bluuebunny/crossref_metadata_2025_split huggingface dataset:
Insulin resistance and liver injury in hepatitis C is not associated with virus-specific changes in adipocytokines
Authors: Cua Ian Homer Y. , Hui Jason M. , Bandara Priyanka , Kench James G. , Farrell Geoffrey C. , McCaughan Geoffrey W. , George Jacob 
Published: June 2007

Abstract

The role of tumor necrosis factor α, interleukin 6, leptin, and adiponectin in the pathogenesis of hepatitis C virus (HCV)-associated insulin resistance (IR) remains controversial. We tested the hypothesis that these adipocytokines contribute to chronic HCV-associated IR and liver injury by first comparing their serum levels and homeostasis model assessment of insulin resistance (HOMA-IR) in 154 untreated, non-diabetic, HCV-infected male subjects with fibrosis stage 0-2, to that in 75 healthy volunteers matched for age, body mass index (BMI), and waist-hip ratio (WHR). We next examined whether the adipocytokine levels were associated with the extent of hepatic steatosis, portal/periportal inflammation and fibrosis in our total cohort of 240 HCV-infected male subjects. Significantly higher levels of HOMA-IR (2.12 versus 1.63,

P

= 0.01), TNFα (1.28 versus 0.60 pg/ml,

P

< 0.001) and IL6 (2.42 versus 1.15 pg/ml,

P

= 0.001) were noted in the HCV cohort compared with healthy controls respectively, but there were no significant differences in leptin and adiponectin concentrations. By multiple linear regression, independent predictors of HOMA-IR included the body mass index, and the serum levels of leptin (positive correlation) and adiponectin (negative correlation), but not that of TNFα and IL6. Only TNFα levels were correlated with the extent of histological injury (portal/periportal inflammation,

P

= 0.02).

Conclusion:

Whereas leptin and adiponectin contribute to IR, none of the adipocytokines accounted for the

elevated

IR in HCV-infected subjects. The adipocytokines were not associated with histological features of chronic HCV infection except for TNFα which correlated with portal/periportal inflammation. HCV-associated IR is most likely an adipocytokine-independent effect of the virus to modulate insulin sensitivity. (HEPATOLOGY 2007;46:66–73.)
On the TRAIL to therapeutic intervention in liver disease
Authors: Herr Ingrid , Schemmer Peter , Büchler Markus W. 
Published: June 2007

Abstract

Hepatocellular carcinoma (HCC) ranks among the 10 most common cancers worldwide. The fact that HCC is resistant to conventional chemotherapy and is rarely amenable to radiotherapy leaves this disease with no effective therapeutic options and a very poor prognosis. Therefore, the development of more effective therapeutic tools and strategies is much needed. HCCs are phenotypically and genetically heterogeneous tumors that commonly emerge on a background of chronic liver diseases, most of which culminate in cirrhosis, such as alcoholic cirrhosis and chronic hepatitis B and C infections. This review outlines recent findings on the progression of liver disease, including our knowledge of the role of apoptotic processes, with an emphasis on the tumor necrosis factor–related apoptosis-inducing ligand (TRAIL). The proapoptotic and antiapoptotic properties of TRAIL, its involvement in liver injury, and its potential as a therapeutic agent in fibrosis and HCC are discussed. Several contradictory and confusing data have not yet been resolved or placed into perspective, such as the influence of factors that determine the TRAIL sensitivity of target cells, including the tumor microenvironment or cirrhotic tissue. Therefore, we assess these data from the perspectives of gastroenterologists (P.S. and M.W.B.) and a molecular oncologist (I.H.) with research interests in liver injury, apoptosis, and experimental therapeutics. (HEPATOLOGY 2007;46:266–274.)
Hypoxia modulates cholinergic but not opioid activation of G proteins in rat hippocampus
Authors: Hambrecht V.S. , Vlisides P.E. , Row B.W. , Gozal D. , Baghdoyan H.A. , Lydic R. 
Published: June 2007

