Miracle-dz/UniFAR-FTUs huggingface dataset:
Newly generated granule cells show rapid neuroplastic changes in the adult rat dentate gyrus during the first five days following pilocarpine‐induced seizures

Long‐term neuroplastic changes to dentate granule cells have been reported after seizures and were shown to contribute to recurrent excitatory circuitry. These changes include increased numbers of newborn granule cells, sprouted mossy fibers, granule cell layer dispersion, increased hilar ectopic granule cells and formation of hilar basal dendrites on granule cells. The goal of the current study was to determine the acute progression of neuroplastic changes involving newly generated granule cells after pilocarpine‐induced seizures. Doublecortin (DCX) immunocytochemical preparations were used to examine the newly generated granule cells 1–5 days after seizures were induced. The results showed that there are rapid neuroplastic changes to the DCX‐labeled cells. At 1 day after seizures were induced, there were significant increases in the percentage of DCX‐labeled cells with hilar basal dendrites and in the progenitor cell population. At 2 days after seizures were induced, an increase in the thickness of the layer of DCX‐labeled cells occurred. At 3 days after seizures were induced, the number of DCX‐labeled cells was significantly increased. At 4 days after seizures were induced, developing synapses were observed on DCX‐labeled hilar basal dendrites. Thus, newly generated granule cells in the adult dentate gyrus display neuroplastic changes by 1 day after pilocarpine‐induced seizures and further changes occur to this population of cells in the subsequent 4 days. The presence of synapses, albeit developing ones, on hilar basal dendrites during this period indicates that newly generated granule cells become rapidly incorporated into dentate gyrus circuitry following seizures.
The Fiscal Austerity and Urban Innovation Project

niger, Richard Berk, Judith Blake, Ronald Burt, Stephen Cutler, Greg Duncan, Robert Groves, Herbert Hyman, Norval Glenn, Karen Mason, John Mueller, Stanley Presser, John Robinson, Peter Rossi (former Chair), James Short, Seymour Sudman, and Stephen Withey. The General Social Survey seeks proposals for future topical modules, as well as smaller proposals seeking to improve the measurement of relevant social phenomena. For a detailed statement describing the guidelines for the development of such proposals, interested readers should write to Duane F. Alwin, Chair, GSS Board of Overseers, Survey Research Center, Institute for Social Research, University of Michigan, Ann Arbor, Ml 481061248.
Antigenic characterization of fimbria preparations from Streptococcus mutans isolates from caries-free and caries-susceptible subjects

The adhesion of pathogenic bacteria to the host surface is an essential step in the development of numerous infections, including dental caries. Attachment of Streptococcus mutans, the main etiological agent of human dental caries, to the tooth surface may be mediated by glucan synthesized by glucosyltransferase (GTF) and by cell surface proteins, such as P1, which bind to salivary receptors. Fimbriae on the surfaces of many microorganisms are known to function in bacterial adhesion. Previous studies in this laboratory have initially characterized the fibrillar surface of S. mutans. The purpose of this investigation was the comparison of the antigenic properties of fimbria preparations of S. mutans isolates from five caries-resistant (CR) and six caries-susceptible (CS) subjects. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis of S. mutans fimbrial preparations revealed five major protein bands at 200, 175, 157, 86, and 66 kDa in preparations from CR and CS subjects. Immunoblot analysis indicated the presence of the same major bands recognized by anti-S. mutans fimbria antisera. Furthermore, the 175- and 157-kDa bands were recognized by antibodies to P1 and GTF, respectively. Immunoblot analysis with antisera to the fimbria preparation, to P1, or to GTF indicated that the levels of fimbria-reactive components and P1 and GTF antigens were higher in S. mutans fimbria preparations from CS subjects than in those from CR individuals. For example, four of six fimbria preparations from CS patients had demonstrable P1, and all had GTF. In contrast, only two of five CR fimbrial preparations exhibited P1 and GTF. Enzyme-linked immunosorbent assay demonstrated similar results for levels of GTF antigen in the fimbrial preparations from CR and CS subjects. The results suggest that differences between the compositions of S. mutans fimbriae in CR and CS individuals may play an important role in the virulence of this microorganism in dental caries.
Abdominal Wall Transplantation: Skin as a Sentinel Marker for Rejection

