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| 2. |
- Nabi, S. A., et al.
(author)
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Is Global Warming likely to cause an increased incidence of Malaria?
- 2009
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In: Libyan Journal of Medicine. - : Informa UK Limited. - 1993-2820 .- 1819-6357. ; 4:1, s. 18-22
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Research review (peer-reviewed)abstract
- The rise in the average temperature of earth has been described as global warming which is mainly attributed to the increasing phenomenon of the greenhouse effect. It is believed that global warming can have several harmful effects on human health, both directly and indirectly. Since malaria is greatly influenced by climatic conditions because of its direct relationship with the mosquito population, it is widely assumed that its incidence is likely to increase in a future warmer world. This review article discusses the two contradictory views regarding the association of global warming with an increased incidence of malaria. On one hand, there are many who believe that there is a strong association between the recent increase in malaria incidence and global warming. They predict that as global warming continues, malaria is set to spread in locations where previously it was limited, due to cooler climate. On the other hand, several theories have been put forward which are quite contrary to this prediction. There are multiple other factors which are accountable for the recent upsurge of malaria: for example drug resistance, mosquito control programs, public health facilities, and living standards.
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| 3. |
- Qader, S S, et al.
(author)
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Sociodemographic risk factors of metabolic syndrome in middle-aged women: results from a population-based study of Swedish women, The Women's Health in the Lund Area (WHILA) Study.
- 2008
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In: Climacteric. - : Informa UK Limited. - 1369-7137 .- 1473-0804. ; 11:6, s. 475-482
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Journal article (peer-reviewed)abstract
- BACKGROUND: Metabolic syndrome (MS) is a common health problem in menopausal women. According to The Adult Treatment Panel (ATP) III, MS includes the combination of three or more of the following risk factors: abdominal obesity, glucose intolerance, high blood pressure, high serum triglycerides and low levels of high density lipoprotein cholesterol. OBJECTIVES: To assess the prevalence of the MS in middle-aged women, and the relationships of sociodemographic factors to the MS. METHODS: This analysis covers 10,766 women born between December 2, 1935 and December 1, 1945, living in the Lund area of Sweden by December 1, 1995. RESULTS: We found that 11.6% of women with a mean (+/-standard deviation) age of 56.9 +/- 3.06 years had MS. Women with MS were older and had higher scores for body weight, body mass index, waist/hip ratio, pulse rate, pulse pressure, serum triglycerides and total serum cholesterol (p < 0.001 for all) compared to the control group. More MS women were smokers, less often consumers of alcohol, and less qualified. In addition, they had low-intensity physical activity at leisure time (p < 0.001) and high-intensity physical activity at work (p = 0.009). Premenopausal women and those treated with hormones had less MS (p < 0.001). Education, physical activity at leisure time, moderate intensity of physical activity at work, alcohol intake and smoking had strong association with MS but work status, household status and dietary habits had no significant association with MS. CONCLUSIONS: Sociodemographic features may contribute to MS. Hence, prevention of MS should encompass sociodemographic features.
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| 5. |
- Ekelund, Mats, et al.
(author)
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Selective induction of inducible nitric oxide synthase in pancreatic islet of rat after an intravenous glucose or intralipid challenge.
- 2006
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In: Nutrition. - : Elsevier BV. - 1873-1244 .- 0899-9007. ; 22:2006 Apr 22, s. 652-660
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Journal article (peer-reviewed)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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| 6. |
- Gharipour, Mojgan, et al.
(author)
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Socioeconomic determinants and metabolic syndrome : Results from the Isfahan Healthy Heart Program
- 2016
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In: Acta Biomedica. - 0392-4203. ; 87:3, s. 291-298
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Journal article (peer-reviewed)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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| 8. |
- Qader, Saleem, et al.
(author)
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Long-term infusion of nutrients (total parenteral nutrition) suppresses circulating ghrelin in food-deprived rats.
