Miracle-dz/UniFAR-FTUs huggingface dataset:
Angiotensin AT2 receptor protects against cerebral ischemia‐induced neuronal injury

Several lines of clinical and experimental evidence suggest an important role of the reninangiotensin system in ischemic brain injury although the cellular regulation of the angiotensin AT1 and AT2 receptors and their potential relevance in this condition have not yet been clearly defined. We first assessed the regulation of brain AT1 and AT2 receptors in response to transient unilateral medial cerebral artery occlusion in rats by real‐time RT‐PCR, Western blot, and immunofluorescence labeling. AT2 receptors in the peri‐infarct zone were significantly upregulated 2 days after transient focal cerebral ischemia. Increased AT2 receptors, which were abundantly distributed in a large number of brain regions adjacent to the infarct area including cerebral frontal cortex, piriform cortex, striatum, and hippocampus, were exclusively expressed in neurons. By contrast, AT1 receptors, which remained unaltered, were mainly expressed in astrocytes. In neurons of ischemic striatum, increased AT2 receptors were associated with intense neurite outgrowth. Blockade of central AT2 receptors with PD123177 abolished the neuroprotective effects of central AT1 receptor blockade with irbesartan on infarct size and neurological outcome. In primary cortical neurons, stimulation of AT2 receptors supported neuronal survival and neurite outgrowth. Our data indicate that cerebral AT2 receptors exert neuroprotective actions in response to ischemia‐induced neuronal injury, possibly by supporting neuronal survival and neurite outgrowth in peri‐ischemic brain areas.
Ultrahigh Data-Rate Transmission Using a Dense Dispersion Map With Two-Fold Periodicity

We demonstrate how intrachannel as well as interchannel nonlinear penalties can be effectively controlled and minimized through the use of dense dispersion management in combination with amplifier site compensation. When applying the ideas to a system operating at 171.2 Gb/s (160 Gb/s+7% overhead), we show that effective wavelength-division-multiplexed transmission can be achieved over more than 1000 km with conservative terrestrial system parameters and without distributed Raman amplification.
Remission of PTSD after victims of intimate partner violence leave a shelter.

Intimate partner violence (IPV) is a significant public health problem associated with high rates of posttraumatic stress disorder (PTSD). Few longitudinal studies have investigated IPV-related PTSD and we know of only 1 longitudinal study to date that has explored IPV-related PTSD in residents of battered women's shelters. The current report describes a prospective study of IPV-related PTSD in an initial sample of 147 residents of battered women's shelters. Baseline correlates of remission of IPV-related PTSD (i.e., PTSD and IPV severity, loss of personal and social resources, cessation of abuse, reunion with abuser, and length of shelter stay) over a 6-month follow-up period were investigated. Although findings are consistent with prior research suggesting a natural recovery of PTSD in IPV-victims, they also show that a significant number (46.8%) of women exhibit chronic PTSD. Participants whose PTSD remitted over follow-up had at baseline less severe IPV-related PTSD (partial η(2) = . 104) and fewer loss of personal and social resources (partial η(2) = . 095), and were less likely to reunite with their abuser after leaving the shelter than participants with chronic PTSD (3.3% and 22.4%, respectively). Clinical implications and limitations of findings are discussed.
Mody-3: novel HNF1A mutation and the utility of glucagon-like peptide (GLP)-1 receptor agonist therapy.

OBJECTIVE An estimated 1 to 2% of cases of diabetes mellitus have a monogenic basis; however, delayed diagnosis and misdiagnosis as type 1 and 2 diabetes are common. Correctly identifying the molecular basis of an individual's diabetes may significantly alter the management approach to both the patient and his or her relatives. We describe a case of mature onset diabetes of the young (MODY) with sufficient evidence to support the classification of a novel HNF1A (hepatocyte nuclear factor-1-α) mutation as a cause of MODY-3. METHODS A 21-year-old Caucasian female presented to our office with a diagnosis of noninsulin-dependent diabetes mellitus (NIDDM) at age 10; glycemia was initially managed with oral antidiabetic (OAD) agents and insulin detemir. The patient reported a strong family history of early-onset NIDDM in both her mother and maternal grandmother, both of whom eventually required insulin therapy to control glycemia. The patient's medical and family history were highly suggestive of maturity-onset diabetes of the young (MODY), and genetic testing was performed. RESULTS Genetic screening detected a mutation p. Arg200Trp in the HNF1A gene in the patient, her mother, and maternal grandmother, suggesting a diagnosis of MODY-3. This finding resulted in a change of antidiabetic therapy in all 3 patients, including the addition of once-daily liraglutide therapy, which helped improve their glycemic control. CONCLUSION Our case report supports the classification of the p. Arg200Trp mutation as a cause of MODY-3. The findings also suggest that glucagon-like peptide-1 (GLP-1) receptor agonist therapy may be of value in managing glycemia in patients with MODY-3.
Morphology of novel XLPE cable systems

