bluuebunny/crossref_metadata_2025_split huggingface dataset:
Rho/Rho kinase is a key enzyme system involved in the angiotensin II signaling pathway of liver fibrosis and steatosis
Authors: Kitamura Kumi , Tada Shinichiro , Nakamoto Nobuhiro , Toda Kyoko , Horikawa Hitomi , Kurita Satoshi , Tsunematsu Satoshi , Kumagai Naoki , Ishii Hiromasa , Saito Hidetsugu , Hibi Toshifumi 
Published: October 2006

AbstractBackground and Aim:  The molecular mechanisms underlying the involvement of the renin‐angiotensin system in hepatic fibrosis are unclear. Recently, it was reported that a Rho kinase inhibitor prevented fibrosis of various tissues and that the Rho/Rho kinase pathway was involved in the renin‐angiotensin system of vascular smooth muscle cells. In this study, the involvement of the Rho/Rho kinase pathway on angiotensin II signaling in liver fibrogenesis and generation of steatosis was investigated.Methods:  Rats were fed a choline‐deficient/L‐amino acid‐defined (CDAA) diet continuously and treated with a Rho kinase inhibitor, Y‐27632, and an angiotensin II receptor blocker, TCV‐116. Liver histology and hepatic stellate cell activation were analyzed. Free radical production was detected by 4‐hydroxynonenal and 8‐hydroxy‐2′‐deoxyguanosine immunostaining and the expression of tumor necrosis factor‐α was examined. Isolated hepatic stellate cells were pretreated with a Rho kinase inhibitor, Y‐27632, or an angiotensin II receptor blocker, CV‐11974, and stimulated with angiotensin II, and mRNA expression of transforming growth factor‐β and α‐smooth muscle actin was analyzed.Results:  Both the angiotensin II receptor blocker and the Rho kinase inhibitor improved fibrosis and steatosis of the liver in CDAA‐fed rats. The increase in the number of hepatocytes positive for 4‐hydroxynonenal and 8‐hydroxy‐2′‐deoxyguanosine in CDAA‐fed rats was significantly prevented by the angiotensin II receptor blocker and the Rho kinase inhibitor. The levels of tumor necrosis factor‐α mRNA in the liver of CDAA‐fed rats were significantly increased and this increase was significantly inhibited by treatment with the angiotensin II receptor blocker and the Rho kinase inhibitor. mRNA expression of transforming growth factor‐β and α‐smooth muscle actin stimulated by angiotensin II was also significantly suppressed by these two drugs.Conclusion:  These results suggest that the Rho/Rho kinase pathway is at least partly involved in the renin‐angiotensin system and plays an important role in hepatic fibrosis and steatosis.
Low incidence of alpha 1‐antitrypsin deficiency among Filipinos with neonatal cholestatis
Authors: Tan Josephine J , Cutiongco‐dela Paz Eva Maria , Avila Jose Maria C , Gregorio Germana V 
Published: October 2006

Aim:  Alpha 1‐antitrypsin (AAT) deficiency is the most common genetic cause of liver disease in children. The Pi*S carrier rate among Filipinos is <1%. Its significance in Filipino infants with neonatal cholestasis has not been investigated. The aim of the study was to determine the incidence of AAT deficiency among Filipino infants presenting with neonatal cholestasis.Methods:  Genotype determination that detects Pi*S and Pi*Z alleles was performed using Elucigene AAT reagents (Cellmark Diagnostics, UK). AAT inclusions were identified by light microscopy using periodic acid‐Schiff (PAS) stain.Results:  Ninety‐six infants (mean age: 89 days, 48 males) with a history of jaundice since 2 weeks old and a direct bilirubin level >20% of the total were recruited. Only one patient (1 month old, male) was positive for Pi*S allele and 95 were negative for Pi*S and Pi*Z alleles, with an annual incidence of 0.7%. Of the 96, 49 infants underwent diagnostic percutaneous liver biopsy. All liver biopsy specimen were subjected to PAS stain and two infants, 2 and 4 months old, both with idiopathic neonatal hepatitis, had suspicious findings of AAT globules that was confirmed on immunostain. Both infants were negative for Pi*S alleles. The only patient positive for Pi*S allele was negative for PAS globule on liver biopsy.Conclusion:  Our results showed a low incidence of AAT deficiency caused by the Pi*S and Pi*Z alleles among Filipino infants presenting with neonatal cholestasis, similar to the low carrier rate in the population.
Descriptive epidemiology of small screen recreation among Australian adolescents
Authors: Hardy Louise L , Dobbins Timothy A , Denney‐Wilson Elizabeth A , Okely Anthony D , Booth Michael L 
Published: October 2006

