bluuebunny/crossref_metadata_2025_split huggingface dataset:
Social and Economic Determinants of Disparities in Professional Help‐Seeking for Child Mental Health Problems: Evidence from a National Sample
Authors: Zimmerman Frederick J. 
Published: September 2005

Objective. To test the role of social determinants—including race, education, income, and demographic factors—of child mental health services use, defined as having had a visit to a mental health professional for depression, attention‐deficit, or for any reason.Data Sources/Study Setting. National Longitudinal Survey of Youth and the Child/Young Adult supplement, a nationally representative sample of 7–14‐year‐old children born to women who were 14–22 years old at the start of data collection, in 1979. African Americans and Latinos were over‐sampled, and population weights are available to make nationally representative inferences.Study Design. Indicators of mental health service use were regressed on social and economic determinants, family structure variables, and insurance variables, controlling for need as captured by several different symptom scales.Principal Findings. Girls are much less likely to obtain needed treatment for externalizing behavior disorders than are boys, and are somewhat less likely to obtain needed treatment for depression than boys. Middle children are less likely to obtain needed treatment for any mental health problem than are oldest, youngest, or only children. The presence of the father inhibits the likelihood that the child will receive treatment, particularly for depression. African Americans and Latinos are less likely than white children to receive treatment. In contrast to these rich results for the social and demographic determinants of children's specialty mental health utilization, the economic and insurance variables (including maternal education and income) seem to hold little predictive power.Conclusions. These results argue for interventions to sensitize parents—especially fathers—to the need to pay attention to the mental health needs of their children, in particular girls and middle children. The analysis also suggests that the literature on intrahousehold decision making and on the gender dimensions of investment in children is worth extending to mental health treatment decisions.
The Impact of Reference Pricing of Nonsteroidal Anti‐Inflammatory Agents on the Use and Costs of Analgesic Drugs
Authors: Grootendorst Paul V. , Marshall John K. , Holbrook Anne M. , Dolovich Lisa R. , O'Brien Bernie J. , Levy Adrian R. 
Published: September 2005

Objective. To estimate the effect of reference pricing (RP) of nonsteroidal anti‐inflammatory drugs (NSAIDs) on drug subsidy program and beneficiary expenditures on analgesic drugs.Data Sources/Study Setting. Monthly claims data from Pharmacare, the public drug subsidy program for seniors in British Columbia, Canada, over the period of February 1993 to June 2001.Study Design. RP limits drug plan reimbursement of interchangeable medicines to a reference price, which is typically equal to the price of the lowest cost interchangeable drug; any cost above that is borne by the patient. Pharmacare introduced two different forms of RP to the NSAIDs, Type 1 in April 1994 and Type 2 in November 1995. Under Type 1 RP, generic and brand versions of the same NSAID are considered interchangeable, whereas under Type 2 RP different NSAIDs are considered interchangeable. We extrapolated average reimbursement per day of NSAID therapy over the months before RP to estimate what expenditures would have been without the policies. These counterfactual predictions were compared with actual values to estimate the impact of the policies; the estimated impacts on reimbursement rates were multiplied by the postpolicy volume of NSAIDS dispensed, which appeared unaffected by the policies, to estimate expenditure changes.Principal Findings. After Type 2 RP, program expenditures declined by $22.7 million (CAN), or $4 million (CAN), annually cutting expenditure by about half. Most savings accrued from the substitution of low‐cost NSAIDs for more costly alternatives. About 20 percent of savings represented expenditures by seniors who elected to pay for partially reimbursed drugs. Type 1 RP produced one‐quarter the savings of type 2 RP.Conclusions. Type 2 RP of NSAIDs achieved its goal of reducing drug expenditures and was more effective than Type 1 RP. The effects of RP on patient health and associated health care costs remain to be investigated.
Earnings Quality, Insider Trading, and Cost of Capital
Authors: ABOODY DAVID , HUGHES JOHN , LIU JING 
Published: September 2005

