bluuebunny/crossref_metadata_2025_split huggingface dataset:
GENETIC POLYMORPHISM OF PEROXISOME PROLIFERATOR‐ACTIVATED RECEPTOR‐γ2 PRO12ALA ON ETHNIC SUSCEPTIBILITY TO DIABETES IN UYGUR, KAZAK AND HAN SUBJECTS
Authors: Li Lin‐Lin , Ma Xiao‐Li , Ran Jian‐Xin , Sun Xiao‐Feng , Xu Li‐Ming , Ren Jun , Mao Xin‐Min 
Published: October 2007

SUMMARY

The aim of the present study was to determine whether the peroxisome proliferator‐activated receptor (PPAR)‐g Pro12Ala polymorphism affects susceptibility to diabetes in Uygur, Kazak and Han subjects in Xinjiang, China.
Uygur, Kazak and Han subjects from Kashi, Yili and Shawan (Xinjiang, China) were enrolled in the present study. The PPAR‐g Pro12Ala polymorphism was determined using restriction fragment length polymorphism. Anthropometric and serum biological indices were monitored among different genotype carriers to examine the PPAR‐g Pro12Ala gene polymorphism and the prevalence of type 2 diabetes.
The distribution frequency of the Pro12Ala genotype did not differ between diabetic and non‐diabetic Uygur, Kazak and Han subjects. However, the frequency of the A allele of Pro12Ala was significant different among non‐diabetics, with frequencies of 11, 9 and 5% in Uygur, Kazak and Han groups, respectively. Using the c2 test, it was shown that the frequency of the A allele in Uygurs (11%) was significantly higher than that in Han subjects (5%). To compare the wild‐type (Pro/Pro) carriers in diabetics from each ethnic group, Ugyur subjects, who carry PPAR‐g Pro12Ala (Pro/Ala), had a larger waist circumference and lower low‐density lipoprotein–cholesterol level, Kazaks subjects showed larger waist circumference and higher high‐density lipoprotein levels and Han subjects exhibited a high waist‐to‐hip ratio and body mass index.
The present study revealed that the allele and genotype frequency did not differ in diabetics and non‐diabetics of each ethnic group. However, the frequency of the A allele was significantly different in non‐diabetics from various ethnic groups. These data suggest that PPAR‐g Pro12Ala may affect blood lipid levels and the abdominal fat storage of diabetic Ugyurs and Kazaks and may be associated with fat storage and insulin resistance in Hans.
TYPE 1 DIABETES AND HYPERCHOLESTEROLAEMIA REVEAL THE CONTRIBUTION OF ENDOTHELIUM‐DERIVED HYPERPOLARIZING FACTOR TO ENDOTHELIUM‐DEPENDENT RELAXATION OF THE RAT AORTA
Authors: Malakul Wachirawadee , Thirawarapan Suwan , Suvitayavat Wisuda , Woodman Owen L 
Published: October 2007

SUMMARYThe present study evaluated the effect of diabetes, hypercholesterolaemia and their combination on the contribution of nitric oxide (NO) and endothelium‐derived hyperpolarizing factor (EDHF) to relaxation of rat isolated aortic rings and the potential contribution of oxidant stress to the disturbance of endothelial function.Thoracic aortic rings from control, diabetic, hypercholesterolaemic and diabetic plus hypercholesterolaemic rats were suspended in organ baths for tension recording. Generation of superoxide by the aorta was measured using lucigenin‐enhanced chemiluminescence.The maximal response to acetylcholine (ACh) was significantly reduced in diabetic or hypercholesterolaemic rats compared with control rats. In rats with diabetes plus hypercholesterolaemia, both the sensitivity and maximal response to ACh was impaired. In control rats, the response to ACh was abolished by the NO synthase inhibitorNG‐nitro‐l‐arginine (l‐NNA) or inhibition of soluble guanylate cyclase with 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ). In contrast, in rats with diabetes, hypercholesterolaemia or both, relaxation to ACh was resistant to inhibition byl‐NNA or ODQ, but abolished by additional inhibition of KCachannels with charybdotoxin plus apamin.The generation of superoxide was not significantly enhanced in aortic rings from either diabetic or hypercholesterolaemic rats, but was significantly increased in aortic rings from rats with diabetes plus hypercholesterolaemia.These results suggest that when diabetes and hypercholesterolaemia impair endothelium‐dependent relaxation, due to a diminished contribution from NO, a compensatory contribution of EDHF to endothelium‐dependent relaxation of the aorta is revealed. The attenuation of NO‐mediated relaxation, at least in the presence of both diabetes and hypercholesterolaemia, is associated with enhanced superoxide generation.
CHANGES IN MUSCARINIC RECEPTORS IN THE TOAD UROTHELIAL CELL LINE TBM‐54 FOLLOWING ACROLEIN TREATMENT
Authors: Giglio D , Andersson M , Aronsson P , Delbro DS , Haraldsson B , Tobin G 
Published: October 2007