Aim:  To describe the epidemiology of small screen recreation (SSR) that is: television, computer, video, and DVD use among school students aged 11–15 years in New South Wales, Australia.Methods:  Cross‐sectional representative population survey (n = 2750) of 45 primary and 48 secondary schools in rural and urban areas. Self‐reported time spent in SSR was categorised according to national guidelines into less than 2 h per day (low users) or 2 or more hours per day (high users).Results:  Of primary and secondary school students, 53% and 72%, respectively, were high users of SSR. Boys spent significantly more time in SSR and were more likely to be high users of SSR compared with girls. For primary students, rural boys had a higher prevalence of high SSR use than urban boys (odds ratio (OR) 1.9, 95% confidence interval (CI) 1.0–3.5), while overweight girls had a higher prevalence than healthy‐weight girls (OR 1.8, 95% CI 1.2–2.8). For secondary students, rural boys had a lower prevalence of high SSR use than urban boys (OR 0.5, 95% CI 0.3–0.6), and girls from high SES backgrounds had a lower prevalence than girls from low socio‐economic status backgrounds (OR 0.6, 95% CI 0.3–1.0).Conclusion:  The majority of school students in New South Wales exceed the national guidelines for SSR. Reducing the time spent in SSR among young people is one potential approach to increasing energy expenditure and reducing adiposity or maintaining a healthy weight. First steps for intervention strategies among school‐age children to reduce SSR could include teaching awareness skills and self‐monitoring techniques.
Atherosclerosis in haemodialysis patients without significant comorbidities: Determinants of progression
Authors: ZUMRUTDAL AYSEGUL , DEMIRCAN SENOL , SEYDAOGLU GULSAH , SINGAN METIN , SEZER SIREN , OZDEMIR F NURHAN , HABERAL MEHMET 
Published: October 2006

SUMMARY:Aim:  The aim of this prospective study was to assess the determinants of the progression of carotid artery intima‐media thickness (CA‐IMT) for 1 year in haemodialysis (HD) patients without significant comorbidities.Methods:  Fifty‐four HD patients younger than 55 years, without diabetes, obesity and any clinical evidence of cardiovascular disease (29 men, 25 women; mean age 33.3 ± 10 years; mean time on HD 49.4 ± 43 months) were included in the 1‐year study. CA‐IMT was assessed at baseline and after 12 months. The difference in IMT between these two points of time was calculated (ΔCA‐IMT). C‐reactive protein (CRP), erythrocyte sedimentation rate (ESR), haematocrit‐corrected ESR, beta‐2 microglobulin, cardiac troponin I, lipid profile, fibrinogen, homocysteine, CaXP product, intact parathyroid hormone, haematocrit, albumin, uric acid levels, anthropometric parameters (age, body mass index), smoking, hypertension and left ventricular hypertrophy were recorded at baseline.Results:  The mean value for CA‐IMT at baseline (0.59 ± 0.05 mm) was significantly lower than that at 12 months (0.64 ± 0.07 mm) (P < 0.001). CA‐IMT had increased in 41 patients (75.9%). Age (P = 0.02), CRP (P = 0.03), beta‐2 microglobulin (P = 0.001) and left ventricular hypertrophy (P = 0.01) were independently related with CA‐IMT at baseline. Age (P = 0.003) and CRP (P = 0.04) were the independent variables related with CA‐IMT, measured at 12 months. ΔCA‐IMT correlated positively with age (r = 0.31, P < 0.05). Age and sex were independent predictors of ΔCA‐IMT (R2 for the model 0.56).Conclusion:  In addition to age and male sex, non‐specific inflammation may have a possible role in the progression of atherosclerosis in HD patients without significant comorbidities.
Roxithromycin inhibits transforming growth factor‐β production by cultured human mesangial cells
Authors: YAMABE HIDEAKI , SHIMADA MICHIKO , KAIZUKA MITSUAKI , NAKAMURA MASAYUKI , KUMASAKA RYUICHIRO , MURAKAMI REI‐ICHI , FUJITA TAKESHI , NAKAMURA NORIO , OSAWA HIROSHI , OKUMURA KEN 
Published: October 2006

