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Normal Control Group (normal + control_group)
Selected AbstractsRole of Echocardiography in Assessing the Mechanism and Effect of Ramipril on Functional Mitral Regurgitation in Dilated CardiomyopathyECHOCARDIOGRAPHY, Issue 4 2005D.M. (Card), F.I.A.E., F.I.A.M.S., F.I.C.C., F.I.C.P., I.B. Vijayalakshmi M.D. The objectives of this article are to determine the possible mechanism of functional mitral regurgitation in patients with dilated cardiomyopathy (DCM) and to know the effect of ramipril on left ventricle (LV) and mitral regurgitation by ECHO. Several postulates are put forth for functional mitral regurgitation in DCM, and mitral annular dilatation is said to be the primary mechanism in the past, but the exact mechanism is not clear. Though angiotensin converting enzyme (ACE) inhibitors are known to remodel the LV, their beneficial effect in patients with DCM with functional mitral regurgitation is not known. Various cardiac dimensions and degree of mitral regurgitation were measured by echocardiography in 30 normal control group and in 30 patients with DCM of various etiologies except ischemic, before and after ramipril therapy. There was a significant difference in all parameters especially sphericity of left ventricle and position of papillary muscles (P < 0.0003) in DCM patients, but mitral valve annulus did not show significant change (P < 0.3) compared to control group. In 50% of the patients, the functional mitral regurgitation totally disappeared. In 30% of patients, it came down from grade II to I or became trivial. In 20% of patients, it remained unchanged. There was remarkable improvement in sphericity, LV dimension, volumes, and EF%, which increased from 31 ± 9.81 to 39.3 ± 8.3% (P < 0.0003). It is concluded that echocardiography clearly demonstrates the increased sphericity of LV in DCM. The lateral migration of papillary muscles possibly plays a major role in functional mitral regurgitation. Ramipril significantly reduces not only sphericity but also functional mitral regurgitation. [source] Lack of association between pro-inflammatory cytokine (IL-6, IL-8 and TNF-,) gene polymorphisms and Graves' diseaseINTERNATIONAL JOURNAL OF IMMUNOGENETICS, Issue 6 2005R.-H. Chen Summary Graves' disease (GD) is a common, autoimmune disease involving the thyroid gland, and it has been previously suggested that pro-inflammatory cytokines are involved in the disease's pathogenesis. The aim of this study was to test whether the interleukin (IL)-6 gene promoter region, or tumour necrosis factor (TNF)-, or IL-8 gene 3,-untranslated region (3,-UTR) polymorphisms could provide useful genetic markers for an individual's susceptibility to GD. A normal control group of 60 healthy people and 95 patients featuring GD were examined. Polymerase chain reaction (PCR)-based restriction analysis was performed for the three gene polymorphisms using endonucleases BsrBI, NcoI and ApaLI, respectively. We found no significant difference between the frequencies of genotype and allelic variants for the IL-6 gene promoter (,572 G/C), the TNF-, gene promoter (,308 A/G) and the IL-8 gene 3,-UTR (2767 A/G) for GD patients and for normal controls. Cytokines are a large group of proteins that may elicit multiple effects upon immunological reactions. It still appears to be very worthwhile to continue to aggressively search for cytokine gene polymorphisms in order to predict the development of such disease. [source] Urokinase gene 3,-UTR T/C polymorphism is associated with oral cancerJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 5 2004Ming-Hsui Tsai Abstract Urokinase is thought to be involved in the formation of oral cancer, although there is a lack of genetic evidence. Our aim was to study single nucleotide polymorphisms in order to investigate the possibility. A total of 130 oral cancer patients and 105 controls were studied. Polymerase chain reaction (PCR) based restriction analysis was used to identify the C/T polymorphism of the urokinase gene, which is located on the 3,-untranslated region (3,-UTR) of chromosome 10. There was a significant difference in the distribution of the urokinase gene 3,-UTR C/T polymorphism frequency between cancer patients and the normal control group (P<0.05). The "T" allele was prominent in the cancer group. The odds ratio for the risk of the "T" allele in cancer patients was 2.71 (95% CI=1.325,5.562). The cancer patients were further categorized according to gender and whether or not they were habitual smokers or betel nut chewers. These clinical parameters were then compared with tumor cell differentiation and tumor progression. No significant differences were