Photonic band gaps and defect states induced by excitations of Bose-Einstein condensates in optical lattices

We study the interaction of a Bose-Einstein condensate, which is confined in an optical lattice, with a largely detuned light field propagating through the condensate. If the condensate is in its ground state it acts as a periodic dielectric and gives rise to photonic band gaps at optical frequencies. The band structure of the combined system of condensed lattice-atoms and photons is studied by using the concept of polaritons. If elementary excitations of the condensate are present, they will produce defect states inside the photonic band gaps. The frequency of localized defect states is calculated using the Koster-Slater model.Comment: 10 pages, 1 figure, RevTe

Sinteza i biološko vrednovanje novih derivata 2-fenil-benzimidazol-1-acetamida kao potencijalnih anthelmintika

The present study describes synthesis of a series of 2-phenyl benzimidazole-1-acetamide derivatives and their evaluation for anthelmintic activity using Indian adult earthworms, Pheretima posthuma. The structure of the title compounds was elucidated by elemental analysis and spectral data. The compounds 4-({[2-(4-nitrophenyl)-1H-benzimidazol-1-yl]acetyl}amino) benzoic acid (3a), N-ethyl-2-[2-(4-nitrophenyl)-1H-benzimidazol-1-yl] acetamide (3c), N-benzyl-2-[2-(4-nitrophenyl)-1H-benzimidazol-1-yl] acetamide (3d), N-(4-hydroxyphenyl)-2-[2-(4-nitrophenyl)-1H-benzimidazol-1-yl] acetamide (3f), 2-[2-(4-nitrophenyl)-1H-benzimidazol-1-yl]-N-phenylacetamide (3h), 2-[2-(4-chlorophenyl)-1H-benzimidazol-1-yl]-N\u27-phenylacetohydrazide (3k), 2-[2-(4-chlorophenyl)-1H-benzimidazol-1-yl]-N-(4-nitrophenyl) acetamide (3n) and 2-[2-(4-chlorophenyl)-1H-benzimidazol-1-yl]-N-phenylacetamide (3q) were better to paralyze worms whereas N-ethyl-2-[2-(4-nitrophenyl)-1H-benzimidazol-1-yl] acetamide (3c), N-(4-nitrophenyl)-2-[2-(4-nitrophenyl)-1H-benzimidazol-1yl] acetamide (3e), 4-({[2-(4-chlorophenyl)-1H-benzimidazol-1-yl] acetyl} amino) benzoic acid (3j), 2-[2-(4-chlorophenyl)-1H-benzimidazol-1-yl]-N-ethylacetamide (3l) and 2-[2-(4-chlorophenyl)-1H-benzimidazol-1-yl]-N-phenylacetamide (3q) were better to cause death of worms compared to the anthelmintic drug albendazole.U radu je opisana sinteza derivata 2-fenil-benzimidazol-1-acetamida i ispitivanje njihovog anthelmintičkog djelovanja na odrasle indijske gliste, Pheretima posthuma. Struktura sintetiziranih spojeva određena je elementarnom analizom i spektroskopskim metodama. Spojevi 4-({[2-(4-nitrofenil)-1H-benzimidazol-1-il]acetil}amino) benzojeva kiselina (3a), N-etil-2-[2-(4-nitrofenil)-1H-benzimidazol-1-il] acetamid (3c), N-benzil-2-[2-(4-nitrofenil)-1H-benzimidazol-1-il] acetamid (3d), N-(4-hidroksifenil)-2-[2-(4-nitrofenil)-1H-benzimidazol-1-il] acetamid (3f), 2-[2-(4-nitrofenil)-1H-benzimidazol-1-il]-N-fenilacetamid (3h), 2-[2-(4-klorfenil)-1H-benzimidazol-1-il]-N\u27-fenilacetohidrazid (3k), 2-[2-(4-klorfenil)-1H-benzimidazol-1-il]-N-(4-nitrofenil) acetamid (3n) i 2-[2-(4-klorfenil)-1H-benzimidazol-1-il]-N-fenilacetamid (3q) jače paraliziraju gliste, a N-etil-2-[2-(4-nitrofenil)-1H-benzimidazol-1-il] acetamid (3c), 2-[2-(4-nitrofenil)-1H-benzimidazol-1-il]-N-fenilacetamid (3h), 4-({[2-(4-klorfenil)-1H-benzimidazol-1-il]acetil}amino) benzojeva kiselina (3j), 2-[2-(4-klorfenil)-1H-benzimidazol-1-il]-N-etilacetamid (3l) i 2-[2-(4-klorfenil)-1H-benzimidazol-1-il]-N-fenilacetamid (3q) učinkovitije usmrćuju gliste nego anthelmintik albendazol