SUMMARY:Background:  Transforming growth factor‐β (TGF‐β) plays an important role in progression of renal injury. However, few materials which inhibit TGF‐β have been known. Roxithromycin (ROX), macrolide antibiotics, is known to have anti‐inflammatory, immunomodulatory and tissue reparative effects besides its bacteriostatic activity, although the exact mechanism of its anti‐inflammatory and immunomodulatory effects was not defined. We examined the effect of ROX on production of TGF‐β and type IV collagen by cultured human mesangial cells (HMC).Methods:  Human mesangial cells were incubated with several concentrations of ROX and TGF‐β and type IV collagen levels in the culture supernatants were measured by enzyme‐linked immunoassay. Amount of TGF‐β mRNA was also quantified by using a colourimetric mRNA quantification kit and semiquantitative reverse transcriptase polymerase chain reaction. We also examined the effect of ROX on tyrosine kinase, MAP kinase and NF‐κB stimulated by thrombin.Results:  Roxithromycin (0.1–10.0 µg/mL) inhibited TGF‐β production by HMC in a dose‐ and time‐dependent manner without inducing cell injury. ROX (10.0 µg/mL) also inhibited mRNA expression of TGF‐β in HMC. Thrombin (5 U/mL) stimulated TGF‐β production by HMC and ROX significantly inhibited the stimulating effect of thrombin on TGF‐β production. ROX also inhibited the increment of type IV collagen production stimulated by thrombin. ROX (10.0 µg/mL) suppressed the thrombin‐induced NF‐κB activation, although ROX did not inhibit the activation of tyrosine kinase and MAP kinase by thrombin.Conclusion:  Roxithromycin has an inhibitory effect on TGF‐β production by HMC possibly via inhibition of NF‐κB. ROX may be a potential agent for the treatment of glomerulosclerosis.
Systemic antioxidant defences during acute exacerbation of chronic obstructive pulmonary disease
Authors: SADOWSKA Anna M. , LUYTEN Chris , VINTS Anne‐Marie , VERBRAECKEN Johan , RANST Dirk Van , BACKER Wilfried A. De 
Published: October 2006

Objective and background:  Existence of an increased oxidative stress has been confirmed in patients with acute exacerbation of COPD. This study aims to examine the extent and time‐course of antioxidant defence in patients with an acute exacerbation of COPD in comparison with stable patients.Methods:  Twelve patients with acute exacerbation were studied at admission, and then 24 h and 48 h following admission and at discharge. The antioxidants assessed were the endogenous antioxidants: glutathione peroxidase, superoxide dismutase, oxidized and reduced glutathione, albumin and exogenous antioxidants: α‐tocopherol and retinol. Trolox equivalent antioxidant capacity as a marker of antioxidant status was also measured.Results:  There was an increase in glutathione peroxidase and superoxide dismutase 48 h after admission (P < 0.05). α‐Tocopherol was the lowest 24 h after admission and increased significantly at discharge (P < 0.05).Conclusions:  There is an increase in antioxidant defence during acute exacerbation of COPD reaching a maximum at 48 h after admission. This rise in the antioxidant defence is not sufficient to prevent depletion of non‐enzymatic antioxidants such as α‐tocopherol.
Effect of a prebiotic‐enriched phytocompound in improving ovalbumin allergenicity
Authors: METUGRIACHUK Yussef , TSUCHIYA Juichiro , MAROTTA Francesco , KAWAKITA Sam , OKURA Ruichi , KUROI Olivia , MINELLI Emilio 
Published: October 2006

