Miracle-dz/UniFAR-FTUs huggingface dataset:
Prediction of symptom remission in schizophrenia during inpatient treatment

Objective: Standardized consensus criteria for remission in schizophrenia were recently proposed. The present study applied the symptom-severity component of these criteria to a sample of inpatients in order to determine the rates of remission during inpatient treatment and to explore predictors of remission. Method: A total of 288 inpatients from a multi-centre follow-up programme who fulfilled ICD-10 criteria for schizophrenia were included in the present analyses. PANSS ratings at admission and at discharge from hospitalization were used to examine remission status. Clinical and sociodemographic variables at admission were tested for their ability to predict remission at discharge. Results: In total, 55% of the sample achieved symptom remission during inpatient treatment; 84% percent showed remission with respect to ‘reality distortion’, 85% with respect to ‘disorganization’ and only 65% with respect to ‘negative symptoms’. Logistic regression analysis revealed that the global functioning (GAF) in the year before admission, the total score of the Strauss–Carpenter Prognostic Scale and the PANSS negative subscore at admission were predictive for symptom remission. The regression model showed a predictive value of about 70% and explained 36% of the observed variance. Conclusion: The results highlight the impact of negative symptoms for the course and treatment response of schizophrenic illness.
A Phase II and Biomarker Study of Ramucirumab, a Human Monoclonal Antibody Targeting the VEGF Receptor-2, as First-Line Monotherapy in Patients with Advanced Hepatocellular Cancer

Purpose: To assess the efficacy and safety of the anti-VEGF receptor-2 (VEGFR-2) antibody ramucirumab as first-line therapy in patients with advanced hepatocellular carcinoma and explore potential circulating biomarkers. Experimental Design: Adults with advanced hepatocellular carcinoma and no prior systemic treatment received ramucirumab 8 mg/kg every two weeks until disease progression or limiting toxicity. The primary endpoint was progression-free survival (PFS); secondary endpoints included objective response rate (ORR) and overall survival (OS). Circulating biomarkers were evaluated before and after ramucirumab treatment in a subset of patients. Results: Forty-two patients received ramucirumab. Median PFS was 4.0 months [95% confidence interval (CI), 2.6–5.7], ORR was 9.5% (95% CI, 2.7–22.6; 4/42 patients had a partial response), and median OS was 12.0 months (95% CI, 6.1–19.7). For patients with Barcelona Clinic Liver Cancer (BCLC) stage C disease, median OS was 4.4 months (95% CI, 0.5–9.0) for patients with Child-Pugh B cirrhosis versus 18.0 months (95% CI, 6.1–23.5) for patients with Child-Pugh A cirrhosis. Treatment-related grade ≥3 toxicities included hypertension (14%), gastrointestinal hemorrhage and infusion-related reactions (7% each), and fatigue (5%). There was one treatment-related death (gastrointestinal hemorrhage). After treatment with ramucirumab, there was an increase in serum VEGF and placental growth factor (PlGF) and a transient decrease in soluble VEGFR-2. Conclusion: Ramucirumab monotherapy may confer anticancer activity in advanced hepatocellular carcinoma with an acceptable safety profile. Exploratory biomarker studies showed changes in circulating VEGF, PlGF, and sVEGFR-2 that are consistent with those seen with other anti-VEGF agents. Clin Cancer Res; 19(23); 6614–23. ©2013 AACR.
Patent foramen ovale does not have a negative impact on early outcomes in patients undergoing liver transplantation

Alba AC, Verocai Flaman F, Granton J, Delgado DH. Patent foramen ovale does not have a negative impact on early outcomes in patients undergoing liver transplantation. Clin Transplant 2011: 25: 151–155. © 2010 John Wiley & Sons A/S.
Assimilation of GPS Radio Occultation Refractivity Data from CHAMP and SAC-C Missions over High Southern Latitudes with MM5 4DVAR

Abstract In this study, the GPS radio occultation (RO) data from the Challenging Minisatellite Payload (CHAMP) and Satellite de Aplicaciones Cientificas-C (SAC-C) missions are assimilated. An updated version of the fifth-generation Pennsylvania State University–National Center for Atmospheric Research Mesoscale Model (MM5) four-dimensional variational data assimilation system (4DVAR) is used to assess the impact of the GPS RO data on analyses and short-range forecasts over the Antarctic. The study was performed during the period of intense cyclonic activity in the Ross Sea, 9–19 December 2001. On average 66 GPS RO soundings were assimilated daily. For the assimilation over a single 12-h period, the impact of GPS RO data was only marginally positive or near neutral, and it varied markedly from one 12-h period to another. The large case-to-case variation was attributed to the low number of GPS RO soundings and a strong dependency of forecast impact on the location of the soundings relative to the rapidly de.
Cell-cycle regulatory proteins in podocyte cell in idiopathic nephrotic syndrome of childhood.