found. Therefore, the urokinase gene 3,-UTR "T" allele is associated with oral cancer and may play a role in oral cancer formation. However, we did not find the relationship between tumor progression and this polymorphism. J. Clin. Lab. Anal. 18:276,279, 2004. © 2004 Wiley-Liss, Inc. [source] TAP1 gene AccI polymorphism is associated with atopic bronchial asthmaJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 2 2003Liang-Wen Hang Abstract Asthma is a hyperresponsive airway disease that may involve inflammation responses. A transporter associated with the antigen processing 1 gene (TAP1) is involved in antigen processing, and is therefore considered to play a role in the pathogenesis of bronchial asthma. The aim of this study was to test whether the polymorphisms of the TAP1 gene are a genetic marker for susceptibility to bronchial asthma. A normal control group comprised of 43 healthy people, and 116 patients with allergic asthma were examined in this study. The polymorphism was detected by polymerase chain reaction (PCR)-based restriction analysis. Associations between atopic bronchial asthma and TAP1 polymorphisms were evaluated. The results revealed no significant differences between normal individuals and asthmatics in regard to the TAP1 gene DpnII polymorphism (P=0.752). However, there was a significant difference between the control and asthma groups as regards the TAP1 gene AccI polymorphism (P=0.020). The odds ratio (OR) of GG homozygotes of the TAP1 AccI polymorphism was 229.8 compared with the AA homozygote group. The results show that the AccI polymorphism may be an indicator for atopic bronchial asthma. J. Clin. Lab. Anal. 17:57,60, 2003. © 2003 Wiley-Liss, Inc. [source] Role of interleukin-18 in the development of acute pulmonary injury induced by intestinal ischemia/reperfusion and its possible mechanismJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2 2007Yong-jie Yang Abstract Background and Aims:, Lung injury is an important target for the systemic inflammatory response associated with intestinal ischemia/reperfusion (I/R). In the present study, the role of interleukin (IL)-18 in the development of acute pulmonary injury induced by intestinal I/R and its possible mechanism in relation to the increased activity of inducible nitric oxide synthase and tumor necrosis factor (TNF)-, were investigated. Methods:, Mice were randomly divided into three groups: normal control group without operation; sham group with sham operation; and I/R group in which mice underwent superior mesenteric artery occlusion for 30 min followed by reperfusion for 3 h. Each group received pretreatment with exogenous IL-18, anti-IL-18 neutralizing antibody or L-NIL, the selective inhibitor of inducible nitric oxide synthase, 30 min before ischemia. The expression of TNF-, was detected by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). Lung injury was evaluated by means of Evans blue dye (EBD) concentration, myeloperoxidase (MPO) activity and morphological analysis. Results:, The experimental results showed that both in the sham-operated and I/R groups of animals, pretreatment with exogenous IL-18 clearly enhanced pulmonary MPO activity, microvascular leakage and the expression of TNF-, mRNA and protein. In contrast, IL-18 did not increase the TNF-, level and degree of lung injury, although it clearly enhanced the pulmonary MPO activity in normal animals. Meanwhile, IL-18 antibody given prior to ischemia led to a reduction in the sequestration of neutrophils, extravasation of EBD and downregulation of the serum level of TNF-, in the I/R group of animals. In addition, selective inhibition of inducible nitric oxide synthase (iNOS) that inhibited plasma extravasation and pulmonary injury without affecting the MPO activity could be demonstrated in all treated animals. Conclusions:, These data suggested a role of IL-18 in the activation and sequestration of neutrophils in lungs. Our results were consistent with the hypothesis that increased sequestration of neutrophils and microvascular leakage might, respectively, relate to the increased IL-18 level and the elevation of TNF-,/iNOS activity, and these two aspects might synergically contribute to intestinal I/R-induced pulmonary dysfunction. [source] Craniofacial morphology in patients with hypophosphataemic vitamin-D-resistant rickets: a cephalometric studyJOURNAL OF ORAL REHABILITATION, Issue 7 2009S. H. AL-JUNDI Summary, Hypophosphataemic vitamin-D-resistant rickets (HVDRR) is a hereditary disease mainly transmitted as an X-linked dominant trait and characterized by certain general clinical signs (Filho HM, de Castro LC, Damiani D. Arq Bras Endocrinol Metab. 