Miracle-dz/UniFAR-FTUs huggingface dataset:
Use of Palm computer as an adjunct to cognitive–behavioural therapy with an ultra‐high‐risk patient: a case report

Aim: Recently, attempts have been made to develop cognitive‐behaviour therapy (CBT) treatment models to target negative symptoms in individuals with schizophrenia, as well as individuals at ultra‐high risk (UHR) for psychosis. Successful CBT treatment is founded on active patient participation including completion of homework assignments such as daily logs of activities and experiences. However, these very negative symptoms may themselves hinder the rate of homework assignment completion. We describe a case report of using experience sampling method with a Palm computer as an adjunct to CBT with a female patient at UHR status with predominantly negative symptoms. Our aim was to assess the feasibility and effectiveness of this methodology to improve homework completion and overcome treatment barriers associated with negative symptoms.
Beta-cell function and the development of diabetes-related complications in the diabetes control and complications trial.

In patients with type 1 diabetes, measurement of connecting peptide (C-peptide), cosecreted with insulin from the islets of Langerhans, permits estimation of remaining beta-cell secretion of insulin. In this retrospective analysis to distinguish the incremental benefits of residual beta-cell activity in type 1 diabetes, stimulated (90 min following ingestion of a mixed meal) C-peptide levels at entry in the Diabetes Control and Complications Trial (DCCT) were related to measures of diabetic retinopathy and nephropathy and to incidents of severe hypoglycemia. Based on the analytical sensitivity of the assay (0.03 nmol/l) and study entry criteria, the DCCT subjects were divided into four groups of stimulated C-peptide responses: <or=0.03, 0.04-0.20, 0.21-0.50 nmol/l at entry, and 0.21-0.50 nmol/l at entry and at least 1 year later (sustained C-peptide secretion). Uniformly in the intensive and partially in the conventional DCCT treatment groups, any C-peptide secretion, but especially at higher and sustained levels of stimulated C-peptide, was associated with reduced incidences of retinopathy (both a single three-step change and a repeated three-step change on the Early Treatment of Diabetic Retinopathy Study [ETDRS] scale at the next 6 month visit) and nephropathy (both albuminuria >40 mg/24 h once and repeated at the next annual visit). There were also differences in severe hypoglycemia across C-peptide levels in both treatment groups. In the intensively treated cohort there were essentially identical prevalences of severe hypoglycemia ( approximately 65% of participants) in the first three groups; however, those subjects with mixed-meal stimulated C-peptide level >0.20 nmol/l for at least baseline and the first annual visit in the DCCT experienced a reduced prevalence of approximately 30%. Therefore, even modest levels of beta-cell activity at entry in the DCCT were associated with reduced incidences of retinopathy and nephropathy. Also, continuing C-peptide (insulin) secretion is important in avoiding hypoglycemia (the major complication of intensive diabetic therapy).
Identification of genetic loci associated with fire blight resistance in Malus through combined use of QTL and association mapping.

Fire blight, incited by the enterobacterium Erwinia amylovora, is a destructive disease of Rosaceae, particularly of apples and pears. There are reports on the molecular mechanisms underlying E. amylovora pathogenesis and how the host activates its resistance mechanism. The host's resistance mechanism is quantitatively controlled, although some major genes might also be involved. Thus far, quantitative trait loci (QTL) mapping and differential expression studies have been used to elucidate those genes and/or genomic regions underlying quantitative resistance present in the apple genome. In this study, an effort is undertaken to dissect the genetic basis of fire blight resistance in apple using both QTL and genome-wide association mapping. On the basis of an F1 pedigree of 'Coop 16' × 'Coop 17' and a genome-wide association study (GWAS) mapping population of Malus accessions (species, old and new cultivars and selections), new QTLs and associations have been identified. A total of three QTLs for resistance to fire blight, with above 95% significant logarithm of odds threshold value of 2.5, have been identified on linkage groups (LGs) 02, 06, and 15 of the apple genome with phenotypic variation explained values of 14.7, 20.1 and 17.4, respectively. Although elevated P-values with signals for marker-trait associations are observed for some LGs, these are not found to be significant. However, a total of 34 significant associations, with P-values ≥0.02, have been detected including 8 for lesion length at 7 days following inoculation (PL1), 14 for lesion length at 14 days following inoculation (PL2), and 12 for shoot length.
Long-term effects of acute exposure to chlorphenvinphos on behavioural responsiveness to amphetamine and scopolamine in rats.

