Cross-cultural study of hotel practices as perceived by Chinese and North American travellers: A data mining analysis.

This paper aims to unearth the different perception styles of Chinese and North American travellers from analytic versus holistic thinking perspectives. Python was utilized to gather online textual data from Chinese and North American travellers, while word frequency analysis, latent Dirichlet allocation (LDA) topic modelling analysis and content analysis were employed to elucidate the perception styles in a cross-cultural context. In general, North American travellers mainly leaned towards analytic thinking, whereas Chinese travellers showcased a blend of holistic and analytic thought processes. The topic of travel, leisure and accommodation showed both holistic and analytic thinking styles. The topics of nature and environment, front desk service, and travel routes and scenic spot areas mainly represented a holistic thinking style. The topics of convenience and facilities, breakfast, transportation, hotel theme and features, and decoration and amenities mainly suggested an analytic thinking style. Hotels should consider the different perception styles of Chinese and North American travellers to facilitate strategies accordingly and to maximize the experience of travellers from different cultural backgrounds.

Optical Simulation Design of a Short Lens Length with a Curved Image Plane and Relative Illumination Analysis.

This study proposes a three-lens design with a short lens length and explores the curved imaging plane and performs a relative illumination analysis. There are two ways to reduce the lens length: shortening the back focal and lens group lengths. We derived the relevant parameter relationships of three lenses using the first-order geometric optics theory. The optical lens length can be controlled within 2 mm. The shorter the lens length, the larger the angle of the chief ray in the image space, resulting in an increase in the field curvature and astigmatism. Third-order Seidel aberrations can be effectively reduced by a curved image plane. We also derived the equations for relative illuminance, solid angle, surface transmittance, and internal transmittance for the short three-lens design. The optical lens design uses a curved image plane to shorten the distance from the off-axis beam image space to the image plane and reduce the incident angle of the chief ray on the image plane. The formula and design results verified by Code V software (version 11.2) show that both the solid angle and relative contrast of the lens can be increased. For the proposed three-lens design with a short lens length, the semi-field angle is 32°, F/# is 2.7, the effective focal length is 1.984 mm, the image plane area is 2.16 mm × 1.22 mm, and the curvature radius of the concave image plane is 3.726 mm. Moroever, the MTF (100 lp/mm) is larger than 52%, the lateral color aberration is less than 2.12 µm, the optical distortion is less than 2.00%, and the relative illumination is greater than 68%.

NOX4 stimulates ANF secretion via activation of the Sirt1/Nrf2/ATF3/4 axis in hypoxic beating rat atria.

Silent information regulator factor 2­related enzyme 1 (Sirt1) is involved in the regulation of cell senescence, gene transcription, energy balance and oxidative stress. However, the effect of Sirt1 on atrial natriuretic factor (ANF) secretion, especially under hypoxic conditions is unclear. The present study aimed to investigate the effect of Sirt1, regulated by NADPH oxidase 4 (NOX4), on ANF secretion in isolated beating rat atria during hypoxia. ANF secretion was analyzed using radioimmunoassays and protein expression levels were determined by western blotting and immunofluorescence staining. Intra­atrial pressure was recorded using a physiograph. Hypoxia significantly upregulated Sirt1 and nuclear factor erythroid­2­related factor 2 (Nrf2) protein expression levels, together with significantly increased ANF secretion. Hypoxia­induced protein expression of Sirt1 was significantly blocked by a NOX4 inhibitor, GLX351322, and Nrf2 protein expression levels were significantly abolished using the Sirt1 inhibitor, EX527. Hypoxia also significantly elevated the protein expression levels of phosphorylated­Akt and sequestosome 1 and significantly downregulated Kelch­like ECH­associated protein 1 protein expression levels. These effects were significantly blocked by EX527, preventing hypoxia­induced Nrf2 expression. An Nrf2 inhibitor, ML385, significantly abolished the hypoxia­induced upregulation of activating transcription factor (ATF)3, ATF4, T cell factor (TCF)3 and TCF4/lymphoid enhancer factor 1 (LEF1) protein expression levels, and significantly attenuated hypoxia­induced ANF secretion. These results indicated that Sirt1 and Nrf2, regulated by NOX4, can potentially stimulate TCF3 and TCF4/LEF1 signaling via ATF3 and ATF4 activation, thereby potentially participating in the regulation of ANF secretion in beating rat atria during hypoxia. In conclusion, intervening with the Sirt1/Nrf2/ATF signaling pathway may be an effective strategy for resisting oxidative stress damage in the heart during hypoxia.