2006;50:802). In literature, only one study had been published in 1965 on the cephalometric findings in patients with HVDRR (Marks SC, Lindahl RL, Bawden JW. J Dent Child. 1965;32:259). This is the first detailed study on craniofacial characteristics of patients with HVDRR in the dental literature. The aim of this study was to determine the effect of HVDRR on the parameters of the craniofacial skeleton of young Jordanian patients using cephalometric analysis. Lateral cephalometric radiographs were made for 22 Jordanian children (aged 2,16 years) diagnosed with HVDRR. The cephalometeric parameters of HVDRR group were compared with those of normal control group matched for gender and chronological age using paired t -test. The HVDRR group had a significant increase in the SNBa angle (P < 0·01); as well as reduced anterior cranial base length (P = 0·01), reduced maxillary length, corpus mandibular length and mandibular height (P = 0·01, 0·04 and 0·008 respectively). The cranial base and gonial angles were significantly increased in diseased individual, but the SNA and ANB angles were significantly reduced (P = 0·018 and 0·000 respectively). The angulation of the lower incisor to mandibular plane was also significantly reduced in the diseased group compared with Jordanian norm (P = 0·004). Patients with HVDRR have deficiency in the anterior cranial base length, ramus height and cranial base angle. Patients with HVDRR also have class III skeletal relationship. [source] Transplantation of mesenchymal stem cells in a canine disc degeneration modelJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 5 2008Akihiko Hiyama Abstract Transplantation of mesenchymal stem cells (MSCs) is effective in decelerating disc degeneration in small animals; much remains unknown about this new therapy in larger animals or humans. Fas-ligand (FasL), which is only found in tissues with isolated immune privilege, is expressed in IVDs, particularly in the nucleus pulposus (NP). Maintaining the FasL level is important for IVD function. This study evaluated whether MSC transplantation has an effect on the suppression of disc degeneration and preservation of immune privilege in a canine model of disc degeneration. Mature beagles were separated into a normal control group (NC), a MSC group, and the disc degeneration (nucleotomy-only) group. In the MSC group, 4 weeks after nucleotomy, MSCs were transplanted into the degeneration-induced discs. The animals were followed for 12 weeks after the initial operation. Subsequently, radiological, histological, biochemical, immunohistochemical, and RT-PCR analyses were performed. MSC transplantation effectively led to the regeneration of degenerated discs. FACS and RT-PCR analyses of MSCs before transplantation demonstrated that the MSCs expressed FasL at the genetic level, not at the protein level. GFP-positive MSCs detected in the NP region 8 weeks after transplantation expressed FasL protein. The results of this study suggest that MSC transplantation may contribute to the maintenance of IVD immune privilege by the differentiation of transplanted MSCs into cells expressing FasL. © 2008 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 26:589,600, 2008 [source] Maternal Oral Intake Mouse Model for Fetal Alcohol Spectrum Disorders: Ocular Defects as a Measure of EffectALCOHOLISM, Issue 10 2006Scott E. Parnell Background: This work was conducted in an effort to establish an oral intake model system in which the effects of ethanol insult that occur during early stages of embryogenesis can be easily examined and in which agents that may modulate ethanol's teratogenicity can be readily tested in vivo. The model system described utilizes the alcohol deprivation effect to obtain teratogenic levels of maternal ethanol intake on days 7 and 8 of pregnancy in C57Bl/6J mice. Ocular defects including microphthalmia and uveal coloboma, which have previously been shown to result from ethanol administered by gavage or via intraperitoneal injection on these days, served as the developmental end point for this study. The ocular defects are readily identifiable and their degree of severity is expected to correlate with concurrently developing defects of the central nervous system (CNS). Methods: Female C57Bl/6J mice were maintained on an ethanol-containing (4.8% v/v) liquid diet for 14 days and then mated during a subsequent abstinence period. Mice were then reexposed to ethanol on days 7 and 8 of pregnancy only. Control as well as ethanol-exposed dams were killed on their 14th day of pregnancy. Fetuses were then weighed, measured for crown rump length, photographed, and analyzed for ocular abnormalities. Globe size, palpebral fissure length, and pupil size and