We investigated the effect of acute exposure to chlorphenvinphos (CVP) (2-chloro-1 (2,4-dichlorophenyl)-vinyl-diethyl-phosphate), an organophosphate anticholinesterase, on the amphetamine- and scopolamine-induced open-field locomotion in Wistar rats. CVP was administered at a single i.p. dose of 1.0 mg/kg (1/10 of LD50). In part of the rats cholinesterase (ChE) was determined. Three hours after CVP injection, the ChE activity decreased by about 27%. It returned to the preinjection level within 14 days after the exposure. In the behavioural part of the experiment, the animals were challenged with 1.0 mg/kg amphetamine or 0.75 mg/kg scopolamine three weeks after CVP exposure, i.e. after a period of time sufficient for cholinesterase recovery. It has been found that in the CVP-exposed rats, the behavioural responses to amphetamine or scopolamine challenge (the increase in locomotor activity) was significantly reduced compared to the controls. This suggests that acute exposure to CVP produced an increase in cholinergic activity which persisted long after ChE activity had returned to normal.
Surveillance of Acute Respiratory Infections Using Community-Submitted Symptoms and Specimens for Molecular Diagnostic Testing

Participatory systems for surveillance of acute respiratory infection give real-time information about infections circulating in the community, yet to-date are limited to self-reported syndromic information only and lacking methods of linking symptom reports to infection types. We developed the GoViral platform to evaluate whether a cohort of lay volunteers could, and would find it useful to, contribute self-reported symptoms online and to compare specimen types for self-collected diagnostic information of sufficient quality for respiratory infection surveillance. Volunteers were recruited, given a kit (collection materials and customized instructions), instructed to report their symptoms weekly, and when sick with cold or flu-like symptoms, requested to collect specimens (saliva and nasal swab). We compared specimen types for respiratory virus detection sensitivity (via polymerase-chain-reaction) and ease of collection. Participants were surveyed to determine receptivity to participating when sick, to receiving information on the type of pathogen causing their infection and types circulating near them. Between December 1 2013 and March 1 2014, 295 participants enrolled in the study and received a kit. Of those who reported symptoms, half (71) collected and sent specimens for analysis. Participants submitted kits on average 2.30 days (95 CI: 1.65 to 2.96) after symptoms began. We found good concordance between nasal and saliva specimens for multiple pathogens, with few discrepancies. Individuals report that saliva collection is easiest and report that receiving information about what pathogen they, and those near them, have is valued and can shape public health behaviors. Community-submitted specimens can be used for the detection of acute respiratory infection with individuals showing receptivity for participating and interest in a real-time picture of respiratory pathogens near them.
The E47 transcription factor binds to the enhancer sequences of recombinant murine leukemia viruses and influences enhancer function

The genomes of most recombinant murine leukemia viruses (MuLVs) inherit pathogenic U3 region sequences from the endogenous xenotropic provirus Bxv-1. However, the U3 regions of about one-third of recombinant MuLVs from CWD mice, such as CWM-T15, have nonecotropic substitutions that are probably derived from an endogenous polytropic provirus. The CWM-T15 U3 region sequences contain five nucleotide substitutions compared with the less pathogenic sequences of the endogenous ecotropic virus parent, Emv-1. Three of these substitutions are located immediately 3' of the enhancer core, and two form part of an E-box motif that is also found in the Bxv-1 sequence. A series of electromobility shift assays revealed that nuclear extracts from S194 cells and the basic helix-loop-helix transcription factor E47 could distinguish between oligonucleotides that contained the core region sequences of CWM-T15 or Emv-1. The E47 homodimers appeared to bind to the CWM-T15 E-box motif and when expressed at high levels in cells transactivated the CWM-T15 but not the Emv-1 enhancer. Taken together, these results suggest that E47 or related basic helix-loop-helix proteins that are expressed in lymphoid cells bind to and transactivate the CWM-T15 enhancer in vivo. This transactivation may explain why the CWM-T15 and Bxv-1 U3 regions accelerate the onset of lymphoid neoplasms and why related enhancer core region sequences are preferentially incorporated into the genomes of recombinant MuLVs and are found in other leukemogenic mammalian retroviruses.
A short-term study of the safety, pharmacokinetics, and efficacy of ritonavir, an inhibitor of HIV-1 protease. European-Australian Collaborative Ritonavir Study Group.