- 2005
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In: Regulatory Peptides. - : Elsevier BV. - 1873-1686 .- 0167-0115. ; 131:Aug 12, s. 82-88
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Journal article (peer-reviewed)abstract
- Background: Ghrelin derives from endocrine cells (A-like cells) in the stomach (mainly the oxyntic mucosa). Its concentration in the circulation increases during fasting and decreases upon re-feeding. This has fostered the notion that the absence of food in the upper gastrointestinal (GI) tract stimulates the secretion of ghrelin. The purpose of the present study was to determine the concentration of ghrelin in serum and oxyntic mucosa after replacing food with intravenous (iv) infusion of nutrients for 8 days using the technique known as total parenteral nutrition (TPN). Materials and methods: Male Sprague-Dawley rats (200-250 g) were given nutrients (lipids, glucose, amino acids, minerals and vitamins) by iv infusion for 8 days during which time they were deprived of food and water; another group was deprived of food for 24-48 h (fasted controls), while fed controls had free access to food and water. Serum ghrelin, gastrin and pancreastatin concentrations were measured together with the ghrelin content of the oxyntic mucosa. Plasma insulin and glucose as well as serum lipid concentrations were also determined. Results: Fasted rats had higher serum ghrelin than TPN rats and fed controls. The oxyntic mucosal ghrelin concentration (and content) was lower in TPN rats than in fasted rats or fed controls. The serum gastrin and pancreastatin concentrations were lower in TPN rats and fasted rats than in fed controls. The plasma insulin concentration was 87 pmol/l +/- 8 (SEM) in TPN rats compared to 101 16 pmol/l in fed controls; it was 26 14 pmol/l in fasted rats. The basal plasma glucose level was 11 +/- 0.6 mmol/l in TPN rats and 12 +/- 0.8 mmol/l in fed controls; it was 7 +/- 0.3 mmol/l in fasted rats. In TPN rats, the serum concentrations of free fatty acids, triglycerides and cholesterol were increased by 100%, 50% and 25%, respectively, compared to fed controls. Fasted rats had higher circulating concentrations of free fatty acids (20%) and lower concentrations of triglycerides (- 40%) than fed controls; fasted rats did not differ from fed controls with respect to serum cholesterol. Conclusion: The circulating ghrelin concentration is high in situations of nutritional deficiency (starvation) and low in situations of nutritional plenty (free access to food or TPN). The actual presence or absence of food in the GI tract seems irrelevant. Circulating insulin and glucose concentrations did not differ much between TPN rats and fed controls, serum lipids, however, were elevated in the TPN rats. We suggest that elevated blood lipid levels contribute to the suppression of circulating ghrelin in rats subjected to TPN for 8 days.
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| 9. |
- Qader, Saleem, et al.
(author)
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Proghrelin-derived peptides influence the secretion of insulin, glucagon, pancreatic polypeptide and somatostatin: A study on isolated islets from mouse and rat pancreas.
- 2008
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In: Regulatory Peptides. - : Elsevier BV. - 1873-1686 .- 0167-0115. ; 146:1-3, s. 230-237
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Journal article (peer-reviewed)abstract
- Proghrelin, the precursor of the orexigenic and adipogenic peptide hormone ghrelin, is synthetized in endocrine (A-like) cells in the gastric mucosa. During its cellular processing, proghrelin gives rise to the 28-amino acid peptide desacyl ghrelin, which after octanoylation becomes active acyl ghrelin, and to the 23-amino acid peptide obestatin, claimed to be a physiological opponent of acyl ghrelin. This study examines the effects of the proghrelin products, alone and in combinations, on the secretion of insulin, glucagon, pancreatic polypeptide (PP) and somatostatin from isolated islets of mice and rats. Surprisingly, acyl ghrelin and obestatin had almost identical effects in that they stimulated the secretion of glucagon and inhibited that of PP and somatostatin from both mouse and rat islets. Obestatin inhibited insulin secretion more effectively than acyl ghrelin. In mouse islets, acyl ghrelin inhibited insulin secretion at low doses and stimulated at high. In rat islets, acyl ghrelin inhibited insulin secretion in a dose-dependent manner but the IC50 for the acyl ghrelin-induced inhibition of insulin release was 7.5 × 10− 8 M, while the EC50 and IC50 values, with respect to stimulation of glucagon release and to inhibition of PP and somatostatin release, were in the 3 × 10− 12–15 × 10− 12 M range. The corresponding EC50 and IC50 values for obestatin ranged from 5 × 10− 12 to 20 × 10− 12 M. Desacyl ghrelin per se did not affect islet hormone secretion. However, at a ten times higher concentration than acyl ghrelin (corresponding to the ratio of the two peptides in circulation), desacyl ghrelin abolished the effects of acyl ghrelin but not those of obestatin. Acyl ghrelin and obestatin affected the secretion of glucagon, PP and somatostatin at physiologically relevant concentrations; with obestatin this was the case also for insulin secretion. The combination of obestatin, acyl ghrelin and desacyl ghrelin in concentrations and proportions similar to those found in plasma resulted in effects that were indistinguishable from those induced by obestatin alone. From the data it seems that the effects of endogenous, circulating acyl ghrelin may be overshadowed by obestatin or blunted by desacyl ghrelin.
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