AbstractIntermittent hypoxia, such as that associated with obstructive sleep apnea, can cause neuronal death and neurobehavioral dysfunction. The cellular and molecular mechanisms through which hypoxia alter hippocampal function are incompletely understood. This study used in vitro [35S]guanylyl‐5′‐O‐(γ‐thio)‐triphosphate ([35S]GTPγS) autoradiography to test the hypothesis that carbachol and DAMGO activate hippocampal G proteins. In addition, this study tested the hypothesis that in vivo exposure to different oxygen (O2) concentrations causes a differential activation of G proteins in the CA1, CA3, and dentate gyrus (DG) regions of the hippocampus. G protein activation was quantified as nCi/g tissue in CA1, CA3, and DG from rats housed for 14 days under one of three different oxygen conditions: normoxic (21% O2) room air, or hypoxia (10% O2) that was intermittent or sustained. Across all regions of the hippocampus, activation of G proteins by the cholinergic agonist carbachol and the mu opioid agonist [D‐Ala2, N‐Met‐Phe4, Gly5] enkephalin (DAMGO) was ordered by the degree of hypoxia such that sustained hypoxia > intermittent hypoxia > room air. Carbachol increased G protein activation during sustained hypoxia (38%), intermittent hypoxia (29%), and room air (27%). DAMGO also activated G proteins during sustained hypoxia (52%), intermittent hypoxia (48%), and room air (43%). Region‐specific comparisons of G protein activation revealed that the DG showed significantly less activation by carbachol following intermittent hypoxia and sustained hypoxia than the CA1. Considered together, the results suggest the potential for hypoxia to alter hippocampal function by blunting the cholinergic activation of G proteins within the DG. © 2007 Wiley‐Liss, Inc.
Integrating associative learning signals across the brain
Authors: Suzuki Wendy A. 
Published: June 2007

AbstractAssociative learning is defined as the ability to link arbitrary stimuli or actions together in memory. The neural correlates of this fundamental form of plasticity were first described in the hippocampus during delay eye blink conditioning and have since been examined using a variety of tasks in both rats and monkeys. In monkeys, the neural correlates of associative learning have been studied using conditional motor learning tasks where animals learn to associate particular visual stimuli with particular motor responses (i.e., touch left or touch right). Similar tasks have also been used to examine learning‐related plasticity in motor‐related areas throughout the frontal lobe and striatum. Here, we review the patterns of learning‐related activity seen in these diverse brain areas during conditional motor learning. While each of these areas exhibits strong associative learning signals, the differential patterns and time courses of these signals provides insight into the unique contribution of each area to associative learning. © 2007 Wiley‐Liss, Inc.
Structural learning and the hippocampus
Authors: Aggleton John P. , Sanderson David J. , Pearce John M. 
Published: June 2007

AbstractIt is argued that while the hippocampus is not vital for all classes of configural learning, it is vital for a specific subclass of configural tasks called “structural learning.” The defining feature of structural learning is that in addition to binding stimulus elements to make unique arrays (as in all configural learning), the relationship of these elements to each other, be it spatial or temporal, is specified. Direct evidence supporting the proposal that the hippocampus is required for structural learning comes from recent lesion studies with rats. While rats with hippocampal lesions were impaired at relearning a set of spatial structural problems, they showed no impairment when relearning two configural tasks (transverse patterning and the biconditional discrimination), neither of which required structural learning. Other support comes from surveys of spatial and temporal learning by amnesic patients with hippocampal damage, and from imaging studies of both humans and rats. While these studies offer consistent support for the structural hypothesis, very few provide a rigorous test as the tasks can often be solved by other strategies. For this reason, the present review details the design features of future stringent tests of the structural hypothesis. © 2007 Wiley‐Liss, Inc.
Which computational mechanisms operate in the hippocampus during novelty detection?
Authors: Kumaran Dharshan , Maguire Eleanor A. 
Published: June 2007

AbstractA fundamental property of adaptive behavior is the ability to rapidly distinguish what is novel from what is familiar in our environment. Empirical evidence and computational work have provided biologically plausible models of the neural substrate and mechanisms underlying the coding of stimulus novelty in the perirhinal cortex. In this article, we highlight the importance of a different category of novelty, namely associative novelty, which has received relatively little attention, despite its clear ecological importance. While previous studies in both animals and humans have documented hippocampal responses in relation to associative novelty, a key issue concerning the computations underlying these novelty signals has not been previously addressed. We argue that this question has importance not only for our understanding of novelty processing, but also for advancing our knowledge of the fundamental computational operations performed by the hippocampus. We suggest a different approach to this problem, and discuss recent evidence supporting the hypothesis that the hippocampus operates as a comparator during the processing of associative novelty, generating mismatch/novelty signals when prior predictions are violated by sensory reality. We also draw on conceptual similarities between associative novelty and contextual novelty to suggest that empirical findings from these two seemingly distant research fields accord with the operation of a comparator mechanism during novelty detection more generally. We therefore conclude that a comparator mechanism may underlie the role of the hippocampus not only in detecting occurrences that are unexpected given specific associatively retrieved predictions, but also events that violate more abstract properties of the experimental context. © 2007 Wiley‐Liss, Inc.
Contribution of Na+/Ca2+exchange to excessive Ca2+loading in dendrites and somata of CA1 neurons in acute slice
Authors: Dietz Robert M. , Kiedrowski Lech , Shuttleworth C. William 
Published: June 2007