Abdominal wall transplantation (AWTX) has revolutionized difficult abdominal closure after intestinal transplantation (ITX). More important, the skin of the transplanted abdominal wall (AW) may serve as an immunological tool for differential diagnosis of bowel dysfunction after transplant. Between August 2008 and October 2014, 29 small bowel transplantations were performed in 28 patients (16 male, 12 female; aged 41 ± 13 years). Two groups were identified: the solid organ transplant (SOT) group (n = 15; 12 ITX and 3 modified multivisceral transplantation [MMVTX]) and the SOT‐AWTX group (n = 14; 12 ITX and 2 MMVTX), with the latter including one ITX‐AWTX retransplantation. Two doses of alemtuzumab were used for induction (30 mg, 6 and 24 h after reperfusion), and tacrolimus (trough levels 8–12 ng/mL) was used for maintenance immunosuppression. Patient survival was similar in both groups (67% vs. 61%); however, the SOT‐AWTX group showed faster posttransplant recovery, better intestinal graft survival (79% vs. 60%), a lower intestinal rejection rate (7% vs. 27%) and a lower rate of misdiagnoses in which viral infection was mistaken and treated as rejection (14% vs. 33%). The skin component of the AW may serve as an immune modulator and sentinel marker for immunological activity in the host. This can be a vital tool for timely prevention of intestinal graft rejection and, more important, avoidance of overimmunosuppression in cases of bowel dysfunction not related to graft rejection.
An Analysis of Ritual Co-Parenthood (Compadrazgo)

A S ANTHROPOLOGISTS have been drawn into the study of Latin American cultures, they have gathered increasing amounts of material on the characteristic ultural mechanisms of compadrazgo. This term designates the particular complex of relationships set up between individuals primarily, though not always, through participation in the ritual of Catholic baptism. This rite involves, among its various aspects, three individuals or groups of individuals. These are: first, an initiate, usually a child; secondly, the parents of the initiate; third, the ceremonial sponsor or sponsors of the initiate. It thus involves three sets of relationships. The first links parents and child, and is set up within the confines of the immediate biological family. The second links the child and his ceremonial sponsor, a person outside the limits of his immediate biological family. This relation is familiar to most Americans as the relation between godfather or godmother and godchild. The third set of relationships links the parents of the child to the child's ceremonial sponsors. In Spanish, these call each other compadres (Latin compater-commater, Spanish compadre-comadre, Italian com-
Does Development Aid Lead to Economic Freedom

For more than 50 years individual countries and international agencies have given aid to third world countries to promote economic development, yet poverty still persists in many recipient nations. In recent years development economists and agencies have increasingly recognized the importance of institutions that support property rights and economic freedom in promoting development. Nevertheless, nations continue to provide aid to less developed countries. This raises two important questions. Does the receipt of aid lead to increases or decreases in economic freedom, and are increases in economic freedom rewarded with more aid or punished with reduced aid? The failure of aid to directly promote development in impoverished countries is well documented. Boone (1996), Vasquez (1998), Easterly and Levine (2001), and Ovaska (2003) all find that development aid fails to systematically improve growth rates. Easterly (2001) summarizes World Bank aid policies that have failed to promote development. Although aid has generally failed to promote development, Burnside and Dollar (2000) argue that aid can be effective if the correct policy environment is in place. This leads us to examine
DOXORUBICINOL, THE METABOLITE OF DOXORUBUCIN, IS MORE CARDIOTOXIC THAN DOXORUBICIN