Nitric oxide impairs spatial learning and memory in a rat model of Alzheimer's disease via disturbance of glutamate response in the hippocampal dentate gyrus during spatial learning.

Nitric oxide (NO)-dependent pathways may play a significant role in the decline of synaptic and cognitive functions in Alzheimer's disease (AD). However, whether NO in the hippocampal dentate gyrus (DG) is involved in the spatial learning and memory impairments of AD by affecting the glutamate (Glu) response during these processes is not well-understood. Here, we prepared an AD rat model by long-term i.p. of D-galactose into ovariectomized rats, and then the effects of L-NMMA (a NO synthase inhibitor) on Glu concentration and amplitude of field excitatory postsynaptic potential (fEPSP) were measured in the DG region during the Morris water maze (MWM) test in freely-moving rats. During the MWM test, compared with the sham group, the escape latency was increased in the place navigation trial, and the percentage of time spent in target quadrant and the number of platform crossings were decreased in the spatial probe trial, in addition, the increase of fEPSP amplitude in the DG was significantly attenuated in AD group rats. L-NMMA significantly attenuated the spatial learning and memory impairment in AD rats, and reversed the inhibitory effect of AD on increase of fEPSP amplitude in the DG during the MWM test. In sham group rats, the Glu level in the DG increased significantly during the MWM test, and this response was markedly enhanced in AD rats. Furthermore, the response of Glu in the DG during spatial learning was recovered by microinjection of L-NMMA into the DG. Our results suggest that NO in the DG impairs spatial learning and memory and related synaptic plasticity in AD rats, by disturbing the Glu response during spatial learning.

L-Carnitine protects against tacrolimus-induced renal injury by attenuating programmed cell death via PI3K/AKT/PTEN signaling.

Reducing immunosuppressant-related complications using conventional drugs is an efficient therapeutic strategy. L-carnitine (LC) has been shown to protect against various types of renal injury. In this study, we investigated the renoprotective effects of LC in a rat model of chronic tacrolimus (TAC) nephropathy. SD rats were injected with TAC (1.5 mg · kg-1 · d-1, sc) for 4 weeks. Renoprotective effects of LC were assessed in terms of renal function, histopathology, oxidative stress, expression of inflammatory and fibrotic cytokines, programmed cell death (pyroptosis, apoptosis, and autophagy), mitochondrial function, and PI3K/AKT/PTEN signaling. Chronic TAC nephropathy was characterized by severe renal dysfunction and typical histological features of chronic nephropathy. At a molecular level, TAC markedly increased the expression of inflammatory and fibrotic cytokines in the kidney, induced oxidative stress, and led to mitochondrial dysfunction and programmed cell death through activation of PI3K/AKT and inhibition of PTEN. Coadministration of LC (200 mg · kg-1 · d-1, ip) caused a prominent improvement in renal function and ameliorated histological changes of kidneys in TAC-treated rats. Furthermore, LC exerted anti-inflammatory and antioxidant effects, prevented mitochondrial dysfunction, and modulated the expression of a series of apoptosis- and autophagy-controlling genes to promote cell survival. Human kidney proximal tubular epithelial cells (HK-2 cells) were treated with TAC (50 µg/mL) in vitro, which induced production of intracellular reactive oxygen species and expression of an array of genes controlling programmed cell death (pyroptosis, apoptosis, and autophagy) through interfering with PI3K/AKT/PTEN signaling. The harmful responses of HK-2 cells to TAC were significantly attenuated by cotreatment with LC and the PI3K inhibitor LY294002 (25 µM). In conclusion, LC treatment protects against chronic TAC nephropathy through interfering the PI3K/AKT/PTEN signaling.

L-carnitine treatment attenuates renal tubulointerstitial fibrosis induced by unilateral ureteral obstruction.