shape were noted for both the right and left eyes of all fetuses and informative comparisons were made. Results: This exposure paradigm resulted in peak maternal blood alcohol concentrations that ranged from 170 to 220 mg/dL on gestational day (GD) 8. Compared with the GD 14 fetuses from the normal control group, the pair-fed, acquisition controls, as well as the ethanol-exposed fetuses, were developmentally delayed and had reduced weights. Confirming previous studies, comparison of similarly staged control and treated GD 8 embryos illustrated reductions in the size of the forebrain in the latter. Subsequent ocular malformations were noted in 33% of the right eyes and 25% of the left eyes of the 103 GD 14 ethanol-exposed fetuses examined. This incidence of defects is twice that observed in the control groups. Additionally, it was found that the palpebral fissure length is directly correlated with globe size. Conclusions: The high incidence of readily identifiable ocular malformations produced by oral ethanol intake in this model and their relevance to human fetal alcohol spectrum disorders (FASD) makes this an excellent system for utilization in experiments involving factors administered to the embryo that might alter ethanol's teratogenic effects. Additionally, the fact that early ethanol insult yields ocular and forebrain abnormalities that are developmentally associated allows efficient specimen selection for subsequent detailed analyses of CNS effects in this in vivo mammalian FASD model. [source] Antioxidant Pretreatment Does Not Ameliorate Alcohol-Induced Purkinje Cell Loss in the Developing Rat CerebellumALCOHOLISM, Issue 7 2005Jedidiah J. Grisel Background: Recent research has suggested that oxidative stress is a potential mechanism for alcohol-induced injury and that supplementation with antioxidants can ameliorate alcohol-induced damage. In this study, two known antioxidants, melatonin and U83836E, were assessed for their effectiveness in blocking the expected alcohol-induced cerebellar Purkinje cell loss in neonatal rat pups. Methods: Sprague-Dawley rat pups were artificially reared from postnatal days (PDs) 4,9 and were exposed to either alcohol or antioxidants (melatonin or U83836E) individually or in combination. A normal control group (raised by rat dams) was included in this study. On PD 9, the brain from each pup was removed and weighed, and the cerebellar vermis was processed for stereological cell counting. Results: Alcohol exposure during the brain growth spurt produced microencephaly, in addition to significant decreases in the number and density of Purkinje cells in lobule I and the volume of lobule I. The antioxidants did not reduce any of the adverse effects observed from alcohol exposure, and they did not decrease the Purkinje cell number when administered alone. Furthermore, antioxidants did not change the only blood alcohol concentration measured on PD 6. Conclusions: The results confirmed alcohol-induced microencephaly and cerebellar Purkinje cell loss from neonatal alcohol exposure, and they showed that neither antioxidant could attenuate these adverse effects on the developing brain. The inability of antioxidants to reduce Purkinje cell loss from neonatal alcohol exposure suggests the existence of alternative mechanisms for developmental alcohol-induced Purkinje cell loss. [source] Bradykinesia, muscle weakness and reduced muscle power in Parkinson's disease,MOVEMENT DISORDERS, Issue 9 2009Natalie E. Allen BAppSc (Physio) Hons Abstract Muscle power (force × velocity) could clarify the relationship between weakness and bradykinesia in Parkinson's disease (PD). The aims of this study were to determine if patients with PD were weaker and/or less powerful in their leg extensor muscles than a neurologically normal control group and to determine the relative contributions of force and movement velocity/bradykinesia to muscle power in PD. Forty patients with PD and 40 controls were assessed. Strength in Newtons (N) was measured as the heaviest load the participant could lift. Power in Watts (W) was measured by having the participant perform lifts as fast as possible. The PD group were 172 N weaker (95% CI 28,315) and 124 W less powerful at peak power (95% CI 32,216) than controls. However, velocity at maximal power was only reduced compared with controls when lifting light to medium loads. When lifting heavy loads bradykinesia was no longer apparent in the PD group. These results suggest that reduced muscle power in PD at lighter loads arises from weakness and bradykinesia combined, but at heavier loads arises only from weakness. The absence of bradykinesia in the PD group when lifting heavy loads warrants