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Sökning: WFRF:(Qader Saleem)

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1.
  • Ekelund, Mikael, et al. (författare)
  • Effects of total parenteral nutrition on rat enteric nervous system, intestinal morphology, and motility.
  • 2005
  • Ingår i: Journal of Surgical Research. - Elsevier. - 1095-8673. ; 124:2, s. 187-193
  • Tidskriftsartikel (refereegranskat)abstract
    • Total parenteral nutrition (TPN) is often crucial for patients not being able to feed enterally or having intestinal absorptive deficits. Enteral nutrition is, however, frequently regarded vital for maintaining functional and structural intestinal integrity. The aim of this study was to investigate possible effects of TPN on rat distal small intestine compared to enterally fed identically housed controls, regarding the enteric nervous system (ENS), motility in vitro, and morphology. This study shows that motor responses evoked by electrical stimulation or exposure to vasoactive intestinal peptide (VIP), pituitary adenylate cyclase activating peptide-27 (PACAP-27), and nitric oxide (NO) donor were unchanged. By using immunohistochemistry, the numbers of submucous (P < 0.05) and myenteric (P < 0.05) nerve cells were found to increase, expressed as numbers per unit length. The percentage of neurons expressing VIP, PACAP-27, NO-synthase, and galanin remained unchanged, however. By in situ hybridization the number of submucous neurons expressing neuropeptide Y-mRNA was found to decrease (P < 0.05); the other populations were unaltered. Morphometry revealed an increased submucosal thickness (P < 0.05), while intestinal circumference markedly decreased (P < 0.0001) in TPN-treated rats. In conclusion, TPN treatment resulted in reduced intestinal circumference leading to condensation of enteric neurons. No marked changes in neurotransmitter expression of the enteric neurons or in motor activity were noted.
2.
  • Ekelund, Mats, et al. (författare)
  • Selective induction of inducible nitric oxide synthase in pancreatic islet of rat after an intravenous glucose or intralipid challenge.
  • 2006
  • Ingår i: Nutrition. - Elsevier. - 1873-1244. ; 22:2006 Apr 22, s. 652-660
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Constant exposure of pancreatic islets to high levels of glucose or free fatty acids can lead to irreversible beta-cell dysfunction, a process referred to as glucotoxicity or lipotoxicity, respectively. In this context a role for nitric oxide generated by pancreatic islet has been suggested. The present investigation examined whether the route of glucose administration, i.e., given orally (OG) or infused intravenously (IVG), could have any effect on the expression and activity of inducible nitric oxide synthase (iNOS) in pancreatic islets. Methods: Rats were infused with glucose (50%) or Intralipid intravenously for 24 h or given glucose orally. A freely fed control group (FF) was also included. At 24 h rats were killed and blood samples were drawn for analysis of plasma insulin, glucagon, and glucose. Pancreatic islets were harvested from each animal and investigated for the occurrence of iNOS by the use of confocal microscopy, western blot, and high-performance liquid chromatographic analysis. The effect of intravenously infused glucose was then compared with the effect of an intravenous infusion of Intralipid (IL). Results: Plasma insulin levels were markedly decreased after 24 h of infusion of glucose (IVG group) or Intralipid (IL group) compared with the FF or OG group. Plasma glucagon and glucose levels were markedly increased in the IVG group, whereas both parameters were decreased in the IL group. No significant differences in plasma insulin, glucagon, or glucose were found between the OG and FF groups. Immunocytochemical (confocal microscopy), western blot, and biochemical (high-performance liquid chromatographic) analyses showed that a sustained increase in plasma level of glucose or free fatty acids by an intravenous infusion of either nutrient for 24 h resulted in a marked expression and activity of iNOS in pancreatic islets. No sign of iNOS expression could, however, be detected in the islets of FF control or OG rats. Conclusion: The data suggest that impaired beta-cell function found after 24 It of an intravenous infusion of glucose or Intralipid might be mediated, at least in part, by the induction of iNOS in pancreatic islets. This may subsequently result in an exclusive production of nitric oxide, which is deleterious for beta-cells. (C) 2006 Elsevier Inc. All rights reserved.
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3.