ABSTRACTPrevious research argues that earnings quality, measured as the unsigned abnormal accruals, proxies for information asymmetries that affect cost of capital. We examine this argument directly in two stages. In the first stage, we estimate firms' exposure to an earnings quality factor in the context of a Fama‐French three‐factor model augmented by the return on a factor‐mimicking portfolio that is long in low earnings quality firms and short in high earnings quality firms. In the second stage, we examine whether the earnings quality factor is priced and whether insider trading is more profitable for firms with higher exposure to that factor. Generally speaking, we find evidence consistent with pricing of the earnings quality factor and insiders trading more profitably in firms with higher exposure to that factor.
Hepatoprotective effect of ginsenoside Rb1 and compound K on tert‐butyl hydroperoxide‐induced liver injury
Authors: Lee Hae‐Ung , Bae Eun‐Ah , Han Myung Joo , Kim Nam‐Jae , Kim Dong‐Hyun 
Published: September 2005

Abstract: Background/Aim: The main component of Panax ginseng, which have been reported by many researchers, are ginsenoside Rb1, Rb2 and Rc. Orally administered ginsenosides are metabolized to 20‐O‐β‐d‐glucopyranosyl‐20(S)‐protopanaxadiol (compound K) by intestinal bacteria and absorbed to blood. To understand its hepatoprotective effect and its mechanism, the effects of ginsenoside Rb1 and its metabolite compound K on chemically injured HepG2 cells and mice were investigated.Methods: Ginsenoside Rb1 and compound K were isolated from ginseng. Hepatotoxicity of HepG2 cells and mice was induced by tert‐butyl hydroperoxide (t‐BHP). Cytotoxicity for HepG2 cells and serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) for mice as markers of hepatoprotective activity were measured.Results: Compound K protected HepG2 cell cytotoxicity induced by t‐BHP. However, ginsenoside Rb1 did not inhibit cytotoxicity. Nevertheless, both ginsenoside Rb1 and compound K significantly inhibited the increment of ALT and AST induced by t‐BHP in mice, when it was orally administered. However, intraperitoneally administered ginsenoside Rb1 did not inhibit the increment of plasma ALT and AST induced by t‐BHP in mice. These compounds did not exhibit antioxidant activity. However, compound K showed the potent membrane stabilizing activity more than ginsenoside Rb1.Conclusion: Compound K, which was produced from ginsenosides of Panax ginseng in intestine, could protect liver injury.
Outcome from molecular adsorbent recycling system (MARS™) liver dialysis following drug‐induced liver failure
Authors: Lee Kang‐Hoe , Lee Margaret Kwee‐Hiang , Sutedja Dede Selamat , Lim Seng‐Gee 
Published: September 2005

Abstract: Rationale: Fulminant liver failure from drug ingestion is associated with a high mortality, and the introduction of liver transplantation has improved the mortality significantly if done in a timely fashion. Recently, molecular adsorbent recycling system (MARS™) liver dialysis has been introduced as a support for liver failure with varying results. We review our experience with drug‐induced liver failure and the impact of MARS™ liver dialysis on the outcome, in a setting where cadaveric liver transplantation is rarely available.Results: A total of 13 patients were treated, and 40 sessions of MARS™ liver dialysis were conducted in the intensive care unit. The majority of cases were because of herbal medicine toxicity. Total bilirubin, conjugated bilirubin, and delta bilirubin were significantly reduced, with no change in unconjugated bilirubin. All patients satisfied the criteria for urgent liver transplantation with an average Model End Stage Liver Disease (MELD) score of 35. Only one patient received a liver transplantation from a live donor (right lobe). Overall mortality was 85%. Median time‐to‐death from the start of MARS™ was 8 days.Conclusions: MARS™ liver dialysis in a setting without timely liver transplantation is associated with a poor outcome. It does, however, provide a window of time for consideration of living donors in the setting of limited cadaveric donors.
Upregulation ofGlypican‐3expression in hepatocellular carcinoma but downregulation in cholangiocarcinoma indicates its differential diagnosis value in primary liver cancers
Authors: Man Xiao‐Bo , Tang Liang , Zhang Bao‐Hua , Li Shen‐Jing , Qiu Xiu‐Hua , Wu Meng‐Chao , Wang Hong‐Yang 
Published: September 2005