BACKGROUND/AIMS: Accumulating evidence indicates that L-carnitine (LC) protects against multiorgan damage through its antioxidant properties and preservation of the mitochondria. Little information is available about the effects of LC on renal fibrosis. This study examined whether LC treatment would provide renoprotection in a rat model of unilateral ureteral obstruction (UUO) and in vitro. METHODS: Sprague-Dawley rats that underwent UUO were treated daily with LC for 7 or 14 days. The influence of LC on renal injury caused by UUO was evaluated by histopathology, and analysis of gene expression, oxidative stress, mitochondrial function, programmed cell death, and phosphatidylinositol 3-kinase (PI3K)/ AKT/forkhead box protein O 1a (FoxO1a) signaling. In addition, H2O2-exposed human kidney cells (HK-2) were treated with LC. RESULTS: LC treatment inhibited expression of proinflammatory and profibrotic cytokines, and was followed by a significant attenuation of tubulointerstitial inflammation and fibrosis. The increased oxidative stress caused by UUO was associated with mitochondrial dysfunction and excessive apoptosis and autophagy via PI3K/AKT/FoxO1a-dependent signaling, and this was abrogated by administration of LC. In H2O2-exposed HK-2 cells, LC decreased intracellular production of reactive oxygen species, and suppressed expression of profibrotic cytokines and reduced the number of apoptotic cells. CONCLUSION: LC protects against the progression of tubulointerstitial fibrosis in an obstructed kidney.

L-carnitine treatment attenuates renal tubulointerstitial fibrosis induced by unilateral ureteral obstruction

Background/Aims@#Accumulating evidence indicates that L-carnitine (LC) protects against multiorgan damage through its antioxidant properties and preservation of the mitochondria. Little information is available about the effects of LC on renal fibrosis. This study examined whether LC treatment would provide renoprotection in a rat model of unilateral ureteral obstruction (UUO) and in vitro. @*Methods@#Sprague-Dawley rats that underwent UUO were treated daily with LC for 7 or 14 days. The influence of LC on renal injury caused by UUO was evaluated by histopathology, and analysis of gene expression, oxidative stress, mitochondrial function, programmed cell death, and phosphatidylinositol 3-kinase (PI3K)/ AKT/forkhead box protein O 1a (FoxO1a) signaling. In addition, H2O2-exposed human kidney cells (HK-2) were treated with LC. @*Results@#LC treatment inhibited expression of proinflammatory and profibrotic cytokines, and was followed by a significant attenuation of tubulointerstitial inflammation and fibrosis. The increased oxidative stress caused by UUO was associated with mitochondrial dysfunction and excessive apoptosis and autophagy via PI3K/AKT/FoxO1a-dependent signaling, and this was abrogated by administration of LC. In H2O2-exposed HK-2 cells, LC decreased intracellular production of reactive oxygen species, and suppressed expression of profibrotic cytokines and reduced the number of apoptotic cells. @*Conclusions@#LC protects against the progression of tubulointerstitial fibrosis in an obstructed kidney.

Analysis of the prevalence and influencing factors of elevated FPG in Liaoning Province / 上海预防医学

Objective To determine the prevalence rate of elevated fasting plasma glucose(FPG)in residents of Liaoning Province and to identify the risk factors, which will help to effectively prevent/alleviate the occurrence and development of diabetes for reduction of socioeconomic burden. Methods A multi-stage stratified random cluster sampling method was used to investigate the residents of 3 towns and 3 rural areas in Liaoning Province. A total of 53 497 adults(aged 35-75 years)were surveyed by questionnaires and the risk or protective factors were analyzed by logistic regression method. Results The prevalence rate of elevated FPG was 24.7% with 23.2% in males and 26.0% in females, respectively. The results of multivariate logistic regression showed that age increase, female, high education, occupation(except farmers), alcohol drinking, obesity, hypertension, and dyslipidemia were risk factors of FPG(P < 0.05 or P < 0.001). Conclusion The prevalence of elevated FPG is high in the study population aged 35-75 years in Liaoning. It is necessary to strengthen the intervention in this part of the population in order to reduce the incidence of diabetes mellitus.

Norepinephrine in the dentate gyrus is involved in spatial learning and memory alteration induced by chronic restraint stress in aged rats.