Health-related quality of life in patients with a germline BRCA mutation and metastatic pancreatic cancer receiving maintenance olaparib

Background: Patients with metastatic pancreatic cancer often have a detriment in health-related quality of life (HRQoL). In the randomized, double-blind, phase III POLO trial progression-free survival was significantly longer with maintenance olaparib, a poly(ADP-ribose) polymerase inhibitor, than placebo in patients with a germline BRCA1 and/or BRCA2 mutation (gBRCAm) and metastatic pancreatic cancer whose disease had not progressed during first-line platinum-based chemotherapy. The prespecified HRQoL evaluation is reported here. Patients and methods: Patients were randomized to receive maintenance olaparib (300 mg b.i.d.; tablets) or placebo. HRQoL was assessed using the European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire Core 30-item module at baseline, every 4 weeks until disease progression, at discontinuation, and 30 days after last dose. Scores ranged from 0 to 100; a ≥10-point change or difference between arms was considered clinically meaningful. Adjusted mean change from baseline was analysed using a mixed model for repeated measures. Time to sustained clinically meaningful deterioration (TSCMD) was analysed using a log-rank test. Results: Of 154 randomized patients, 89 of 92 olaparib-arm and 58 of 62 placebo-arm patients were included in HRQoL analyses. The adjusted mean change in Global Health Status (GHS) score from baseline was <10 points in both arms and there was no significant between-group difference [-2.47; 95% confidence interval (CI) -7.27, 2.33; P = 0.31]. Analysis of physical functioning scores showed a significant between-group difference (-4.45 points; 95% CI -8.75, -0.16; P = 0.04). There was no difference in TSCMD for olaparib versus placebo for GHS [P = 0.25; hazard ratio (HR) 0.72; 95% CI 0.41, 1.27] or physical functioning (P = 0.32; HR 1.38; 95% CI 0.73, 2.63). Conclusions: HRQoL was preserved with maintenance olaparib treatment with no clinically meaningful difference compared with placebo. These results support the observed efficacy benefit of maintenance olaparib in patients with a gBRCAm and metastatic pancreatic cancer. ClincalTrials.gov number: NCT02184195

European guidelines for the diagnosis and treatment of pancreatic exocrine insufficiency: UEG, EPC, EDS, ESPEN, ESPGHAN, ESDO, and ESPCG evidence-based recommendations

\ua9 2024 The Author(s). United European Gastroenterology Journal published by Wiley Periodicals LLC on behalf of United European Gastroenterology.Pancreatic exocrine insufficiency (PEI) is defined as a reduction in pancreatic exocrine secretion below the level that allows the normal digestion of nutrients. Pancreatic disease and surgery are the main causes of PEI. However, other conditions and upper gastrointestinal surgery can also affect the digestive function of the pancreas. PEI can cause symptoms of nutritional malabsorption and deficiencies, which affect the quality of life and increase morbidity and mortality. These guidelines were developed following the United European Gastroenterology framework for the development of high-quality clinical guidelines. After a systematic literature review, the evidence was evaluated according to the Oxford Center for Evidence-Based Medicine and the Grading of Recommendations Assessment, Development, and Evaluation methodology, as appropriate. Statements and comments were developed by the working groups and voted on using the Delphi method. The diagnosis of PEI should be based on a global assessment of symptoms, nutritional status, and a pancreatic secretion test. Pancreatic enzyme replacement therapy (PERT), together with dietary advice and support, are the cornerstones of PEI therapy. PERT is indicated in patients with PEI that is secondary to pancreatic disease, pancreatic surgery, or other metabolic or gastroenterological conditions. Specific recommendations concerning the management of PEI under various clinical conditions are provided based on evidence and expert opinions. This evidence-based guideline summarizes the prevalence, clinical impact, and general diagnostic and therapeutic approaches for PEI, as well as the specifics of PEI in different clinical conditions. Finally, the unmet needs for future research are discussed

