No cases fulfilled the Hunter Criteria for serotonin toxicity. One case published since the original report does not meet either criteria, and subsequently reported cases involving triptan monotherapy include insufficient details to confirm a diagnosis of serotonin syndrome. Recommendations.— With only Class IV evidence available in the literature and available through the FDA registration of adverse events, inadequate data are available to determine the risk of serotonin syndrome

with the addition of a triptan to SSRIs/SNRIs or with triptan monotherapy. The currently available evidence does not support limiting the use of triptans with SSRIs or SNRIs, or the use of triptan monotherapy, due to concerns NVP-AUY922 for serotonin syndrome (Level U). However, given the seriousness of serotonin syndrome, caution is certainly warranted and clinicians should be vigilant to serotonin toxicity symptoms and signs to insure prompt treatment. Health care providers should report potential cases to MedWatch and consider submitting them for publication. On July 19, 2006, the United States Food and Drug Administration (FDA) issued an alert, “Potentially Life-Threatening Serotonin Syndrome with Combined Use of SSRIs or SNRIs and Triptan Medications.”1 (An update Everolimus datasheet was issued on November 24, 2006 adding sibutramine).2 The FDA reported that there is the potential for life-threatening

serotonin syndrome in patients taking 5-hydroxytryptamine receptor agonists (triptans) and concomitantly taking selective serotonin reuptake inhibitors (SSRIs) or selective serotonin/norepinephrine reuptake inhibitors (SNRIs) (listed in Table 1). As summarized in the FDA alert, the recommendation is based on 29 case reports of serotonin syndrome that occurred in patients concomitantly treated with triptans and SSRIs/SNRIs, with the assumption of biological plausibility of such a reaction in persons receiving 2 serotonergic medications.1 The FDA recommended that patients receiving a triptan and SSRI/SNRI medications be informed of the possible risk

of serotonin syndrome.1 The FDA now requires that this information be included as part of the prescribing information for see more triptans. Based upon this alert, numerous patients and physicians have received warnings or recommendations from pharmacists that at least one of the medications (triptan or SSRI/SNRI) be discontinued. However, this recommendation is based on a limited number of anecdotal clinical reports. Consequently, using established criteria for diagnosing serotonin syndrome (eg, Sternbach Criteria and Hunter Serotonin Toxicity Criteria), an evidence-based review of the published clinical reports available to date is clearly warranted and provided below. Migraine Is Co-Morbid With Depression, Anxiety, Panic, and Bipolar Disorder.

Involvement of TRIF-dependent pathways in IL-28B production was shown by the significant inhibition of IL-28B with TRIF inhibitor. selleck chemicals Nevertheless, active HCV replication in the cells is not required. Based on our data, we considered that BDCA3+ DCs recognize HCV genome mainly by an endosome and TRIF-dependent mechanism. Although the results with UV-irradiated HCVcc, anti-CD81 blocking Ab,

and chloroquine were quite similar, the TRIF-specific inhibitor failed to suppress IL-28B from pDCs (Fig. 6, Fig. S9). In the coculture with JFH-transfected Huh7.5.1 cells, BDCA3+ DCs presumably receive some signals for IL-28B production by way of cell-to-cell dependent and independent mechanisms. In the present study, most of the stimuli to BDCA3+ DCs for IL-28B production may be the released HCVcc from Huh7.5.1 cells, judging from the inability of suppression with transwells. However, a contribution of contact-dependent mechanisms cannot be excluded in the coculture experiments. HCV genome is transmissible GSK1120212 cell line from infected hepatocytes to uninfected ones through tight junction molecules, such as claudin-1 and occuludin. Further investigation is needed to clarify whether such cell-to-cell transmission of viral genome is operated or not in BDCA3+ DCs. The relationship

between IL-28B expression and the induction of ISGs has been drawing much research attention. In primary human hepatocytes, it is reported that HCV primarily induces IFN-λ, instead of type-I IFNs, subsequently enhancing ISG expression.7 Of particular interest is that