Crosslinked polyethylene (XLPE) insulated cables are used widely for the transmission and distribution of electrical power. Although XLPE has many desirable characteristics, the addition of other polymers constitutes one way in which properties can be modified to suit particular applications. This paper describes a modified permanganic etching technique that has been optimized to permit the study of such systems by transmission electron microscopy. The approach is then applied to a range of triple-extruded (semicon/insulation/semicon) XLPE-based cables that exhibit both one and two-phase microstructures. The morphologies seen are described and the origin of preferential lamellar growth perpendicular to the semicon/insulation interface is explored. It is also shown that the apparent presence of carbon black particles well away from the dielectric interface is an artifact associated with sample preparation.
Biomechanical Comparison of Instrumented Posterior Lumbar Interbody Fusion With One or Two Cages by Finite Element Analysis

Study Design. Using finite element models to study the biomechanics of lumbar instrumented posterior lumbar interbody fusion (PLIF) with one or two cages. Objective. Analyzing the biomechanics of instrumented PLIF with one or two cages as to evaluate whether a single cage is adequate for instrumented PLIF. Summary of Background Data. Implantation of a single cage in instrumented PLIF of lumbar spine is still controversial. Methods. Three validated finite element models of L3–L5 lumbar segment were established [intact model (INT), one cage model (LS-1), and two cages model (LS-2)]. The available finite element program ANSYS 6.0 (Swanson Analysis System Inc., Houston, TX) was applied. To analyze the biomechanics of these models, 10 Nm flexion, extension, rotation, and lateral bending moment with 150 N of preload were respectively imposed on the superior surfaces of the L3. Results. Compared with the INT model, the decrease of ROM in the LS-1 and LS-2 models were exaggerated from 0.67° to 3.73° and ranged from 37.2% to 86.1% in all motions. The mean subsidence was found to be slightly higher in the LS-1 model. Most of the cage dislodgement in both models was less than 0.03 mm. The mean dislodgement was slightly higher in the LS-1 model. The stress of cage was found to be high in the LS-2 model. The mean stress of screw was raised to 4.5% to 9.7% in the LS-1, which was higher than that in the LS-2 model. In general, stress of adjacent disc was more pronounced in the LS-2 model. The most stress distributed at the anterior portion of the adjacent disc, which could be used to interpret the clinical findings of the early adjacent disc degeneration. Conclusions. A single cage inserted in an instrumented PLIF gains approximate biomechanical stability, slight greater subsidence, and a slight increase in screw stress but less early degeneration in adjacent disc. Adjusting these factors, instrumented PLIF with one cage could be encouraged in clinical practice.
Association of Interleukin 13 +2044G/A Polymorphism with Bronchial Asthma Development, Severity and Immunoglobulin E levels in an Egyptian Population

Background: Asthma is a chronic, inflammatory disease of the respiratory tract, which is characterized by bronchial hyperreactivity and respiratory obstruction in which many cells and cellular elements play a role. Interleukin 13 (IL-13) is a type 2 helper T cells (Th2) cytokine that has been shown to be pivotal in the induction of allergic inflammation of the airways. Moreover, Several IL-13 genetic polymorphisms have been linked with susceptibility to bronchial asthma. Aim: The aim of this study was to evaluate the association of IL-13 + 2044G/A polymorphism with bronchial asthma development, severity and total serum immunoglobulin E (IgE) levels in Egyptian patients with bronchial asthma. Subjects and methods: This study included 50 asthmatic patients and 30 controls. Restriction Fragment Length Polymorphism (RFLP) PCR was used for the analysis of the studied polymorphism. Also, the serum was analyzed for total IgE levels by enzyme-linked immunosorbent assay (ELISA). Results: The frequency of the A allele was significantly higher in asthmatic patients as compared to control subjects. On the contrary, the G allele was less frequent in the asthmatic patients as compared to control subjects. In addition the A allele was more frequent in severe asthmatic patients and on the other hand the G allele was less frequent in severe asthmatic patients. Moreover, the presence of the A allele was significantly associated with higher total serum IgE levels whether in homozygous or heterozygous state. Conclusions: The results showed that the IL-13 +2044 A allele is a risk factor for bronchial asthma. There is a significant association between the A allele and more severe asthma, however the G allele is significantly associated with less severe asthma. In addition, the A allele is significantly associated with higher total serum IgE levels.
Dual Psychiatric Diagnosis and Substance Abuse in Pathological Gamblers

