Miracle-dz/UniFAR-FTUs huggingface dataset:
Immunological characterization of the gag gene products of bovine immunodeficiency virus

The bovine immunodeficiency virus (BIV) gag gene encodes a 53-kDa precursor (Pr53gag) that is involved in virus particle assembly and is further processed into the putative matrix (MA), capsid (CA), and nucleocapsid (NC) functional domains in the mature virus. Gag determinants are also found in the Gag-Pol polyprotein precursor. To immunologically identify the major precursors and processed products of the BIV gag gene, monospecific rabbit sera to recombinant BIV MA protein and Pr53gag and peptides predicted to correspond to the CA and NC proteins and the MA-CA cleavage site were developed and used in immunoprecipitations and immunoblots of BIV antigens. Monospecific antisera to native and recombinant human immunodeficiency virus type 1 proteins were also used to identify analogous BIV Gag proteins and to determine whether cross-reactive epitopes were present in the BIV Gag precursors or processed products. The BIV MA, CA, and NC Gag proteins were identified as p16, p26, and p13, respectively. In addition to BIV Pr53gag, the major Gag precursor, two other Gag-related precursors of 170 and 49 kDa were identified that have been designated pPr170gag-pol and Pr49gag, respectively; pPr170gag-pol is the Gag-Pol polyprotein precursor, and Pr49gag is the transframe Gag precursor present in pPr170gag-pol. Several alternative Gag cleavage products were also observed, including p23, which contains CA and NC determinants, and p10, which contains a peptide sequence conserved in the CA proteins of most lentiviruses. The monospecific antisera to human immunodeficiency virus type 1 CA (p24) and NC (p7) proteins showed cross-reactivity to and aided in the identification of analogous BIV proteins. Based on the present data, a scheme for the processing of BIV Gag precursors is proposed.
No association between socio‐economic status and white blood cell telomere length

It has been hypothesized that more socio‐economically deprived individuals age faster and, thus, have shorter telomeres than their more affluent counterparts. A weak association between white blood cell telomere length and socio‐economic status in a large heterogeneous sample of females has recently been reported. In 318 individuals from a homogeneous birth cohort, we found no evidence of an association between any measure of socio‐economic status and peripheral blood mononucleocyte telomere length at age 50 after control for lifestyle variables, gender and paternal age at birth. The results of this, and the previous study, suggest that there is little evidence of a strong or consistent correlation between white blood cell telomere length and markers of socio‐economic status.
Erythropoietin Administration In Vivo Increases Vascular Nitric Oxide Synthase Expression

This study was designed to determine whether recombinant human erythropoietin (rHuEpo) administration increases vascular nitric oxide (NO) production in healthy rats. We hypothesized that rHuEpo hypertension is associated with increased endothelial expression of nitric oxide synthase and augmented NO-dependent vasodilation. Male rats were instrumented with pulsed Doppler flow probes around their ascending aorta and with arterial and femoral catheters. Rats were treated for 14 days with rHuEpo (2 U/d) or vehicle. rHuEpo elevated hematocrit and increased mean arterial pressure (142 ± 3 versus 116 ± 4 mm Hg). Thoracic aorta segments from rHuEpo rats had a modest increase in NO-dependent relaxation assessed by acetylcholine (10−10 to 10−5 mol/L) relaxation of phenylephrine (PE) (10−6 mol/L) contracted arteries. Relaxation to NO-donor, s-nitrosyl acetylpenicillamine, and PE contraction were not different from control arteries. The NO synthase inhibitor, N-ω-nitro-l-arginine, increased blood pressure and total peripheral resistance more in rHuEpo rats at both 10 and 30 mg/kg. NOS expression in rHuEpo aorta and plasma NOx concentrations were increased compared with control. Thus, it appears that vascular eNOS expression is increased and causes basal vasodilation in rHuEpo hypertensive rats.
Prioritizing Patient‐Reported Outcomes in Breast Cancer Surgery Quality Improvement

