Sano Motoharu No Damage Rar Extractor

Motoharu Sano - No Damage Source: CDDA Genre. Unlimited access to all sources file with one click direct. Motoharu sano no damage rar - SuckX.me - Free Porn Videos Diana Siefert - Rar Clip - Vhs Ripped. The content of this module cannot be visible by unauthenticated users. Please login in order to. Plasma Levels of Middle Molecules to Estimate Residual Kidney Function in Haemodialysis without Urine Collection Cover. Oxidant stress evoked damage in rat hepatocyte leading to triggered nitric oxide synthase (NOS) levels on long term consumption of aspartame. Tanito M, Sano I, Ohira A.

• Zaitone, Sawsan A; Abo-Elmatty, Dina M; Elshazly, Shimaa M 2012-01-01 To evaluate the neuroprotective effect of the nootropic drugs, piracetam (PIR) and vinpocetine (VIN), in rotenone- induced Parkinsonism in rats. Sixty male rats were divided into 6 groups of 10 rats each. The groups were administered vehicle, control (rotenone, 1.5 mg/kg/48 h/6 doses, s.c.), PIR (100 and 200 mg/kg/day, p.o.) and VIN (3 and 6 mg/kg/day, p.o.). The motor performance of the rats was evaluated by the open field and pole test.

Striatal dopamine level, malondialdehyde (MDA), reduced glutathione (GSH) and tumor necrosis factor-α (TNF-α) were assayed. Histopathological study of the substantia nigra was also done. Results showed that rotenone-treated rats exhibited bradykinesia and motor impairment in the open-field test. In addition, GSH level was decreased whereas MDA and TNF-α increased in striata of rotenone-treated rats as compared to vehicle-treated rats. Marked degeneration of the substantia nigra pars compacta (SNpc) neurons and depletion of striatal dopamine was also observed in the rotenone-treated rats. Treatment with PIR or VIN significantly reversed the locomotor deficits and increased striatal dopamine level.

Treatment with VIN significantly (P. • Lobina, Carla; Carai, Mauro A M; Loi, Barbara; Gessa, Gian Luigi; Riva, Antonella; Cabri, Walter; Petrangolini, Giovanna; Morazzoni, Paolo; Colombo, Giancarlo 2014-05-01 This study investigated the protective effect of a standardized extract of Panax ginseng on multiple cisplatin- induced 'sickness behaviors' (model of cancer- induced cachexia) in rats.

Cisplatin was administered twice weekly (1-2 mg/kg, intraperitoneal) for 5 consecutive weeks. Panax ginseng extract (0, 25 and 50 mg/kg, intragastric) was administered daily over the 5-week period of cisplatin exposure. Malaise, bodyweight and temperature, pain sensitivity, and endurance running were recorded at baseline and at 5 weekly intervals. Treatment with cisplatin produced severe signs of malaise, marked loss of bodyweight, hypothermia, hyperalgesia and reduction in running time. Treatment with Panax ginseng extract completely prevented all cisplatin- induced alterations. These data indicate that treatment with Panax ginseng extract exerted a protective effect in a rat model of cachexia and suggest that Panax ginseng extract may be a therapeutic promising tool for supportive care in oncology. • Kiss, Peter; Vadasz, Gyongyver; Kiss-Illes, Blanka; Horvath, Gabor; Tamas, Andrea; Reglodi, Dora; Koppan, Miklos 2013-01-01 Perinatal asphyxia during delivery produces long-term disability and represents a major problem in neonatal and pediatric care.

Numerous neuroprotective approaches have been described to decrease the effects of perinatal asphyxia. Enriched environment is a popular strategy to counteract nervous system injuries.

The aim of the present study was to investigate whether enriched environment is able to decrease the asphyxia- induced neurobehavioral developmental delay in neonatal rats. Asphyxia was induced in ready-to-deliver mothers by removing the pups by caesarian section after 15 min of asphyxia. Somatic and neurobehavioral development was tested daily and motor coordination weekly. Our results show that rats undergoing perinatal asphyxia had a marked developmental delay and worse performance in motor coordination tests. However, pups kept in enriched environment showed a decrease in the developmental delay observed in control asphyctic pups. Rats growing up in enriched environment did not show decrease in weight gain after the first week and the delay in reflex appearance was not as marked as in control rats. In addition, the development of motor coordination was not as strikingly delayed as in the control group.

Short-term neurofunctional outcome are known to correlate with long-term deficits. Our results thus show that enriched environment could be a powerful strategy to decrease the deleterious developmental effects of perinatal asphyxia. PMID:24232451 • Peter Kiss 2013-11-01 Full Text Available Perinatal asphyxia during delivery produces long-term disability and represents a major problem in neonatal and pediatric care. Numerous neuroprotective approaches have been described to decrease the effects of perinatal asphyxia. Enriched environment is a popular strategy to counteract nervous system injuries. The aim of the present study was to investigate whether enriched environment is able to decrease the asphyxia- induced neurobehavioral developmental delay in neonatal rats.

Asphyxia was induced in ready-to-deliver mothers by removing the pups by caesarian section after 15 min of asphyxia. Somatic and neurobehavioral development was tested daily and motor coordination weekly. Our results show that rats undergoing perinatal asphyxia had a marked developmental delay and worse performance in motor coordination tests. However, pups kept in enriched environment showed a decrease in the developmental delay observed in control asphyctic pups. Rats growing up in enriched environment did not show decrease in weight gain after the first week and the delay in reflex appearance was not as marked as in control rats.

In addition, the development of motor coordination was not as strikingly delayed as in the control group. Short-term neurofunctional outcome are known to correlate with long-term deficits. Our results thus show that enriched environment could be a powerful strategy to decrease the deleterious developmental effects of perinatal asphyxia. • Al-Harbi, Naif O; Imam, Faisal; Al-Harbi, Mohammed M; Iqbal, Muzaffar; Nadeem, Ahmed; Sayed-Ahmed, Mohammed M; Alabidy, Ali D; Almukhallafi, Ali F 2014-01-01 Tacrolimus, a calcineurin inhibitor, is clinically used as an immunosuppressive agent in organ transplantation, but its use is limited due to its marked nephrotoxicity.

The present study investigated the effect of olmesartan (angiotensin receptor blocker) on tacrolimus- induced nephrotoxicity in rats. A total of 24 rats were divided into four groups, which included control, tacrolimus, tacrolimus + olmesartan, and olmesartan groups. Tacrolimus- induced nephrotoxicity was assessed biochemically and histopathologically. Tacrolimus significantly increased BUN and creatinine level. Treatment with olmesartan reversed tacrolimus- induced changes in the biochemical markers (BUN and creatinine) of nephrotoxicity. Tacrolimus significantly decreased GSH level and catalase activity while increasing MDA level. Sound Horizon Elysion Rarlab. Olmesartan also attenuated the effects of tacrolimus on MDA, GSH, and catalase.

In tacrolimus group histological examination showed marked changes in renal tubule, mitochondria, and podocyte processes. Histopathological and ultrastructural studies showed that treatment with olmesartan prevented tacrolimus- induced renal damage. These results suggest that olmesartan has protective effects on tacrolimus- induced nephrotoxicity, implying that RAS might be playing role in tacrolimus- induced nephrotoxicity.

Al-Harbi 2014-01-01 Full Text Available Tacrolimus, a calcineurin inhibitor, is clinically used as an immunosuppressive agent in organ transplantation, but its use is limited due to its marked nephrotoxicity. The present study investigated the effect of olmesartan (angiotensin receptor blocker on tacrolimus- induced nephrotoxicity in rats. A total of 24 rats were divided into four groups, which included control, tacrolimus, tacrolimus + olmesartan, and olmesartan groups. Tacrolimus- induced nephrotoxicity was assessed biochemically and histopathologically. Tacrolimus significantly increased BUN and creatinine level. Treatment with olmesartan reversed tacrolimus- induced changes in the biochemical markers (BUN and creatinine of nephrotoxicity. Tacrolimus significantly decreased GSH level and catalase activity while increasing MDA level.

Olmesartan also attenuated the effects of tacrolimus on MDA, GSH, and catalase. In tacrolimus group histological examination showed marked changes in renal tubule, mitochondria, and podocyte processes. Histopathological and ultrastructural studies showed that treatment with olmesartan prevented tacrolimus- induced renal damage. These results suggest that olmesartan has protective effects on tacrolimus- induced nephrotoxicity, implying that RAS might be playing role in tacrolimus- induced nephrotoxicity.

• Zabrodin, O. 1980-01-01 The mechanism of development of experimental gastric ulcers, induced in rats by combined immobilization and electric shock, was analyzed pharmacologically with peripheral neurotropic agents. It is concluded that: (1) The most marked preventive effect in the development of the experimentally induced gastric ulcers was displayed by agents capable of blocking the ascending activation system of the reticular formation.