Abstract: Background/Aim:Expression alteration ofGlypican‐3(GPC3) is associated with several malignancies and has been identified as an overexpressed gene in hepatocellular carcinoma (HCC). In this studyGPC3expression in intrahepatic chanlangiocarcinoma (ICC), gallbladder cancer and HCC was quantitatively detected.Methods:Real‐time quantitative reverse transcription polymerase chain reaction was used to detect the expression level ofGPC3.Results:GPC3expression was elevated more than two‐fold in HCC compared with adjacent tissue in 90 of 100 HCC cases. The average expression level ofGPC3was significantly higher in HCC than that in adjacent liver tissues (P<0.0001). Only in four of 21 ICC casesGPC3expression was upregulated more than two‐fold in tumor tissues.GPC3expression was downregulated in gallbladder cancer in 12 of 13 cases and the average expression level was significantly lower than that in normal gallbladder tissues (P<0.05).Conclusion:The different expression patterns ofGPC3in HCC and ICC suggested that it might play a different role in theses tumors and could serve as a biomarker for differential diagnosis of HCC and ICC.
Mortality predictors in liver transplant recipients with recurrent hepatitis C cirrhosis
Authors: Saab Sammy , Niho Henry , Comulada Scott , Hiatt Jonathan , Durazo Francisco , Han Steven , Farmer Douglas G. , Holt Curtis , Yersiz Hasan , Goldstein Leonard I. , Ghobrial R. Mark , Busuttil Ronald W. 
Published: September 2005

Abstract: Background/Aim:Recipients of orthotopic liver transplant for hepatitis C (HCV) invariably develop recurrent disease. The risk factors for death and retransplantation following the development of cirrhosis from HCV are unclear. The aim of this study was to identify predictors of survival in liver transplant recipients who develop cirrhosis from recurrent HCV.Methods:We reviewed records of patients who underwent liver transplantation for cirrhosis due to HCV between January 1990 and December 2001. Prognostic factors of patient survival following the development of recurrent cirrhosis were identified through multivariate analysis.Results:During the study period, 511 patients underwent transplantation for HCV cirrhosis. Of these, 65 patients (13%) developed biopsy proven recurrent cirrhosis from HCV; 43 (8%) were relisted for transplantation, and 24 (5%) underwent retransplantation. The overall Kaplan–Meier patient survival rates after the histologic diagnosis of cirrhosis at 1 and 5 years were 66% and 30%, respectively. A multivariate Cox proportional hazards model showed patients with higher last (i.e. at follow‐up or prior to retransplantation) International normalized ratio (INR) values (hazard ratios (HR)=2.02, 95% confidence interval 1.26, 3.24,P<0.01) to have an increased risk of death.Conclusion:Our results suggested survival was decreased after the diagnosis of cirrhosis from recurrent HCV. Higher INR was associated with an increased risk of death following the development of cirrhosis.
High glucose stimulates hepatic stellate cells to proliferate and to produce collagen through free radical production and activation of mitogen‐activated protein kinase
Authors: Sugimoto Rie , Enjoji Munechika , Kohjima Motoyuki , Tsuruta Satoshi , Fukushima Marie , Iwao Masataka , Sonta Toshiyo , Kotoh Kazuhiro , Inoguchi Toyoshi , Nakamuta Makoto 
Published: September 2005

Abstract: Background: Nonalcoholic steatohepatitis is a clinicopathologic condition that may progress to liver fibrosis. Hyperglycemia is supposed to be one of the factors inducing hepatic fibrogenesis, but the mechanism has not been fully clarified. Oxidative stress is increasingly found in patients with diabetes/hyperglycemia in which conditions reactive oxygen species (ROS) are produced.Methods: We performed experiments using hepatic stellate cells (HSCs) in culture in order to confirm the effect of high glucose concentrations on cell proliferation, type I collagen production, ROS production and activation of mitogen‐activated protein (MAP) kinase pathway.Results: High glucose stimulated cell growth of HSCs and up‐regulated the levels of activated/phosphorylated extracellular signal‐regulated kinase 1/2 and free radical production in HSCs. The MAP kinase phosphorylation and cell proliferation were suppressed by diphenylene iodonium chloride, an NADPH oxidase inhibitor, and by calphostin C, a protein kinase C (PKC)‐specific inhibitor. Increased type I collagen mRNA and protein levels were also observed in HSCs at high glucose concentrations.Conclusions: Our findings indicate that high glucose concentrations may stimulate ROS production through PKC‐dependent activation of NADPH oxidase, and induce MAP kinase phosphorylation subsequent to proliferation and type I collagen production by HSCs.
Tumor growth‐promoting cellular host response during liver atrophy after portal occlusion
Authors: Mueller Lars , Goettsche Juliane , Abdulgawad Awad , Vashist Yogesh K. , Meyer Jannine , Wilms Christian , Hillert Christian , Rogiers Xavier , Broering Dieter C. 
Published: September 2005