Breast‐cancer‐specific tools that measure health‐related quality of life (HRQOL) were developed for use in research or clinical practice, and little is known about these tools’ performance ability for quality improvement. Furthermore, existing tools may not fully reflect all issues that contribute to quality care as seen by patients. Work is needed to identify and validate patient‐reported outcome measures for use in quality improvement in breast cancer surgical care. We conducted an exploratory qualitative study in order to better understand what HRQOL domains and processes of care define high quality surgical care for women undergoing mastectomy for breast cancer from both the patient and clinician perspective. We conducted focus groups and one‐on‐one interviews with 15 women and administered a prioritization questionnaire to participants. We also conducted a prioritization questionnaire among surgical oncologists, general surgeons, and reconstructive surgeons who are members of the Washington State Medical Association. Both the patient and surgeon prioritization questionnaire asked participants to prioritize HRQOL and treatment satisfaction‐related aspects of their breast cancer surgical care at key time points before and after mastectomy. A Stakeholder Advisory Panel was convened to review focus group, interview, and prioritization questionnaire results and make recommendations as to patient‐reported outcome domains to focus on and existing instruments to use for quality improvement. Patients and clinicians largely agreed on important HRQOL domains, including emotional well‐being, education, communication, and process of care. The Stakeholder Advisory Panel, composed of 12 clinicians and five patients, reviewed study findings and existing patient‐reported outcomes measurement tools. The panel recommended that the BREAST‐Q, a flexible tool with independently validated modules designed for research and clinical care, is an ideal tool to begin developing novel quality improvement benchmarks focused on patient‐reported outcomes.
Application of canonical coordinate methods to the characterization of a family of error minimizing signal compression techniques

Mean-square-error minimizing signal compression techniques, such as Autoregressive Analysis or Linear Predictive Coding and Principal Component or Karhunen-Loeve Analysis, can be systematically characterized in terms of canonical coordinate or generalized eigenvector procedures. This approach provides considerable insight into the interrelationships between a variety of seemingly different signal compression methods. The approach also provides a convenient mechanism for introducing the types of non-Euclidean error measures that are needed to adjust the signal performance optimization criteria to take into account different types of a priori statistical and dynamical information relating to both the desired signal and to various interference processes.
The clinical phenotype of familial and sporadic late onset Alzheimer's disease

Familial factors are clearly associated with an increased risk of developing late onset Alzheimer's disease (LOAD). However, there is emerging evidence to suggest that familial factors may also influence clinical phenotype. To date, most studies have focussed on familial influences upon age of onset or duration of illness and few studies have compared the frequency of non‐cognitive symptoms between familial and sporadic LOAD.
Frequency and pattern of Congenital Heart Defects in children with Down’s Syndrome

Background: Patients with Down’s syndrome are prone to have congenital heart defects. This study was conducted to evaluate the frequency of various congenital heart defects in children with Down’s syndrome in Khyber Pukhtunkhwa province. Material & Methods: This descriptive study was conducted at Department of Pediatrics, Lady Reading Hospital Peshawar, from July 2011 to June 2012. Fifty-five phenotypically Down’s syndrome children born in Khyber Pukhtunkhwa province, age 2 days to 13 years were included in this study. After detailed history and physical examination, all these patients were subjected to 2-dimentional echocardiography in addition to routine laboratory investigations. Results: Congenital heart defects were found in 31 out of 55 patients (56.36%). Among the affected patients, 19(61.3%) were males and 12(38.7%) females with male to female ratio of 1.5:1. Ventricular septal defect was the commonest defect (22.6%), followed by patent ductus arteriosus (19.4%), atrioventricular septal defect (19.4%), atrial septal defect (16.1%) and tetralogy of Fallots (6.4%). Conclusion: Congenital heart defects are common in children with Down’s syndrome. The commonest one is ventricular septal defect in our set-up. All children with Down’s syndrome should have a cardiac evaluation at birth.
Distributed affective space represents multiple emotion categories across the brain

