinetic differences exist between the binding of C3d and iC3b to CR2, which may be due to an additional binding site found on the C3c region of iC3b; and 3) iC3b binds to CR2 with different kinetics, depending on whether the iC3b is in solution or immobilized on the surface. These findings suggest that binding of CR2 to iC3b and C3d is more complex than previously thought.

Alanine↗
PubMed2001

Evidence that neurotensin mediates the central effect of leptin on food intake in rat.

Recent evidence suggests that leptin's action on food intake and body weight regulation is mediated by a number of orexigenic and anorectic neuronal systems in the hypothalamus. Our previous demonstration that central injections of leptin induce hypothalamic neurotensin (NT) gene expression in association with a reduced food intake and decreased body weight in rats indicates that NT, an anorectic peptide, is involved in mediating leptin's action on feeding and body weight regulation. To begin to examine the relative role of NT in this regard we evaluated the effects of NT antiserum (NT-AS) or NT receptor antagonist, SR 48692, on the satiety action of leptin in rats. In the first experiment, 3rd cerebroventricular (i.c.v.) administration of either 1 or 5 microl of NT-AS, 30 min prior to leptin (4 microg) injection, completely blocked the effects of leptin on food deprivation (FD)-induced feeding. In the second experiment, intraperitoneal (i.p.) administration of SR 48692 (40 microg/kg) also completely prevented leptin's satiety action on FD-induced feeding. These results showing the reversal of leptin's satiety action by either NT immunoneutralization or NT-receptor antagonism support our hypothesis that NT is involved in mediating leptin's action on feeding and further suggest that this neuropeptide is a quantitatively important component of the leptin sensitive neural circuitry.

Animals↗
PubMed2001

Could reduced cerebrospinal fluid (csf) galanin contribute to restricted eating in anorexia nervosa?

Galanin (GAL) and gamma amino butyric acid (GABA) are orexigenic neuropeptides that could contribute to the pathogenesis of anorexia nervosa (AN). To avoid the confounding effects of the ill state, we studied women who were recovered (> 1 year, normal weight, and regular menstrual cycles, no binging or purging) from AN (REC AN) and matched healthy control women (NC). CSF GAL was reduced in REC AN (64.4 +/- 8.6 pg/ml) compared to NC (72.0 +/- 11.6 pg/ml; p <.05), GABA was similar between groups. In the brain, GAL stimulates appetite and fat consumption. These data raise the question of whether alterations in brain GAL activity plays a role in clinical symptoms in AN, such as food restriction and fat avoidance.

Adult↗
PubMed2001

Structure and biology of complement protein C3, a connecting link between innate and acquired immunity.

Complement protein C3 is a central molecule in the complement system whose activation is essential for all the important functions performed by this system. After four decades of research it is now well established that C3 functions like a double-edged sword: on the one hand it promotes phagocytosis, supports local inflammatory responses against pathogens, and instructs the adaptive immune response to select the appropriate antigens for a humoral response; on the other hand its unregulated activation leads to host cell damage. In addition, its interactions with the proteins of foreign pathogens may provide a mechanism by which these microorganisms evade complement attack. Therefore, a clear knowledge of the molecule and its interactions at the molecular level not only may allow the rational design of molecular adjuvants but may also lead to the development of complement inhibitors and new therapeutic agents against infectious diseases.

Amides↗
PubMed2001

Pituitary follistatin and activin gene expression, and the testicular regulation of FSH in the adult Rhesus monkey (Macaca mulatta).

In rats, FSHbeta gene expression and FSH secretion are increased and decreased, respectively, by pituitary activin and follistatin. Because little information is available on the paracrine control of FSH secretion in the primate, follistatin and activin/inhibin beta(B) messenger RNA (mRNA) levels were measured in pituitaries of adult male rhesus monkeys 6 weeks after castration or sham surgery (n = 5/group). Follistatin mRNA was determined by quantitative RT-PCR assay using oligonucleotide primers designed to span exons 3-5 of the human follistatin gene. Activin/inhibin beta(B) mRNA levels were measured by ribonuclease protection. Orchidectomy resulted in a 100-fold increase in plasma FSH concentrations and a 60-fold rise in those of LH. In castrated monkeys, levels of mRNA encoding FSHbeta, LHbeta, alpha- subunit, and GnRH receptor (GnRH-R) were increased 21-, 2.1-, 1.7-, and 1.7-fold, respectively (P < 0.01). Levels of pituitary follistatin and activin/inhibin beta(B) mRNAs, however, were similar in castrated and intact animals. These data suggest that the paracrine control of FSH secretion in the male differs substantially in primates and rodents. Specifically, the relatively greater postcastration rise in FSHbeta gene expression and FSH secretion in the adult male monkey may result because in this species pituitary follistatin gene expression does not increase after orchidectomy, as it does in the rat.

Activins↗
PubMed2000

Binding kinetics, structure-activity relationship, and biotransformation of the complement inhibitor compstatin.

We have previously identified a 13-residue cyclic peptide, Compstatin, that binds to complement component C3 and inhibits complement activation. Herein, we describe the binding kinetics, structure-activity relationship, and biotransformation of Compstatin. Biomolecular interaction analysis using surface-plasmon resonance showed that Compstatin bound to native C3 and its fragments C3b and C3c, but not C3d. While binding of Compstatin to native C3 was biphasic, binding to C3b and C3c followed the 1:1 Langmuir binding model; the affinities of Compstatin for C3b and C3c were 22- and 74-fold lower, respectively, than that of native C3. Analysis of Compstatin analogs synthesized for structure-function studies indicated that 1) the 11-membered ring between disulfide-linked Cys2-Cys12 constitutes a minimal structure required for optimal activity; 2) retro-inverso isomerization results in loss of inhibitory activity; and 3) some residues of the type I beta-turn segment also interact with C3. In vitro studies of Compstatin in human blood indicated that a major pathway of biotransformation was the removal of Ile1, which could be blocked by N-acetylation of the peptide. These findings indicate that acetylated Compstatin is stable against enzymatic degradation and that the type I beta-turn segment is not only critical for preservation of the conformational stability, but also involved in intermolecular recognition.

Amino Acid Sequence↗
PubMed2000

Neuropeptide Y: A hypothalamic brake restraining the onset of puberty in primates.

The adult reproductive axis is driven by an intermittent discharge of gonadotropin-releasing hormone (GnRH) generated by a network of hypothalamic neurons known as the GnRH pulse generator. Although this signal generator is operational in infant primates, puberty in these species is delayed by activation shortly after birth of a central neural mechanism that holds GnRH release in check during juvenile development. Here, we show that, in the male rhesus monkey, the postnatal pattern in GnRH pulse generator activity is inversely related to that in neuropeptide Y (NPY) gene and protein expression in the mediobasal hypothalamus and that central administration of an NPY Y(1) receptor antagonist to juvenile animals elicits precocious GnRH release. Cell imaging indicated that the developmentally regulated NPY neurons may be located in regions dorsal to the arcuate nucleus. These findings lead us to propose that NPY is a fundamental component of the neurobiological brake restraining the onset of puberty in primates.

Animals↗