The role of norepinephrine of the hippocampal dentate gyrus in spatial learning and memory alteration induced by chronic restraint stress (CRS, 3 h/day, 6 weeks) was investigated in aged rats. Spatial learning and memory were assessed by the Morris water maze (MWM), and the extracellular concentration of norepinephrine and amplitude of field excitatory postsynaptic potential (fEPSP) were measured in the dentate gyrus during MWM test in freely-moving rats. Next, the involvement of ß-adrenoceptors in spatial learning and memory of CRS rats was examined by microinjection of its antagonist (propranolol) into the dentate gyrus. In addition, we observed the expression of brain-derived neurotrophic factor (BDNF) protein and activation of cAMP-response element binding protein (CREB) in the dentate gyrus. Compared with the control group, the basal level of norepinephrine, BDNF expression and CREB activation in the dentate gyrus were increased, and the spatial learning and memory abilities were enhanced in CRS rats. In the control group, the norepinephrine concentration and fEPSP amplitude in the dentate gyrus were increased on the second to fourth days of MWM test, and these responses were significantly enhanced in CRS rats. Furthermore, in CRS rats, propranolol significantly decreased the spatial learning and memory abilities, and attenuated the fEPSP response during MWM test, and the BDNF expression and CREB activation in the dentate gyrus. Our results suggest that norepinephrine activation of ß-adrenoceptors in the hippocampal dentate gyrus is involved in spatial learning and memory enhancement induced by CRS in aged rats, in part via modulations of synaptic efficiency and CREB-BDNF signaling pathway.

Exogenous pancreatic kininogenase protects against renal fibrosis in rat model of unilateral ureteral obstruction.

Tissue kallikrein has protective function against various types of injury. In this study, we investigated whether exogenous pancreatic kininogenase (PK) conferred renoprotection in a rat model of unilateral ureteral obstruction (UUO) and H2O2-treated HK-2 cells in vitro. SD rats were subjected to UUO surgery, then PK (7.2 U/g per day, ip) was administered for 7 or 14 days. After the treatment, rats were euthanized; the obstructed kidneys were harvested for further examination. We found that PK administration significantly attenuated interstitial inflammation and fibrosis, and downregulated the expression of proinflammatory (MCP-1, TLR-2, and OPN) and profibrotic (TGF-ß1 and CTGF) cytokines in obstructed kidney. UUO-induced oxidative stress, closely associated with excessive apoptotic cell death and autophagy via PI3K/AKT/FoxO1a signaling, which were abolished by PK administration. We further showed that PK administration increased the expression of bradykinin receptors 1 and 2 (B1R and B2R) mRNA and the production of NO and cAMP in kidney tissues. Coadministration with either B1R antagonist (des-Arg9-[Leu8]-bradykinin) or B2R antagonist (icatibant) abrogated the renoprotective effects of PK, and reduced the levels of NO and cAMP in obstructed kidney. In H2O2-treated HK-2 cells, addition of PK (6 pg/mL) significantly decreased ROS production, regulated the expression of oxidant and antioxidant enzymes, suppressed the expression of TGF-ß1 and MCP-1, and inhibited cell apoptosis. Our data demonstrate that PK treatment protects against the progression of renal fibrosis in obstructed kidneys.

Expression of brain-derived neurotrophic factor in kidneys from normal and cyclosporine-treated rats.

BACKGROUND: Accumulating evidence suggests that a decrease in brain-derived neurotrophic factor (BDNF) level induces a variety of psychiatric and neurological disorders. However, the expression and role of BDNF in the kidney have not been explored. The present study examined the expression of BDNF and tropomyosin-related kinase (Trk) receptors in an experimental model of chronic cyclosporine A (CsA) nephropathy. METHODS: Sprague-Dawley rats on a salt-deplete diet were treated daily for four weeks with vehicle or CsA. Urine profiles, apoptotic cell death, oxidative stress (8-hydroxy-2'-deoxyguanosine, 8-OHdG), and expression of BDNF and Trk receptors (TrkB and TrkC) were compared between groups. The impact of vasopressin infusion on the urine-concentrating ability was examined by measuring the expression of aquaporin-2 (AQP-2) and BDNF and urine profiles in normal and CsA-treated rats. RESULTS: Compared with the vehicle-treated rats, rats given CsA had enhanced urine volume and declined urine osmolality. Immunohistochemistry and immunoblotting showed that BDNF and Trk receptors were constitutively expressed in kidneys from vehicle-treated rats. This was confirmed by double immunofluorescent staining for Na-K-ATPase-α1, AQP-1, and AQP-2. By contrast, the expression of these factors decreased in kidneys from CsA-treated rats (BDNF: 51.1 ± 19.5% vs. 102.0 ± 30.3%, p < 0.01). Downregulation of BDNF was accompanied by impairment of urine osmolality, and this was reversed by exogenous infusion of vasopressin. Notably, the number of TUNEL-positive cells correlated negatively with BDNF expression and positively with urinary 8-OHdG excretion. CONCLUSIONS: BDNF is expressed in the collecting duct of the kidney and may be associated with urine-concentrating ability in an experimental model of chronic CsA-induced nephropathy. Our study provides a new avenue for further investigation of chronic CsA nephropathy.