OBJECTIVE:  The aim of the present study was to test a prebiotic‐phytotherapic compound in an experimental model of oral allergenicity.METHODS:  Antigen‐specific immunoglobulin E (IgE) elevated mice were prepared by injecting them intraperitoneally with 10 µg of ovalbumin. Subsequently, the mice were exposed to ovalbumin solution intranasally and blood samples were obtained on weekly intervals for 4 weeks to measure serum‐ovalbumin‐specific IgE and total immunoglobulin G. Mice with high titers of ovalbumin‐IgE were intragastrically administered with 0.3 mL of phosphate buffered solution containing either 20 mg of ovalbumin, the same solution with 5 mL of milk, or 20 mg milk added to prebiotic‐phytocompound.RESULTS:  Ovalbumin administration caused a significant increase of plasma ovalbumin concentration in sensitized mice while prebiotic‐phytocompound‐supplemented mice showed a significantly reduced peak value (P < 0.05). Prebiotic‐phytocompound added to milk exerted a significant effect in lowering the ovalbumin‐IgE level and the total immunoglobulin G level as compared to control plain milk (P < 0.01).CONCLUSION:  This study provides a rationale basis for a feasible non‐pharmacological therapeutic strategy in food allergen hypersensitivity syndromes.
Abnormal expression of Smurf2 during the process of rat liver fibrosis
Authors: CAI Yu , SHEN Xi Zhong , ZHOU Chao Hui , WANG Ji Yao 
Published: October 2006

OBJECTIVE:  Liver fibrosis is a prelude of liver cirrhosis. Currently the molecular mechanism of liver fibrosis is not clear. The purpose of this study is to screen the abnormally expressed genes of liver fibrosis and to illustrate the changes of Smurf2 expression in the process of liver fibrosis.METHODS:  A liver fibrosis model was established in rats by injection of tetrachlormethane (CCl4). A cDNA microarray analysis was performed on the liver at mid‐stage of fibrosis. Thereafter, a semi‐quantitative RT‐PCR, Western blot analysis and immunohistochemistry test were performed for determining Smurf2, Smad2 and SnoN at week 1, 2, 4 and 8 of establishing the liver fibrosis model.RESULTS:  Smurf2, FGG, PTAFR, CYP2D6, among others, increased in the fibrosis liver and a semi‐quantitative RT‐PCR confirmed the reliability of the cDNA microarray analysis. Smurf2 in the liver fibrosis model group was at the same level as that of control group at week 1, but decreased at week 2 and 8 and increased at the week 4. Smad2 increased at week 2 and 8 but increased at week 4. However, Smad2 mRNA increased to the same level at week 4 as that at week 2 and 8. The decrease of Smad2 at week 4 may be due to the enhancement of ubiquitination and proteolytic degradation of Smad2 by the increase of Smurf2. SnoN decreased at week 4 and 8 because of the ubiquitination and degradation caused by Smurf2. The decrease of SnoN may explain the progress of liver fibrosis in spite of the decrease of Smad2 at week 4.CONCLUSION:  This study screened the abnormally expressed genes of liver fibrosis and illustrated the changes of Smurf2, Smad2 and SnoN during the process of liver fibrosis.
CENTRAL PANCREATECTOMY FOR BENIGN PANCREATIC PATHOLOGY/TRAUMA: IS IT A REASONABLE PANCREAS‐PRESERVING CONSERVATIVE SURGICAL STRATEGY ALTERNATIVE TO STANDARD MAJOR PANCREATIC RESECTION?
Authors: Johnson Maria A. , Rajendran Shanmugasundaram , Balachandar Tirupporur G. , Kannan Devy G. , Jeswanth Satyanesan , Ravichandran Palaniappan , Surendran Rajagopal 
Published: October 2006