BACKGROUND Reverse-transcriptase inhibitors have only moderate clinical efficacy against the human immunodeficiency virus type 1 (HIV-1). Ritonavir is an inhibitor of HIV-1 protease with potent in vitro anti-HIV properties and good oral bioavailability. METHODS We evaluated the antiviral activity and safety of ritonavir in a double-blind, randomized, placebo-controlled phase 1 and 2 study of 84 HIV-positive patients with 50 or more CD4+ lymphocytes per cubic millimeter. The patients were randomly assigned to one of four regimens of ritonavir therapy, or to placebo for four weeks and then (by random assignment) to one of the ritonavir regimens. RESULTS During the first 4 weeks, increases in CD4+ lymphocyte counts and reductions in the log number of copies of HIV-1 RNA per milliliter of plasma were similar among the four dosage groups, but in the three lower-dosage groups there was a return to base-line levels by 16 weeks. After 32 weeks, in the seven patients in the highest-dosage group (600 mg of ritonavir every 12 hours), the median increase from base line in the CD4+ lymphocyte count was 230 cells per cubic millimeter, and the mean decrease in the plasma concentration of HIV-1 RNA (as measured by a branched-DNA assay) was 0.81 log (95 percent confidence interval, 0.40 to 1.22). In a subgroup of 17 patients in the two higher-dosage groups, RNA was also measured with an assay based on the polymerase chain reaction, and after eight weeks of treatment there was a mean maximal decrease in viral RNA of 1.94 log (95 percent confidence interval, 1.37 to 2.51). Adverse events included nausea, circumoral paresthesia, elevated hepatic aminotransferase levels, and elevated triglyceride levels. Ten withdrawals from the study were judged to be related to ritonavir treatment. CONCLUSIONS In this short-term study, ritonavir was well tolerated and had potent activity against HIV-1, but its clinical benefits remain to be established.
Extracellular high mobility group box chromosomal protein 1 is a coupling factor for hypoxia and inflammation in arthritis.

OBJECTIVE Tissue hypoxia is closely associated with arthritis pathogenesis, and extracellular high mobility group box chromosomal protein 1 (HMGB-1) released from injured cells also has a role in arthritis development. This study was thus undertaken to investigate the hypothesis that extracellular HMGB-1 may be a coupling factor between hypoxia and inflammation in arthritis. METHODS Concentrations of tumor necrosis factor alpha, interleukin-6, vascular endothelial growth factor, lactic acid, lactate dehydrogenase, and HMGB-1 were measured in synovial fluid (SF) samples from patients with inflammatory arthropathy (rheumatoid arthritis and pseudogout) and patients with noninflammatory arthropathy (osteoarthritis). The localization of tissue hypoxia and HMGB-1 was also examined in animal models of collagen-induced arthritis (CIA). In cell-based experiments, the effects of hypoxia on HMGB-1 release and its associated cellular events (i.e., protein distribution and cell viability) were studied. RESULTS In SF samples from patients with HMGB-1-associated inflammatory arthropathy (i.e., samples with HMGB-1 levels >2 SD above the mean level in samples from patients with noninflammatory arthropathy), concentrations of HMGB-1 were significantly correlated with those of lactic acid, a marker of tissue hypoxia. In CIA models in which the pathologic phenotype could be attenuated by HMGB-1 neutralization, colocalization of HMGB-1 with tissue hypoxia in arthritis lesions was also observed. In cell-based experiments, hypoxia induced significantly increased levels of extracellular HMGB-1 by the cellular processes of secretion and/or apoptosis-associated release, which was much more prominent than the protein release in necrotic cell injury potentiated by oxidative stress. CONCLUSION These findings indicate that tissue hypoxia and its resultant extracellular HMGB-1 might play an important role in the development of arthritis.
Proteomic analysis of proteins expressed by Helicobacter pylori under oxidative stress