Abstract: Background/Aims: Clinical observations suggest cancer progression after preoperative segmental portal vein occlusion, a procedure to prevent liver failure after major hepatic resections. The aim of this study was to determine whether portal occlusion induces host reactions which promote cancer invasion and angiogenesis.Methods: The rat model of portal branch ligation (PBL) was compared with partial hepatectomy (PH) and sham operation (SO) and evaluated for the expression of heat shock protein‐70 (hsp70), heme oxygenase‐1 (hmox1), early growth response gene‐1 (Egr‐1) and urokinase‐type plasminogen activator (uPA), its inhibitor (PAI‐1) and receptor (uPAR).Results:
Portal deprivation after PBL was associated with a regression of liver tissue to 25% of its original mass within 8 days with only modest fibrotic changes. During the progression of atrophy, there were significant inductions of hsp70‐, hmox1‐ and Egr‐1‐mRNA in comparison with regenerating liver tissue. PAI‐1‐specific mRNA was transiently elevated at 3 – 48 h after PBL in the atrophying lobes, whereas uPA and uPAR were unaffected in comparison with PH or SO.Conclusion:
Hepatic atrophy caused by PBL is associated with increased expression of genes known to promote tumor growth. These host events represent a possible explanation for the tumor progression after portal occlusion and require further evaluation.
Expression of hypoxia inducible factor‐1α during liver regeneration induced by partial hepatectomy in rats
Authors: Maeno Hiroshi , Ono Takashi , Dhar Dipok Kumar , Sato Takashi , Yamanoi Akira , Nagasue Naofumi 
Published: September 2005

Abstract: Background/Aims: It has been well established that hypoxia inducible factor‐1α (HIF‐1α) transcribes essential factors in cell preservation, including angiogenesis, during hypoxia. However, the transition of HIF‐1α expression during liver regeneration remains unknown. In this study, a role of HIF‐1α was experimentally elucidated in relation to sinusoidal endothelial reconstruction during liver regeneration.Methods: Expression of HIF‐1α was evaluated in the regenerating liver following 70% hepatectomy in rats. Expressions of nuclear HIF‐1α, vascular endothelial growth factor (VEGF) and fms‐like tyrosine kinase‐1 (flt‐1) were measured by Western blot and liver blood flow by a laser Doppler. Sinusoidal endothelial cell area (SECA) and HIF‐1α were localized by immunohistochemistry. HIF‐1α mRNA was measured by reverse transcription‐polymerase chain reaction.Result: Liver blood flow and SECA were lowest 36 and 72 h following hepatectomy, respectively. Nuclear HIF‐1α peaked at 24 h and continuously increased 72–120 h following hepatectomy. This transition was fully supported by histological HIF‐1α expression and HIF‐1α mRNA up‐regulation. VEGF and flt‐1 peaked at 120 and 12 h, respectively.Conclusions: A significant evaluation in HIF‐1α expression was revealed in regenerating rat livers. HIF‐1α expression was preceded by VEGF and flt‐1 expression and thus may be related to sinusoidal endothelial reconstruction.
Endocannabinoids and liver disease – review
Authors: Gabbay Ezra , Avraham Yosefa , Ilan Yaron , Israeli Eran , Berry Elliot M. 
Published: September 2005