the level of hepatic IFN-λs is closely correlated with the strength of ISG response.26 These reports strongly suggest that hepatic IFN-λs are a crucial driver of ISG induction and subsequent HCV eradication. Besides, it is likely that BDCA3+ DCs, as a bystander IFN-λ producer in the liver, have a significant impact on hepatic ISG induction. In support of this possibility, we demonstrated in this study that BDCA3+ DCs are capable of producing large amounts of IFN-λs in response to HCV, thereby inducing ISGs in the coexisting liver cells. Controversial results have been reported regarding the relationship between IL28B genotypes and the levels of IL-28 expression. Nevertheless, in chronic hepatitis C patients with IL-28B major genotype, the IL-28 transcripts in PBMCs are reported learn more to be higher than those with minor genotype.2 In this study, by focusing on a prominent IFN-λ producer (BDCA3+ DCs) and using the assay specific for IL-28B, we showed that the subjects with IL-28B major genotype could respond to HCV by releasing more IL-28B. Of interest, such a superior capacity of BDCA3+ DCs was observed only in response to HCV but not to poly IC. Since the pathways downstream of TLR3-TRIF leading to IL-28B in BDCA3+ DCs should be the same, either HCV or poly IC stimulation, two plausible explanations exist for such a distinct IL-28B response.

Bleeding PF-01367338 concentration lesions included Dieulafoy’s ulcer, Mallory- Weiss tear, duodenal ulcer, post surgical anastomosis bled and gastric ulcer after polypectomy. After basic life support was provided, all patients underwent emergent and elective endoscopy. Results: These comprised 49 (66.2%) males and 25 (33.8%) females. The mean age was 48.2 ± 6.4years for males and 40.6 ± 2.2years for females. Mallory-Weiss tear and Dieulafoy’s lesion constituted the majority of bleeding lesions 26 and 17 respectively requiring EBL. Other causes were: pre-pyloric ulcer 11; duodenal ulcer 9;

ulcers in antrum 5; post polypectomy bled 3; Anastomosis bleed 1; malignant lesions 2. Bleeding stopped after endoscopic therapy in 96.5% of patients. The single failure was in bleeding from a pre pylori lesion which was treated by using injection

sclerotherapy with 1:10000 adrenaline solution where EBL was not successful. LY294002 manufacturer Conclusion: EBL provides safe and effective modality for hemostasis in NVUGIB. EBL could be considered as a primary or alternative method of choice for treatment of endoscopic hemostasis in patients with NVGIB. Key Word(s): 1. haemostasis; ; 2. EBL; 3. NVUGIB; Presenting Author: ILZE KIKUSTE Additional Authors: ANITA LAOINA, KONRADS FUNKA, ALDIS RUTKIS, HERBERTS KURS, VIKTORS SAULE, PAVELS JANOVICS, MARCIS LEJA Corresponding Author: ILZE KIKUSTE Affiliations: University of Latvia; Riga East University Hospital; Riga East University selleck inhibitor Hospital; Riga East University Hospital Objective: The aim of the study was TO assess conventional white light gastroscopy findings in patients with changed serum pepsinogen

tests (high risk group) and calculate the sensitivity and specificity of endoscopy for the diagnosis of atrophy based on histological diagnosis of atrophy. Methods: The study was a subanalysis of a larger randomly selected cross-sectional sample of the general population in Latvia recruited from November 2008 to July 2009 with the primary objective of exploring cardiovascular risk factors. The selected individuals underwent a structured interview and blood sample collection. From the total number of 6000 invitees, in 3807 cases pepsinogen I (PgI) and pepsinogen II (PgII) was measured in plasma by Eiken (Eiken Chemical Co., Tokyo, Japan) pepsinogen test systems and PgI/PgII ratio was calculated. Patients with a PgI level <70 ng/ml and PgI/PgII ratio <3 (indicating any degree gastric mucosal atrophy) were invited for upper gastrointestinal cconventional white light endoscopy from January 2012 to July 2012. For adequate staging and grading of gastric mucosa atrophy, at least four non-targeted biopsies of two topographic sites (at the lesser and greater curvature, from both the antrum and the corpus) were taken and clearly labelled in separate vials; additional target biopsies of lesions were also taken.

We have known for a long time that HRS represented a spectrum of pathology and pathophysiology, and this culminated in the publication in 1996 of the new criteria for the definition of HRS by the International Ascites Club of type 1 HRS and type 2 HRS.1 Without going into the definitions,

in essence type 1 HRS is the rapid onset of renal failure that occurs in patients with rapid decompensation of cirrhosis due to either alcoholic hepatitis, or acute on chronic liver failure, or acute liver failure. Type 2 HRS is the type of renal impairment observed in patients with refractory ascites, with renal function fluctuating over a relatively long period of time. This definition was born out of necessity, mainly to facilitate research LY2157299 in the area since, prior to this date, patients tended to be clumped together when it was clear that clinically and presumably their underlying pathophysiology were different. Neratinib chemical structure While these definitions have helped us move on in terms of identifying mechanisms, the definitions have by virtue of their criteria probably held us back, by identifying patients late, and with relatively advanced renal