Background:  The aim of this study was to assess the technical feasibility, safety and outcome of central pancreatectomy (CP) with pancreaticogastrostomy or pancreaticojejunostomy in appropriately selected patients with benign central pancreatic pathology/trauma. Benign lesions/trauma of the pancreatic neck and proximal body pose an interesting surgical challenge. CP is an operation that allows resection of benign tumours located in the pancreatic isthmus that are not suitable for enucleation.Methods:  Between January 2000 and December 2005, eight central pancreatectomies were carried out. There were six women and two men with a mean age of 35.7 years. The cephalic pancreatic stump is oversewn and the distal stump is anastomosed end–to–end with a Roux‐en‐Y jejunal loop in two and with the stomach in six patients. The indications for CP were: non‐functional islet cell tumours in two patients, traumatic pancreatic neck transection in two and one each for insulinoma, solid pseudopapillary tumour, splenic artery pseudoaneurysm and pseudocyst. Pancreatic exocrine function was evaluated by a questionnaire method. Endocrine function was evaluated by blood glucose level.Results:  Morbidity rate was 37.5% with no operative mortality. Mean postoperative hospital stay was 10.5 days. Neither of the patients developed pancreatic fistula nor required reoperations or interventional radiological procedures. At a mean follow up of 26.4 months, no patient had evidence of endocrine or exocrine pancreatic insufficiency, all the patients were alive and well without clinical and imaging evidence of disease recurrence.Conclusion:  When technically feasible, CP is a safe, pancreas‐preserving pancreatectomy for non‐enucleable benign pancreatic pathology/trauma confined to pancreatic isthmus that allows for cure of the disease without loss of substantial amount of normal pancreatic parenchyma with preservation of exocrine/endocrine function and without interruption of enteric continuity.
Developmental and regional expression of NADPH‐diaphorase/nitric oxide synthase in spinal cord neurons correlates with the emergence of limb motor networks in metamorphosing Xenopus laevis
Authors: Ramanathan Sankari , Combes Denis , Molinari Micol , Simmers John , Sillar Keith T. 
Published: October 2006

AbstractMetamorphosis in anuran amphibians requires a complete transformation in locomotor strategy from undulatory tadpole swimming to adult quadrupedal propulsion. The underlying reconfiguration of spinal networks may be influenced by various neuromodulators including nitric oxide, which is known to play an important role in CNS development and plasticity in diverse species, including metamorphosis of amphibians. Using NADPH‐diaphorase (NADPH‐d) staining and neuronal nitric oxide synthase (nNOS) immunofluorescence labelling, the expression and developmental distribution of NOS‐containing neurons in the spinal cord and brainstem were analysed in all metamorphic stages of Xenopus laevis. Wholemount preparations of the spinal cord from early stages of metamorphosis (coincident with emergence of the fore‐ and hindlimb buds) revealed two clusters of NOS‐positive neurons interspersed with areas devoid of stained somata. These cells were distributed in three topographic subgroups, the most ventral of which had axonal projections that crossed the ventral commissure. Motoneurons innervating the fore‐ and hindlimb buds were retrogradely labelled with horseradish peroxidase (HRP) to determine their position in relation to the two NOS‐expressing cord regions. Limb motoneurons and NOS‐positive cells did not overlap, indicating that during early stages of metamorphosis nitrergic neurons are excluded from regions where spinal limb circuits are forming. As metamorphosis progresses, NOS expression became distributed along the length of the spinal cord together with an increase in the number and intensity of labelled cells and fibers. NOS expression reached a peak as the forelimbs emerge then declined. These findings are consistent with a role for nitric oxide (NO) in the developmental transition from undulatory swimming to quadrupedal locomotion.
Persistent penetration of MPTP through the nasal route induces Parkinson's disease in mice
Authors: Rojo Ana I. , Montero Celia , Salazar María , Close Ryan M. , Fernández‐Ruiz Javier , Sánchez‐González Miguel A. , De Sagarra María Rosa , Jackson‐Lewis Vernice , Cavada Carmen , Cuadrado Antonio 
Published: October 2006