The clinical utility of the cancer chemotherapeutic agent doxorubicin (DOX) is limited by its cardiotoxicity. Doxorubicinol (DOXol), the major biometabolite of DOX, preferentially accumulates in heart during chronic DOX administration. We now find that DOXol is cardioactive, increasing resting stress in isometrically contracting papillary muscles isolated from rabbit heart. Values in the table were measured after the addition of 50 ug/ml of DOXol or DOX and expressed as the percent (X ± SE) of pretreatment control values.An increase in resting stress indicates failure of myofibrils to relax and may be related to intracellular calcium ([Ca]i). The table also shows that the greater potency of DOXol, relative to DOX, to increase resting stress correlates with DOXol's greater potency to inhibit, in-vitro, two major determinants of resting [Ca]i, isotopic Na/Ca exchange rate of membrane vesicles enriched in sarcolemma (SL) and Ca pump activity of membrane vesicles enriched in sarcoplasmic reticulum (SR). Thus we speculate that the abnormalities in myocardial relaxation noted in the chronic cardiotoxicity of DOX may be related to the effects of DOXol on membrane regulation of [Ca]i.
The yield of universal antibody to hepatitis B core antigen donor screening in the Netherlands, a hepatitis B virus low‐endemic country

In the Netherlands, universal antibody to hepatitis B core antigen (anti‐HBc) donor screening was introduced in July 2011 to intercept potentially infectious donations slipping through hepatitis B surface antigen (HBsAg) and hepatitis B virus (HBV) DNA minipool screening (HBV DNA MP6).
A review of traditional and contemporary assays for direct and indirect detection of Equid herpesvirus 1 in clinical samples

Equid herpesvirus 1 (EHV-1) is one of the most economically important equine viral pathogens. Its clinical manifestations in horses vary from acute upper respiratory tract disease, abortion, or neonatal death, to neurological disease termed equine herpesviral myeloencephalopathy, which may lead to paralysis and a fatal outcome. Successful identification of EHV-1 infection in horses depends on a variety of factors such as suitable case selection with emphasis on timing of sample collection, selection of appropriate sample(s) based on the clinical manifestations, application of relevant diagnostic technique(s) and/or test(s), and careful evaluation and interpretation of laboratory results. Several traditional serologic and virus isolation assays have been described; however, these assays have inherent limitations that prevent rapid and reliable detection of EHV-1. The advent of molecular biologic techniques has revolutionized the diagnosis of infectious diseases in humans and animal species. Specifically, polymerase chain reaction (PCR)–based assays have allowed detection of nucleic acid in clinical specimens precisely and rapidly as compared to the traditional methods that detect the agent or antigen, or agent-specific antibodies in serum. The new molecular methods, especially real-time PCR, can be a very useful means of EHV-1 detection and identification. Veterinarians involved in equine practice must be aware of the advantages and disadvantages of various real-time PCR assays, interpretation of viral genetic marker(s), and latency in order to provide the best standard of care for their equine patients.
Inhibition of p53 Transactivation Function by the Human T-Cell Lymphotropic Virus Type 1 Tax Protein

ABSTRACT Human T-cell lymphotropic virus type 1 (HTLV-1) is the etiologic agent for adult T-cell leukemia. HTLV-1 transforms lymphocytes, and there is increasing evidence that the virus-encoded protein, Tax, plays a primary role in viral transformation. We have shown that wild-type p53 in HTLV-1-transformed cells is stabilized. This study was initiated to directly analyze whether the p53 in HTLV-1-transformed cell lines was transcriptionally active and to identify the viral gene product responsible for stabilization and inactivation. Transfection experiments using a p53-responsive reporter plasmid and γ-irradiation studies demonstrate that the wild-type p53 in HTLV-1-transformed cell lines is not fully active. Further, we demonstrate that the HTLV-1-transforming protein, Tax, stabilizes and inactivates p53 function. Cotransfection of Tax with p53 results in a greater than 10-fold reduction in p53 transcription activity. Using Gal4-p53 fusion proteins, we demonstrate that Tax inhibition of p53 transactivation function is independent of sequence-specific DNA binding. Moreover, Tax inhibits p53 function by interfering with the activity of the N-terminal activation domain (amino acids 1 to 52). We conclude that Tax is involved in the inactivation of p53 function and stabilization of p53 in HTLV-1-infected cells. The functional interference of p53 function by Tax may be important for transformation and leukemogenesis.
Carotid intima–media thickness in coronary slow flow: relationship with plasma homocysteine levels