(2) Sympathetic fibers, which disrupt the trophism of the gastric wall, form the efferent portion of the reflex arc. (3) Gastric secretion does not appear to be the primary cause of ulceration. • Al-Roujayee, Abdulaziz S 2017-04-01 Objective To evaluate the effect of the phenolic compound naringenin on thermal burn- induced inflammatory responses and oxidative stress in rats. Methods First degree thermal burn injuries were induced in shaved rats by 10 s immersion of the back surface in water at 90℃. Naringenin treatment (25, 50 and 100 mg/kg/day) was initiated 24 h following burn injury, and continued for 7 days. On treatment day 7, serum tumour necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, nitric oxide (NO), prostaglandin (PG)E2, caspase-3, leukotriene (LT)-B4 and nuclear factor (NF)-κB levels were quantified. Skin sample glutathione (GSH) and thiobarbituric acid reactive substances (TBARS) levels, and catalase, superoxide dismutase (SOD), glutathione-S-transferase (GST) and glutathione peroxidase (GPx) activities, were also measured.

Results Serum inflammatory biomarkers were significantly increased in thermal-burn injured rats versus uninjured controls. Naringenin significantly inhibited the increased proinflammatory markers at day 7 of treatment. Increased TBARS levels and decreased GSH levels in wounded skin were significantly restored by naringenin treatment at day 7. SOD, catalase, GPx and GST activities were markedly inhibited in wounded skin tissues, and were significantly increased in naringenin-treated rats.

Conclusion Naringenin treatment showed anti-inflammatory and antioxidant effects in rats with thermal burn- induced injury. • Mulyanto; Suparyatmo, Joseph Benedictus; Andayani, I Gusti Ayu Sri; Khalid; Takahashi, Masaharu; Ohnishi, Hiroshi; Jirintai, Suljid; Nagashima, Shigeo; Nishizawa, Tsutomu; Okamoto, Hiroaki 2014-01-22 Rat hepatitis E virus (HEV) strains have recently been isolated in several areas of Germany, Vietnam, the United States, Indonesia and China. However, genetic information regarding these rat HEV strains is limited. A total of 369 wild rats (Rattus rattus) captured in Central Java (Solo) and on Lombok Island, Indonesia were tested for the presence of rat HEV-specific antibodies and RNA. Overall, 137 rats (37.1%) tested positive for rat anti-HEV antibodies, while 97 (26.3%) had rat HEV RNA detectable on reverse transcription-PCR with primers targeting the ORF1-ORF2 junctional region.

The 97 HEV strains recovered from these viremic rats were 76.3-100% identical to each other in an 840-nucleotide sequence and 75.4-88.4% identical to the rat HEV strains reported in Germany and Vietnam. Five representative Indonesian strains, one from each of five phylogenetic clusters, whose entire genomic sequence was determined, were segregated into three genetic groups (a German type, Vietnamese type and novel type), which differed from each other by 19.5-23.5 (22.0 ± 1.7)% over the entire genome. These results suggest the presence of at least three genetic groups of rat HEV and indicate the circulation of polyphyletic strains of rat HEV belonging to three distinct genetic groups in Indonesia. Copyright © 2013 Elsevier B.V.

All rights reserved. • Yousef, Hany N; Aboelwafa, Hanaa R 2017-02-08 Nephrotoxicity is common with the use of the chemotherapeutic agent 5-Fluorouracil (5-FU). The current study aimed to investigate the probable protective effect of taurine (TAU) against 5-FU- induced nephrotoxicity in rats using biochemical, histological and ultrastructural approaches. Twenty-four rats were equally divided into control, TAU, 5-FU and 5-FU+TAU groups. 5-FU significantly elevated levels of blood urea nitrogen (BUN), creatinine, and uric acid; while it reduced activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). Also, 5-FU induced significant elevation in malondialdehyde (MDA) levels accompanied with marked decline in γ-glutamyltranspeptidase (GGT) and alkaline phosphatase (AP) levels in kidney tissues.

These biochemical alterations were accompanied by histopathological changes marked by destruction of the normal renal structure, in addition to ultrastructural alterations represented by thickened and irregular glomerular basement membranes, congested glomerular capillaries, damaged lining fenestrated endothelium, mesangial cells hyperplasia with expanded mesangial matrix, and distorted podocyte's processes. Also, the proximal (PCT) and distal (DCT) convoluted tubules showed thickened basement membranes, destructed apical microvilli and loss of basal infoldings of their epithelial cells. Administration of TAU to 5-FU-treated rats reversed most of the biochemical, histological, and ultrastructural alterations. These results indicate that TAU has a protective effect against 5-FU- induced nephrotoxicity. • Bejar, Wacim; Hamden, Khaled; Ben Salah, Riadh; Chouayekh, Hichem 2013-12-01 This study aimed to assess the potential of the probiotic strain Lactobacillus plantarum TN627 for preventing alloxan- induced diabetes in rats. The oral administration of this probiotic was noted to significantly improve the immunological parameters, protect the pancreatic tissues, and reduce the pancreatic and plasmatic α-amylase activities and level of plasma glucose in the treated as compared to the control group of rats. Furthermore, this probiotic treatment was observed to markedly reduce pancreatic and plasmatic lipase activities and serum triglyceride and LDL-cholesterol rates and to increase the level of HDL-Cholesterol.

It also exerted efficient protective effects on the liver and kidney functions evidenced by significant decreases in serum aspartate transaminase, alanine transaminase, lactate dehydrogenase, and gamma-glutamyl transpeptidase activities, as well as creatinine and urea contents. Taken together, the findings indicate that L.

Plantarum TN627 exhibits attractive in vivo antidiabetic effects that may be helpful in preventing diabetic complications in adult rats. • Lee, Ji-Young; Kim, Bong Jo; Sim, Gyujin; Kim, Gyu-Tae; Kang, Dawon; Jung, Jae Hun; Hwa, Jeong Seok; Kwak, Yeon Ju; Choi, Yeon Jin; Park, Young Sook; Han, Jaehee; Lee, Cheol Soon; Kang, Kee Ryeon 2011-06-01 The influence of spinal cord injury (SCI) on protein expression in the rat urinary bladder was assessed by proteomic analysis at different time intervals post-injury. After contusion SCI between T9 and T10, bladder tissues were processed by 2-DE and MALDI-TOF/MS at 6 hr to 28 days after SCI to identify proteins involved in the healing process of SCI- induced neurogenic bladder.

Approximately 1,000 spots from the bladder of SCI and sham groups were visualized and identified. At one day after SCI, the expression levels of three protein were increased, and seven spots were down-regulated, including heat shock protein 27 (Hsp27) and heat shock protein 20 (Hsp20). Fifteen spots such as S100-A11 were differentially expressed seven days post-injury, and seven proteins including transgelin had altered expression patterns 28 days after injury. Of the proteins with altered expression levels, transgelin, S100-A11, Hsp27 and Hsp20 were continuously and variably expressed throughout the entire post-SCI recovery of the bladder.

The identified proteins at each time point belong to eight functional categories. The altered expression patterns identified by 2-DE of transgelin and S100-A11 were verified by Western blot. Transgelin and protein S100-A11 may be candidates for protein biomarkers in the bladder healing process after SCI.

• Zubin Zhou 2017-08-01 Full Text Available Osteomyelitis is commonly caused by Staphylococcus aureus. Both erythromycin and curcumin can suppress S. Aureus growth, but their roles in osteomyelitis are barely studied. We aim to explore the activities of erythromycin and curcumin against chronical osteomyelitis induced by methicillin-resistant S. Aureus (MRSA. Chronicle implant- induced osteomyelitis was established by MRSA infection in male Wistar rats. Four weeks after bacterial inoculation, rats received no treatment, erythromycin monotherapy, curcumin monotherapy, or erythromycin plus curcumin twice daily for 2 weeks.

Bacterial levels, bone infection status, inflammatory signals and side effects were evaluated. Rats tolerated all treatments well, with no death or side effects such as, diarrhea and weight loss. Two days after treatment completion, erythromycin monotherapy did not suppress bacterial growth and had no effect in bone infection, although it reduced serum pro-inflammatory cytokines tumor necrosis factor (TNF-α and interleukin (IL-6. Curcumin monotherapy slightly suppressed bacterial growth, alleviated bone infection and reduced TNF-α and IL-6. Erythromycin and curcumin combined treatment markedly suppressed bacterial growth, substantially alleviated bone infection and reduced TNF-α and IL-6. Combination of erythromycin and curcumin lead a much stronger efficiency against MRSA induced osteomyelitis in rats than monotherapy.

Our study suggests that erythromycin and curcumin could be a new combination for treating MRSA induced osteomyelitis. • Xu, Lin-Lin; Liu, Meng-Ling; Wang, Jing-Lei; Yu, Mei; Chen, Jia-Xiang 2016-04-01 Tri-ortho-cresyl phosphate (TOCP) has been widely used as plasticizers, plastic softeners, and flame-retardants in industry, which can be metabolized to High-toxic saligenin cyclic-o-tolyl phosphate (SCOTP). Our previous results found that TOCP could disrupt the seminiferous epithelium in the testis and induce autophagy of rat spermatogonial stem cells. Little is known about the toxic effect of SCOTP on rat spermatogonial stem cells. The present study showed that SCOTP decreased viability of rat spermatogonial stem cells in a dose-dependent manner. Both LC3-II and the ratio of LC3-II/LC3-I were significantly increased; autophagy proteins atg5 and Beclin 1 were also markedly increased after treatment with SCOTP, indicating SCOTP could induce autophagy of the cells. Ultrastructural observation under the transmission electron microscopy (TEM) indicated that there were autophagic vacuoles in the cytoplasm in the SCOTP-treated cells.