Prevalence and influencing factors of main chronic diseases among urban residents in Liaoning Province / 预防医学

Objective To investigate the prevalence of main chronic diseases and explore its influencing factors among urban residents in Liaoning Province. Methods Using multistage stratified and cluster random sampling method, 30 953 urban residents of 14 districts were investigated with a standard questionnaire and physical examination. The logistic regression was applied to explore the influencing factors of main chronic diseases. Results The prevalence rate of chronic diseases was 39.25% and the standardized prevalence rate was 32.29%. The top three chronic diseases were hypertension, diabetes mellitus, and dyslipidemia, and the standardized prevalence rates were 21.13%, 9.48% and 5.25%. The results of the logistic regression analysis showed that the three chronic diseases shared older age(OR: 1.266-7.325)and overweight or obesity(OR:1.107-2.982)as the risk factors .In addition, there existed certain interactions among hypertension, diabetes mellitus and dyslipidemia(OR: 2.424-3.121). Conclusion Hypertension, diabetes mellitus and dyslipidemia which shared older age, overweight and obesity as the risk factors are the main chronic diseases to damage the health of urban residents in Liaoning. The corresponding prevention and treatment strategies should be taken based on the key groups and related influencing factors.

miRNA-141 attenuates UV-induced oxidative stress via activating Keap1-Nrf2 signaling in human retinal pigment epithelium cells and retinal ganglion cells.

Activation of NF-E2-related factor 2 (Nrf2) signaling could protect cells from ultra violet (UV) radiation. We aim to provoke Nrf2 activation via downregulating its inhibitor Keap1 by microRNA-141 ("miR-141"). In both human retinal pigment epithelium cells (RPEs) and retinal ganglion cells (RGCs), forced-expression of miR-141 downregulated Keap1, causing Nrf2 stabilization, accumulation and nuclear translocation, which led to transcription of multiple antioxidant-responsive element (ARE) genes (HO1, NOQ1 and GCLC). Further, UV-induced reactive oxygen species (ROS) production and cell death were significantly attenuated in miR-141-expressing RPEs and RGCs. On the other hand, depletion of miR-141 via expressing its inhibitor antagomiR-141 led to Keap1 upregulation and Nrf2 degradation, which aggravated UV-induced death of RPEs and RGCs. Significantly, Nrf2 shRNA knockdown almost abolished miR-141-mediated cytoprotection against UV in RPEs. These results demonstrate that miR-141 targets Keap1 to activate Nrf2 signaling, which protects RPEs and RGCs from UV radiation.

α1-Adrenoceptors in the hippocampal dentate gyrus involved in learning-dependent long-term potentiation during active-avoidance learning in rats.

The hippocampus is the key structure for learning and memory in mammals and long-term potentiation (LTP) is an important cellular mechanism responsible for learning and memory. The influences of norepinephrine (NE) on the modulation of learning and memory, as well as LTP, through ß-adrenoceptors are well documented, whereas the role of α1-adrenoceptors in learning-dependent LTP is not yet clear. In the present study, we measured extracellular concentrations of NE in the hippocampal dentate gyrus (DG) region using an in-vivo brain microdialysis and high-performance liquid chromatography techniques during the acquisition and extinction of active-avoidance behavior in freely moving conscious rats. Next, the effects of prazosin (an antagonist of α1-adrenoceptor) and phenylephrine (an agonist of the α1-adrenoceptor) on amplitudes of field excitatory postsynaptic potential were measured in the DG region during the active-avoidance behavior. Our results showed that the extracellular concentration of NE in the DG was significantly increased during the acquisition of active-avoidance behavior and gradually returned to the baseline level following extinction training. A local microinjection of prazosin into the DG significantly accelerated the acquisition of the active-avoidance behavior, whereas a local microinjection of phenylephrine retarded the acquisition of the active-avoidance behavior. Furthermore, in all groups, the changes in field excitatory postsynaptic potential amplitude were accompanied by corresponding changes in active-avoidance behavior. Our results suggest that NE activation of α1-adrenoceptors in the hippocampal DG inhibits active-avoidance learning by modulation of synaptic efficiency in rats.