The functional organization of human emotion systems as well as their neuroanatomical basis and segregation in the brain remains unresolved. Here we used pattern classification and hierarchical clustering to reveal and characterize the organization of discrete emotion categories in the human brain. We induced 14 emotions (6 “basic”, such as fear and anger; and 8 “non-basic”, such as shame and gratitude) and a neutral state in participants using guided mental imagery while their brain activity was measured with functional magnetic resonance imaging (fMRI). Twelve out of 14 emotions could be reliably classified from the fMRI signals. All emotions engaged a multitude of brain areas, primarily in midline cortices including anterior and posterior cingulate and precuneus, in subcortical regions, and in motor regions including cerebellum and premotor cortex. Similarity of subjective emotional experiences was associated with similarity of the corresponding neural activation patterns. We conclude that the emotions included in the study have discrete neural bases characterized by specific, distributed activation patterns in widespread cortical and subcortical circuits, and highlight both overlaps and differences in the locations of these for each emotion. Locally differentiated engagement of these globally shared circuits defines the unique neural fingerprint activity pattern and the corresponding subjective feeling associated with each emotion.
Dexamethasone induces rapid actin assembly in human endometrial cells without affecting its synthesis

Dexamethasone exerts a stimulatory effect of rapid‐onset on the polymerization of actin. This has been documented in human endometrial adenocarcinoma Ishikawa cells, resulting in an acute, dose‐dependent decrease in the G/total‐actin ratio. In the present study we completely characterized this fast and apparently nongenomic effect of dexamethasone on actin assembly. We followed the morphological alterations of actin cytoskeleton and measured the time‐dependent dynamics of actin polymerization both by ruling out any changes of total actin in the cells and by measuring its transcript. Rapid changes in actin polymerization were accurately measured using a highly sensitive and quantitative rhodamine‐phalloidin fluorimetric assay. Ishikawa cells, exposed to 0.1 μM dexamethasone for various time periods up to 24 h, showed a highly significant, rapid, and transient increase in the polymerization of actin starting within 15 min of dexamethasone exposure and lasting 2 h. Treated cells showed a significant (1.79‐fold) enhancement of the fluorescent signal compared to untreated cells at 15 min. This value decreased continuously in a time‐dependent manner, reaching control levels after 120 min and remained so for the next 24 h. Confocal laser scanning microscopy studies confirmed these findings. Intensive coloration of microfilaments over several scanning sections suggested an enhanced degree of actin polymerization in cells preincubated for 15 min with 0.1 μM dexamethasone. Moreover, actin filaments were more resistant to cytochalasin B. Additionally, quantitative immunoblot analysis showed that the content of total cellular actin remained the same during this period, suggesting that the biosynthesis of actin was unaffected. Northern blot analysis showed that the concentration of the actin transcript was also unaffected. Our data suggest that glucocorticoids induce a fast and self‐limited polymerization of actin in human endometrial cells without affecting its synthesis. These findings strengthen the hypothesis that glucocorticoids exert rapid, nongenomic cellular effects and that the actin‐based cytoskeleton is an integral part of this pathway, playing an essential role in receiving and mediating steroid signals for the modulation of cellular responses. J. Cell. Biochem. 65:492–500. © 1997 Wiley‐Liss Inc.
Neutrophil defensins but not interleukin‐6 in vaginal fluid after preterm premature rupture of membranes predict fetal/neonatal inflammation and infant neurological impairment