AbstractThe aetiology of idiopathic Parkinson's disease (PD) is poorly defined but environmental aggressions may be relevant. Here, we report a new model of PD in mice, based on chronic inoculation with neurotoxins in the nasal cavity, which is a natural route of contact with the environment. C57BL/6 mice, submitted to daily intranasal inoculation with MPTP for 30 days, developed motor deficits that correlated with a progressive and severe depletion of striatal dopamine levels, and loss of tyrosine hydroxylase and dopamine transporter staining in substantia nigra and striatum. Moreover, mice intranasally inoculated with MPTP developed strong astrogliosis and microgliosis in substantia nigra and striatum. Consistent with these observations, a role for oxidant aggression was demonstrated by increased levels of Mn‐superoxide dismutase. However, α‐synuclein aggregation was not observed. This new animal model provides a new tool for studying PD symptoms that develop slowly over time, and it may be used to asses risk from environmental neurotoxins.
Effects of hypocretin‐1 in 192‐IgG–saporin‐lesioned rats
Authors: Blanco‐Centurion Carlos A. , Shiromani Anjelica , Winston Elizabeth , Shiromani Priyattam J. 
Published: October 2006

AbstractHypocretin, also known as orexin, is a neuropeptide located in the perifornical region of the lateral hypothalamus; this region projects to all the major arousal centres including the basal forebrain. The basal forebrain contains a mixed population of neurons, some of which are cholinergic. To identify the relative contribution of the noncholinergic neurons to arousal, here we utilized 192‐IgG–saporin to lesion the basal forebrain cholinergic neurons and determine whether microinjection of hypocretin‐1 to the basal forebrain is still effective in inducing arousal. In Sprague–Dawley rats given 192‐IgG–saporin (intraventricular, 6 µg; n = 7) 92% of the basal forebrain cholinergic neurons were destroyed compared to nonlesioned rats (n = 5). In the lesioned rats microinjection of hypocretin‐1 (0.0625, 0.125 or 0.25 nmol in 250 nL) to the basal forebrain increased waking and suppressed sleep (both non‐REM and REM) in a concentration‐dependent manner and to the same extent as in nonlesioned rats. These results suggest that, in the absence of the basal forebrain cholinergic neurons, the basal forebrain noncholinergic neurons are able to convey hypocretin's arousal signal unabated.
Florivory: the intersection of pollination and herbivory
Authors: McCall Andrew C. , Irwin Rebecca E. 
Published: October 2006

AbstractPlants interact with many visitors who consume a variety of plant tissues. While the consequences of herbivory to leaves and shoots are well known, the implications of florivory, the consumption of flowers prior to seed coat formation, have received less attention. Herbivory and florivory can yield different plant, population and community outcomes; thus, it is critical to distinguish between these two types of consumption. Here, we consider the ecological and evolutionary consequences of florivory. A growing number of studies recognize that florivory is common in natural systems and in some cases surpasses leaf herbivory in magnitude and impact. Florivores can affect male and female plant fitness via direct trophic effects and through altered pathways of species interactions. In particular, florivory can affect pollination and have consequences for plant mating and floral sexual system evolution. Plants are not defenceless against florivore damage. Concepts of resistance and tolerance can be applied to plant–florivore interactions. Moreover, extant theories of plant chemical defence, including optimal defence theory, growth rate hypothesis and growth differentiation–balance hypothesis, can be used to make testable predictions about when and how plants should defend flowers against florivores. The majority of the predictions remain untested, but they provide a theoretical foundation on which to base future experiments. The approaches to studying florivory that we outline may yield novel insights into floral and defence traits not illuminated by studies of pollination or herbivory alone.