[Effect of 5-HT1A receptors in the hippocampal DG on active avoidance learning in rats].

OBJECTIVE: To investigate the effects of serotonin (5-HTIA) receptors in the hippocampal dentate gyrus (DG) on active avoidance learning in rats. METHODS: Totally 36 SD rats were randomly divided into control group, antagonist group and agonist group(n = 12). Active avoidance learning ability of rats was assessed by the shuttle box. The extracellular concentrations of 5-HT in the DG during active avoidance conditioned reflex were measured by microdialysis and high performance liquid chromatography (HPLC) techniques. Then the antagonist (WAY-100635) or agonist (8-OH-DPAT) of the 5-HT1A receptors were microinjected into the DG region, and the active avoidance learning was measured. RESULTS: (1) During the active avoidance learning, the concentration of 5-HT in the hippocampal DG was significantly increased in the extinction but not establishment in the conditioned reflex, which reached 164.90% ± 26.07% (P <0.05) of basal level. (2) The microinjection of WAY-100635 (an antagonist of 5-HT1A receptor) into the DG did not significantly affect the active avoidance learning. (3) The microinjection of 8-OH-DPAT(an agonist of 5-HT1A receptor) into the DG significantly facilitated the establishment process and inhibited the extinction process during active avoidance conditioned reflex. CONCLUSION: The data suggest that activation of 5-HT1A receptors in hipocampal DG may facilitate active avoidance learning and memory in rats.

Effect of 5-HT1A receptors in the hippocampal DG on active avoidance learning in rats / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the effects of serotonin (5-HTIA) receptors in the hippocampal dentate gyrus (DG) on active avoidance learning in rats.</p><p><b>METHODS</b>Totally 36 SD rats were randomly divided into control group, antagonist group and agonist group(n = 12). Active avoidance learning ability of rats was assessed by the shuttle box. The extracellular concentrations of 5-HT in the DG during active avoidance conditioned reflex were measured by microdialysis and high performance liquid chromatography (HPLC) techniques. Then the antagonist (WAY-100635) or agonist (8-OH-DPAT) of the 5-HT1A receptors were microinjected into the DG region, and the active avoidance learning was measured.</p><p><b>RESULTS</b>(1) During the active avoidance learning, the concentration of 5-HT in the hippocampal DG was significantly increased in the extinction but not establishment in the conditioned reflex, which reached 164.90% ± 26.07% (P <0.05) of basal level. (2) The microinjection of WAY-100635 (an antagonist of 5-HT1A receptor) into the DG did not significantly affect the active avoidance learning. (3) The microinjection of 8-OH-DPAT(an agonist of 5-HT1A receptor) into the DG significantly facilitated the establishment process and inhibited the extinction process during active avoidance conditioned reflex.</p><p><b>CONCLUSION</b>The data suggest that activation of 5-HT1A receptors in hipocampal DG may facilitate active avoidance learning and memory in rats.</p>

Synergistic effects of leflunomide and benazepril in streptozotocin-induced diabetic nephropathy.

BACKGROUND: Leflunomide (LEF) and benazepril have renoprotective effects on diabetic nephropathy (DN) through their anti-inflammatory and anti-fibrotic activities. This study investigated whether combined treatment using LEF and benazepril affords superior protection compared with the respective monotherapies. METHODS: Diabetes was induced with streptozotocin (STZ, 65 mg/kg) by intraperitoneal injection in male Wistar rats. Two weeks after STZ injection, diabetic rats were treated daily for 12 weeks with LEF (10 mg/kg), benazepril (10 mg/kg), or a combination of both. Basic parameters (body weight, fasting blood glucose level, and 24 h urinary protein excretion), histopathology, inflammatory [inflammatory cell infiltration (ED-1), monocyte chemoattractant protein-1 (MCP-1), and Toll-like receptor-2 (TLR-2)] and glomerulosclerotic factors [transforming growth factor-ß1 (TGF-ß1) and connective tissue growth factor (CTGF)], and oxidative stress (8-hydroxy-2'-deoxyguanosine, 8-OHdG) were studied. RESULTS: Benazepril or LEF treatment significantly prevented body weight loss and 24 h urinary protein excretion induced by diabetes; combined treatment with LEF and benazepril further improved these parameters compared with giving each drug alone (all p < 0.01). Increased expression of inflammatory (MCP-1 and TLR-2) and glomerulosclerotic (TGF-ß1 and CTGF) factors in diabetic rat kidney was reduced by treatment with either LEF or benazepril and was further reduced by the combined administration of the two drugs (p < 0.01). These effects were accompanied by suppression of urinary 8-OHdG excretion. There was no significant between-group difference in blood glucose level. CONCLUSIONS: LEF treatment lessens DN, and combined treatment with LEF and benazepril provides synergistic effects in preventing DN.

