MATERIALS AND METHODS: Honey and some of its components, which include the sugars, the proteins, the hydrogen peroxide produced, and the phenolics, were exposed to cultured fibroblasts. The MTT colorimetric assay was used to assess cell viability and proliferation.
RESULTS: The stimulatory effect of honey on fibroblast proliferation was observed to be time- and dose-dependent. The continuous production of hydrogen peroxide by the honey-glucose oxidase system also acts to stimulate cell proliferation in a time- and dose-dependent manner. The presence of phenolics with antioxidant properties, on the other hand, renders protection to the cells against the toxic effect of hydrogen peroxide. However, the presence of a growth factor-like substance in honey could not be ascertained.
CONCLUSION: For the first time, honey and its major components were shown to exert stimulatory effects on cultured fibroblasts. Honey is therefore potentially useful in medicinal practices.
METHODS: A retrospective database analysis at a university-affiliated hospital in Thailand was used. Diabetic patients receiving glucose-lowering medications from July 2008 to June 2011 were included. Patients were categorized into those exposed and not exposed to thiazolidinediones (TZDs). PSs were estimated by using conventional PS and CTS-PS. In the CTS-PS, PS was separately estimated for three specific calendar time periods. Patients were matched 1:1 using caliper matching. The outcomes were cardiovascular and all-cause hospitalizations. The TZD and non-TZD groups were compared with Cox proportional hazard models.
RESULTS: A total of 2165 patients were included. The average conventional PS was 0.198 (95% confidence interval [CI] 0.195-0.202), while the average PS in the CTS-PS approach was 0.212 (0.206-0.218), 0.180 (0.173-0.188), and 0.205 (0.197-0.213) for July 2008 to June 2009, July 2009 to June 2010, and July 2010 to June 2011, respectively. The average difference in PS was 0.012 (P < 0.001), -0.009 (P ≤ 0.002), and 0.000 (P = 0.950) in the three calendar time periods. The adjusted hazard ratios of the conventional PS-matched cohort were 0.97 (95% CI 0.39-2.45) and 0.97 (95% CI 0.78-1.20) for CVD-related and all-cause hospitalizations, while the adjusted hazard ratios of the CTS-PS-matched cohort were 1.11 (95% CI 0.43-2.88) and 1.12 (95% CI 0.91-1.39), respectively.
CONCLUSION: CTS-PS is different from PS estimated by using the conventional approach. CTS-PS should be considered when a pattern of medication use has changed over the study period.
Methods: Pseudopregnancy (pc) was induced in cyclic Sprague-Dawley rats by sterile mating. Subcutaneous injection of nicotine tartrate (7.5 mg/kg/day) was scheduled from day 1 through day 5, day 5 through day 9 or day 1 through day 9 of pc. In another group of pseudopregnant rats, concomitant treatment of nicotine tartrate concurrently with progesterone (2 mg/day) was scheduled from day 1 through day 9 pc. Control groups received subcutaneous injections of vehicle only. Endometrial decidualization was induced on day 5 pc. On day 10 pc, animals were sacrificed.The degree of decidual growth and circulating levels of estrogen and progesterone were measured.
Results: The decidual growth in all the first three nicotine-treated groups of animals was significantly reduced, particularly in the animals treated with nicotine from day 1 through day 9 pc. Plasma estrogen levels were significantly elevated in animals treated with nicotine from day 1 through day 9 pc. Conversely, levels of plasma progesterone were found to be significantly attenuated in the same group of nicotine-treated animals compared to controls. Exogenous replacement of progesterone, however, caused a higher degree of endometrial decidualization compared to the nicotine-treated group but it was slightly less than when compared to control.
Conclusions: In conclusion, nicotine-induced progesterone deficiency with a corresponding elevation of estrogen may possibly attenuate the degree of endometrial decidualization in pseudopregnant rats.
Methods: A retrospective study of a total of 106 microbiologically febrile episodes in hospitalized adult neutropenic cancer patients, who were admitted from May 2009 to May 2013, at King Fahad Specialist Hospital, Dammam, Saudi Arabia, was conducted.