failure. Thus, the definitions involve absolute serum creatinine values which we now know are inappropriate. Thus, a serum creatinine in a heavily built black muscular man are treated the same as an emaciated white female with advanced alcoholic liver disease. This definition bit us back when two clinical trials of terlipressin in HRS showed a response rate to treatment of 34%-40%,2, 3 probably because patients were randomized too late for true efficacy. We are now seeing articles that state predictability of response to terlipressin is determined by serum creatinine.4 Another way of putting this is that patients with early HRS respond better to treatment than patients

with advanced kidney failure. In many ways this is “kind of obvious,” so we need new criteria that can be adapted to individual patients. This was also recognized in the working party report of Wong et al.5 The development of HRS is due to four main factors. These are: (1) altered systemic hemodynamics with vasodilatation and lowering of arterial pressure; (2) activation of the sympathetic nervous system, this website which alters renal autoregulation such that renal blood flow becomes more dependent on arterial pressure; (3) a terminal decline in cardiac function due to cirrhotic cardiomyopathy, which renders patients unable to maintain an adequate cardiac output as they decompensate; and (4) increased circulating or intrarenal vasoactive mediators, the role of which remain unknown. Importantly, the role of each of these factors probably varies from patient to patient. The advent of the new definition of acute kidney injury (AKI) by the AKI network has led to a reevaluation and proposed new definitions for HRS.5 What is well recognized by all is that current criteria for HRS recognize and treat patients too late.

[75] showed significant correlation of FVIII

half-life with pre-infusion VWF antigen levels during Saracatinib treatment of haemophilia A patients with recombinant FVIII; (iii) DDAVP-induced VWF increase altered high-purity FVIII kinetics in haemophilia A patients [76] and (iv) Eikenboom et al. [77] evaluated the FVIII/VWF ratios in different types of VWD showing that the ratio increased when VWF synthesis was reduced, but remained 1 when VWF clearance was increased. It has to be emphasized that FVIII half-life significantly correlated with the VWF level over a wide concentration range between 1 U mL−1 and 3 U mL−1 VWF:Ag, i.e. there was sufficient stabilization of FVIII throughout the entire range to prevent proteolytic FVIII cleavage. The molar ratio of VWF monomers and FVIII at the physiological VWF:FVIII ratio of 1:1 unit is theoretically 50:1 and has been experimentally determined as 20:1, probably due to the globular ‘ball-of-yarn’-structure of circulating VWF presenting only a fraction of FVIII binding sites on its surface. The huge excess of FVIII-binding sites theoretically allows stabilization of www.selleckchem.com/products/CP-690550.html up to 20-times FVIII relative to VWF, i.e. up to 20 U FVIII:Ag by 1 U VWF:Ag before saturation of VWF. Following the thesis that (i) FVIII passively follows VWF clearance, (ii) a constant clearing rate of VWF is assumed and (iii) bearing in mind the multimeric structure of VWF, it becomes immediately

apparent that the number of FVIII molecules cleared over time strongly depends on the FVIII loading of VWF, i.e. the actual VWF:Ag/FVIII:Ag ratio. Higher loading of circulating VWF multimers increases the number of cleared FVIII molecules per VWF clearing event. This is essentially what was observed during the pharmacokinetic

study by Kessler et al. [62]: almost physiological FVIII half-life for the concentrate exhibiting a 1:1 VWF:RCo/FVIII:C-ratio and a prolonged FVIII half-life for the concentrate with a roughly 2.3:1 VWF:RCo/FVIII:C-ratio. However, the most exciting consequence of VWF-dependent FVIII clearance is the fact that this mechanism intrinsically constitutes a self-regulating mechanism of the physiological VWF/FVIII ratio in plasma. At situations of high VWF/FVIII ratios click here (i.e. low FVIII plasma concentrations), FVIII clearance is lower, whereas at low VWF/FVIII ratios (i.e. high FVIII plasma concentrations) FVIII clearance increases. At the physiological situation of a 1:1-ratio, VWF-dependent FVIII clearance and synthesis of FVIII and VWF are in equilibrium [Fig. 11 (C. Kannicht, Unpublished data)]. Kannicht et al. are in the process of setting up a mathematical model considering intrinsic FVIII synthesis, known VWF-clearance rates and possible clearance of free FVIII to simulate FVIII clearance in VWD patients dependent on pre-infusion VWF levels and administered VWF/FVIII ratios. There has been much work on inhibitors in haemophilia, but not in VWD.