Helicobacter pylori is a spiral, slow growing gram‐negative microaerophilic bacterium. It has been shown to be the etiological agent of gastroduodenal diseases, such as chronic gastritis, gastric and duodenal ulcers, and gastric cancer. To address the influence of oxidative stress and its underlying mechanisms, we have compared proliferation, urease activity and protein expression profile of H. pylori incubated under normal microaerophilic (5% O2) and aerobic stress (20% O2) conditions. Oxidative‐stress cells displayed coccoid morphology and time‐dependent decrease in proliferation. The urease activity was completely abrogated after 32 h. We have further compared the protein expression profiles of H. pylori under normal growing and oxidative‐stress conditions by a global proteomic analysis, which includes high‐resolution 2‐DE followed by MALDI‐TOF‐MS and bioinformatic databases search/peptide‐mass comparison. The results revealed that more than ten proteins were differentially expressed under oxidative stress. Most notably, the protein expression levels of urease accessory protein E (UreE, an essential metallochaperone for urease activity) and alkylhydroperoxide reductase (AhpC) with antioxidant potential are greatly decreased under stress conditions. Measurements of messenger RNA transcription level by performing RT‐PCR on total mRNA also confirmed that gene expressions for these two proteins are consistently repressed under oxygen tension. These changes form a firm basis to account for the loss of urease activity and anti‐oxidative ability of H. pylori after long‐term exposure to reactive oxygen. Conceivably, UreE and AhpC may thus be listed as potential targets for the development of therapeutic drugs against H. pylori.
Avian Influenza in North and South America, 2002–2005

Abstract Between 2002 and 2005, three outbreaks of highly pathogenic avian influenza (HPAI) occurred in the Americas: one outbreak in Chile (H7N3) in 2002, one outbreak in the United States (H5N2) in 2004, and one outbreak in Canada (H7N3) in 2004. The outbreak in Chile was limited to a large broiler breeder operation and a nearby turkey flock and represented the first outbreak of HPAI in that country. The outbreak of HPAI in the United States occurred in Texas and was limited to one premise where chickens were raised for sale in nearby live-bird markets. The outbreak in Canada was the largest of the three HPAI outbreaks, involving 42 premises and approximately 17 million birds in the Fraser Valley, British Columbia. In each of the HPAI outbreaks, the disease was successfully eradicated by depopulation of infected farms. All other reports of infections in poultry and isolations from wild bird species pertained to low pathogenicity avian influenza (LPAI) viruses. Animal Health Officials in Canada reported subtypes H3, H5, and H6 in domestic poultry, and H3, H5, H11, and H13 from imported and/or wild bird species. An LPAI H5N2 virus continues to circulate in Mexico and the Central American countries of Guatemala and El Salvador. Each country reported isolations of H5N2 virus from poultry and the large-scale use of inactivated and recombinant H5 vaccines in their AI control programs. In Colombia, AI was reported for the first time when antibodies to H9N2 were detected in chickens by routine surveillance. Intensive surveillance activities in the United States detected AI virus or specific antibodies to 13 of the 16 hemagglutinin (H1–H13) and all nine neuraminidase subtypes in live-bird markets, small holder farms, and in commercial poultry from 29 states. The largest outbreak of LPAI in the United States occurred in 2002, when 197 farms were depopulated (4.7 million birds) to control an outbreak in Virginia and surrounding states. The outbreak was caused by an LPAI H7N2 virus closely related to an H7N2 virus that has been circulating in the live-bird marketing system in the northeastern United States since 1994.
EEG spectral analysis and coherence in children with hemiparetic cerebral palsy.