SUMMARY

In cyclophosphamide‐induced cystitis in the rat, cholinergic function of the bladder and muscarinic receptor expression are altered. In the present study, we investigated whether the toad urothelial cell line TBM‐54 expresses functional muscarinic receptors and whether changes in muscarinic receptors can be induced in vitro by treating cells with acrolein, a metabolite of cyclophosphamide causing cystitis.
The occurrence of muscarinic receptors on cells was assessed by microphysiometry, a method analysing receptor function by measuring changes in the extracellular acidity rate (ECAR) in response to receptor stimulation.
Challenging untreated cells with the muscarinic receptor agonist carbachol gave rise to a concentration‐dependent increase in changes in ECAR, with a maximal response at 1 mmol/L carbachol of 51 ± 6%. Pre‐incubating cells with different muscarinic receptor antagonists (i.e. pirenzepine (M1 receptor selective), methoctramine (M2/M4 receptor selective) and 4‐diphenylacetoxy‐N‐methylpiperidine methobromide (4‐DAMP; M3/M1/M5 receptor selective)), gave rise to a concentration‐dependent decrease in the effects of carbachol (0.5 mmol/L) on changes in ECAR.
Western blot analysis was used to determine the expression of all muscarinic receptor subtypes (M1–M5) by the cell line. Following acrolein treatment, cells were markedly less sensitive to carbachol and the expression of muscarinic M2 receptors was decreased, whereas the expression of muscarinic M3 receptors was increased.
In conclusion, the urothelial cell line TBM‐54 expresses functional muscarinic receptors and exposure to acrolein leads to a modulation in the expression of muscarinic receptors. Consequently, acrolein may have direct effects on muscarinic receptor function and expression that contribute to the pathogenesis of cyclophosphamide‐induced cystitis.
EVIDENCE THAT HYDROXYSAFFLOR YELLOW A PROTECTS THE HEART AGAINST ISCHAEMIA–REPERFUSION INJURY BY INHIBITING MITOCHONDRIAL PERMEABILITY TRANSITION PORE OPENING
Authors: Liu Yi‐Na , Zhou Zhong‐Min , Chen Peng 
Published: October 2007