However, cell cycle arrest was not observed by flow cytometry; and the mRNA levels of p21, p27, p53 and cyclin D1 in the cells were also not affected by SCOTP. Meanwhile, SCOTP didn't induce apoptosis of the cells. In summary, we showed that SCOTP could induce autophagy of rat spermatogonial stem cells, without affecting cell cycle and apoptosis. • Raghavendran, Hanumantha Rao Balaji; Rekha, Sathyanath; Shin, Jang-Woo; Kim, Hyeong-Geug; Wang, Jing-Hua; Park, Hye-Jung; Choi, Min-Kyung; Cho, Jung-Hyo; Son, Chang-Gue 2011-01-01 In the present study, we investigate the effect of Korean ginseng root extract (KG) on cisplatin- induced pica in a rat model. Rats were treated with KG before (25, 50, and 100 mg/kg) or after (12.5, 25, and 50 mg/kg) a single intraperitoneal injection of cisplatin (7 and 6 mg/kg, respectively). We examined intake of kaolin and normal food as an indicator of the emetic stimulus every 24 h for 120 h.

Changes in body weight, haematology and histopathology were additionally assessed. Pre-treatment with KG (25 and 50 mg/kg) significantly attenuated cisplatin- induced kaolin intake (24, 48, and 72 h) and markedly improved intake of normal food by rats at 48, 72, 96, and 120 h. Cisplatin- induced kaolin intake was markedly decreased upon post-treatment of rats with KG (12.5, 25, and 50 mg/kg) at 24 h. Notably, post-treatment with the lowest KG dose resulted in a significant anti-pica effect and improved food intake until 72 h. The magnitude of body weight reduction was significantly diminished in rats pre-treated/post-treated with 25, 50, and 12.5 mg/kg KG. The anti-pica effects of KG were further confirmed with haematological and histopathological findings.

Our findings collectively indicate that KG improves the resistance of rats against emesis. • Cui-ling LIU; Yu HUANG; Ching-yuen NGAI; Yuk-ki LEUNG; Xiao-qiang YAO 2006-01-01 Aim: To test the possible involvement of TRPC3 in agonist- induced relaxation and flow- induced vasodilation in rat small mesenteric arteries. Methods: Male Sprague-Dawley rats were used in the present study. After 72 h-treatment of antisense oligo via tail vein injection, isometric tension and isobaric diameter measurement were carried out with isolated mesenteric artery segments by using either a Pressure Myograph or a Multi Myograph system. Endothelial [Ca2+]i changes were measured with a MetaFluor imaging system in response to flow or to 30 nmol/L bradykinin. Results: Immunohistochemical study showed that the 72 h-treatment of antisense oligo via tail vein injection markedly decreased the TRPC3 expression in mesenteric arteries, indicating the effectiveness of the antisense oligo. Isometric tension and isobaric diameter measurement showed that, although the antisense oligo treatment did not affect histamine-, ATP-, and CPA- induced relaxation, it did reduce the magnitude of flow- induced vasodilation by approximately 13% and decreased bradykinin- induced vascular relaxation with its EC50 value raised by nearly 3-fold.

Endothelial [Ca2+]i measurement revealed that treatment of the arteries with antisense oligos significantly attenuated the magnitude of endothelial [Ca2+]i rise in response to flow and to 30 nmol/L bradykinin. Conclusion: The results suggest that TRPC3 is involved in flow- and bradykinin- induced vasodilation in rat small mesenteric arteries probably by mediating the Ca2+ influx into endothelial cells. • Elbe, H; Esrefoglu, M; Vardi, N; Taslidere, E; Ozerol, E; Tanbek, K 2015-09-01 In this study, effects of melatonin, quercetin and resveratrol on hepatocellular injury in streptozotocin (STZ)- induced experimental diabetes were aimed to be investigated by histological and biochemical methods. Thirty-five male Wistar albino rats were divided into five groups, namely, control, diabetes (STZ 45 mg/kg/single dose/intraperitoneally (ip)), diabetes + melatonin (10 mg/kg/30 days/ip), diabetes + quercetin (25 mg/kg/30 days/ip) and diabetes + resveratrol (10 mg/kg/30 days/ip). Initial and final blood glucose levels and body weights (BWs) were measured.

At the end of the experimentation, following routine tissue processing procedure, sections were stained with haematoxylin-eosin (H-E), periodic acid Schiff and Masson's trichrome. Tissue malondialdehyde (MDA) and glutathione (GSH) levels and superoxide dismutase (SOD) and catalase (CAT) activities were examined. The diabetic rats had significantly higher blood glucose levels than those of control rats (p = 0.0001). Mean BWs of diabetic rats were significantly decreased when compared with the control rats (p = 0.0013). Histopathological alterations including cellular glycogen depletion, congestion, sinusoidal dilatation, inflammation and fibrosis were detected in diabetes group. On the other hand, histopathological changes markedly reduced in all of the treatment groups (p = 0.001). Mean tissue MDA level was increased but mean tissue CAT and SOD activities and GSH levels were decreased in the diabetes group.

Melatonin, quercetin and resveratrol administered diabetic rats showed an increase in CAT activities and GSH levels and a decrease in MDA levels (p Melatonin, quercetin and resveratrol administrations markedly reduced hepatocellular injury in STZ- induced experimental diabetes. • Jung, S; Choi, H-J; Park, H-K; Jo, W; Jang, S; Ryu, J-E; Kim, W-J; Yu, E-S; Son, W-C 2014-08-01 The Sleeping Beauty (SB) transposon system is an important tool for genetic studies. It is used to insert a gene of interest into the host chromosome, thus enabling permanent gene expression. However, this system is less useful in higher eukaryotes because the transposition frequency is low. Efforts to improve the efficacy of the SB transposon system have focused on the method of gene delivery, but although electroporation has recently attracted much attention as an in vivo gene delivery tool, the simultaneous use of electroporation and the SB transposon system has not been studied for gene transfer in mice.

In this study, electroporation was used in a model of SB transposon- induced insertional tumorigenesis. Electroporation increased the rate of tumor development to three times that of the control group. There was no difference in phenotype between tumors induced with the SB transposon system alone and those induced by the SB transposon and electroporation.

Electroporation therefore may be an efficient means of improving the efficacy of gene transfer via the SB transposon system. • Adriana Borriello Full Text Available BACKGROUND: The introduction of specific BCR-ABL inhibitors in chronic myelogenous leukemia therapy has entirely mutated the prognosis of this hematologic cancer from being a fatal disorder to becoming a chronic disease. Due to the probable long lasting treatment with tyrosine-kinase inhibitors (TKIs, the knowledge of their effects on normal cells is of pivotal importance.

DESIGN AND METHODS: We investigated the effects of dasatinib treatment on human bone marrow-derived mesenchymal stromal cells (MSCs. RESULTS: Our findings demonstrate, for the first time, that dasatinib induces MSCs adipocytic differentiation. Particularly, when the TKI is added to the medium inducing osteogenic differentiation, a high MSCs percentage acquires adipocytic morphology and overexpresses adipocytic specific genes, including PPARγ, CEBPα, LPL and SREBP1c. Dasatinib also inhibits the activity of alkaline phosphatase, an osteogenic marker, and remarkably reduces matrix mineralization. The increase of PPARγ is also confirmed at protein level.

The component of osteogenic medium required for dasatinib- induced adipogenesis is dexamethasone. Intriguingly, the increase of adipocytic markers is also observed in MSCs treated with dasatinib alone. The TKI effect is phenotype-specific, since fibroblasts do not undergo adipocytic differentiation or PPARγ increase.

CONCLUSIONS: Our data demonstrate that dasatinib treatment affects bone marrow MSCs commitment and suggest that TKIs therapy might modify normal phenotypes with potential significant negative consequences. • Irizar, A; Ioannides, C 1998-04-03 The objective of the present study was to investigate the expression of major xenobiotic-metabolising cytochrome P450 proteins, and of other enzyme systems, in hepatic and extrahepatic tissues of rabbits rendered atherosclerotic by the dietary administration of 1% cholesterol diets for 8 weeks. Individual cytochrome P450 proteins were monitored using diagnostic substrates and immunologically in Western blot analysis. The activity of all hepatic isoforms studied was depressed in the atherosclerotic animals; when, however, apoprotein levels were determined immunologically, no major differences were evident between the control and the atherosclerotic rabbits. In vitro studies indicated that neither cholesterol nor palm oil inhibited cytochrome P450 activity.