AbstractMultiple Ca2+entry routes have been implicated in excitotoxic Ca2+loading in neurons and reverse‐operation of sodium–calcium exchangers (NCX) has been shown to contribute under conditions where intracellular Na+levels are enhanced. We have investigated effects of KB‐R7943, an inhibitor of reverse‐operation NCX activity, on Ca2+elevations in single CA1 neurons in acute hippocampal slices. KB‐R7943 had no significant effect on input resistance, action potential waveform, or action potential frequency adaptation, but reduced L‐type Ca2+entry in somata. Nimodipine was therefore included in subsequent experiments to prevent complication from effects of L‐type influx on evaluation of NCX activity. NMDA produced transient primary Ca2+increases, followed by propagating secondary Ca2+increases that initiated in apical dendrites. KB‐R7943 had no significant effect on primary or secondary Ca2+increases generated by NMDA. The Na+/K+ATPase inhibitor ouabain (30 μM) produced degenerative Ca2+overload that was initiated in basal dendrites. KB‐R7943 significantly reduced initial Ca2+increases and delayed the propagation of degenerative Ca2+loads triggered by ouabain, raising the possibility that excessive intracellular Na+loading can trigger reverse‐operation NCX activity. A combination of NMDA and ouabain produced more rapid Ca2+overload, that was contributed to by NCX activity. These results suggest that degenerative Ca2+signaling can be triggered by NMDA in dendrites, before intracellular Na+levels become sufficient to reverse NCX activity. However, since Na+/K+ATPase inhibition does appear to produce significant reverse‐operation NCX activity, this additional Ca2+influx pathway may operate in ATP‐deprived CA1 neurons and play a role in ischemic neurodegeneration. © 2007 Wiley‐Liss, Inc.
Long‐term administration of the low‐dose risperidone in schizotaxia subjects
Authors: Rybakowski Janusz K. , Drozdz Wiktor , Borkowska Alina 
Published: June 2007

AbstractThe term schizotaxia is currently defined as a syndrome of neuropsychological deficits and negative symptoms found in relatives of schizophrenic patients. The aim of this study was to assess the effect of long‐term treatment with the low‐dose risperidone on cognitive and social functioning in seven schizotaxia patients. There were four males and three females, aged between 17 and 44 years, first‐degree (four patients) or second‐degree (three patients) relatives of schizophrenic patients. Schizotaxia was recognized in them on account of neuropsychological and social function impairment. They all consented to risperidone administration, 1–2 mg/day. Duration of risperidone treatment has ranged between 3–7 years. In all subjects, the continuous treatment with risperidone brought about a marked improvement in their cognitive, social, and vocational functioning. Neuropsychological testing after 6–24 months showed significant improvement on such tests as Wisconsin Card Sorting Test (WCST), Trail Making Test (TMT), and Stroop Test. Discontinuation of treatment after 3–4 years did not cause deterioration of functioning. Copyright © 2007 John Wiley & Sons, Ltd.
Reduction of discharge hydrograph and flood stage resulted from upstream detention ponds
Authors: Chen Ching‐Nuo , Tsai Chih‐Heng , Tsai Chang‐Tai 
Published: June 2007