In general, IL-6 binds to its corresponding gp80 receptor located on hepatocytes and induces dimerization of the gp130 signal chain. Consequently, the Janus kinases associated with the gp130 chains also dimerize and autophosphorylate. Once activated, the Janus kinases then phosphorylate gp130 to activate STAT3 monomers. Phosphorylated STAT3 then forms dimers and translocates into the nuclei to induce expression of a wide

array of genes, including anti-apoptotic and anti-oxidative genes that protect against hepatocyte damage. The protective role of hepatic STAT3 has been well documented in studies with hepatocyte-specific gp130 or STAT3 knockout mice; these mice have shown to be more susceptible to hepatocellular damage induced by various toxins.23-25 Moreover, a conditional ablation of the STAT3 gene in myeloid

linage selleck compound cells (for example, macrophages) have shown markedly enhanced systemic and liver inflammation,26-28 which clearly suggests the anti-inflammatory functions of STAT3 in myeloid cells. In Small Molecule Compound Library this investigation, we found that myeloid-specific STAT3 knockout (STAT3) mice are more susceptible to CCl4-induced liver inflammation, but are surprisingly resistant to CCl4-induced necrosis. Further study revealed that the enhanced inflammation observed is associated with elevated hepatic STAT3 activation, which may explain the reduced necrosis observed in these mice. ALT, alanine aminotransferase; CCl4, carbon tetrachloride; CCR2, CC chemokine receptor 2; ConA, concanavalin A; CYP2E1, p450 cytochrome p450 2E1; GSH, glutathione; IFN, interferon; IL, interleukin; KO, knockout; MPO, myeloperoxidase; OSM, oncostatin M; STAT, signal transducer and activator of transcription; TNF-α, tumor necrosis factor alpha. Eight-week-old to ten-week-old male mice were used in all experiments. Hepatocyte-specific STAT3 knockout (KO) mice (STAT3) and myeloid-specific STAT3 KO mice (STAT3)were generated as described previously.27

The STAT3 mice were described previously as M/N-STAT3KO mice.27 The corresponding littermates of the wild-type mice were used as controls. For deletion of STAT3 in both hepatocytes and 上海皓元医药股份有限公司 myeloid cells, STAT3 and STAT3 were bred to generate four lines of mice, including double KO (STAT3), STAT3, STAT3, and littermate wild-type controls. All mice were fed regular chow unless specified. All animal experiments were conducted in accordance with National Institutes of Health guidelines and approved by the Institutional Animal Care and Use Committee of the National Institute on Alcohol Abuse and Alcoholism. Liver injury was induced by intraperitoneal injection with 2 mL/kg body weight 10% CCl4 (Sigma) dissolved in olive oil (Sigma). Data are expressed as mean ± SD. To compare values obtained from two groups, the Student t test was performed. To compare values obtained from three or more groups, one-factor analysis of variance was used, followed by Tukey’s post hoc test. Statistical significance was taken at the P < 0.05 level.

In response to LPS, NICD1 translocates to mitochondria as demonstrated by confocal and electron microscopy, and enriches at the mtDNA D-loop comprising promoters of mitochondria genome as assessed by ChlP. Finally, systemic administration of DAPT attenuates Nos2 upregulation, nitrosative stress, and ASH in the model. [Conclusion] Our findings reveal a novel mechanism of MO M1 activation in ASH, which involves Notch activation FK506 manufacturer to shift metabolism to glucose oxidation through induction of mtDNA and nuclear genes encoding mitochondrial complex proteins and consequent generation of mtROS enhancing M1 Nos2 activation. Disclosures: Hidekazu īsukamoto – Consulting: Shionogi & Co.,