The effects of cholesterol treatment leading to atherosclerosis on kidney, heart and lung cytochrome P450 activities were isoform- and tissue-specific; no change was evident in the heart activities, but in the lung and kidney cytochrome P450 activities were clearly modulated by the treatment with cholesterol. Apoprotein levels did not always parallel the changes in activities. Western blot analysis of aortic cytochromes P450 revealed that administration of cholesterol-rich diets enhanced CYP2B and CYP3A apoprotein levels. Cholesterol feeding to rabbits gave rise to a marked decrease in hepatic glutathione S-transferase activity but did not influence glutathione reductase or total glutathione levels.

Antonio Jose Sonata Pdf To Excel. The same treatment had no effect on catalase, glutathione peroxidase and superoxide dismutase. It is concluded that treatment of rabbits with cholesterol-rich diets leading to atherosclerosis gives rise to profound changes in the expression of cytochrome P450 proteins in the liver and other tissues; possible mechanisms are discussed. • Burguera, B; Hofbauer, L C; Thomas, T; Gori, F; Evans, G L; Khosla, S; Riggs, B L; Turner, R T 2001-01-01. Serum leptin levels are strongly and directly related to fat body mass.

We report here the effects of leptin administration compared with estrogen therapy on ovariectomy- induced bone loss in rats. • Purushothaman, Ayyakkannu; Nandhakumar, Elumalai; Shanthi, Palanivelu; Sachidanandam, Thiruvaiyaru Panchanatham 2015-10-01 A herbal preparation, Shemamruthaa (SM), was formulated to investigate the molecular mechanism by which it exhibits anticancer effects in mammary carcinoma bearing rats. Female Sprague-Dawley rats were used for the study, and mammary carcinoma was induced by administration of 7,12-dimethylbenz(a)anthracene, intragastrically.

After 3 months of induction period, the rats were treated with SM (400 mg/kg body weight) for 14 days. Our study shows that SM-treated mammary carcinoma rats showed regression in tumor volume with concomitant increase in p(53), Bax, caspase-3, and caspase-9 mRNA and protein levels compared with mammary carcinoma- induced rats. Proliferating cell nuclear antigen and anti-apoptotic Bcl-2 were markedly increased in mammary carcinoma- induced rats, whereas the SM treatment significantly decreased the expression of these proteins. The expression pattern of apoptotic signaling molecules analyzed in the present study signifies the therapeutic efficacy of SM against breast cancer. • Benter, Ibrahim F. 2017-01-01 Molecular mechanisms of the beneficial effects of angiotensin-(1-7), Ang-(1-7), in diabetes-related complications, including erectile dysfunction, remain unclear. We examined the effect of diabetes and/or Ang-(1-7) treatment on vascular reactivity and cyclic guanosine monophosphate (cGMP) phosphodiesterase (PDE) in corpus cavernosum.

Male Wistar rats were grouped as (1) control, (2) diabetic (streptozotocin, STZ, treated), (3) control + Ang-(1-7), and (4) diabetic + Ang-(1-7). Following 3 weeks of Ang-(1-7) treatment subsequent to induction of diabetes, rats were sacrificed.

Penile cavernosal tissue was isolated to measure vascular reactivity, PDE gene expression and activity, and levels of p38MAP kinase, nitrites, and cGMP. Carbachol- induced vasorelaxant response after preincubation of corpus cavernosum with PE was significantly attenuated in diabetic rats, and Ang-(1-7) markedly corrected the diabetes- induced impairment. Gene expression and activity of PDE and p38MAP kinase were significantly increased in cavernosal tissue of diabetic rats, and Ang-(1-7) markedly attenuated STZ- induced effects. Ang-(1-7) significantly increased the levels of nitrite and cGMP in cavernosal tissue of control and diabetic rats.

Cavernosal tissue of diabetic rats had significantly reduced cGMP levels and Ang-(1-7) markedly prevented the STZ- induced cGMP depletion. This study demonstrates that attenuation of diabetes- induced PDE activity might be one of the key mechanisms in the beneficial effects of Ang-(1-7). • Maharshi Bhaswant 2015-09-01 Full Text Available Both black (B and green (G cardamom are used as flavours during food preparation.

This study investigated the responses to B and G in a diet- induced rat model of human metabolic syndrome. Male Wistar rats were fed either a corn starch-rich diet (C or a high-carbohydrate, high-fat diet with increased simple sugars along with saturated and trans fats (H for 16 weeks. H rats showed signs of metabolic syndrome leading to visceral obesity with hypertension, glucose intolerance, cardiovascular remodelling and nonalcoholic fatty liver disease. Food was supplemented with 3% dried B or G for the final eight weeks only. The major volatile components were the closely related terpenes, 1,8-cineole in B and α-terpinyl acetate in G.

HB (high-carbohydrate, high-fat + black cardamom rats showed marked reversal of diet- induced changes, with decreased visceral adiposity, total body fat mass, systolic blood pressure and plasma triglycerides, and structure and function of the heart and liver. In contrast, HG (high-carbohydrate, high-fat + green cardamom rats increased visceral adiposity and total body fat mass, and increased heart and liver damage, without consistent improvement in the signs of metabolic syndrome. These results suggest that black cardamom is more effective in reversing the signs of metabolic syndrome than green cardamom.

• Bhaswant, Maharshi; Poudyal, Hemant; Mathai, Michael L; Ward, Leigh C; Mouatt, Peter; Brown, Lindsay 2015-09-11 Both black (B) and green (G) cardamom are used as flavours during food preparation. This study investigated the responses to B and G in a diet- induced rat model of human metabolic syndrome. Male Wistar rats were fed either a corn starch-rich diet (C) or a high-carbohydrate, high-fat diet with increased simple sugars along with saturated and trans fats (H) for 16 weeks. H rats showed signs of metabolic syndrome leading to visceral obesity with hypertension, glucose intolerance, cardiovascular remodelling and nonalcoholic fatty liver disease.

Food was supplemented with 3% dried B or G for the final eight weeks only. The major volatile components were the closely related terpenes, 1,8-cineole in B and α-terpinyl acetate in G. HB (high-carbohydrate, high-fat + black cardamom) rats showed marked reversal of diet- induced changes, with decreased visceral adiposity, total body fat mass, systolic blood pressure and plasma triglycerides, and structure and function of the heart and liver. In contrast, HG (high-carbohydrate, high-fat + green cardamom) rats increased visceral adiposity and total body fat mass, and increased heart and liver damage, without consistent improvement in the signs of metabolic syndrome. These results suggest that black cardamom is more effective in reversing the signs of metabolic syndrome than green cardamom. • Subbuswamy K.

Prabu 2011-05-01 Full Text Available We have previously shown a tissue-specific increase in oxidative stress in the early stages of streptozotocin (STZ- induced diabetic rats. In this study, we investigated oxidative stress-related long-term complications and mitochondrial dysfunctions in the different tissues of STZ- induced diabetic rats (>15 mM blood glucose for 8 weeks. These animals showed a persistent increase in reactive oxygen and nitrogen species (ROS and RNS, respectively production.

Oxidative protein carbonylation was also increased with the maximum effect observed in the pancreas of diabetic rats. The activities of mitochondrial respiratory enzymes ubiquinol: cytochrome c oxidoreductase (Complex III and cytochrome c oxidase (Complex IV were significantly decreased while that of NADH:ubiquinone oxidoreductase (Complex I and succinate:ubiquinone oxidoreductase (Complex II were moderately increased in diabetic rats, which was confirmed by the increased expression of the 70 kDa Complex II sub-unit. Mitochondrial matrix aconitase, a ROS sensitive enzyme, was markedly inhibited in the diabetic rat tissues. Increased expression of oxidative stress marker proteins Hsp-70 and HO-1 was also observed along with increased expression of nitric oxide synthase. These results suggest that mitochondrial respiratory complexes may play a critical role in ROS/RNS homeostasis and oxidative stress related changes in type 1 diabetes and may have implications in the etiology of diabetes and its complications. • Kohda, Yuka; Hiramatsu, Jun; Gemba, Munekazu 2003-07-20 We have previously reported that free radical-mediated injury induced by cephaloridine (CER) is enhanced by phorbol 12-myristate 13-acetate (PMA), a protein kinase C (PKC) activator, in rat renal cortical slices. We have also shown that PKC activation in mitochondria is involved in CER- induced nephrotoxicity in rats.

We investigated the role of a downstream PKC pathway, a MEK/ERK pathway, in free radical- induced injury in rat renal cortical slices exposed to CER. Immediately after preparing slices from rat renal cortex, the slices were incubated in the medium containing MEK inhibitors. ERK1/2 activation was determined by Western blot analysis for phosphorylated ERK (pERK) 1/2 protein in nucleus fraction prepared from the slices exposed to CER. Prominently, CER caused not only increases in lipid peroxidation as an index of free radical generation and in LDH leakage as that of cell injury in the slices, but also marked activation of ERK1/2 in nucleus fraction. PD98059 and U0126, MEK1/2 inhibitors, significantly attenuated CER- induced increases in lipid peroxidation and LDH leakage in the slices.