  • Gharipour, Mojgan, et al. (författare)
  • Socioeconomic determinants and metabolic syndrome : Results from the Isfahan Healthy Heart Program
  • 2016
  • Ingår i: Acta Biomedica. - L'Ateneo Parmense. - 0392-4203. ; 87:3, s. 291-298
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: The prevalence of metabolic syndrome (MetS) is increasing in Iran. We assessed the relationship between socioeconomic status (SES) and Mets components in the Iranian population. Materi- als and Methods: The sample for this study comprised a random cross-section of men and women from two province districts who participated in the Isfahan Healthy Heart Program (IHHP) in 2007. Each participant completed a questionnaire, underwent anthropometric testing and blood pressure measurements, and pro- vided a blood sample. Mets was defined based on ATPIII criteria. Several SES dimensions, such as education, occupation, and number of children, as well as home, car, and personal computer ownership, were assessed to determine the participant’s SES. Results: A higher-than-average income, car ownership, owning or renting a private home, and having a computer are increasing towards increment in SES. All MetS components were more prevalent in participants defined as having a lower SES, while low HDL levels were more common in participants having an SES II (P>0.001). A multivariate analysis showed that having the lowest SES (I) increased the risk of MetS by 1.72 [1.44-2.07], whereas subjects having an SES III had a 1.23 [1.04-1.47] lower risk for MetS. Conclusions: The relationship between SES and Mets is due largely to behavioural factors, such as practicing unhealthy eating habits. Given the high prevalence of Mets in Iran, we propose that regular health check-ups may be useful in the early detection of the syndrome and, consequently, in the prevention of its effects. In addition, the early detection of MetS may result in the early diagnosis and prevention of car- diovascular diseases. (www.actabiomedica.it)
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5.
  • Grapengiesser, Eva, et al. (författare)
  • Glucose Induces Glucagon Release Pulses Antisynchronous with Insulin and Sensitive to Purinoceptor Inhibition.
  • 2006
  • Ingår i: Endocrinology. - Endocrine Society. - 0013-7227. ; 147:2006 Apr 13, s. 3472-3477
  • Tidskriftsartikel (refereegranskat)abstract
    • Both increase of the glucose concentration and activation of purinoceptors are known to affect pancreatic alpha-cells. Effects obtained with various purino derivatives at 2.8 and 8.3 mmol/ liter glucose have been taken to indicate that external ATP is less potent than adenosine as a stimulator of glucagon release. However, when making a corresponding comparison at 20 mmol/ liter glucose, we observed marked stimulation of glucagon release from isolated rat islets with 100 mu mol/liter adenosine-5- O-2-thiodiphosphate but inhibition with 10 mu mol/liter adenosine. Analyses of 30-sec samples of perfusate from rat pancreas indicated that a rise of the glucose concentration from 3 to 20 mmol/ liter rapidly induces a glucagon peak followed by regular 4- to 5-min pulses. The glucagon pulses preceded those of insulin with a phase shift (1.8 +/- 0.1 min) near half the interpeak interval. Because of the antisynchrony, the maximal glucagon effect on liver cells will be manifested during periods with low concentrations of insulin. In support for the idea that neural P2Y(1) receptors are important for coordinating the secretory activity of the islets, both the insulin and glucagon pulses disappeared in the presence of the purinoceptor inhibitor MRS 2179 (10 mu mol/liter). However, in contrast to what was observed for insulin, MRS 2179 lowered average glucagon release to the level of the oscillatory nadirs.
6.
  • Njuguna, J., et al. (författare)
  • Challenges Associated with Scaling up Artemisinin Combination Therapy in Sub-Saharan Africa A Review Article
  • 2008
  • Ingår i: Libyan Journal of Medicine. - Univ Alfateh, Fac Med. - 1993-2820. ; 3:1, s. 42-48
  • Forskningsöversikt (refereegranskat)abstract
    • Malaria is the leading cause of morbidity and mortality in Sub-Saharan Africa. One key strategic intervention is provision of early diagnosis and prompt effective treatment. A major setback has been the development of drug resistance to commonly used antimalarials. To overcome this, most countries in Sub-Saharan Africa have adopted Artemisinin Combination Therapy (ACT) as a first line treatment for uncomplicated malaria. Artemether Lumefantrine (AL) and Artesunate Amodiaquine (ASAQ) are the main drugs of choice. There are key implementation issues, which may have a bearing on the scaling up of this new treatment. This article reviewed the published papers on ACT with focus on sustainability, compliance, and diagnosis. ACTs are costly, but highly effective. Their scaling up is the most cost effective malaria intervention currently available. Most countries rely heavily on the Global Fund for their scaling up. AL has a short shelf life, a complicated six-dose regimen that requires intake with fat to ensure sufficient bioavailability. High rates of adherence have been reported. Use of parasitic diagnosis is advocated to ensure rational use. Parasitic diagnostics like rapid test and microscopy are currently inadequate. The majority of malaria cases may continue to be diagnosed clinically leading to over prescription of drugs. ACTs are currently not available at the community level for home based management of malaria. Issues related to safety and rational use need to be addressed before their use in the informal health sector like community drug sellers and community health workers. The majority of malaria cases at the community level could go untreated or continue to be treated using less effective drugs. We conclude that ACTs are highly effective. A major challenge is ensuring rational use and access at the household level. It is hoped that addressing these issues will increase the likelihood that ACT achieves its intended goals of reducing morbidity and mortality due to malaria, and delaying the onset of drug resistance.
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8.