further investigation. © 2009 Movement Disorder Society [source] Effect of activin A on tubulointerstitial fibrosis in diabetic nephropathyNEPHROLOGY, Issue 3 2009XIAO-JUN REN SUMMARY Aim: The effect of activin A on tubulointerstitial fibrosis in diabetic nephropathy (DN) using streptozotocin (STZ)-induced diabetic rats and high glucose-cultured HK-2 cells was investigated. Methods: Male Wistar rats were randomized into a normal control group (NC) and diabetes mellitus group (DM). Diabetes was induced by i.p. injection of STZ. Six rats were respectively killed 4, 8, 12 and 16 weeks after model establishment in each group. The changes of kidney weight/bodyweight (KW/BW), urine albumin excretion rate (AER) and creatinine clearance rate (Ccr) were determined. The morphology of tubulointerstitium was observed by light microscopy. Further biochemical analysis was provided using immunohistochemistry and real-time polymerase chain reaction. The different parameters in high glucose-cultured HK-2 cells were monitored by western blotting or enzyme-linked immunosorbent assay (ELISA) and the intervention of rh-follistatin on them was investigated. Results: Compared with the NC group, there was marked enlargement in the levels of KW/BW, AER, Ccr and interstitial fibrosis index, and the production of P-Smad2/3 and fibronectin in the DM group from 8 to 16 weeks. Activin ,A, mainly located in tubular epithelial cells, was significantly higher in the DM group than that in the NC group throughout the study periods. Follistatin was abundant in the NC group, but was diminished gradually in the DM group. High glucose may facilitate the synthesis of activin ,A, transforming growth factor (TGF)-,, P-Smad2/3 and fibronectin in HK-2 cells while rh-follistatin inhibited them except TGF-,. Conclusion: Activin A is involved in tubulointerstitial fibrosis in DN by inducing the production of fibronectin through Smad signal pathway. [source] FSFI Scores of Women with Persistent Genital Arousal Disorder Compared with Published Scores of Women with Female Sexual Arousal Disorder and Healthy ControlsTHE JOURNAL OF SEXUAL MEDICINE, Issue 2 2009Sandra R. Leiblum PhD ABSTRACT Introduction., Although persistent genital arousal disorder (PGAD) has been mistaken for hypersexuality, there is no research documenting the sexual functioning of PGAD women to support or refute such an assumption. Aim., To compare the Female Sexual Function Index (FSFI) scores of PGAD women to that of women diagnosed with female sexual arousal syndrome (FSAD) and healthy controls. Methods., The FSFI scores of heterosexual women who met all five features qualifying for a diagnosis of PGAD (N = 172) on an online questionnaire were compared with previously published FSFI scores of women diagnosed with FSAD (N = 128) and healthy controls (N = 131). Main Outcome Measure., Total and subscale scores on the FSFI. Results., On every subscale of the FSFI with the exception of desire, the PGAD women obtained scores between that of the FSAD and the healthy control group. The FSAD women displayed the greatest problems in desire, arousal, lubrication, orgasm, and pain while women with PGAD reported somewhat more desire than the control group but did not meet the cutoff score for sexual dysfunction. PGAD women are more similar to the normal control group than women with FSAD. Conclusions., There is no evidence to support the belief that women who meet criteria for a diagnosis of PGAD are "hypersexual." In fact, their overall sexual functioning falls within the normal range and is significantly better than that of women diagnosed with FSAD. Leiblum SR, and Seehuus M. FSFI scores of women with persistent genital arousal disorder compared with published scores of women with female sexual arousal disorder and healthy controls. J Sex Med 2009;6:469,473. [source] A Pilot Study of Quantitative Aspiration in Patients with Symptoms of Obstructive Sleep Apnea: Comparison to a Historic Control Group,THE LARYNGOSCOPE, Issue 6 2004Michael Beal MD Abstract Objective: It has been shown that many healthy people aspirate secretions at night. Patients with obstructive sleep apnea (OSA) have frequent episodes of gasping at night that may predispose them to aspiration. The purpose of this study was to determine whether patients with symptoms of OSA are predisposed to pharyngeal aspiration. Study Design: A prospective study in which patients with symptoms of OSA were compared with a historic group of normal controls by using the same methodology. Methods: The study was offered to patients with symptoms of OSA undergoing a sleep study. The radiotracer Technicium99 was infused through a plastic tube placed in the nasopharynx after