S. P. Pharmaceutics; Grant/Research Support: The Toray

Co. The following people have nothing to disclose: Jun Xu, Feng Chi, Samuel W. French Background: Danger signals released from damaged cells trigger inflammatory response and tissue injury. N〇D-like receptors, such as NLRP3, are intracellular sensors of danger signals that activate the inflammasome, an intracellular complex which converts pro-interleukin (IL)−1β into mature IL-1β and perpetuates inflammation. Inflammasomes and IL-1β are key determinants of alcoholic liver disease (ALD), but the signals driving their activation are yet to be identified. Ivacaftor cell line Aim: To determine the role of danger signals in activation of inflammasomes and IL-1β in ALD. Methods: We co-cultured primary hepatocytes with macrophages in vitro, or fed Lieber-DeCarli ethanol (EtOH) diet to wild-type (WT), ATp receptor 2×7 (P2rx7)- or NLRP3-deficient (KO) mice, and to two strains of transgenic mice overexpressing uricase (UOX-Tg). Some mice were treated with probenecid or allopurinol. Results: Administration of EtOH to WT mice caused hepatocyte damage and inflammasome medchemexpress activation in the liver. Co-culture experiments revealed that damaged hepatocytes release signals that drive inflammasome activation and IL-1 β release in liver immune cells and identified extracellular adenosine triphosphate (ATP) as a mediator of this cross-talk.

Administration of EtOH to mice, or treatment of hepatocytes with EtOH resulted in extracellular ATP release. Absence of ATP receptors in P2rx7-K〇 mice or inhibition of ATP signaling in mice treated with probenecid prevented inflammasome activation in the liverand attenuated ALD. In addition to blocking ATP signaling, probenecid also depletes uric acid, another endogenous molecule released upon tissue injury. Indeed, we observed significantly increased hepatocyte-derived uric in vitro and in vivo, and found that depletion of uric acid in UOX-Tg mice or inhibition of uric acid synthesis with allopurinol prevented inflammasome activation and attenuated ALD. As the protection from ALD in P2rx7-K〇 or in UOX-Tg mice was substantial, yet incomplete, we asked whether ATP and uric acid activated inflammasomes in a complementary fashion.

These findings confirm that the prognostic role of alpha-fetoprotein reported in other studies may be due to the heterogeneous liver- and tumor-related characteristics, and different modalities of HCC treatment in the studied populations.11, 16 In fact, it seems that the predictive ability of alpha-fetoprotein is highly dependent on tumor size and treatment strategy, being more apparent in

patients with advanced HCC and in those treated with palliative intention, and less evident in patients with small tumors and in those who underwent curative treatment.11-14, 30, 35 Indeed, in studies where patients with advanced liver disease and/or advanced HCC were excluded from the analyses, the prognostic role of alpha-fetoprotein was dramatically diluted.12, 30 These considerations are also supported by the evidence that in FG-4592 clinical trial our

series there was no “therapeutic disparity,” and that mortality and causes of death were evenly distributed across patients with normal, mildly, and markedly elevated alpha-fetoprotein levels, likely ruling out the presence of other possible prognostic confounding factors. Some studies have shown that the rate of rise of serum alpha-fetoprotein levels may have prognostic meaning in HCC patients awaiting liver transplantation, yet these studies did not identify static alpha-fetoprotein levels as a predictor of survival or HCC recurrence after liver transplantation.36-38 As serial alpha-fetoprotein determinations were not available in our patients, we were not able to assess TGF-beta inhibitor the possible prognostic role of

dynamic alpha-fetoprotein determinations in the clinical setting of this study. In this study we selected the 3-cm cutoff to define small HCC, as several studies have shown an excellent outcome after curative treatment in these patients, and this threshold is also accepted for curative treatment by the Asian Pacific 上海皓元 Association for the Study of the Liver.9, 39, 40 However, we also performed the same analyses in patients with an HCC ≤2 cm, as other studies have shown that the prevalence of the two main negative prognostic factors, microvascular invasion and satellite nodules, tends to increase in lesions above this threshold.41-43 We confirmed, also in this group of HCC classified “very early” (stage 0) by the BCLC system, that serum alpha-fetoprotein had no prognostic role, thus confuting the hypothesis that adding this tumor marker to the BCLC classification might increase its prognostic yield for patients with very early (stage 0) and early (stage A) HCCs.11, 16 Noteworthy, in our cohort the 5-year survival rate was ≈60% in both patients with alpha-fetoprotein serum levels below and above 200 ng/mL. This result is in keeping with those previously obtained in similar patient populations treated with RFTA and hepatic resection, and compares favorably with the results of liver transplantation.