Objective. To determine whether neutrophil defensins (HNP1–3) and interleukin‐6 (IL‐6) in vaginal fluid after preterm premature rupture of membranes predict fetal inflammatory response syndrome (FIRS), neurological impairment or chorioamnionitis. Design. Prospective study. Setting. Tertiary referral university hospital. Population. Forty‐two patients with preterm premature rupture of membranes at <32 weeks. Methods. Levels of HNP1–3 and IL‐6 were measured in vaginal fluid obtained by swabs. Mann–Whitney U‐test was used to compare HNP1–3 and IL‐6 levels in groups with vs. without FIRS, infant death or neurological impairment, and chorioamnionitis (p<0.05 significant). Logistic regression was used to control for potential confounders. Diagnostic accuracies of HNP1–3 and IL‐6 were determined by receiver operator characteristics analysis. Main Outcome Measures. Fetal inflammatory response syndrome was defined as neonatal inflammation within 72hours postpartum. Neurological impairment was defined as motor and/or tone abnormalities at one year of corrected age. Chorioamnionitis was diagnosed histologically. Results. Levels of HNP1–3, but not IL‐6, were higher in 12 cases of FIRS (p=0.019 and p=0.256, respectively). Levels of HNP1–3, but not IL‐6, were higher in 14 cases of infant death or neurological impairment (p=0.015 and p=0.100, respectively) and, when only survivors were analyzed, in nine cases of neurological impairment (p=0.030 and p=0.187, respectively). Levels of HNP1–3 and IL‐6 were higher in 29 cases of chorioamnionitis (p=0.005 and p=0.003, respectively). The differences remained significant after adjustment for gestational age. Levels of HNP1–3 predicted FIRS, infant death or neurological impairment and chorioamnionitis with an area under the curve of 0.75, 0.79 and 0.78, respectively. Conclusions. Elevated vaginal fluid HNP1–3 and IL‐6 levels are associated with histological chorioamnionitis. Elevated HNP1–3 can also identify FIRS and predict infant death or neurological impairment.
Elevation change measurement of the East Antarctic Ice Sheet, 1978 to 1988, from satellite radar altimetry

Seasat and Geosat satellite radar altimeter measurements over the East Antarctic Ice Sheet (EAIS) are analyzed to determine surface elevation change over the period from 1978 to 1988. The results show that the average elevation change over 1.7 /spl times/10/sup 6/ km/sup 2/ of the EAIS is -0.4/spl plusmn/1.8 cm/yr and is therefore not significantly different than zero. This result is in very good agreement with ERS-1/2 radar altimeter estimates of EAIS elevation change from 1992 to 1996. The combined results suggest that the EAIS has been close to a state of balance for two decades. This further reduces the likelihood that recent changes in snow accumulation have masked a long-term mass imbalance in the EAIS.
Public health case studies in diabetes prevention and control: innovation, partnerships, and funding.

BACKGROUND In 2006, we conducted case studies of 4 North Carolina local health departments (LHDs) that scored highly on an index of diabetes prevention and control performance, to explore characteristics that may serve as barriers or facilitators of diabetes prevention and control services. METHODS Case studies involving in-depth interviews were conducted at 4 LHDs. Sites were selected on the basis of 2 variables, known external funding for diabetes services and population size, that were associated with performance in diabetes prevention and control in a 2005 survey of all North Carolina LHDs. Fourteen interviews (individual and group) were conducted among 17 participants from the 4 LHDs. The main outcome measures were LHD characteristics that facilitate or hinder the performance of diabetes programs and services. RESULTS Interviews revealed that all 4 high-performing LHDs had received some sort of funding from a source external to the LHD. Case study participants indicated that barriers to additional service delivery included low socioeconomic status of the population and lack of financial resources. Having a diabetes self-management education program that was recognized by the American Diabetes Association appeared to be a facilitator of diabetes services provision. Other facilitators were leadership and staff commitment, which appeared to facilitate the leveraging of partnerships and funding opportunities, leading to enhanced service delivery. LIMITATIONS The small number of LHDs participating in the study and the cross-sectional study design were limitations. CONCLUSION Leadership, staff commitment, partnership leveraging, and funding appear to be associated with LHD performance in diabetes prevention and control services. These factors should be further studied in future public health systems and services research.
Elevated Nerve Growth Factor Levels in Cerebrospinal Fluid Associated with Progressive Cortical Atrophy

Using a two-site enzyme-linked immunosorbent assay, we measured nerve growth factor (NGF) levels in cerebrospinal fluid (CSF) from 40 patients with or without brain atrophy due to various neurologic disorders. White matter and cortical atrophies were assessed by frontal horn index (FHI) and subarachnoid space area/inner skull space area (SSA/ISSA) ratio, respectively. CT findings of 40 patients were classified into 4 grades: normal (< mean + 2SD), grade I (mean + 2SD < or = or < mean + 4SD), grade II (mean + 4SD < or = < mean + 8SD), and grade III (mean + 8SD < or =). NGF levels in CSF were significantly elevated in 3 of 6 patients with grade III cortical atrophy and normal in 2 with grade II atrophy, 4 with grade I atrophy and 28 without atrophy. Cortical atrophy was progressive in the 3 with NGF elevation in CSF. With respect to white matter atrophy, NGF elevation was observed in none of 3 with grade III white matter atrophy, two of 4 with grade II atrophy, none of 3 with grade I atrophy and one of 30 without atrophy. The symptoms of the two of three with NGF elevation were progressive at the time of obtaining the CSF samples, while those of other patients without NGF elevation were non-progressive. The present study suggests that NGF elevation in CSF may reflect extensive cortical degenerative change.
Incidence, risk and prognosis of acute and chronic fatigue syndromes and psychiatric disorders after glandular fever