  • Qader, Saleem, et al. (författare)
  • Could Quality of Life Impact the Prevalence of Metabolic Syndrome? Results from a Population-Based Study of Swedish Women: The Women's Health in the Lund Area Study.
  • 2008
  • Ingår i: Metabolic syndrome and related disorders. - Mary Ann Liebert, Inc.. - 1557-8518.
  • Tidskriftsartikel (refereegranskat)abstract
    • Abstract Background: The metabolic syndrome is regarded as an important risk factor for diabetes mellitus and cardiovascular disease. Metabolic syndrome could be associated with impaired quality of life (QoL). Methods: The Women's Health in the Lund Area (WHILA) project covers 10,766 women born between December 2, 1935, and December 1, 1945, living in the Lund area, of Sweden by December 1, 1995. The primary objectives of this project were to survey perimenopausal women in this area and to evaluate their health status and lifestyles. We used the criteria for the metabolic syndrome, as defined by the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III), which include three or more of five risk factors: central obesity, elevated serum triglycerides, low high-density lipoprotein cholesterol (HDL-C), and elevated blood pressure and fasting glucose. Analysis of most aspects of daily life and QoL according to the Gothenburg Quality of Life Instrument (GQL) was done. GQL refers to the WHO definition of health. Results: A total number of 6913 (64.2%) women with a mean age (56.1) years fulfilled the criteria for screening procedure in the WHILA study. A positive association between women with metabolic syndrome and the following aspects of quality of life were found: "Partnership," "free time," "memory," and being "appreciated outside home." However, "economy," "health," "body image," and "fitness" had a negative association to the metabolic syndrome. Conclusion: QoL is an important factor for metabolic syndrome. Apart from traditional biological factors, prevention of metabolic syndrome should also encompass QoL.
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9.
  • Qader, Saleem, et al. (författare)
  • Could Spontaneous Retroperitoneal Haematoma Present with Scrotal Mass?
  • 2009
  • Ingår i: Libyan Journal of Medicine. - Univ Alfateh, Fac Med. - 1993-2820. ; 4:3, s. 117-119
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Retroperitoneal haematoma could be caused by different factors. It is increasing due to an increase in the use of antithrombotic and anticoagulant therapy. Diagnosis of retroperitoneal haematoma forms a big challenge in daily clinical practice. Patients with retroperitoneal haematoma could present with leg paresis, abdominal pain, shock or abdominal compartment syndrome. Retroperitoneal haematoma could be treated conservatively but surgical interference or embolization of the bleeding vessels is always an option. Objectives: To present a case with spontaneous retroperitoneal haematoma presenting with scrotal haematoma together with a mini- review of retroperitoneal haematoma. Conclusions: Retroperitoneal haematoma may present with a scrotal swelling and could be treated conservatively depending on the presentation and severity of the bleeding.
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10.
  • Qader, Saleem, et al. (författare)
  • Expression of islet iNOS and inhibition of glucose stimulated insulin release after long-term lipid infusion in the rat is counteracted by PACAP27.
  • 2007
  • Ingår i: American Journal of Physiology: Endocrinology and Metabolism. - American Physiological Society. - 1522-1555. ; 292:5, s. 1447-1455
  • Tidskriftsartikel (refereegranskat)abstract
    • Chronic exposure of pancreatic islets to elevated plasma lipids ( lipotoxicity) can lead to beta-cell dysfunction, with overtime becoming irreversible. We examined, by confocal microscopy and biochemistry, whether the expression of islet inducible nitric oxide synthase ( iNOS) and the concomitant inhibition of glucose-stimulated insulin release seen after lipid infusion in rats was modulated by the islet neuropeptide pituitary adenylate cyclase-activating polypeptide ( PACAP) 27. Lipid infusion for 8 days induced a strong expression of islet iNOS, which was mainly confined to beta-cells and was still evident after incubating islets at 8.3 mmol/l glucose. This was accompanied by a high iNOS-derived NO generation, a decreased insulin release, and increased cyclic GMP accumulation. No iNOS expression was found in control islets. Addition of PACAP27 to incubated islets from lipid-infused rats resulted in loss of iNOS protein expression, increased cyclic AMP, decreased cyclic GMP, and suppression of the activities of neuronal constitutive ( nc) NOS and iNOS and increased glucose-stimulated insulin response. These effects were reversed by the PKA inhibitor H-89. The suppression of islet iNOS expression induced by PACAP27 was not affected by the proteasome inhibitor MG-132, which by itself induced the loss of iNOS protein, making a direct proteasomal involvement less likely. Our results suggest that PACAP27 through its cyclic AMP- and PKA-stimulating capacity strongly suppresses not only ncNOS but, importantly, also the lipid-induced stimulation of iNOS expression, possibly by a nonproteasomal mechanism. Thus PACAP27 restores the impairment of glucose-stimulated insulin release and additionally might induce cytoprotection against deleterious actions of iNOS-derived NO in beta-cells.
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