the patient achieved stage II sleep. A chest radionuclide scan determined the amount of material aspirated. The Wilcoxon-rank sum test was used to compare the mean amount aspirated between the experimental and historic control groups. Results: Fourteen patients successfully completed the study. One normal volunteer in our study aspirated a quantity similar to the historic normal control group. The amount of aspirated material in the study group ranged from 0.152 to 3.648 mL, with a mean of 1.24 mL ± 0.905 (SD). When compared with the historic normal control group, the patients with symptoms of OSA aspirated significantly more radio-tracer (P <.01). There was a lack of association between respiratory disturbance index and amount aspirated. Conclusions: The results suggest there is an apparent risk of increased pharyngeal aspiration in patients with symptoms of OSA. [source] Lack of association of ,2-glycoprotein I polymorphisms Val247Leu and Trp316Ser with antiphospholipid antibodies in patients with thrombosis and pregnancy complicationsBRITISH JOURNAL OF HAEMATOLOGY, Issue 6 2003Raymond S. Camilleri Summary. Beta2 -glycoprotein I (,2GPI) is an important target antigen for antiphospholipid antibodies (aPL) and thus ,2GPI polymorphisms may influence aPL production and the development of antiphospholipid syndrome. We have studied the relationship between the Val247Leu and Trp316Ser ,2GPI polymorphisms and the aPL status of 230 patients referred for aPL screening. Sixty-one (26·5%) had persistent aPL [anticardiolipin antibodies (IgG and/or IgM), lupus anticoagulants and/or IgG anti-,2GPI antibodies]. A comparison of the genotypic and allelic frequencies of these two polymorphisms between the Caucasian patient population and an ethnic-matched normal control group (n = 308) showed no significant differences between aPL-positive patients, aPL-negative patients and the normal control group. This suggests that the Val or Leu allele at position 247 and the Trp or Ser allele at position 316 of ,2GPI do not play a role in the production of aPL. There was a significantly decreased prevalence of the Ser316 allele in aPL-negative women (n = 98) when compared with female normal control subjects (n = 249) {0·020 [95% confidence interval (CI) 0·00,0·04]vs 0·060 (95% CI 0·04,0·08), P = 0·0286}. Subgroup analysis showed no significant difference between female patients with thrombosis and female normal control subjects. Thus, the Ser316 allele may protect women from developing pregnancy complications by influencing an anticoagulant function of ,2GPI via a mechanism distinct from aPL production. [source] Therapeutic Effects and Anti-inflammatory Mechanisms of Heparin on Acute Lung Injury in RabbitsACADEMIC EMERGENCY MEDICINE, Issue 7 2008Meitang Wang MD Abstract Objectives:, The objectives were to investigate the potential beneficial effects and molecular mechanisms of heparin and low-molecular-weight heparin (LMWH) on acute lung injury (ALI). Methods:, Forty-eight rabbits were randomized into four groups: normal control group (Group A), lipopolysaccharide (LPS) group (Group B), LPS + heparin group (Group C), and LPS + LMWH group (Group D). The rabbit ALI model was established by intravenous (IV) injection with LPS. Alveolar,arterial O2 difference (PA-aO2), serum tumor necrosis factor , (TNF-,), circulating p38 mitogen-activated protein kinase (p38 MAPK) levels, lung nuclear factor (NF)-,B levels, and lung dry/wet (D/W) ratio were measured, and the lung injury scores were calculated. Results:, Lipopolysaccharide caused significant increases in PA-aO2, serum TNF-,, expression of p38 MAPK in polymorphonuclear neutrophils (PMNs), the lung injury scores, and nuclear factor-,B (NF-,B) activity in the lung tissue and caused a decrease in lung D/W ratio. A positive linear correlation was found between p38 MAPK and TNF-, at 1, 2, 4, and 6 hours (r = 0.68, 0.92, 0.93, and 0.93, respectively) and between NF-,B and p38 MAPK and TNF-, at 6 hours (r = 0.94 and 0.83, respectively). IV heparin or LMWH given after LPS treatment attenuated these changes in inflammatory response, oxygenation, p38 MAPK expression, and NF-,B activation. Conclusions:, The anti-inflammatory mechanisms of heparin in ALI may be inhibiting p38 MAPK and NF-,B activities, and then TNF-, overexpression, thus alleviating the inflammatory reaction. [source] Corneal thickness in glaucoma: an important parameter?ACTA OPHTHALMOLOGICA, Issue S232 2000P. Brusini Summary Central corneal thickness was measured by pachometry in 49 patients with primary open-angle glaucoma (POAG), 41 with ocular hypertension (OHT), 14 with normal tension glaucoma (NTG) and 48 normal subjects. The mean corneal thickness