PD98059 also suppressed ERK1/2 activation in nucleus fraction prepared from the slices treated with CER. Inhibition of other MAP kinase pathways, p38 MAP kinase and c-Jun N-terminal kinase (JNK) had no effect on CER- induced increases in lipid peroxidation level and LDH leakage in the slices. The present results suggest that a MEK/ERK pathway down stream of a PKC pathway is probably involved in free radical- induced injury in rat renal cortical slices exposed to CER.

• Saxena, Beenam; Sharma, Shiv 2015-01-01 Objective: Certain dietary constituents can induce toxicity and play a critical role in the development of several hepatic disorders. Tartrazine, metanil yellow and sunset yellow are widely used azo dyes in food products, so the present study is aimed to investigate the food color induced hepatotoxicity in Swiss albino rats. Materials and Methods: Swiss albino rats were divided into four groups, each group having six animals. Group I served as control, Group II, Group III and Group IV were ad. • Poulsen, Steen Seier 1980-01-01 Duodenal ulcers can be produced in rats within 24 h by a single subcutaneous administration of cysteamine. To determine the role of gastric acid secretion in the pathogenesis of these ulcers, secretory and pathoanatomic studies were performed in chronic fistula rats ater an ulcerogenic dose. Of cysteamine.

A prolonged increase of acid secretion was seen after cysteamine, reaching fourfold the basal level after 5 h. The acid response lasted for 10 to 11 h. After vagotomy cysteamine- induced acid secretion was markedly reduced. Ulcer formation was prevented by vagotomy and by drainage of the gastric.

For ulcer formation, the hypersecretion of acid induced by cysteamine is not the only factor responsible for the development of duodenal ulcer. • Mojtahedin, Ali; Tamaddonfard, Esmaeal; Zanboori, Ali 2008-01-01 In the present study, effects of intracerebroventricular (icv) administration of histamine, mepyramine (H1-receptor antagonist) and famotidine (H2-receptor antagonist) have been investigated on the formalin test in rats. Subcutaneous injection of formalin (50 microl, 1%) into the ventral surface of the left hind paw produced a marked biphasic pain response (first phase: 0-5 min and second phase: 15-45 min). All the performed treatments did not significantly influence the first phase of pain.

Histamine at the doses of 10 and 40 microg and mepyramine and famotidine at the same doses of 20 and 80 microg, significantly (P histamine (40 microg)- induced antinociception. These results indicate that brain histamine produces antinociception, and both central H1 and H2 receptors may involve in the histamine- induced antinociception in the formalin test in rats. • Adaramoye, Oluwatosin Adekunle; Adedara, Isaac Adegboyega; Popoola, Bosede; Farombi, Ebenezer Olatunde 2010-01-01 Ionizing radiation is an important environmental risk factor and, a major therapeutic agent for cancer treatment. This study was designed to evaluate the protective effect of extract of Xylopia aethiopica (XA) on gamma-radiation- induced testicular damage in rats. Vitamin C (VC) served as the reference antioxidant during the study. The study consists of 4 groups of 11 rats each.

Group I received corn oil (vehicle), groups II and IV were pretreated with XA (250 mg/kg) and VC (250mg/kg) for 6 weeks before and 8 weeks after exposure to gamma-radiation; group III was exposed to a single dose of gamma-radiation (5 Gy). Biochemical analysis revealed that gamma-irradiation caused a significant increase (p testicular lipid peroxidation (LPO) levels by 217% and 221%, respectively. Irradiated rats had markedly decreased testicular catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GST), and reduced glutathione (GSH) levels. Irradiation resulted in 59% and 40% decreases in spermatozoa motility and live/dead sperm count, respectively, and a 161% increase in total sperm abnormalities. Histologically, testes of the irradiated rats showed extensive degenerative changes in the seminiferous tubules and defoliation of spermatocytes. Supplementation of XA and VC reversed the adverse effects of gamma-radiation on biochemical and histological indices of the rats.

These findings demonstrated that Xylopia aethiopica has a protective effect by inhibiting oxidative damage in testes of irradiated rats. • Collares, E.F.; Vinagre, A.M.; Collares-Buzato, C.B. 2017-01-01 Atropine (AT) and dipyrone (Dp) induce a delay of gastric emptying (GE) of liquids in rats by inhibiting muscarinic receptors and activating β2-adrenergic receptors, respectively. The objective of the present study was to determine the effects of pretreatment with AT and Dp, given alone or in combination, on the effect of hypoglycemia in the liquid GE in rats. Male Wistar adult rats (280-310 g) were pretreated intravenously with AT, Dp, AT plus Dp or their vehicle and then treated 30 min later with iv insulin or its vehicle (n=8-10 animals/group).

Thirty min after treatment, GE was evaluated by determining, in awake rats, the percent gastric retention (%GR) of a saline meal labeled with phenol red administered by gavage. The results indicated that insulin induced hypoglycemia in a dose-dependent manner resulting in a significant reduction in%GR of liquid only at the highest dose tested (1 U/kg). Pretreatment with AT significantly increased%GR in the rats treated with 1 U/kg insulin. Surprisingly, after pretreatment with AT, the group treated with the lowest dose of insulin (0.25 U/kg) displayed significantly lower%GR compared to its control (vehicle-treated group), which was not seen in the non-pretreated animals. Pretreatment with Dp alone at the dose of 40 mg/kg induced an increase in%GR in both vehicle and 0.25 U/kg-treated rats. A higher dose of Dp alone (80 mg/kg) significantly reduced the effect of a marked hypoglycemia induced by 1 U/kg of insulin on GE while in combination with AT the effect was completely abolished. The results with AT suggest that moderate hypoglycemia may render the inhibitory mechanisms of GE ineffective while Dp alone and in combination with AT significantly overcame the effect of hypoglycemia on GE.

PMID:28876363 • E.F. Collares 2017-08-01 Full Text Available Atropine (AT and dipyrone (Dp induce a delay of gastric emptying (GE of liquids in rats by inhibiting muscarinic receptors and activating β2-adrenergic receptors, respectively.

The objective of the present study was to determine the effects of pretreatment with AT and Dp, given alone or in combination, on the effect of hypoglycemia in the liquid GE in rats. Male Wistar adult rats (280-310 g were pretreated intravenously with AT, Dp, AT plus Dp or their vehicle and then treated 30 min later with iv insulin or its vehicle (n=8-10 animals/group. Thirty min after treatment, GE was evaluated by determining, in awake rats, the percent gastric retention (%GR of a saline meal labeled with phenol red administered by gavage. The results indicated that insulin induced hypoglycemia in a dose-dependent manner resulting in a significant reduction in%GR of liquid only at the highest dose tested (1 U/kg. Pretreatment with AT significantly increased%GR in the rats treated with 1 U/kg insulin. Surprisingly, after pretreatment with AT, the group treated with the lowest dose of insulin (0.25 U/kg displayed significantly lower%GR compared to its control (vehicle-treated group, which was not seen in the non-pretreated animals. Pretreatment with Dp alone at the dose of 40 mg/kg induced an increase in%GR in both vehicle and 0.25 U/kg-treated rats.

A higher dose of Dp alone (80 mg/kg significantly reduced the effect of a marked hypoglycemia induced by 1 U/kg of insulin on GE while in combination with AT the effect was completely abolished. The results with AT suggest that moderate hypoglycemia may render the inhibitory mechanisms of GE ineffective while Dp alone and in combination with AT significantly overcame the effect of hypoglycemia on GE. • Jintao Yu; Dalian Ding; Hong Sun; Richard Salvi; Jerome A. Roth 2016-01-01 Trimethyltin (TMT) is an occupational and environmental health hazard behaving as a potent neurotoxin known to affect the central nervous system as well as the peripheral auditory system. However, the mechanisms underlying TMT- induced ototoxicity are poorly understood.

To elucidate the effects of TMT on the cochlea, a single injection of 4 or 8 mg/kg TMT was administered intraperitoneally to adult rats. The compound action potential (CAP) threshold was used to assess the functional status of the cochlea and histological techniques were used to assess the condition of the hair cells and auditory nerve fibers. TMT at 4 mg/kg produced a temporary CAP threshold elevation of 25e60 dB that recovered by 28 d post-treatment. Although there was no hair cell loss with the 4 mg/kg dose, there was a noticeable loss of auditory nerve fibers particularly beneath the inner hair cells. TMT at 8 mg/kg produced a large permanent CAP threshold shift that was greatest at the high frequencies.

The CAP threshold shift was associated with the loss of outer hair cells and inner hair cells in the basal, high-frequency region of the cochlea, considerable loss of auditory nerve fibers and a significant loss of spiral ganglion neurons in the basal turn. Spiral ganglion neurons showed evidence of soma shrinkage and nuclear condensation and fragmentation, morphological features of apoptotic cell death.

TMT- induced damage was greatest in the high-frequency, basal region of the cochlea and the nerve fibers beneath the inner hair cells were the most vulnerable structures. Copyright © 2016, PLA General Hospital Department of Otolaryngology Head and Neck Surgery. Production and hosting by Elsevier (Singapore) Pte Ltd. This is an open access article under the CC BY-NC-ND license (• Ahmad, Mousa Numan; Amr, Amira Mohammad 2017-06-05 Cocoa has been known for many health benefits, but its lipid-lowering activity still remains unresolved.