BACKGROUND Hemiparetic cerebral palsy (HCP) is described as having two main forms: arm-dominant, associated with large cortical/subcortical lesions and leg-dominant, associated with central white matter lesions. MATERIAL/METHODS Twelve children with HCP underwent clinical assessment and imaging studies. For each child, 20 artifact-free EEG epochs, each of 2s duration, were selected for spectral analysis and coherence functions. The objective of this research was to estimate EEG spectral power, interhemispheric coherence (ICoh), and intrahemispheric (Hcoh) coherence in children with HCP as compared to healthy children. RESULTS Significant differences between the HCP and control children were detected in the distribution of alpha, theta, delta and beta rhythms over the left and right hemispheres. The ICoh values in the alpha band in the temporal, parietal and occipital regions were significantly lower in the HCP patients than in the controls. There was a significant ICoh increase in the HCP in the theta and delta band, involving frontal and temporal derivations. The significantly lower ICoh values in the HCP children in the beta band involved the frontal, central, parietal and occipital derivations. A higher HCoh value in the HCP children in the alpha band was detected at the right hemisphere. CONCLUSIONS The lower ICoh at the temporal, parietal and occipital derivations in the alpha band implies hypoconnectivity between the right and left hemispheres. HCoh asymmetry, which implies relative hypoconnectivity within the left hemisphere as compared with the right, suggests that functional hemispheric differentiation may be diminished.
Moderate influenza vaccine effectiveness with variable effectiveness by match between circulating and vaccine strains in Australian adults aged 20–64 years, 2007–2011

Please cite this paper as: Kelly et al. Moderate influenza vaccine effectiveness with variable effectiveness by match between circulating and vaccine strains in Australian adults aged 20–64 years, 2007–2011. Influenza and Other Respiratory Viruses DOI:10.1111/irv.12018.
Expression of membrane‐type 1 matrix metalloproteinase in rheumatoid synovial cells

Membrane‐type 1 matrix metalloproteinase (MT1‐MMP) is thought to be a putative regulator of pro‐gelatinase A (MMP‐2) in the rheumatoid synovium. In this study, we examined the effects of IL‐1β, one of the inflammatory cytokines, on the expression of MT1‐MMP and the activation of pro‐MMP‐2 using rheumatoid synovial cells. We also studied the effects of KE‐298 (2‐acetylthiomethyl‐4‐(4‐methylphenyl)‐4‐oxobutanoic acid), a new disease‐modifying anti‐rheumatic drug (DMARD), on MT1‐MMP expression of rheumatoid synovial cells. Type B synovial cells (fibroblast‐like synovial cells) were cultured with KE‐298 (25–100 µg/ml) in the presence of IL‐1β for 48 h. Activation of pro‐MMP‐2 secreted from synovial cells was analysed by gelatin zymography. Reverse transcription–polymerase chain reaction (RT–PCR) methods were used to detect MT1‐MMP mRNA. MT1‐MMP protein expression on synovial cells was examined by anti‐MT1‐MMP immunoblot. An active form of MMP‐2 was demonstrated in the culture media conditioned by IL‐1β‐stimulated synovial cells. In addition, MT1‐MMP mRNA and protein expression of rheumatoid synovial cells were increased by IL‐1β treatment. KE‐298 blocked this IL‐1β‐induced pro‐MMP‐2 activation and MT1‐MMP expression, but did not affect IL‐1β‐induced tissue inhibitor of metalloproteinase‐2 (TIMP‐2) secretion from rheumatoid synovial cells. These findings indicate that activation of rheumatoid synovial cells by IL‐1β results in the induction of MT1‐MMP expression. Given that MT1‐MMP promotes matrix degradation by activating pro‐MMP‐2, these results suggest a novel mechanism whereby cytokine may contribute to articular destruction in rheumatoid arthritis (RA). KE‐298 may prevent this process by down‐regulating MT1‐MMP expression.