Β-adrenoceptors in the hypothalamic paraventricular nucleus modulate the baroreflex in conscious rats.

The role of ß-adrenoceptors of the hypothalamic paraventricular nucleus (PVN) in modulation of the baroreflex was investigated in conscious rats. The baroreflex was induced by intravenous injection of phenylephrine, and then the extracellular concentration of norepinephrine in the PVN region determined using microdialysis and high-performance liquid chromatography. Next, the role of the ß-adrenoceptor in modulation of the baroreflex was investigated by perfusion of its antagonist or agonist into the PVN using microdialysis. Intravenous injection of phenylephrine increased the norepinephrine concentration in the PVN by 35.83 ± 5.71%. Propranolol (an antagonist of the ß-adrenoceptor) significantly decreased the gain of reflex bradycardia, but did not affect the magnitude of blood-pressure increases in the baroreflex, resulting in reduced baroreflex sensitivity. Isoprenaline (an agonist of the ß-adrenoceptor) significantly increased the gain of reflex bradycardia without affecting blood-pressure increases, leading to increased baroreflex sensitivity. Our results suggest that norepinephrine in the PVN facilitates the phenylephrine-induced baroreflex via ß-adrenoceptors.

Establishment of reverse genetics system for infectious bronchitis virus attenuated vaccine strain H120.

Infectious bronchitis virus (IBV) strain H120 was successfully rescued as infectious clone by reverse genetics. Thirteen 1.5-2.8 kb fragments contiguously spanning the virus genome were amplified and cloned into pMD19-T. Transcription grade complete length cDNA was acquired by a modified "No See'm" ligation strategy, which employed restriction enzyme Bsa I and BsmB I and ligated more than two fragments in one T4 ligase reaction. The full-length genomic cDNA was transcribed and its transcript was transfected by electroporation into BHK-21 together with the transcript of nucleocapsid gene. At 48 h post transfection, the medium to culture the transfected BHK-21 cells was harvested and inoculated into 10-days old SPF embryonated chicken eggs (ECE) to replicate the rescued virus. After passage of the virus in ECE five times, the rescued H120 virus (R-H120) was successfully recovered. R-H120 was subsequently identified to possess the introduced silent mutation site in its genome. Some biological characteristics of R-H120 such as growth curve, EID50 and HA titers, were tested and all of them were very similar to its parent strain H120. In addition, both R-H120 and H120 induced a comparable titer of HA inhibition (HI) antibody in immunized chickens and also provided up to 85% of immune protection to the chickens that were challenged with Mass41 IBV strain. The present study demonstrated that construction of infectious clone from IBV vaccine strain H120 is possible and IBV-H120 can be use as a vaccine vector for the development of novel vaccines through molecular recombination and the modified reverse genetics approach.

Expression of avian infectious bronchitis virus multi-epitope based peptide EpiC in Lactococcus lactis for oral immunization of chickens.

The avian infectious bronchitis virus (IBV) multi-epitope based peptide EpiC was found to be effective in inducing strong humoral and cellular responses against IBV. In this study, the gene EpiC was introduced into Lactococcus lactis NZ3900, and three recombinant strains expressing EpiC in intracellular and extracellular forms were constructed. SDS-PAGE and Western blot results indicated that EpiC was successfully expressed and had good immunoreactivity with chicken anti-IBV serum. Fusion of the signal pepitide gene SPusp45 and the nine-peptide LEISSTCDA encoding oligonucleotide to EpiC increased the secretion of EpiC, but reduced the total yields of EpiC. Oral immunization to specific-pathogen-free (SPF) chickens with recombinant strains induced significantly higher levels of humoral immune responses, and provided protection against lethal dose challenge by the IBV SAIBk strain. These results indicate that it is feasible to use L. lactis as an antigen delivery vehicle in developing oral vaccines against IBV infection.