SUMMARY

The present study was conducted to investigate whether hydroxysafflor yellow A (HSYA) has a protective effect against heart injury after ischaemia–reperfusion and to determine the possible mechanism involved.
Hearts isolated from male Sprague‐Dawley rats were perfused on a Langendorff apparatus and subjected to 30 min global ischaemia, followed by 120 min reperfusion. Infarct size and the level of lactate dehydrogenase (LDH) in the coronary effluent were determined. In mitochondria from isolated perfused hearts, Ca2+‐induced swelling was observed. In isolated ventricular myocytes, depolarization of the mitochondrial membrane was determined by tetramethyl‐rhodamine ethyl ester (TMRE) fluorescence. Furthermore, levels of phosphorylated endothelial nitric oxide synthase (eNOS) protein were measured by western blot.
Pretreatment with HSYA for 5 min before ischaemia reduced infarct size and the release of LDH. Administration of 20 µmol/L atractyloside, an opener of the mitochondrial permeability transition pore, and 10 µmol/L NG‐nitro‐l‐arginine methyl ester (l‐NAME), an inhibitor of NOS, attenuated the protective effects of HSYA. In mitochondria isolated from hearts pretreated with 0.1 mmol/L HSYA for 5 min, a significant inhibition of Ca2+‐induced swelling was observed and this inhibition was attenuated by l‐NAME. In isolated ventricular myocytes, pretreatment with HSYA prevented ischaemia‐induced cell death and depolarization of the mitochondrial membrane, whereas atractyloside or l‐NAME attenuated the effects of HSYA. Levels of phosphorylated eNOS protein were significantly enhanced in the HSYA‐treated group.
The findings of the present study indicate that HSYA protects the myocardium against ischaemia–reperfusion injury by inhibiting mitochondrial permeability transition pore opening. The effect of HSYA on mitochondrial permeability transition pore opening may be mediated through enhanced nitric oxide production by eNOS activation.
Peripheral and central administration of exogenous urocortin 1 disrupts the fasted motility pattern of the small intestine in rats via the corticotrophin releasing factor receptor 2 and a cholinergic mechanism
Authors: Yin Yan , Dong Lei , Yin Dong 
Published: October 2007

AbstractBackground and Aim:  The action of the corticotrophin releasing factor (CRF) receptor on the small intestinal motility has been rarely investigated. The present study aimed to determine the effects of urocortin 1 on small intestinal motility in rats and the CRF receptor subtypes and autonomic pathways mediating the effects.Methods:  Fasted or fed rats were used to investigate the effect of intravenous or intracerebroventricular urocortin 1 on duodenum and jejunum motility. NBI‐27914 and astressin2‐B (CRF receptor 1 and 2 antagonists, respectively), atropine (an M‐receptor antagonist), phentolamine (an α‐receptor antagonist), propranolol (a β‐receptor antagonist) and Nω‐Nitro‐l‐arginine (a nitric oxide synthase [NOS] inhibitor) were applied to determine the involved CRF receptor subtypes and autonomic pathways.Results:  In fasted rats, intravenous or intracerebroventricular injection of urocortin 1 disrupted duodenal and jejunal migrating myoelectric complex pattern, leading to an irregular spiking activity similar to the fed motility pattern. When urocortin 1 was given in the fed state, the fed motility pattern remained unchanged. In addition, urocortin 1 also inhibited small intestinal transit function. Astressin2‐B injected intraperitoneally or intracerebroventricularly blocked urocortin 1‐induced change, while NBI‐27914 had no effect. The disruption of migrating myoelectric complex induced by urocortin 1 was abolished by atropine, but not affected by phentolamine, propranolol and Nω‐Nitro‐l‐arginine.Conclusion:  Intravenous or intracerebroventricular injection of urocortin 1 acts, respectively, on peripheral and central CRF receptor 2 to disrupt the intestinal migrating myoelectric complex through an M‐receptor‐dependent mechanism, and such change has an inhibitory effect as proved by measuring the small intestinal transit function.
Percutaneous radiofrequency ablation of hepatocellular adenoma: Initial experience in 10 patients
Authors: Rhim Hyunchul , Lim Hyo K , Kim Young‐sun , Choi Dongil 
Published: October 2007

AbstractBackground and Aim:  The purpose of this study was to assess the therapeutic efficacy and safety of percutaneous radiofrequency (RF) ablation for hepatocellular adenoma.Methods:  We performed percutaneous RF ablation in 10 patients with pathologically proven hepatocellular adenomas. Eight patients were asymptomatic and two patients had a recurrent tumor after surgical resection. The size of the tumors was 2.25 ± 0.76 cm (range: 1.5–4.5 cm) in the largest diameter. All ablation procedures were percutaneously performed with an internally cooled RF electrode system under ultrasound (US) guidance. We evaluated the therapeutic efficacy and safety of the procedure by clinical follow‐up data with regular follow‐up computed tomography (CT) for 2–35 months (mean, 17.5 months).Results:  All patients well tolerated percutaneous RF ablation procedure without any incident. Contrast‐enhanced CT (n = 7) or contrast‐enhanced US (n = 3) obtained immediately (<24 h) after the procedure revealed complete ablation of the tumor in all cases. There was no case of local tumor progression or new recurrence during the follow‐up period. We found neither procedure‐related mortality nor major complication requiring specific treatment.Conclusion:  Percutaneous RF ablation of hepatocellular adenoma without overt complication can be a new potential alternative to close imaging follow‐up or elective surgery.
Altered expression of glucagon‐like peptide‐1 and dipeptidyl peptidase IV in patients with HCV‐related glucose intolerance
Authors: Itou Minoru , Kawaguchi Takumi , Taniguchi Eitaro , Sumie Shuji , Oriishi Tetsuharu , Mitsuyama Keiichi , Tsuruta Osamu , Ueno Takato , Sata Michio 
Published: October 2007