Background and objectiveCoronary slow-flow phenomenon is characterized by delayed opacification of coronary vessels in a normal coronary angiogram. Although clinical and pathological features have been previously described, the underlying pathophysiology has not been fully elucidated. Thus, it still remains to be determined whether either microvascular or epicardial diffuse atherosclerotic disease is related to slow flow. In this study, we aimed to determine the carotid artery intima–media thickness, which is a marker of atherosclerosis in patients with coronary slow flow, and its possible relationship with the total homocysteine level. MethodThe study population consisted of 88 patients who underwent coronary angiography because of typical and quasi-typical symptoms of angina. Forty-four patients with angiographically proven coronary slow flow and 44 individuals with normal coronary flow pattern with similar risk profiles were enrolled in the study. Coronary flow patterns of the latter were determined by the thrombolysis in myocardial infarction frame count method. Intima–media thickness was measured by recording ultrasonographic images of both the left and the right common carotid artery with a 12-MHz linear array transducer. Plasma homocysteine, folate and B12 levels were measured from blood samples. ResultsPlasma homocysteine levels (μmol/l) and carotid intima–media thickness (mm) of patients with coronary slow flow were found to be significantly higher than that of controls (12.4±4.9 vs. 8.5±2.8, P=0.0001; 0.75±0.08 vs. 0.69±0.06, P=0.0001, respectively). The plasma folate level (ng/ml) was lower in coronary slow-flow patients than in controls (13.8±4.4 vs. 16.5±5.6, P=0.014). The plasma homocysteine level was significantly positively correlated with the mean thrombolysis in myocardial infarction frame count and intima–media thickness of the carotid artery in correlation analysis (r=0.58, P=0.0001; r=0.41, P=0.0001; respectively). ConclusionHomocysteine levels and carotid intima–media thickness increased but folate levels decreased in patients with coronary slow flow. The present findings allow us to conclude that the possible disturbance in the metabolism of homocysteine in patients with coronary slow flow may have a role in the etiopathogenesis of this phenomenon by causing generalized atherosclerosis.
The bundlin pilin protein of enteropathogenic Escherichia coli is an N‐acetyllactosamine‐specific lectin

Synthetic N‐acetyllactosamine (LacNAc) glycoside sequences coupled to BSA competitively inhibit enteropathogenic Escherichia coli (EPEC) localized adherence (LA) to human intestinal biopsy specimens and tissue culture cell monolayers. The LacNAc‐specific adhesin appears to be associated with the bundle‐forming pili (BFP) expressed by EPEC during the early stages of colonization. Herein, we report that recombinant bundlin inhibits EPEC LA to HEp‐2 cells and binds to HEp‐2 cells. Recombinant bundlin also binds, with millimolar association constants (Kassoc), to synthetic LacNAc‐Benzene and LacNAc‐O(CH2)8CONH2 glycosides as assessed in the gas phase by nanoelectrospray ionization mass spectrometry. Furthermore, LacNAc‐BSA inhibits LA only of EPEC strains that express α bundlin alleles, suggesting putative locations for the LacNAc‐binding pocket in the α bundlin monomer. Collectively, these results suggest that α bundlin possesses lectin‐like properties that are responsible for LacNAc‐specific initial adherence of α bundlin‐expressing EPEC strains to host intestinal epithelial cells.
Traditional resuscitative practices fail to resolve metabolic acidosis in morbidly obese patients after severe blunt trauma.

BACKGROUND Obesity is a risk factor for postinjury complications; in particular, obese patients develop multiple organ failure (MOF) at a greater rate than do normal weight counterparts. Evaluation of differences in resuscitative practices altered by body mass index (BMI) might provide an explanation for the increased risk of MOF seen in these high-risk patients. METHODS We used prospectively collected multicenter data to retrospectively compare patients grouped by BMI with regard to resuscitation volumes and traditional end points during the first 48 hours after injury. Marshall MOF score was used as the primary outcome measure. RESULTS One thousand sixty-six patients were analyzed, with 877 meeting inclusion and exclusion criteria. All patients received similar volumes of resuscitation per kilogram lean and ideal body weight. Morbidly obese patients attained greater central venous pressures but otherwise differed little in attainment of standard cardiovascular end points. Despite this, morbidly obese patients resolved base deficit more slowly and remained in metabolic acidosis for 48 hours postinjury. Morbidly obese patients with persistent metabolic acidosis developed MOF at a significantly greater rate than did normal weight patients with or without persistent metabolic acidosis. CONCLUSIONS Morbidly obese trauma patients show prolonged metabolic acidosis despite receiving similar volumes and attaining similar end points of resuscitation when compared with patients in other BMI groups. Inadequate resuscitation based on inaccurate end points and metabolic disturbances associated with increased BMI are likely responsible; identification of the etiology, sources, and consequences of this acidosis may provide further insight into the susceptibility of the morbidly obese patient to develop postinjury organ failure.
Mortality Salience and Positive Affect Influence Adolescents' Attitudes Toward Peers with Physical Disabilities: Terror Management and Broaden and Build Theories