BACKGROUND The podocyte cell is believed to play an important role in idiopathic nephrotic syndrome (INS) of childhood. In adults with cellular and collapsing focal segmental glomerulosclerosis (FSGS), the expression of cell-cycle regulatory proteins such as p27, p57, and cyclin D is decreased and expression of cyclin A, Ki-67, and p21 is observed in podocyte cells suggestive of a dysregulated podocyte phenotype. We investigated for alterations in the expression of cyclin kinase inhibitors, p27, p57, p21, and cyclins D and A in the podocyte cell of children with INS. METHODS Forty-two kidney biopsies were investigated; 14 with minimal-change disease (MCD), seven with diffuse mesangial hypercellularity (DMH), 12 with FSGS, four with Alport syndrome (AS), and five normal biopsies. The sections were examined by immunohistochemistry using dual staining method. Podocyte cells were first identified by Wilm's tumor-1 staining after which expressions of cell-cycle regulatory proteins were analyzed. A quantitative analysis was performed for the proportion of podocyte cells that expressed each cell cycle regulatory protein. RESULTS On light microscopy, all podocyte cells expressed p27, while p57 and p21 expression was seen in a portion of podocyte cells in normal kidney biopsies. Cyclin D was expressed in a small percent of podocyte cells though the expression was more marked in mesangial and endothelial cells. Cyclin A expression was not seen in normal biopsies. The mean expression of p27 decreased significantly in order from normal (100%), MCD (45.9%), DMH (22.4%), and FSGS (16.7%), and the difference between MCD and FSGS was significant. p21 was significantly and equally reduced in MCD (2.3%), DMH (0%), and FSGS (0.7%) compared to normal (66.6%). There was no significant difference in expression of p57, cyclin D and cyclin A in the podocyte cells between normal and children with INS. Children with AS showed a significant decrease in p27 and p21 expression, while the expression of p57, cyclin D and cyclin A were unchanged from normal, thus demonstrating a pattern similar to INS. CONCLUSION The podocyte cell in children with INS down-regulates expression of cyclin kinase inhibitors such as p21 and p27, but not p57, but does not up-regulate cyclin D and cyclin A that are needed to overcome the G1/S transition and move the cell forward in the cell cycle process. Thus, the podocyte cell remains trapped in the G1 arrest phase. In children with INS or AS, the dysregulated podocyte phenotype is different than the one described in adults with cellular or collapsing FSGS.
REPRESENTATION AS A FACTOR OF PROPENSITY FOR COOPERATION IN INTERNATIONAL RELATIONS

En esta investigacion utilizamos la cooperacion de estados en la lucha contra el terrorismo internacional como un ejemplo de cooperacion estatal. En el campo de las relaciones internacionales es habitual pensar que el deseo de cooperacion entre los estados surge de la existencia de una amenaza comun; se supone que la cooperacion entre ellos como miembros de una union antiterrorista solo es fortalecida por la existencia de nuevas amenazas. Sin embargo, somos testigos de lo contrario: la union antiterrorista de estados se desintegro poco despues de su creacion. En nuestra investigacion comprobamos que el supuesto de que la existencia de un problema comun, incluso una amenaza externa comun, es un requisito pero no una condicion suficiente para la emergencia de cooperacion. Comparamos la representacion de las amenazas terroristas de los lideres politicos de Rusia y EE.UU. como miembros de la coalicion antiterrorista durante la operacion militar en Irak en 2003.
Atlantic Salmon Type I IFN Subtypes Show Differences in Antiviral Activity and Cell-Dependent Expression: Evidence for High IFNb/IFNc–Producing Cells in Fish Lymphoid Tissues