Abstract:
Aims: Endocannabinoids are endogenous compounds that bind to the same receptors as tetrahydrocannabinol, the active component in marijuana and hashish. They have been found to have many physiological and patho‐physiological functions, including mood alteration, control of feeding and appetite, motor and co‐ordination activities, analgesia, immune modulation and gut motility. In this review we aim to elucidate current knowledge as to their role in liver physiology and disease.Methods: The major findings published to date concerning endocannabinoids and liver disease are described, and their implications with regard to understanding disease mechanisms, and the development of new treatments is considered.Results: Recently, endocannabinoids have been implicated in the hemodynamic alterations occurring in cirrhosis. These changes appear to be mediated via specific cannabinoid receptors (CB1) on splanchnic and hepatic vascular endothelium. Plasma levels of endocannabinoids also seem to be elevated in hepatitis, and are involved in apoptosis of hepatocytes by a membrane mechanism not related to a specific receptor. Other studies suggest a beneficial role for cannabinoids in reducing the inflammation of experimental hepatitis. In an animal model of acute hepatic failure, both endocannabinoids and the antagonist to the CB1 receptor have been found to have a beneficial effect on neurological and cognitive function.Conclusions: Endocannabinoids appear to be involved in several aspects of acute and chronic liver disease, including vascular changes, modulation of inflammatory process and neurological function, Further research may provide new insights into the pathophysiology of liver disease, as well as a basis for novel treatment modalities.
Population Structure in the Mediterranean Basin: A Y Chromosome Perspective
Authors: Capelli C. , Redhead N. , Romano V. , Calì F. , Lefranc G. , Delague V. , Megarbane A. , Felice A. E. , Pascali V. L. , Neophytou P. I. , Poulli Z. , Novelletto A. , Malaspina P. , Terrenato L. , Berebbi A. , Fellous M. , Thomas M. G. , Goldstein D. B. 
Published: September 2005

AbstractThe Mediterranean region has been characterised by a number of pre‐historical and historical demographic events whose legacy on the current genetic landscape is still a matter of debate. In order to investigate the degree of population structure across the Mediterranean, we have investigated Y chromosome variation in a large dataset of Mediterranean populations, 11 of which are first described here. Our analyses identify four main clusters in the Mediterranean that can be labelled as North Africa, Arab, Central‐East and West Mediterranean. In particular, Near Eastern samples tend to separate according to the presence of Arab Y chromosome lineages, suggesting that the Arab expansion played a major role in shaping the current genetic structuring within the Fertile Crescent.
Retigabine: Bending Potassium Channels to Our Will
Authors: Lagrange Andre 
Published: September 2005

The New Anticonvulsant Retigabine Favors Voltage-dependent Opening of the Kv7.2 (KCNQ2) Channel by Binding to Its Activation Gate Wuttke TV, Seebohm G, Bail S, Maljevic S, Lerche H Mol Pharmacol 2005;67:1009–1017 Retigabine (RTG) is an anticonvulsant drug with a novel mechanism of action. It activates neuronal KCNQ-type K+ channels by inducing a large hyperpolarizing shift of steady-state activation. To identify the structural determinants of KCNQ channel activation by RTG, we constructed a set of chimeras by using the neuronal KV7.2 ( KCNQ2) channel, which is activated by RTG, and the cardiac KV7.1 ( KCNQ1) channel, which is not affected by this drug. Substitution of either the S5 or the S6 segment in KV7.2 by the respective parts of KV7.1 led to a complete loss of activation by RTG. Trp236 in the cytoplasmic part of S5 and the conserved Gly301 in S6 (KV7.2), considered as the gating hinge (Ala336 in KV7.1), were found to be crucial for the RTG effect: mutation of these residues could either knock out the effect in KV7.2 or restore it partially in KV7.1/KV7.2 chimeras. We propose that RTG binds to a hydrophobic pocket formed upon channel opening between the cytoplasmic parts of S5 and S6 involving Trp236 and the channel's gate, which could well explain the strong shift in voltage-dependent activation.
Cytokines: A Link between Fever and Seizures
Authors: Mazarati Andrey M. 
Published: September 2005

Interleukin-1β Contributes to the Generation of Experimental Febrile Seizures Dube C, Vezzani A, Behrens M, Bartfai T, Baram TZ Ann Neurol 2005;57:152–155 Fever can provoke “febrile” seizures (FSs). Because complex FSs may promote development of temporal lobe epilepsy, understanding their mechanisms is clinically important. By using an immature rodent model and transgenic technology, we examined the role of interleukin-1 β, (IL-1 β), a pyrogenic, proinflammatory cytokine, in FSs. IL-1 β receptor–deficient mice were resistant to experimental FSs. This resistance appeared independent of genetic background and was attributed to lack of IL-1 β signaling, because exogenous cytokine reduced the seizure threshold in wild-type but not receptor-deficient mice, independent of strain. In addition, high IL-1 β doses induced seizures only in IL-1 β receptor-expressing mice. These data indicate that IL-1 β signaling contributes critically to fever-induced hyperexcitability underlying FS, constituting a potential target for their prevention.