AbstractBackground and Aim:  The pathogenesis of hepatitis C virus (HCV)‐associated glucose intolerance remains unclear. Glucagon‐like peptide‐1 (GLP‐1), a gut hormone, synthesizes hepatic glycogen and is inactivated by dipeptidyl peptidase IV (DPPIV). The aims of this study were to investigate the alterations in the expression of GLP‐1 and DPPIV in HCV‐associated glucose intolerance.Methods:  We enrolled patients with HCV‐ or hepatitis B virus (HBV)‐related liver disease (n = 94 and 37, respectively), patients with inflammatory bowel disease (IBD; n = 14) as disease controls, and healthy controls (n = 48). The serum or tissue GLP‐1 and DPPIV expression levels were determined by enzyme immunoassay, immunoblotting, or immunostaining. The hepatic glycogen content was assayed by periodic acid–Schiff staining.Results:  The serum GLP‐1 levels were significantly decreased in the HCV group (4.9 ± 0.3 ng/mL) than those in the controls (7.5 ± 0.6 ng/mL), the HBV group (7.0 ± 0.5 ng/mL), or the IBD group (10.8 ± 1.0 ng/mL, P < 0.01). Although the ileum GLP‐1 expression was not significantly different between the controls and the HCV group, the DPPIV expression was significantly increased in the ileum, liver, and serum in the HCV group. Hepatic glycogen content was decreased to a greater extent in the HCV group than that in the HBV group (127.5 ± 5.3 vs 187.7 ± 6.6 arbitrary units; n = 19, P < 0.01).Conclusion:  We demonstrated the altered expressions of GLP‐1 and DPPIV in patients with HCV‐associated glucose intolerance. Since hepatic glycogen synthesis, a GLP‐1 action, was impaired, the altered expressions of GLP‐1 and DPPIV may be involved in the development of HCV‐associated glucose intolerance.
How to characterize non‐hypervascular hepatic nodules on contrast‐enhanced computed tomography in chronic liver disease: Feasibility of contrast‐enhanced ultrasound with a microbubble contrast agent
Authors: Yoshizumi Hiroaki , Maruyama Hitoshi , Okugawa Hidehiro , Kobayashi Satoshi , Akiike Taro , Yoshikawa Masaharu , Ebara Masaaki , Yokosuka Osamu , Matsutani Shoichi , Kondo Fukuo , Kamiyama Naohisa 
Published: October 2007