9 hours ± 7.1 hours) compared to control siRNA (5.6 hours ± 0.9 hours). Interestingly, the depletion of IGF2BP1 and CNOT1 simultaneously had no additive effect on HULC up-regulation, indicating that both proteins are mechanistically linked to each other (Supporting Fig. 4). Thus, we propose a model in which HULC expression is negatively regulated by way of binding to IGF2BP1. By associating directly or indirectly with CNOT1,

IGF2BP1 recruits the CCR4-NOT deadenylase complex onto its RNA substrate (Fig. 4E). To understand the mechanisms underlying hepatocarcinogenesis, a large number of genetic and epigenetic profiling studies had been conducted.[3] These studies mainly focused on the role of protein-coding genes and rarely included long, nonprotein-coding transcripts. www.selleckchem.com/products/ch5424802.html selleck products Our study validated the significant up-regulation of HULC, a liver-enriched lncRNA in human HCC samples. Moreover, we showed for the first time that the expression of HULC is significantly higher in low-stage and low-grade tumors, which points towards a functional role of HULC in the early steps of tumor development. Chronic inflammation, caused, e.g., by viral infections or alcohol abuse, is a critical factor that triggers liver carcinogenesis. In our analysis, we could

not detect a positive correlation with HBV or HCV infections. This is surprising in light of recent reports that established a link between HULC expression and HBV status, MCE公司 and showed that the HBx protein up-regulates HULC by way of CREB.[26, 27] Based on the necessarily limited size of every patient cohort, we cannot formally exclude the possibility of a correlation with viral infections, but we do not see any trend towards HULC induction in primary patient samples infected with HBV. Previously, no direct association with HBV or HCV infection in patient samples was shown, but only cell culture models were used to establish this connection. Future studies with larger patient cohorts may further detail the correlations

with different etiologies. After confirming the high up-regulation of HULC in liver cancer, we wanted to explore the regulation of this transcript in human liver cancer cells. First, we could not verify the previously described regulation of HULC by miR-372 in three different liver cancer cell lines. Thus, we performed RNA affinity purification experiments to identify RNA-binding proteins that bind and potentially regulate HULC posttranscriptionally. Through this approach, we identified a novel and unexpected function of the well-known RNA-binding protein IGF2BP1. IGF2BP1 acts as a trans-acting factor that represses HULC stability and expression. Moreover, IGF2BP1 associates with CNOT1 and thereby brings HULC into close proximity to the CCR4-NOT deadenylase complex, which initiates RNA degradation from the 3′ end.

Thus, it may be possible to recommend selleck prescription of tolvaptan with minimal risk of prevalence of serious adverse event. In conclusion, it is expected that tolvaptan can resolve several aforementioned problems in cirrhotic patients. In the near future, a novel indication of tolvaptan for the improvement of hepatic edema will be approved in Japan for the first time in the world. As a future study, confirmation of preventive

effect on recurrence of hepatic edema status by long-term administration of tolvaptan may be required. “
“A strong association between family function and irritable bowel syndrome (IBS) has been observed. Parental rearing styles, as a comprehensive mark for family function, may provide new clues to the etiology of IBS. This study aimed to explore which dimensions of parental rearing styles were risk factors or protective factors for IBS in adolescents. Two thousand three hundred twenty adolescents were recruited from one middle school and

one high school randomly selected from Jiangan District (an urban district in Wuhan City). Data were collected using two Chinese versions of validated self-report questionnaires including the Rome III diagnostic criteria for pediatric IBS and the Egna Minnen Beträffande Uppfostran: One’s Memories of Upbringing for perceived parental rearing styles. Ninety-six subjects diagnosed as pediatric IBS were compared with 1618 controls. The click here IBS patients reported less both paternal and maternal emotional warmth (all P < 0.01) and more both paternal and 上海皓元 maternal punishment, overinterference,

rejection, and overprotection (only for father) (all P < 0.01) than the controls. Furthermore, the IBS patients had higher total scores of parental rearing styles (all P < 0.001) than the controls. With univariate logistic regression, standardized regression coefficients and odds ratios of parental rearing variables were calculated. Multivariate logistic regression revealed that paternal rejection (P = 0.001) and maternal overinterference (P = 0.002) were independent risk factors for IBS in adolescents. Parental emotional warmth is a protective factor for IBS in adolescents and parental punishment, overinterference, rejection, and overprotection are risk factors for IBS in adolescents. "
“Galectin-1 (Gal-1), a widely expressed β-galactoside–binding protein, exerts pleiotropic biological functions. Gal-1 is up-regulated in hepatocarcinoma cells, although its role in liver pathophysiology remains uncertain. We investigated the effects of Gal-1 on HepG2 hepatocellular carcinoma (HCC) cell adhesion and polarization. Soluble and immobilized recombinant Gal-1 (rGal-1) promoted HepG2 cell adhesion to uncoated plates and also increased adhesion to laminin. Antibody-mediated blockade experiments revealed the involvement of different integrins as critical mediators of these biological effects.