AbstractThe models of physiographic inundation and flood routing for channel network were used in this study to analyse the influence of the Tainan Scientific Base Industrial Park (TSBIP) and Feng‐Hua detention ponds on the inundated potential, inundated volume, flood damage, and flood stage of peak flow along the Yen‐Shui creek in 2‐day flood for the 2‐, 10‐ and 50‐year return periods, respectively. The computed results show that the TSBIP detention ponds are able to reduce the inundated area and flood damage. However, the decrease in inundated area is not obvious for the 50‐year return‐period flood. Construction of the Feng‐Hua detention pond resulted in a significant decrease in the flood stage along the Yen‐Shui creek in the downstream reach. Moreover, the decrease in peak flow and lag of time‐to‐peak become increasingly evident in the downstream direction for the 2‐ and 10‐year return‐period events. For the 50‐year return period, the lag of time‐to‐peak is not apparent, but the decrease in peak flow is still noticeable. In respect to the performance of detention ponds, the slopes of hydrographs in the rising and recession segments are smoother than those without detention ponds. Meanwhile, the shapes of peak become flatter if the detention ponds are installed. Copyright © 2007 John Wiley & Sons, Ltd.
Electrochemical treatment of olive mill wastewater
Authors: Giannis Apostolos , Kalaitzakis Michael , Diamadopoulos Evan 
Published: June 2007

AbstractBackground Olive mill wastewater (OMW) constitutes a very strong agro‐industrial wastewater posing severe environmental threats in olive oil producing countries. The main objective of this study was to treat olive mill wastewater by electrochemical oxidation. The variables studied included the type and concentration of electrolyte solutions, voltage and time applied.Results: The electrolyte type and concentration significantly affected the degradation efficiency of the electrochemical oxidation. Optimal conditions for NaCl concentration were 3% (w/v) and 16 V. At these conditions chemical oxygen demand (COD) removal reached 70.8% after 8 h of electrochemical treatment, while color and turbidity were completely removed after short periods of treatment. However, bio‐assays indicated that the ecotoxicity of the treated wastewater remained unchanged, possibly due to the formation of chlorinated by‐products. Na2SO4 did not demonstrate sufficient efficiency. The simultaneous use of FeCl3 and NaCl contributed to electro‐coagulation of OMW. After settlement, two separate phases were formed: the supernatant phase and the settled solids. Under optimal conditions (2% Na2SO4 + 1% FeCl3; 24 V), the removal efficiency of COD reached 85.5% at the supernatant phase.Conclusion: NaCl was an effective electrolyte for OMW treatment. The electro‐coagulation process was also a successful process, but as in the case of NaCl the remaining acute toxicity of treated OMW was high. Copyright © 2007 Society of Chemical Industry
Determining the source of nosocomial transmission in hemodialysis units in Tunisia by sequencing NS5B and E2 sequences of HCV
Authors: Hmaïed Fatma , Mamou Myriam Ben , Dubois Martine , Pasquier Christophe , Sandres‐Saune Karine , Rostaing Lionel , Slim Amine , Arrouji Zakia , Redjeb Saïda Ben , Izopet Jacques 
Published: June 2007

AbstractHepatitis C virus infection is a significant problem in hemodialysis units. HCV is very variable genetically with six genotypes. Clinical and epidemiological investigation of a new infection requires the determination of both the genotype and the strain of the HCV involved. A prospective, epidemiologic study of 395 dialysis patients in Tunisia was conducted from November 2001 to November 2003 to identify the source of nosocomial transmission using phylogenetic analysis of NS5b and E2 sequences. Hepatitis C infection was diagnosed by screening for anti‐HCV antibodies and HCV RNA in sera using third generation ELISA and a qualitative RT‐PCR assay. HCV strains were genotyped by sequencing the NS5b region. The genetic relatedness of the HCV strains was studied by sequencing the NS5b and the HVR‐1 regions of the HCV genome. Two de novo cases of HCV infection were detected during the follow‐up. One of them has been described previously. The case described in this study occurred in a center in which 12 patients were already infected with HCV strains belonging to genotypes 1b (n = 8) and 1a (n = 4). Phylogenetic analysis of the NS5b region from the HCV strains circulating in this center disclosed four clusters, confirmed by analysis of the HVR‐1 region, providing strong evidence for nosocomial infection. Epidemiological data showed that these patients were dialyzed during the same shift and in the same area. Phylogenetic analysis of NS5b sequences is useful for determining the HCV genotype and providing evidence of nosocomial transmission. J. Med. Virol. 79: 1089–1094, 2007. © 2007 Wiley‐Liss, Inc.
Latent membrane protein 1 encoded by Epstein–Barr virus induces telomerase activity via p16INK4A/Rb/E2F1 and JNK signaling pathways
Authors: Ding Lin , Li Lili , Yang Jing , Zhou Shanghui , Li Wei , Tang Min , Shi Ying , Yi Wei , Cao Ya 
Published: June 2007