Attitudes toward teenagers with and without physical disabilities, and their social acceptance, were examined from the perspective of terror management theory and the broaden and build theory. Participants (n = 390, aged 13–17) were divided into 3 experimental conditions: positive emotions, mortality salience, and control. Then, they were shown either a picture depicting an adolescent sitting on a regular chair or in a wheelchair and were asked to assess the characteristics of the person in the picture and their willingness to be in his or her company. The findings suggest that both types of manipulations enhanced the personality assessment and social acceptance of adolescents with disabilities compared to adolescents without disabilities and compared to the control condition. Girls reported more favorable attitudes toward another adolescent than boys did. The study indicates that seemingly contradictory manipulations may lead to social acceptance of adolescents with disabilities.
Gait Speed in Relation to Categories of Functional Ambulation After Spinal Cord Injury

Objective. The aim of the present study was to assess gait speeds that distinguished between levels of functional ambulation in subjects with a spinal cord injury. Methods. The data of 886 spinal cord injury subjects were derived from the European Multicenter Study for Human Spinal Cord Injury and analyzed at 1, 3, 6, and 12 months after injury. The indoor and outdoor mobility items from the Spinal Cord Independence Measure were combined into 5 clinically relevant categories: (1) wheelchair-dependent, (2) supervised walker with outdoor wheelchair dependency, (3) indoor walker with outdoor wheelchair dependency, (4) walker with aid, and (5) walker without aid. The preferred walking speed that distinguished between ambulation categories was derived from the 10-meter walking test and determined using receiver operating characteristic curves. Results. The walking speed correlated well (>0.84) with the ambulation categories. The average walking speed for each category was (1) 0.01 m/s, (2) 0.34 m/s, (3) 0.57 m/s, (4) 0.88 m/s, and (5) 1.46 m/s. The average (± SD) speed that distinguished between the categories was 0.09 ± 0.01 m/s (1 vs 2), 0.15 ± 0.08 m/s (2 vs 3), 0.44 ± 0.14 m/s (3 vs 4), and 0.70 ± 0.13 m/s (4 vs 5). The averaged sensitivity and specificity were above 0.98 and 0.94, respectively. Conclusion. In subjects with spinal cord injury, the preferred walking speed as assessed in the clinic can be used to estimate functional ambulation during daily life. The walking speed can distinguish between ambulation categories with high sensitivity and specificity.
Conditional Coalescent Trees With Two Mutation Rates and Their Application to Genomic Instability

Humans have invested several genes in DNA repair and fidelity replication. To account for the disparity between the rarity of mutations in normal cells and the large number of mutations present in cancer, an hypothesis is that cancer cells must exhibit a mutator phenotype (genomic instability) during tumor progression, with the initiation of abnormal mutation rates caused by the loss of mismatch repair. In this study we introduce a stochastic model of mutation in tumor cells with the aim of estimating the amount of genomic instability due to the alteration of DNA repair genes. Our approach took into account the difficulties generated by sampling within tumoral clones and the fact that these clones must be difficult to isolate. We provide corrections to two classical statistics to obtain unbiased estimators of the raised mutation rate, and we show that large statistical errors may be associated with such estimators. The power of these new statistics to reject genomic instability is assessed and proved to increase with the intensity of mutation rates. In addition, we show that genomic instability cannot be detected unless the raised mutation rates exceed the normal rates by a factor of at least 1000.