of the OHT patients was significantly greater than that of the normal control group. The NTG patients, on the other hand, had a cornea on average thinner than the normals. These differences may cause misclassification of normals with a thick cornea as ocular hypertensive eyes or, contrarywise, cause those normals whose IOP is underestimated because of a thin cornea to be classed as NTG patients. [source] PROTECTION BY AND ANTI-OXIDANT MECHANISM OF BERBERINE AGAINST RAT LIVER FIBROSIS INDUCED BY MULTIPLE HEPATOTOXIC FACTORSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 3 2008Ben-Jian Zhang SUMMARY 1The aim of the present study was to investigate the effect and mechanism of berberine, an alkaloid extracted from the traditional Chinese medicine coptis, on rat liver fibrosis induced by multiple hepatotoxic factors. 2Male Wistar rats were separated into five groups, a normal control group, a fibrotic control group and fibrotic groups treated with three different doses of berberine. The fibrotic models were established by introduction of multiple hepatotoxic factors, including CCl4, ethanol and high cholesterol. Rats in the treatment groups were administered 50, 100 or 200 mg/kg berberine, intragastrically, daily for 4 weeks. Serum levels of alanine aminotransferase (ALT) and serum aspartate aminotransferase (AST), hepatic activity of superoxide dismutase (SOD) and hepatic malondialdehyde (MDA) and hepatic hydroxyproline (Hyp) content were determined. Liver biopsies were obtained for histological and immunohistochemical studies to detect the expressions of a-smooth muscle actin (SMA) and transforming growth factor (TGF)-b1. 3The results showed that, compared with the fibrotic control group, serum levels of ALT and AST and hepatic content of MDA and Hyp were markedly decreased, but the activity of hepatic SOD was significantly increased in berberine-treated groups in a dose-dependent manner. In addition, histopathological changes, such as steatosis, necrosis and myofibroblast proliferation, were reduced and the expression of a-SMA and TGF-b1 was significantly downregulated in the berberine-treated groups (P < 0.01). 4These results suggest that berberine could be used to prevent experimental liver fibrosis through regulation of the anti-oxidant system and lipid peroxidation. [source] UPREGULATED ENDOTHELIN SYSTEM IN DIABETIC VASCULAR DYSFUNCTION AND EARLY RETINOPATHY IS REVERSED BY CPU0213 AND TOTAL TRITERPENE ACIDS FROM FRUCTUS CORNICLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2007Wei Su SUMMARY 1The aims of the present study were to examine whether: (i) upregulation of the endothelin (ET) pathway is involved in impairment of vascular relaxation and early retinopathy in diabetic rats; and (ii) vascular and retinal abnormalities respond to the total triterpene acid (TTA) isolated from Fructus Corni compared with responses to the novel endothelin receptor antagonist CPU0213 and aminoguanidine (AMG), a special antagonist for advanced glycation end-products (AGE) and inducible nitric oxide synthase (iNOS). 2Male Sprague-Dawley rats were randomized into five groups, namely a normal control and four diabetic groups, which included an untreated diabetic group and groups treated with AMG (100 mg/kg, i.g.), CPU0213 (30 mg/kg, s.c.) or TTA (50 mg/kg, i.g.). Diabetes was induced by single injection of streptozotocin (60 mg/kg, i.p.) on the 1st day. The mRNA expression of prepro-endothelin-1 (ppET-1), endothelin-converting enzyme (ECE) and iNOS in the thoracic aorta and mRNA for ETA receptors and iNOS in the retina were detected by reverse transcription,polymerase chain reaction. Vasorelaxation to acetylcholine (ACh) and functional assessment of nitric oxide (NO) bioavailability was determined in the thoracic aorta. 3We observed upregulated mRNA expression of iNOS, ppET-1 and ECE in the thoracic aorta and upregulated mRNA for the ETA receptor and iNOS in the retina in the untreated diabetic group. Vasodilatation mediated by ACh and NO bioavailability were markedly reduced in the thoracic aorta compared with the normal control group. These abnormalities were essentially reversed by TTA, CPU0213 or AMG, with the exception with that AMG did not modify vasodilatation to ACh. 4These data suggest that upregulation of gene transcription of the ET system mediates depressed vasorelaxation, NO bioavailability and changes in iNOS and ETA receptors that reflect early retinopathy in diabetic rats. Total triterpene acid, in terms of pharmacological properties resembling the endothelin receptor antagonist CPU0213, is effective in normalizing expression of the ET system and iNOS in early diabetic retinopathy and vasculaopathy. [source] | ||||||||||