This work reveals distinct roles of the two-cysteine–containing type I IFNs, IFNa and IFNd, and the four-cysteine–containing IFNb and IFNc in antiviral immunity of Atlantic salmon. IFNa and IFNc showed similar antiviral activities and ability to induce antiviral genes, IFNb was less active, and IFNd showed no activity. Expression of IFNs was compared by treatment of cells or fish with the dsRNA polyinosinic–polycytidylic acid [poly(I:C)], which induces IFNs via the viral RNA receptors MDA5 and TLR3/TLR22 and with the imidazoquinoline R848, which induces IFNs via TLR7. Poly(I:C) strongly induced IFNa in cell lines, whereas the other IFNs showed little response, indicating that IFNa is the main IFN subtype induced through the RIG-I/MDA5 pathway. In contrast, IFNb and IFNc are the main IFNs induced through the TLR7 pathway because R848 induced high transcript levels of IFNb and IFNc and low transcript levels of IFNa in the head kidney and spleen. IFNd was constitutively expressed in cells and organs but showed no response to poly(I:C) or R848. Fluorescence in situ hybridization studies showed that poly(I:C) induced IFNa and IFNc in a variety of cells in the head kidney, spleen, gills, liver, and heart, whereas R848 induced coexpression of IFNb and IFNc in distinct cells in head kidney and spleen. These cells are likely to be specialized high IFN producers because they were few in numbers despite high IFNb/IFNc transcript levels in the same organs. High IFN expression in response to TLR7 ligation is a feature shared by mammalian plasmacytoid dendritic cells.
Extracellular Glutamate During Focal Cerebral Ischaemia in Rats: Time Course and Calcium Dependency

Abstract: The time course of changes in extracellular glutamic acid levels and their Ca2+ dependency were studied in the rat striatum during focal cerebral ischaemia, using microdialysis. Ischaemia‐induced changes were compared with those produced by high K+‐evoked local depolarization. To optimize time resolution, glutamate was analysed continuously as the dialysate emerged from the microdialysis probe by either enzyme fluorimetry or biosensor. The Ca2+ dependency of glutamate changes was examined by perfusing the probe with Ca2+‐free medium. With normal artificial CSF, ischaemia produced a biphasic increase in extracellular glutamate, which started from the onset of ischaemia. During the first phase lasting ∼10 min, dialysate glutamate level increased from 5.8 ± 0.9 µM· min−1 to 35.8 ± 6.2 µM where it stabilized for ∼3 min. During the second phase dialysate glutamate increased progressively to its maximum (82 ± 8 µM), reached after 55 min of ischaemia, where it remained for as long as it was recorded (3 h). The overall changes in extracellular glutamate were similar when Ca2+ was omitted from the perfusion medium, except that the first phase was no longer detectable and, early in ischaemia, extracellular glutamate increased at a significantly slower rate than in the control group (2.2 ± 1 µM· min−1; p < 0.05). On the basis of these data, we propose that most of the glutamate released in the extracellular space in severe ischaemia is of metabolic origin, probably originating from both neurons and glia, and caused by altered glutamate uptake mechanisms. Comparison with high K+‐induced glutamate release did not suggest that glutamate “exocytosis,” early after middle cerebral artery occlusion, was markedly limited by deficient ATP levels.
Lexical access and vocabulary development in very young bilinguals

This study compares lexical access and expressive and receptive vocabulary development in monolingual and bilingual toddlers. More specifically, the link between vocabulary size, production of translation equivalents, and lexical access in bilingual infants was examined as well as the relationship between the Communicative Development Inventories and the Computerized Comprehension Task. Twenty-five bilingual and 18 monolingual infants aged 24 months participated in this study. The results revealed significant differences between monolingual and bilinguals’ expressive vocabulary size in L1 but similar total vocabularies. Performance on the Computerized Comprehension Task revealed no differences between the two groups on measures of both reaction time and accuracy, and a strong convergent validity of the Computerized Comprehension Task with the Communicative Development Inventories was observed for both groups. Bilinguals with a higher proportion of translation equivalents in their expressive vocabulary showed faster access to words in the Computerized Comprehension Task.
The S promoter of hepatitis B virus is regulated by positive and negative elements

The S promoter, one of the major hepatitis B virus (HBV) promoters, directs the synthesis of mRNA for surface antigen. Transient expression studies revealed that this promoter is highly active in the Alexander hepatoma cell line but not in SK-Hep1 and HeLa cells. We found that a distal element of the promoter (-103 to -48) confers this cell-type-specific behavior through a mechanism in which the promoter activity is repressed in HeLa and SK-Hep1 cells but increased in Alexander cells. By using an inhibitor of protein synthesis, we obtained evidence that a labile repressor(s) confers the negative effect in SK-Hep1 cells. We also found an enhancerlike activity associated with a small DNA segment of the S promoter (-27 to + 30). This proximal element was active in HeLa and SK-Hep1 cells only in the absence of the distal negative element. Finally, analysis of S promoter deletion mutants demonstrated that the -27 to -17 region of the S promoter is crucial for its activity.
Hypertonic resuscitation of hemorrhagic shock upregulates the anti-inflammatory response by alveolar macrophages.