To investigate effects of varying amounts of defatted cocoa on serum lipids in cholesterol-fed rats. Forty-eight male Sprague-Dawley rats were randomly assigned into four cholesterol-free (control) and four cholesterol-supplemented (experimental) diets containing 0, 1, 2 or 3% defatted cocoa (DC) and given ad libitumto the rats for ten weeks. Serum total cholesterol (TC), low- and very low-density lipoprotein cholesterol (LDL-C and VLDL-C), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG) were quantified, atherogenic index (AI) was calculated, and other biological parameters were assessed. Food intake and body weight did not respond to DC.

Compared to 0% DC, 3% DC had the most prominent effect on serum lipids inducing significant fall in LDL-C and TG, and rise in TC/TG in cholesterol-deprived rats, and increase in VLDL-C and AI, and decrease in HDL-C in cholesterol-fed rats. Compared to cholesterol-deprived rats, 3% DC caused significant rise in VLDL-C, AI and TC/TG, and fall in TG in cholesterol-fed rats. This lipid-modifying effect was markedly substantiated by corresponding linear trend responses to DC. Differences in lipid variables of rats fed on DC diets were less evident.

Results suggest that, in contrast to cholesterol-free situations, defatted cocoa is seemingly incapable of counteracting the atherogenic effect of cholesterol in rats, perhaps in an interaction that is likely to have clinical implications in cardiometabolic conditions. • Kobayashi, Y; Suzuki, M; Ohshiro, N; Sunagawa, T; Sasaki, T; Tokuyama, S; Yamamoto, T; Yoshida, T 2001-08-01 We examined the effect of climbazole on the induction of rat hepatic microsomal cytochrome P450 (P450), and compared the induction potency with other N-substituted azole drugs such as clorimazole. We found that climbazole is found to be a potent inducer of rat hepatic microsomal P450 as clorimazole. Induced level of P450 by climbazole was almost similar in extent to clorimazole when compared with other imidazole drugs in a dose- and time-dependent manner. Parallel to the increase in P450, climbazole increased aminopyrine and erythromycin N-demethylase, ethoxycoumarin O-deethylase, and androstenedione 16 beta- and 15 alpha/6 beta hydroxylase activities; however, clorimazole did not induce aminopyrine N-demethylase activity irrespective of its marked increase in P450 content.

Immunoblot analyses revealed that climbazole induced CYP2B1, 3A2 and 4A1. The present findings indicate that climbazole is a new potent inducer of hepatic microsomal P450 and drug-metabolizing enzymes like clorimazole, but it may have some differential mechanism(s) for these enzymes' induction in rat liver. Teixeira Full Text Available Uroguanylin (UGN is an endogenous peptide that acts on membrane-bound guanylate cyclase receptors of intestinal and renal cells increasing cGMP production and regulating electrolyte and water epithelial transport. Recent research works demonstrate the expression of this peptide and its receptor in the central nervous system. The current work was undertaken in order to evaluate modifications of electroencephalographic spectra (EEG in anesthetized Wistar rats, submitted to intracisternal infusion of uroguanylin (0.0125 nmoles/min or 0.04 nmoles/min. The current observations demonstrate that 0.0125 nmoles/min and 0.04 nmoles/min intracisternal infusion of UGN significantly enhances amplitude and frequency of sharp waves and evoked spikes (p = 0.03.

No statistical significance was observed on absolute alpha and theta spectra amplitude. The present data suggest that UGN acts on bioelectrogenesis of cortical cells by inducing hypersynchronic firing of neurons.

This effect is blocked by nedocromil, suggesting that UGN acts by increasing the activity of chloride channels. • Teixeira, M D A; Nascimento, N R F; Fonteles, M C; Vale, O C 2013-08-01 Uroguanylin (UGN) is an endogenous peptide that acts on membrane-bound guanylate cyclase receptors of intestinal and renal cells increasing cGMP production and regulating electrolyte and water epithelial transport. Recent research works demonstrate the expression of this peptide and its receptor in the central nervous system. The current work was undertaken in order to evaluate modifications of electroencephalographic spectra (EEG) in anesthetized Wistar rats, submitted to intracisternal infusion of uroguanylin (0.0125 nmoles/min or 0.04 nmoles/min). The current observations demonstrate that 0.0125 nmoles/min and 0.04 nmoles/min intracisternal infusion of UGN significantly enhances amplitude and frequency of sharp waves and evoked spikes (p = 0.03). No statistical significance was observed on absolute alpha and theta spectra amplitude. The present data suggest that UGN acts on bioelectrogenesis of cortical cells by inducing hypersynchronic firing of neurons.

This effect is blocked by nedocromil, suggesting that UGN acts by increasing the activity of chloride channels. • Farombi, Ebenezer Olatunde; Abarikwu, Sunday O; Adedara, Isaac A; Oyeyemi, Matthew O 2007-01-01 The present study was carried out to evaluate the ameliorative effects of kolaviron (a biflavonoid from the seeds of Garcinia kola) and curcumin (from the rhizome, Curcuma longa L.) on the di-n-butylphthalate (DBP)- induced testicular damage in rats.

Administration of DBP to rats at a dose of 2 g/kg for 9 days significantly decreased the relative testicular weights compared to the controls, while the weights of other organs remained unaffected. Curcumin or kolaviron did not affect all the organ weights of the animals. While only DBP treatment significantly increased the testicular malondialdehyde level and gamma-glutamyl transferase activity (gamma-GT), it markedly decreased glutathione level, the testicular catalase, glucose-6-phosphate dehydrogenase, superoxide dismutase, sperm gamma-GT activities and serum testosterone level compared to the control group.

Data on cauda epididymal sperm count and live/dead ratio were not significantly affected in the DBP-treated rats. Alone, DBP treatment resulted in a 66% decrease in spermatozoa motility and a 77% increase in abnormal spermatozoa in comparison to control. DBP-treated rats showed marked degeneration of the seminiferous tubules with necrosis and defoliation of spermatocytes. The DBP- induced injuries in biochemical, spermatological parameters and histological structure of testis were recovered by treatment with kolaviron or curcumin.

The pattern in the behaviour of these compounds might be correlated with their structural variations. Our results indicate that kolaviron and curcumin protect against testicular oxidative damage induced by DBP. The chemoprotective effects of these compounds may be due to their intrinsic antioxidant properties and as such may prove useful in combating phthalate- induced reproductive toxicity. • Li, Zhiqiang; Huang, Lihua; Yu, Xiao; Yu, Can; Zhu, Hongwei; Li, Xia; Han, Duo; Huang, Hui 2017-01-01 The study aimed to explore the alteration of autophagy in rat pancreas treated with exenatide. Normal Sprague-Dawley rats and diabetes-model rats induced by 2-month high-sugar and high-fat diet and streptozotocin injection were subcutaneously injected with exenatide, respectively, for 10 weeks, with homologous rats treated with saline as control.

Meanwhile, AR42J cells, pancreatic acinar cell line, were cultured with exenatide at doses of 5 pM for 3 days. The pancreas was disposed, and several sections were stained with hematoxylin-eosin.

Immunohistochemistry was used to measure the expressions of glucagon-like peptide 1 receptor (GLP-1R) and cysteine-aspartic acid protease-3 in rat pancreas, and Western blot was used to test the expressions of GLP-1R, light chain 3B-I and -II, and p62 in rat pancreas and AR42J cells. The data were expressed as mean (standard deviation) and analyzed by unpaired Student's t-test. Exenatide can induce pathological changes in rat pancreas. The GLP-1R, p62, light chain 3B-II, and cysteine-aspartic acid protease-3 in rat pancreas and AR42J cells treated with exenatide were significantly overexpressed.

Exenatide can activate and upregulate its receptor, GLP-1R, then impair autophagy flux and activate apoptosis in the pancreatic acinar cell, thus damaging rat pancreas. • Reddy, Vaddi Damodara; Padmavathi, Pannuru; Hymavathi, Reddyvari; Maturu, Paramahamsa; Varadacharyulu, N Ch 2014-06-01 The protective effect of Emblica officinalis fruit extract (EFE) against alcohol- induced oxidative damage in liver microsomes was investigated in rats.

EFE (250mg/kg b.wt/day) and alcohol (5g/kg b.wt/day, 20%, w/v) were administered orally to animals for 60 days. Alcohol administration significantly increased lipid peroxidation, protein carbonyls with decreased sulfhydryl groups in microsomes, which were significantly restored to normal levels in EFE and alcohol co-administered rats. Alcohol administration also markedly decreased the levels of reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) in the liver microsomes, which were prevented with EFE administration. Further, alcohol administration significantly increased the activities of cytochrome P-450, Na(+)/K(+) and Mg(2+) ATPases and also membrane fluidity. But, administration of EFE along with alcohol restored the all above enzyme activities and membrane fluidity to normal level.