Results: Among 106 microbiologically documented febrile neutropenic episodes, the majority of malignancies were solid tumors accounting for 53.8% (57/106) and hematological malignancies accounted for 46.23% (49/106). The most common malignancies were non-Hodgkin's lymphoma 19.81% (21/106) followed by acute myeloid leukemia 15.09% (16/106), then colorectal cancer 13.21% (14/106), pancreatic cancer and acute lymphoblastic leukemia accounting for 5.66% (6/106) each, multiple myeloma 4.72% (5/106), gall bladder cancer 3.77% (4/106), and lung cancer 2.83% (3/106). A total of 138 bacterial isolates were identified. The overall prevalence of gram-negative bacteria was 65.94% (91/138) and for gram-positive bacteria was 34.06% (47/138). The most common bacterial isolation sites were blood 33.32% (46 isolates), urine 29.71% (41 isolates), wound 19.55% (27 isolates), body fluids 9.41% (13 isolates) and sputum 7.96% (11 isolates). The most predominant pathogens were Escherichia coli 30.43 (42/138), Klebsiella pneumonia 14.49% (20/138), Staphylococcus aureus 13.04% (18/138), Sptreptococcus spp. 7.25% (10/138), Pseudomonas spp. 7.25% (10/138), Enterococcus spp. 5.80% (8/138), Staphylococcus spp. 4.35% (6/138), Corynebacterium spp. 3.62% (5/138), Enterobacter spp. 3.62% (5/138), Acinobacter spp. 2.90% (4/138), Serratia marcescens 2.17% (3/138), Proteus mirabilis 1.45% (2). Aeromonas hydrophylia, Citrobacter freundii, Providencia stuartii, Sphingomonas paucimobilis and Stenotropomonas multipholia contributed to 0.72% with one isolate each. For gram-negative Escherichia coli and Klebsiella pneumonia, the extended-spectrum beta-lactamases producers (ESBLs) rates were 38% and 22.22% respectively. For Pseudomonas aerugenosa imipenem-cilastatin resistance rate was 18.84%. For gram-positive bacteria, methicillin-resistant Staphylococcus aureus (MRSA) rate was 28.62%. The vancomycin-resistant Enterococci (VRE) rate was 1.18%.
Conclusion: Gram-negative bacteria were more prevalent as a cause of infection in adult cancer patients with febrile neutropenia at our institution, with Escherichia coli and Klebsiella pneumonia with high ESBLs rates being the most common pathogens. Blood stream infections followed by urinary tract infections were the most common sites of infection. The use of initial antibiotic therapy in febrile neutropenic episodes should be based on local bacterial spectrum and susceptibility/sensitivity patterns to prevent treatment failure with increased morbidity and mortality.
METHOD: Cleistanthins A and B were isolated from the leaves of Cleistanthus collinus. Both the compounds were administered orally for 90 days at the concentration of 12.5, 25 and 50 mg/kg, and the effects on blood pressure, biochemical parameters and histology were assessed. The dose for sub-chronic toxicology was determined by fixed dose method according to OECD guidelines.
RESULT: Sub-chronic toxicity study of cleistanthins A and B spanning over 90 days at the dose levels of 12.5, 25 and 50 mg/kg (once daily, per oral) revealed a significant dose dependant toxic effect in lungs. The compounds did not have any effect on the growth of the rats. The food and water intake of the animals were also not affected by both cleistanthins A and B. Both the compounds did not have any significant effect on liver and renal markers. The histopathological analysis of both cleistanthins A and B showed dose dependent morphological changes in the brain, heart, lung, liver and kidney. When compared to cleistanthin A, cleistanthin B had more toxic effect in Wistar rats. Both the compounds have produced a dose dependent increase of corpora amylacea in brain and induced acute tubular necrosis in kidneys. In addition, cleistanthin B caused spotty necrosis of liver in higher doses.
CONCLUSION: The present study concludes that both cleistanthin A and cleistanthin B exert severe toxic effects on lungs, brain, liver, heart and kidneys. They do not cause any significant pathological change in the reproductive system; neither do they induce neurodegenerative changes in brain. When compared to cleistanthin A, cleistanthin B is more toxic in rats.