AbstractElevated telomerase activity is observed in about 90% of human cancers. This activity correlates strictly with human telomerase reverse transcriptase (hTERT). Previously, it was shown that the Epstein–Barr virus‐encoded latent membrane protein 1 (LMP1) induced telomerase activity in nasopharyngeal carcinoma cells. In this study, it was indicated that LMP1 inhibited p16INK4A expression, promoted phosphorylation of p105 Rb and upregulated E2F1 expression as well as transactivation, and overexpression of E2F1 alone was sufficient to upregulate telomerase activity. The JNK kinase cascade could also promote telomerase activity modulated by LMP1, that inhibition of JNK by JIP and TAM 67 dominant negative mutant abrogated telomerase activity. The data show that p16INK4A/Rb/E2F1 and JNK signaling pathways are involved in the regulation of telomerase activity via LMP1. The present study provides new perspectives on carcinogenesis of nasopharyngeal carcinoma that may be exploited for novel therapeutic strategies. J. Med. Virol. 79: 1153–1163, 2007. © 2007 Wiley‐Liss, Inc.
Humoral immune responses against norovirus infections of children
Authors: Iritani Nobuhiro , Seto Toshiyuki , Hattori Hideji , Natori Katsurou , Takeda Naokazu , Kubo Hideyuki , Yamano Tsunekazu , Ayata Minoru , Ogura Hisashi , Seto Yoshiyuki 
Published: June 2007

AbstractIn 2 infants with gastroenteritis associated with Norovirus (NoV), serum immunoglobulin (Ig) G, IgM, IgA, and fecal IgA antibody responses against NoV were examined by enzyme‐linked immunosorbent assay using 11 different antigenic and genetic types of NoV virus‐like particles expressed in insect cells. These two cases were putative primary single NoV infections, because antibodies against NoVs were not detected in acute‐phase serums. In one of two cases, long‐term excretion of virus RNA for 33 days was observed. Serum IgG responses demonstrated strong seroresponse to the homologous type, and weak seroresponse to the heterologous types within the genogroup. After more than 2 years, the IgG antibody titer remained high to the homologous type and low to the heterologous type within the genogroup. IgM and IgA were specific to the homologous type. IgM was short lived and the serum IgA antibody titer remained low to the homologous type for a long period. These results improve our understanding of the humoral immune response to NoV infection. J. Med. Virol. 79: 1187–1193, 2007. © 2007 Wiley‐Liss, Inc.
Human cytomegalovirus glycoprotein B genotypes in Brazilian mothers and their congenitally infected infants
Authors: Yamamoto Aparecida Yulie , Mussi‐Pinhata Marisa Marcia , de Deus Wagatsuma Virginia Mara , Marin Lauro Juliano , Duarte Geraldo , Figueiredo Luis Tadeu Moraes 
Published: June 2007

AbstractA case‐control study design was used in order to compare the distribution of human cytomegalovirus (HCMV) glycoprotein B (gB) genotypes in 48 mothers of 49 congenitally infected infants with that observed in 144 mothers of 146 uninfected infants to study genetic variation of HCMV strains and maternal‐fetal transmission. Congenital infection with HCMV was characterized by DNA detection and virus isolation from two urine or saliva samples collected prior to the third week of life. Genotyping of HCMV was carried out by a polymerase chain reaction‐restriction fragment length polymorphism analysis of the variable region of the gB gene, testing for four genotypes. Genotype frequency was similar among the 28 non‐transmitting mothers who were shedding virus (gB1: 25%; gB2: 28.6%; gB3: 42.8%; gB4: 0%), the 37 transmitting mothers (gB1: 21.6%; gB2: 46%; gB3: 27%; gB4: 0%), and the 49 infected infants (gB1: 39%; gB2: 37%; gB3: 24%; gB4: 0%). The same genotype was detected at different body sites (urine, saliva, and blood) of each infected newborn and in the respective mother (breast milk, urine, and saliva). Co‐infection with multiple genotypes was observed in the immediate postpartum period in two mothers of infected infants (5.4%) and one non‐transmitting mother (3.6%). The gB genotype was not correlated with intrauterine HCMV transmission. The genotype distribution found reflects the overall frequency of wild strains circulating in this geographic region. A single genotype is responsible for congenital HCMV infection. Co‐infection with more than one strain, as characterized by gB genotype, was infrequent in women who were presumably immunocompetent. J. Med. Virol. 79: 1164–1168, 2007. © 2007 Wiley‐Liss, Inc.