BACKGROUND Resuscitated hemorrhagic shock predisposes patients to the development of acute respiratory distress syndrome (ARDS). Hypertonic saline (HTS) has been shown to inhibit immune cell activation in response to lipopolysaccharide (LPS) in vitro and to reduce lung damage when used for resuscitation of hemorrhagic shock in vivo. We hypothesize that HTS resuscitation of hemorrhagic shock may exert this anti-inflammatory effect by modulating alveolar macrophage function leading to an altered balance between the proinflammatory and the counter-inflammatory response. METHODS A 2-hit rat model of shock resuscitation was used. Alveolar macrophages were harvested by bronchoalveolar lavage (BAL), and tumor necrosis factor (TNF)-alpha and interleukin (IL)-10 were quantified in the cell culture supernatants by enzyme-linked immunosorbent assay (ELISA). Alternatively, 1 hour after resuscitation, animals received endotracheal LPS followed by endotracheal anti-IL-10 neutralizing antibody. Lung injury was determined by measuring BAL neutrophil counts 4 hours after LPS in vivo administration. RESULTS Systemic administration of HTS significantly modulates the responsiveness of alveolar macrophages. Specifically, HTS resuscitation inhibited LPS-induced TNF-alpha production while enhancing IL-10 release in response to LPS administered ex vivo and in vivo. Anti-IL-10 antibody in vivo partially reversed the lung protective effect of HTS resuscitation. CONCLUSIONS HTS resuscitation exerts an immunomodulatory effect on alveolar macrophages by shifting the balance of pro- and counter-inflammatory cytokine production in favor of an anti-inflammatory response. The in vivo data suggest a causal role for HTS-induced augmented IL-10 as protective. These findings suggest a novel mechanism for the in vivo salutary effect of HTS resuscitation on lung injury after resuscitated hemorrhagic shock.
In vitro analysis of the role of DCC in mucus‐secreting intestinal differentiation

The deleted in colorectal cancer (DCC) gene was initially described as a colon cancer‐associated tumor suppressor gene and subsequently proposed to be involved in goblet cell differentiation, but its precise role in normal intestine physiology and in cancer remains to be established. We have analyzed DCC mRNA expression in a panel of human colorectal cancer cell lines with a variety of differentiation phenotypes by reverse transcription‐polymerase chain reaction (RT‐PCR) and have shown that (1) most cell lines showed lower levels of DCC mRNA than normal colonic tissue; (2) only 1 cell line lacked detectable levels of DCC mRNA expression; (3) a discrepancy was found between the detectability of RT‐PCR products corresponding to the extracellular and intracellular domains of DCC; and (4) there was no association between the presence of DCC transcripts and the differentiation phenotype. Specifically, DCC was not exclusively associated with the mucus‐secreting phenotype, as determined by Alcian blue staining and Northern blotting with mucin gene probes. This was further supported by immunohistochemical results on DCC product and mucins in normal colon: DCC was detected in both goblet and absorptive cells. The introduction of full‐length DCC cDNA in undifferentiated HT‐29 cells did not have any effect on their differentiation phenotype, as shown by morphological studies and analysis of markers for this process in colon, such as mucins, dipeptidylpeptidase IV, villin and sucrase‐isomaltase. There were no effects on cell proliferation in vitro. Our results indicate that DCC is not selectively involved in the mucosecretory differentiation pathway and that it is neither sufficient nor essential for normal intestinal differentiation. Int. J. Cancer 81:799–807, 1999. © 1999 Wiley‐Liss, Inc.
Quaternary tectonic evolution of the Pamir‐Tian Shan convergence zone, Northwest China