Background The role of viruses in the aetiology of both chronic fatigue syndrome (CFS) and depressive illness is uncertain. Method A prospective cohort study of 250 primary care patients, presenting with glandular fever or an ordinary upper respiratory tract infection (URTI). Results The incidence of an acute fatigue syndrome was 47% at onset, after glandular fever, compared with 20% with an ordinary URTI (relative risk 2.3, 95% CI 1.3–4.1). The acute fatigue syndrome lasted a median (interquartile range) of eight weeks (4–16) after glandular fever, but only three weeks (2–4) after an URTI. The prevalence of CFS was 9–22% six months after glandular fever, compared with 0–6% following an ordinary URTI, with relative risks of 2.7–5.1. The most conservative measure of the incidence of CFS was 9% after glandular fever, compared with no cases after an URTI. A conservative estimate is that glandular fever accounts for 3113 (95% C11698–4528) new cases of CFS per annum in England and Wales. New episodes of major depressive disorder were triggered by infection, especially the Epstein – Barr virus, but lasted a median of only three weeks. No psychiatric disorder was significantly more prevalent six months after onset than before. Conclusions Glandular fever is a significant risk factor for both acute and chronic fatigue syndromes. Transient new major depressive disorders occur close to onset, but are not related to any particular infection if they last more than a month.
An Unusual Cause of Cerebral Venous Thrombosis in a Four‐Year‐Old Child

Background and Purpose: Inherited protein S deficiency has been associated with an increased risk of thromboembolic disease. It is possible that such a coagulopathy could predispose children to the development of strokes by permitting clot formation in response to stimuli that ordinarily would be insufficient to cause thrombus formation. Case Description: We evaluated a previously well 4‐year‐old boy who developed cerebral venous thrombosis after suffering minor head trauma. Crossed‐immunoelectrophoresis of his plasma showed a marked decrease of the free, active form of protein S. Family studies revealed that the patient's father and other paternal relatives had a similar abnormality of protein S. Conclusions: We suggest that the cerebral venous thrombosis in this child was initially precipitated by minor head trauma and pathological thrombus formation was then potentiated by inherited protein S deficiency. This case extends the clinical spectrum for protein S deficiency and emphasizes the importance of evaluating family members to establish a specific diagnosis and therapeutic intervention. (Stroke 1993;24:603‐605)
Functional interactions between potassium and phosphate homeostasis in Saccharomyces cerevisiae

Maintenance of ion homeostatic mechanisms is essential for living cells, including the budding yeast Saccharomyces cerevisiae. Whereas the impact of changes in phosphate metabolism on metal ion homeostasis has been recently examined, the inverse effect is still largely unexplored. We show here that depletion of potassium from the medium or alteration of diverse regulatory pathways controlling potassium uptake, such as the Trk potassium transporters or the Pma1 H+‐ATPase, triggers a response that mimics that of phosphate (Pi) deprivation, exemplified by accumulation of the high‐affinity Pi transporter Pho84. This response is mediated by and requires the integrity of the PHO signaling pathway. Removal of potassium from the medium does not alter the amount of total or free intracellular Pi, but is accompanied by decreased ATP and ADP levels and rapid depletion of cellular polyphosphates. Therefore, our data do not support the notion of Pi being the major signaling molecule triggering phosphate‐starvation responses. We also observe that cells with compromised potassium uptake cannot grow under limiting Pi conditions. The link between potassium and phosphate homeostasis reported here could explain the invasive phenotype, characteristic of nutrient deprivation, observed in potassium‐deficient yeast cells.