AbstractBackground and Aim:  Although hypervascular appearance is characteristic in hepatocellular carcinoma (HCC), hepatic nodules without hypervascular appearance are sometimes found in patients with chronic liver disease (CLD). The aim of the present study was to clarify the efficacy of contrast‐enhanced ultrasound (CEUS) with Levovist to characterize small, non‐hypervascular hepatic nodules on contrast‐enhanced computed tomography (CECT) in patients with CLD.Methods:  The subject was 41 hepatic nodules (<30 mm, 18.5 ± 5.6 mm) which showed non‐hypervascular appearance on CECT in 35 patients with CLD; their histological results were 31 HCC (15 well, 14 moderate, and two poor) and 10 regenerative nodules (RN). CEUS with Levovist was performed under intermittent scanning (1‐s interval) using APLIO at the early phase and the liver‐specific phase, and the contrast enhancement of the nodule was assessed in comparison to that of the surrounding liver parenchyma. The contrast‐enhanced findings with the time‐intensity analysis were compared with the histological results.Results:  Twelve nodules with weak enhancement in the liver‐specific phase were HCC, regardless of their early‐phase appearances. The other 29 nodules with equivalent or weak enhancement in the early phase and equivalent enhancement in the liver‐specific phase were 19 HCC and 10 RN. Among them, the maximum‐intensity ratio of tumor to non‐tumor in the early phase was significantly higher in HCC than in RN (P < 0.01, n = 16), and the receiver‐operating characteristic analysis showed a sensitivity of 1.0 and a specificity of 0.83 for their characterization.Conclusion:  CEUS with Levovist may be an alternative to biopsy to characterize small, non‐hypervascular hepatic nodules on CECT in patients with CLD.
Prospective evaluation of the management of moderate to severe cellulitis with parenteral antibiotics at a paediatric day treatment centre
Authors: Gouin Serge , Chevalier Isabelle , Gauthier Marie , Lamarre Valérie 
Published: October 2007

Aim:  To assess the clinical outcome of patients with moderate to severe cellulitis managed at a paediatric day treatment centre (DTC).Methods:  Prospective observational study of all patients (3 months to 18 years) with a presumed diagnosis of moderate to severe cellulitis made in a university‐affiliated paediatric emergency department (ED) (September 2003 to September 2005). Patients treated at the DTC were given ceftriaxone or clindamycin.Results:  During the study period, a presumed diagnosis of moderate to severe cellulitis was made in 224 patients in the ED. Ninety‐two patients were treated at the DTC (41%). The cellulitis had a median width of 7.0 cm (range: 1.0–50.0 cm) and a median length of 6.5 cm (range: 1.0–40.0 cm). Blood cultures were performed in 95.7%; one was positive for Staphylococcus aureus. After a mean of 2.5 days of intravenous therapy (first injection in the ED and a mean of 1.5 days at the DTC), 73 patients (79.3%) were successfully discharged from the DTC and switched to an oral agent. For these patients no relapse occurred. Nineteen patients (20.7%) required inpatient admission for further therapy. No patient was diagnosed with necrotizing fasciitis in the course of therapy. Seventy‐eight satisfaction questionnaires were handed in and revealed very good to excellent parental satisfaction with treatment at the DTC in 94.8%.Conclusion:  Treatment with parenteral antibiotic at a DTC is a viable alternative to hospitalisation for moderate to severe cellulitis in children.
Clinical and urodynamic outcomes of pubovaginal sling procedure with autologous rectus fascia for stress urinary incontinence
Authors: Mitsui Takahiko , Tanaka Hiroshi , Moriya Kimihiko , Kakizaki Hidehiro , Nonomura Katsuya 
Published: October 2007

Aim:  We report the clinical and urodynamic outcomes of the pubovaginal sling procedure with autologous rectus fascia for stress urinary incontinence (SUI) and determined the urodynamic parameters that could predict the occurrence of postoperative voiding difficulty.Methods:  Between 1998 and 2005, a total of 29 consecutive women with SUI underwent pubovaginal sling surgery with autologous rectus fascia. Patients were preoperatively and postoperatively evaluated with regard to symptoms and urodynamic findings including uroflowmetry (UFM), postvoid residual urine volume (PVR), filling cystometry (CMG) and pressure flow study (PFS).Results:  Overall SUI was cured in 23 patients (80%) and improved in 3 patients (10%). Three patients (10%) who developed persistent urinary retention or severe voiding difficulty after surgery underwent urethrolysis. Of 17 patients who had urgency before the pubovaginal sling, urgency was cured postoperatively in seven, while de novo urgency appeared in one patient. Maximum flow rate (Qmax) in UFM was significantly decreased (P < 0.05) and PVR was increased (P = 0.08) after surgery. PFS showed a significant increase in detrusor opening pressure and detrusor pressure at Qmax (P < 0.01) after surgery. Eight patients (28%) needed prolonged intermittent self‐catheterization. Patients who had PVR >100 mL (P < 0.05) or Qmax ≤20 mL/s (P = 0.09) in preoperative UFM were more likely to require prolonged intermittent catheterization after surgery.Conclusions:  The pubovaginal sling procedure with autologous rectus fascia is an effective treatment for SUI. A comparison of preoperative and postoperative urodynamic parameters indicates an increase in urethral resistance after pubovaginal sling surgery. PVR >100 mL and Qmax ≤20 mL/s before surgery are risk factors for postoperative voiding difficulty.
Rhythmic auditory stimulation modulates gait variability in Parkinson's disease
Authors: Hausdorff Jeffrey M. , Lowenthal Justine , Herman Talia , Gruendlinger Leor , Peretz Chava , Giladi Nir 
Published: October 2007