Nitric oxide levels in response to the patients with different stage of diabetes

The association between hyperglycaemia and serum nitric oxide (NO) levels has not yet been fully clarified. Thus, it was aimed to evaluate the concentration of NO metabolites (nitrate, nitrite) in diabetic patients and to find the relationship between hyperglycaemia and serum NO levels in diabetic and prediabetic patients, and control groups. In this study, 100 subjects were divided into 3 groups: healthy control (n=20), prediabetic (n=40) and diabetic (n=40). Glycemic control was assessed using glycated hemoglobin (HbA1c). Nitrate and nitrite levels were measured using the Griess reagent. NO was obtained from the sum of nitrates and nitrites. The serum NO level was higher in diabetic (53.4 +/- 2.0 mu M) and prediabetic patients (51.6 +/- 1.6 mu M) as compared to that in the control (45.6 +/- 1.2 mu M), (p< 0.05). The NO level was not significantly different in diabetic and prediabetic patients. Higher levels of serum glucose, insulin and HOMA-IR may be responsible for the activation of endothelial cells to increase NO levels. This study supports the role of insulin resistance in increased NO levels in both diabetic and prediabetic patients

Effects of exercise on ghrelin

Ghrelin, a gastric derived acylated peptide, was discovered in 1999 as a mediator of growth hormone secretiation. Since then, ghrelin has been found to significant impacts on many physiological functions of body systems. Ghrelin has a potential on appetite stimulation that influence on regulation of energy metabolism. It is known that exercise has a marked impact on energy homeostasis and consequently many research focused on the interaction between exercise stimulus and ghrelin response. This review provides an overwiew of research relating to the acute and chronic effects of exercise on (total, acyl and desacyl) ghrelin levels and also impact of exercise intensity on ghrelin levels. Although there is uncertainty among the results of previous studies, our review suggests that acute exercise transiently enterferes with the acly and total ghrelin levels. However, chronic exercise may acause increase in ghrelin levels in contrast to acute exercise with related to change of body weight. In adition, inenstiy of exercise may also reveales various results concerning the relationship between exercise and circulation ghreline levels. The discovery of ghrelin has raised our knowledge of food intake regulation, energy homeostasis and metabolic function mechanism. Further studies should be focused betwen the impact of exercise (type, duration and intensity) on circulation ghreline levels. Exercise induced ghrelin levels will likely generate new pharmacological approaches to many metabolic diseases based on inbalance in body energy homeostasis

Serum Nesfatin-1 Levels in Patients With Different Glucose Tolerance Levels

The aim of this study was to compare the levels of nesfatin-1 in healthy subjects with those in prediabetic and diabetic patients who have different glucose tolerance levels. Overall, 100 subjects were divided into 5 groups healthy control (C), impaired fasting glycemia (IFG), impaired glucose tolerance (IGT), metabolic syndrome (MS) and type 2 diabetes mellitus, (Type 2 DM). Glycated hemoglobin (HbA1c) assessed the glycemic control. Homeostasis model assessment of insulin resistance (HOMA-IR) was determined using computer analyses. Nesfatin-1 levels were measured using ELISA method. IFG and IGT (prediabetic groups) from MS and Type 2 DM (diabetic groups) differed significantly in HOMA-IR. The nesfatin-1 levels were lower, although not statistically significant, in IFG (0.937±0.03 ng/ml, p=0.07) and IGT (1.039±0.06 ng/ml, p=0.5) groups compared to healthy subjects (1.094±0.07 ng/ml). However, the nesfatin-1 levels were lower in patients with Type 2 DM (0.867±0.02 ng/ml, p=0.007) and MS (0.885±0.01 ng/ml, p=0.01) compared to healthy subjects. Nesfatin-1 levels were significantly lower in diabetic patients compared to healthy subjects. This study supports the role of insulin resistance in decreased nesfatin-1 levels in patients with Type 2 DM and MS.</jats:p