The Pamir‐Tian Shan collision zone in the western Tarim Basin, northwest China, formed from rapid and ongoing convergence in response to the Indo‐Eurasian collision. The arid landscape preserves suites of fluvial terraces crossing structures active since the late Neogene that create fault and fold scarps recording Quaternary deformation. Using geologic and geomorphic mapping, differential GPS surveys of deformed terraces, and optically stimulated luminescence dating, we create a synthesis of the active structures that delineate the timing, rate, and migration of Quaternary deformation during ongoing convergence. New deformation rates on eight faults and folds, when combined with previous studies, highlight the spatial and temporal patterns of deformation within the Pamir‐Tian Shan convergence zone during the Quaternary. Terraces spanning ~130 to ~8 ka record deformation rates between ~0.1 and 5.6 mm/yr on individual structures. In the westernmost Tarim Basin, where the Pamir and Tian Shan are already juxtaposed, the fastest rates occur on actively deforming structures at the interface of the Pamir‐Tian Shan orogens. Farther east, as the separation between the Pamir‐Tian Shan orogens increases, the deformation has not been concentrated on a single structure, but rather has been concurrently distributed across a zone of faults and folds in the Kashi‐Atushi fold‐and‐thrust belt and along the NE Pamir margin, where shortening rates vary on individual structures during the Quaternary. Although numerous structures accommodate the shortening and the locus of deformation shifts during the Quaternary, the total shortening across the western Tarim Basin has remained steady and approximately matches the current geodetic rate of 6–9 mm/yr.
Nitric-oxide-dependent pial arteriolar dilation in the female rat: effects of chronic estrogen depletion and repletion.

In this study, we compared endothelial nitric oxide synthase (eNOS)-mediated cerebral vasodilating responses in intact female rats, chronically ovariectomized (OVX) rats, and OVX rats treated for 2 weeks with 17beta-estradiol (E(2)). Under anesthesia, using intravital microscopy and a closed cranial window system, pial arteriolar diameter changes were monitored during sequential cortical suffusions of an eNOS-dependent dilator [acetylcholine (ACh)] and a direct NO donor [S-nitrosoacetylpenicillamine (SNAP)]. In separate rats from the same groups, we compared eNOS and caveolin-1 (CAV-1) protein abundance in pial arterioles (via immunofluorescence analyses). In untreated and low-dose E(2)-treated (1.0 microg x kg(-1) x day(-1)) OVX rats, ACh-induced vasodilations were virtually absent. High-dose E(2) treatment (100 microg x kg(-1) x day(-1)) restored ACh-induced pial arteriolar dilations to levels seen in intact females. The vasodilations elicited by SNAP and ADO were unaffected by chronic estrogen changes, indicating no direct estrogen influence on vascular smooth muscle (VSM) reactivity. Pial arteriolar eNOS protein abundance was diminished by ovariectomy and restored by high-dose E(2) treatment. Pial arteriolar CAV-1 expression was higher in OVX versus intact and E(2)-treated OVX females. These results suggest that long-term changes in estrogen directly influence brain eNOS functional activity. The estrogen-related changes in eNOS-dependent vasodilating function appear to be related, in part, to a capacity for E(2) to increase eNOS protein expression and, in part, to an E(2)-associated diminution in endothelial CAV-1 expression.
PlGF in a clinical setting of pregnancies at risk of preeclampsia and/or intrauterine growth restriction

Abstract Placental growth factor (PlGF) is an angiogenic molecule produced by the placenta and implicated in the pathogenesis of preeclampsia (PE) and intrauterine growth restriction (IUGR). We have evaluated utility and applicability of the PlGF test in a clinical setting of pregnancies at risk of PE or complicated by IUGR in order to assess its relationship with pregnancy outcomes. Seventy-three pregnancies were enrolled between 19 and 35 weeks: 57 pregnancies at risk of PE and 16 at diagnosis of IUGR. Maternal circulating PlGF levels were measured by the Triage PlGF test (Alere, San Diego, CA). Pregnancy outcomes were evaluated in relation to three categories of plasma PlGF levels: very low (<12 pg/ml), low (12–100 pg/ml) and normal (≥100 pg/ml). Uterine artery Doppler velocimetry (UADV) pulsatility index (PI) was measured in the same patients on the day of maternal sampling. Pregnancies at risk with very low plasma PlGF levels had significantly lower gestational age at delivery than patients with low or normal PlGF. The rate of emergency C-section was significantly higher in the group with PlGF <12 pg/ml. IUGR pregnancies with very low and low PlGF delivered earlier than patients with normal PlGF. All IUGR with very low and low PlGF had UADV PI > 95th percentile. Our data indicate that PlGF may provide useful information to identify fetuses requiring increased surveillance and possibly urgent delivery in pregnancies at risk of adverse outcomes. Furthermore, in IUGR, PlGF can predict adverse pregnancy outcomes that may be secondary to placental insufficiency.