Thus, EFE showed protective effects against alcohol- induced oxidative damage by possibly reducing the rate of lipid peroxidation and restoring the various membrane bound and antioxidant enzyme activities to normal levels, and also by protecting the membrane integrity in rat liver microsomes. In conclusion, the polyphenolic compounds including flavonoid and tannoid compounds present in EFE might be playing a major role against alcohol- induced oxidative stress in rats.

“Not the gun but the word is the symbol of authority.” Charles Lindblom, former American political scientist and economist. Public discussion and debate are essential in a social democracy such as Barbados. Indeed, effective political language and communication are healthy for good governance, especially in a context where there is a contest of alternative policies and programmes by competing political parties. There is a held view in Political Science that “politics without communication is like having blood without veins and arteries: it’s not really going anywhere.” Surely, Barbadians are prompted to ask what is the logic or intent of Prime Minister Freundel Stuart’s abysmal communication style? Stuart’s intrinsic disinclination to engage the nation is problematic, and the lack of substance coming from the Democratic Labour Party (DLP) is taking Barbados nowhere favourable.

While the policy orientations of the Ministers of Cabinet may have flowed from manifesto promises or to address Barbados’ systemic shortcomings, their discursive practices – contextually constructed phenomena reflecting their power positions – have singed the local landscape by being shambolic. The fact is, policy-making is a constant discursive struggle in which strategic communication is a prerequisite for national solutions. Political language fused into broader communication dynamics happens to be one of the main tools of policymaking.

Strategic political communication refers to a multiplicity of techniques that reach out to audiences to build and maintain relationships and, to coordinate activities that can mobilize supporters and rally the nation. This type of communication helps to persuade and/or convince the audience to actively support the efforts being articulated.

However, one must not fall into the trap of thinking that political communication and propaganda are one and the same thing. Propaganda is‘systematic strategic mass communication conveyed by an organization’ such as our political parties, to ‘shape perceptions and manipulate the cognitions of a specific audience’ so as to achieve the goal of directing ‘the audience’s behaviour to achieve a response that furthers the political objectives’ of the organization. It is not necessarily framed in or for the national interest, nor is it conducive to encouraging constructive criticism.

By their definitions, political communication and propaganda can be informative. However, strategic communication will be inclusionary, but propaganda will not engender deliberation and participation. Propaganda does not tolerate discussion and by its very nature, it rejects contradiction and discussion. The propagandist posturing evident in Barbados, is precisely the way Stuart and the DLP function. They have resorted more to propaganda than on fixing the problems which occurred under Stuart’s stewardship. On the verge of what is expected to be a stubbornly fought general election, the language of politics will become more divisive, and increasingly unclear and conflicting. Numerous Barbadians have become aware that Stuart often reveals a greater propensity to scuttle national consensus-building than inspire through effective, transformational leadership.

Stuart’s limited communication reveals that he can be utterly dismissive, thus producing disruptive national outcomes. Popular discourse indicates that Barbadians in droves are ready to again express dissatisfaction with the current DLP Government.

This displeasure goes beyond the previously held marches of protest and disgust. There are Barbadians hopeful of solace and are gravitating towards the inspiration of the Leader of the Opposition and the Barbados Labour Party (BLP). To a lesser extent, small portions of the Barbados society are also drawn to emergent political entities. Noteworthy, is that the‘third’ political parties have no relevant or proven track record of performing and delivering in the national interest, although all things are possible. The next prime minister must seal a by far better deal for all Barbadians. Urgently required is an empathetic leader who will talk, can inspire, and will prioritize the needs of Barbados. That leader must communicate a clear vision arising from nothing short of‘rubbing shoulders’ with the electorate and listening to the expectations and complaints of the nation.

Barbadians are craving for truthful information. Admittedly, Prime Minister Stuart means well, but he has been ineffective on leadership. He does not seek to motivate and enhance national performances or even productivity. Strategic and effective political communication has escaped his attention.

Indiscipline within his Cabinet divulges the validity of that sentiment. Furthermore, when there is necessity to inform Barbadians about the state’s priorities and the ills affecting society, or the means for achieving national goals, Stuart is frequently mute.

Stuart’s breastplate overly relies on serendipity, while this conundrumis amplified by an ongoing mismatch between Stuart’s DLP as the key speakers and Barbadians as the listeners. There is definite gross misunderstanding between the expectations of the governed and the objectives of the governing. Stuart, invariably, buckles when it comes to utilizing and maximizing soft power. Soft power arises from factors such as consideration for traditions, drawing on local political culture, and inculcating the dominant values that would have emerged in the post-independence period. Stuart’s resistance to local value systems and attributes that were essential in guiding Barbados’ local practices and policies since 1966, regularly scuttles his ability to obtain the DLP’s vision of ‘continuing on the pathways to progress’. Stuart’s woeful stance has redirected the DLP to becoming more autocratic while relishing on secrecy, coercion, and of course, propaganda. Why hasn’t Stuart seized the moment and the DLP utilize strategic communication and stakeholder deliberation as the means for igniting national reforms in governance?

With strategic communication and the use of soft power, PM Stuart could have achieved many positive things for Barbados. Surely, Barbadians are being short-changed by this DLP government. The hiatus in governance continues to widen due to the paltry efforts at communicating with the public. For example, it is true that Barbados ought to soon have a Teaching Service Commission. Yet, teachers have not had adequate input into the constitutive elements of this innovation. The void is likely to throw out another set of avoidable controversies for the DLP.

Stuart’s refusal to use soft power, also fosters resentment on taxation. The DLP is unlikely to overcome Barbadians’ rejection of the National Social Responsibility Levy (NSRL). The Finance Minister tersely pushed the NSRL up by 400% from its original two per cent, but last week, he boasted that the tax was raking in more than expected since implementation. Sinckler’s brag was followed by the lukewarm defence of Minister Donville Inniss, and retreat by Stuart. Surely, the $50 million in revenues are intended to enhance benefits for the people. With the credibility of the DLP near rock-bottom, how does one explain the authoritarian disdain?

Today, Barbadians still need to understand where the country’s economy lurks. How many more sacrifices will be necessary to stop the entire country from falling over the cliff? Secrecy and surprise are normally essential weapons of war, but these are undermining Barbados’ social democracy. There can be no war among ourselves. Acting Governor of the Central Bank, Cleviston Haynes interestingly stated more than a year ago that: “We must bring new energy and bold strategies to the challenges which we all face. The real enemy is not each other, but unemployment, poverty and the need to renew our confidence in the Barbados economy.”. Important Jewels and Jadeite, Hong Kong, 12 Oct 2017, 02:00 PM comment5, Hitler, 454, Arms Production in the United Kingdom: Problems and Prospects, 9732, Heaven Knows, 062, Jumanji, ljrwar, Roads for the West Country, 3894, The Architecture of Europe,%-DD, Moose Country 2002 Calendar: 16 Month, 55533, At Home With the Word 2001: Sunday Scriptures and Reflections, >:-), We provide Training, Interview support (Male/Female) & Job support for almost all IT courses / technologies in market.

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Today, prescription and synthetic opioids crowd America’s medicine cabinets and streets, driving a modern crisis that. Opioids claimed 53,000 lives in the U.S. Last year, from the Centers for Disease Control and Prevention —. How did we arrive here? Here’s a look at why our brains get hooked on opioids.

The pain divide Let’s start with. They go by different names depending on which scientist you ask. Peripheral versus central pain. Nociceptive versus neuropathic pain.

The distinction is the sensation of actual damage to your body versus your mind’s perception of this injury. Your body quiets your pain nerves through the production of natural opioids called endorphins. Stuff that damages your skin and muscles — pin pricks and stove burns — is considered peripheral/nociceptive pain. Pain fibers sense these injuries and pass the signal onto nerve cells — or neurons — in your spine and brain, the duo that makes up your central nervous system. In a normal situation, your pain fibers work in concert with your central nervous system. Someone punches you, and your brain thinks “ow” and tells your body how to react. Stress-relieving hormones get released.

Your immune system counteracts the inflammation in your wounded arm. Your body quiets your pain nerves through the production of natural opioids called endorphins.

The trouble is when these pain pathways become overloaded or uncoupled. One receptor to rule them all Say you have chronic back pain. Your muscles are inflamed, constantly beaming pain signals to your brain. Your natural endorphins aren’t enough and your back won’t let up, so your doctor prescribes an opioid painkiller like oxycodone.

Prescription opioids and natural endorphins both land on tiny docking stations — called receptors — at the ends of your nerves. Most receptors catch chemical messengers — called neurotransmitters — to activate your nerve cells, triggering electric pulses that carry the signal forward. The Mu-opiate receptor is responsible for the major effects of all opiates, whether it’s heroin, prescription pills like oxycodone or synthetic opioids like fentanyl. The Mu-opiate receptor is responsible for the major effects of all opiates, whether it’s heroin, prescription pills like oxycodone or synthetic opioids like fentanyl, said Chris Evans, director of Brain Research Institute at UCLA. “The depression, the analgesia [pain numbing], the constipation and the euphoria — if you take away the Mu-opioid receptor, and you give morphine, then you don’t have any of those effects,” Evans said. Opioids receptors trigger such widespread effects because they govern more than just pain pathways.