AbstractPatients with Parkinson's disease (PD) walk with a shortened stride length and high stride‐to‐stride variability, a measure associated with fall risk. Rhythmic auditory stimulation (RAS) improves stride length but the effects on stride‐to‐stride variability, a marker of fall risk, are unknown. The effects of RAS on stride time variability, swing time variability and spatial‐temporal measures were examined during 100‐m walks with the RAS beat set to 100 and 110% of each subject's usual cadence in 29 patients with idiopathic PD and 26 healthy age‐matched controls. Carryover effects were also evaluated. During usual walking, variability was significantly higher (worse) in the patients with PD compared with the controls (P < 0.01). For the patients with PD, RAS at 100% improved gait speed, stride length and swing time (P < 0.02) but did not significantly affect variability. With RAS at 110%, reductions in variability were also observed (P < 0.03) and these effects persisted 2 and 15 min later. In the control subjects, the positive effects of RAS were not observed. For example, RAS increased stride time variability at 100 and 110%. These results demonstrate that RAS enables more automatic movement and reduces stride‐to‐stride variability in patients with PD. Further, these improvements are not simply a by‐product of changes in speed or stride length. After walking with RAS, there also appears to be a carryover effect that supports the possibility of motor plasticity in the networks controlling rhythmicity in PD and the potential for using RAS as an intervention to improve mobility and reduce fall risk.
Involvement of protein‐tyrosine phosphatase PTPMEG in motor learning and cerebellar long‐term depression
Authors: Kina Shin‐ichiro , Tezuka Tohru , Kusakawa Shinji , Kishimoto Yasushi , Kakizawa Sho , Hashimoto Koichi , Ohsugi Miho , Kiyama Yuji , Horai Reiko , Sudo Katsuko , Kakuta Shigeru , Iwakura Yoichiro , Iino Masamitsu , Kano Masanobu , Manabe Toshiya , Yamamoto Tadashi 
Published: October 2007

AbstractAlthough protein‐tyrosine phosphorylation is important for hippocampus‐dependent learning, its role in cerebellum‐dependent learning remains unclear. We previously found that PTPMEG, a cytoplasmic protein‐tyrosine phosphatase expressed in Purkinje cells (PCs), bound to the carboxyl‐terminus of the glutamate receptor δ2 via the postsynaptic density‐95/discs‐large/ZO‐1 domain of PTPMEG. In the present study, we generated PTPMEG‐knockout (KO) mice, and addressed whether PTPMEG is involved in cerebellar plasticity and cerebellum‐dependent learning. The structure of the cerebellum in PTPMEG‐KO mice appeared grossly normal. However, we found that PTPMEG‐KO mice showed severe impairment in the accelerated rotarod test. These mice also exhibited impairment in rapid acquisition of the cerebellum‐dependent delay eyeblink conditioning, in which conditioned stimulus (450‐ms tone) and unconditioned stimulus (100‐ms periorbital electrical shock) were co‐terminated. Moreover, long‐term depression at parallel fiber–PC synapses was significantly attenuated in these mice. Developmental elimination of surplus climbing fibers and the physiological properties of excitatory synaptic inputs to PCs appeared normal in PTPMEG‐KO mice. These results suggest that tyrosine dephosphorylation events regulated by PTPMEG are important for both motor learning and cerebellar synaptic plasticity.