When opioid drugs infiltrate a part of, their receptors slow respiration, cause constipation, lower blood pressure and decrease alertness., where opioids receptors switch off a batch of nerve cells called GABAergic neurons. GABAergic neurons are themselves an off-switch for the brain’s euphoria and pleasure networks. When it comes to addiction, opioids are an off-switch for an off-switch.

Opioids hold back GABAergic neurons in the midbrain, which in turn keep another neurotransmitter called dopamine from flooding a brain’s pleasure circuits. Image by Adam Sarraf Once opioids shut off GABAergic neurons, the pleasure circuits fill with another neurotransmitter called dopamine. At one stop on this pleasure highway — the nucleus accumbens — dopamine triggers a surge of happiness. When the dopamine rolls into amygdala, the brain’s fear center, it relieves anxiety and stress.

Both of these events reinforce the idea that opioids are rewarding. These areas of the brain are constantly communicating with decision-making hubs in the prefrontal cortex, which make value judgments about good and bad. When it hears “This pill feels good.

Let’s do more,” the mind begins to develop habits and cravings. Taking the drug soon becomes second nature or habitual, Evans said, much like when your mind zones out while driving home from work. The decision to seek out the drugs, rather than participate in other life activities, becomes automatic. The opioid pendulum: When feeling good starts to feel bad. It is the surge of withdrawal from opioids that makes the drugs so inescapable. Opioid addiction becomes entrenched after a person’s neurons adapt to the drugs.

The GABAergic neurons and other nerves in the brain still want to send messages, so they begin to adjust. They produce three to four times more cyclic AMP, a compound that primes the neuron to fire electric pulses, said Thomas Kosten, director of the division of alcohol and addiction psychiatry at the Baylor College of Medicine.

That means even when you take away the opioids, Kosten says, “the neurons fire extensively.” The pendulum swings back. Now, rather than causing constipation and slowing respiration, the brain stem triggers diarrhea and elevates blood pressure. Instead of triggering happiness, the nucleus accumbens and amygdala reinforce feelings of dysphoria and anxiety. All of this negativity feeds into the prefrontal cortex, further pushing a desire for opioids. While other drugs like cocaine and alcohol can also feed addiction through the brain’s pleasure circuits, it is the surge of withdrawal from opioids that makes the drugs so inescapable. Could opioid addiction be driven in part by people’s moods? Chronic pain patients have a very high risk of becoming addicted to opioids if they are also coping with a mood disorder.

Photo by Roy Morsch/via Getty Cathy Cahill, a pain and addiction researcher at UCLA, said these big swings in emotions likely factor into the, especially with those with chronic pain. A person with opioid use disorder becomes preoccupied with the search for the drugs. Certain contexts become triggers for their cravings, and those triggers start overlapping in their minds.

“The basic view is some people start with the pain trigger [the chronic back problem], but it gets partially substituted with the negative reinforcement of the opioid withdrawal,” Cahill said. That’s why Cahill, Evans and other scientists think the opioid addiction epidemic might be driven, in part, by our moods. Patients on morphine experience 40 percent less pain relief from the drug if they have mood disorder. Chronic pain patients have a very high risk of becoming addicted to opioids if they are also coping with a mood disorder. A 2017 study — 81 percent — whose addiction started with a chronic pain problem also had a mental health disorder.

Another found patients on morphine experience 40 percent less pain relief from the drug if they have mood disorder. They need more drugs to get the same benefits.

People with mood disorders alone are also more likely to abuse opioids. A 2012 survey found patients with depression. “So, not only does a mood disorder affect a person’s addiction potential, but it also influences if the opioids will successfully treat their pain,” Cahill said. Meanwhile, the country is living through sad times. Some research suggests social isolation. While the opioid epidemic started long before the recession,, with every 1 percent increase in unemployment. Can the brain swing back?

As an opioid disorder progresses, a person needs a higher quantity of the drugs to keep withdrawal at bay. A person typically overdoses when they take so much of the drug that the brain stem slows breathing until it stops, Kosten said. Many physicians have turned to opioid replacement therapy, a technique that swaps highly potent and addictive drugs like heroin with compounds like methadone or buprenorphine (an ingredient in Suboxone). These substitutes outcompete heroin when they reach the opioid receptors, but do not activate the receptors to the same degree. By doing so, they reduce a person’s chances for overdosing.

These replacement medications also stick to the receptors for a longer period of time, which curtails withdrawal symptoms. Buprenorphine, for instance, while morphine only hangs on for a few milliseconds. Science correspondent Miles O’Brien discovers future pain treatments may rely on virtual reality.

For some, this solution is not perfect. The patients need to remain on the replacements for the foreseeable future, and some recovery communities. Plus, opioid replacement therapy does not work for fentanyl, the synthetic opioid.

Kosten’s lab is one of many working on a opioid vaccine that would direct a person’s immune system to clear drugs like fentanyl before they can enter the brain. But those are.

And Evans and Cahill said many clinics in Southern California are combining psychological therapy with opioid replacement prescriptions to combat the mood aspects of the epidemic. “I don’t think there’s going to be a magic bullet on this one,” Evans said. “It’s really an issue of looking after society and looking after of people’s psyches rather than just treatment.” The post appeared first on. Manager of Litigation Support and eDiscovery Duties: Manage and support all litigation and technological services and requirements for the delivery of advocacy and dispute resolution services involving electronically stored information and eDiscovery. Preparing paperless workflows; Identifying, purchasing and implementing new technology beneficial to paperless workflows; Working directly with IT and. The demand in the smart toys market, a sector born out of industrial and technological convergence, is projected for an impressive CAGR during the forecast period of 2017 to 2022. Albany, NY -- () -- -- A fresh market study by the researchers at Transparency Market Research (TMR) reports that the global smart toys market is heavily dependent on product innovation, and that an increasing number of players are venturing into the competitive landscape, eating out significant chunk of the total shares.

That being said, a few companies do hold a respectable position in the global smart toys market, such as Activision Blizzard Inc., Fisher-Price Inc., The Hasbro Inc., LeapFrog Enterprises, Inc., Spin Master Corp, Seebo Interactive Ltd, Wow Wee Group Ltd, Genesis Toy Co. Ltd, Reach Robotics Ltd, and SmartGurlz ApS. While Activision Blizzard is a little ahead of the curve, Hasbro is concentrating on revisiting the most popular toys and games.

LEGO too has made heavy investments for research and development in the recent past to emerge as a notable competitor in the global smart toys market. View and Download TOC of Smart Toys Market Research Report@ Nascent Market Has Strong Potential for Product Innovation The demand in the smart toys market, a sector born out of industrial and technological convergence, is projected for an impressive CAGR during the forecast period of 2017 to 2022.

However, the market for smart toys is still at its early stage, with Sphero BB8 App-Enabled Droid being the only one that has achieved broad consumer appeal in the toys to life segment. In the near future, currently ongoing R&D efforts by the market leaders is expected to bear fruits and newer products are anticipated to make an impression on a wider population. That is when the demand in the global smart toys market will witness an escalation. Based on toy-type, the global smart toys market gains maximum demand for voice or image recognition toys, accounting for US$2,271.7 mn in 2017 and projected for a CAGR of 3.7% during the forecast period of 2017 to 2022. This segment is growing at US$ 89.7 mn annually over the course of the forecast period, and this absolute growth is larger than the any other segment, viz.

Request and Download Sample Report@ App-enabled mechanical toys, screenless toys, toys-to-life, puzzles and building games, health tracking toys, wearables, and others. North America is identified as the most lucrative regional market for smart toys, promising a revenue worth US$2,119.2 mn by 2022. On the other hand, the demand for smart toys in the region of Asia Pacific expect Japan (APEJ) is anticipated to expand at an above-average CAGR of 3.9% during the same forecast period. Increased Disposable Income of Urban Population Driving Demand Urban population is growing increasing inclined towards restless lifestyle and while they have managed to add to their disposable income, time for personalized parenting is diminishing. Smart toys utilize artificial intelligence, and are punctuated with microprocessors, input and output devices, and volatile or nonvolatile memory units.

Smart toys goes beyond just being educational toys, as they can recognize speech as well as react to their surroundings in order to provide a comprehensive entertainment and engagement to children between the age group of five to 14. The growth of the global smart toys market is also a reflection of increasing awareness towards the smart toys and the availability of diverse indoor and outdoor sports and educational toys. On the other hand, high cost of these products, the lack of awareness among large masses, particularly in the emerging economies, regulatory issues for overseas distribution, and impending innovations are some of the challenges that are hindering the prosperity of the global smart toys market. The emergence of the Internet of Things (IoT) is having tremendous positive effect on the global smart toys market too. With IoT, modern toys are increasingly becoming a potential area wherein connectivity and existing toy types can be collaborated together to innovate appealing new devices, referred to as connected or 'smart toys'.