Abstract Background: Pathological Gambling (PG) is a highly prevalent and disabling impulse control disorder. Recent studies have consistently shown that PG patients have responded well to treatment with SSRIs, mood stabilizers, and opioid antagonists. These findings have supported the observation that PG is strongly associated with both mood and anxiety disorders as well as substance abuse. The aim of the study is to evaluate the comorbid psychiatric diagnoses in our sample of pathological gamblers. Methods: Thirty-six female, and forty-two male PGs were enrolled in our study. A comprehensive psychiatric diagnostic evaluation was performed on all patients, and patients were screened for symptoms of depression and anxiety using the Hamilton Depression Rating Scale, the Hamilton Anxiety Rating Scale, the Yale-Brown Obsessive Compulsive Scale, and the Frost Multidimensional Perfectionism Scale. In addition, the patients completed self-report questionnaires about their demographic status and substance abuse. Results: The majority of patients were married with full or part-time employment. The study results demonstrated that PG in males is correlated with substance and alcohol abuse. Diagnoses which were prevalent among our cohort of female PGs included major depression, affective disorders, anxiety disorders, and eating disorders. Conclusion: In our sample of PGs, the men and women had different patterns of psychiatric comorbidity. The different patterns of psychiatric comorbidity seen in our male versus female PGs raises the question of whether the underlying etiopathology in PG may differ according to gender.
BRCA1 Downregulation Leads to Premature Inactivation of Spindle Checkpoint and Confers Paclitaxel Resistance

BRCA1 germline mutations predispose women to early onset, familial breast and ovariancancer. BRCA1 has been recently implicated in the cellular response to agents that disruptthe mitotic spindle. In this report, we studied BRCA1 contribution to paclitaxel response inMCF-7 breast cancer cells. We show that MCF-7 cells transfected with BRCA1 siRNAdisplay a significant increase in resistance to paclitaxel compared with the control cells. Wenext demonstrate that down-regulation of BRCA1 reduces the mitotic index and triggerspremature cyclin B1 degradation and decrease in Cdk1 activity following paclitaxel treatment,suggesting that BRCA1 down-regulation results in precocious inactivation of the spindlecheckpoint. These findings were confirmed by showing that BRCA1 down-regulation inducespremature sister–chromatids separation in MCF-7 cells following spindle damage.Furthermore, we show that BRCA1 up-regulates the expression of the protein kinase BubR1,essential component of the functional spindle checkpoint, whose down-regulation is known toresult in paclitaxel resistance in MCF-7 cells. Altogether, our findings support the notion thatdown-regulation of BRCA1 expression mediates paclitaxel resistance through prematureinactivation of spindle checkpoint in MCF-7 breast cancer cells. They link BRCA1 to themitotic checkpoint that plays an essential role in the maintenance of chromosomal stability.
N-acetylcysteine administration confers lung protection in different phases of lung ischaemia-reperfusion injury.

OBJECTIVES To verify the effects of N-acetylcysteine (NAC) administered before and after ischaemia in an animal model of lung ischaemia-reperfusion (IR) injury. METHODS Twenty-four Wistar rats were subjected to an experimental model of selective left pulmonary hilar clamping for 45 min followed by 2 h of reperfusion. The animals were divided into four groups: control group (SHAM), ischaemia-reperfusion, N-acetylcysteine-preischaemia (NAC-Pre) and NAC-postischaemia (NAC-Post). We recorded the haemodynamic parameters, blood gas analysis and histology. We measured the thiobarbituric acid reactive substances concentration; the expression of superoxide dismutase (SOD), inducible nitric oxide synthase (iNOS), nitrotyrosine, cleaved caspase 3, nuclear factor κB (NF-κB), NF-kappa-B inhibitor alpha (IκB-α), tumour necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β); myeloperoxidase activity (MPO). RESULTS No significant differences were observed in the haemodynamic parameters, blood gas analysis and SOD activity among the groups. Lipid peroxidation was significantly higher in the IR and NAC-Pre groups (P < 0.01). The expression of nitrotyrosine, cleaved caspase 3, NF-κB, IκB-α, TNF-α and IL-1β were significantly higher in the IR group when compared with the SHAM and NAC groups (P < 0.01). The NAC-Pre group showed a significantly higher expression of these proteins when compared with the SHAM and NAC-Post groups (P < 0.05). After reperfusion, the expression of iNOS increased almost uniformly in all groups when compared with the SHAM group (P < 0.01). The histological analysis showed fewer inflammatory cells in the NAC groups. CONCLUSIONS The intravenous administration of NAC demonstrated protective properties against lung IR injury. The use of NAC immediately after reperfusion potentiates its protective effects.
Understanding Noncompetition Agreements: The 2014 Noncompete Survey Project

In recent years, scholars and policymakers have devoted considerable attention to the potential consequences of employment noncompetition agreements and to whether legislatures ought to reform the laws that govern the enforcement of these controversial contractual provisions. Unfortunately, much of this interest — and the content of proposed reforms — derives from anecdotal tales of burdensome noncompetes among low-wage workers and from scholarship that is either limited to slivers of the population (across all studies, less than 1%) or relies on strong assumptions about the incidence of noncompetition agreements. Better understanding of the use of noncompetes and effective noncompetition law reform requires a more complete picture of the frequency and distribution of noncompetes at the individual employee level. Accordingly, in 2014, we administered a nationwide survey of individuals in the labor force to ask them about their employment status, history, and future expectations — including their experience with and understanding of noncompetition agreements. In this Article, we describe the methods we used to carry out this survey and refine the data for analysis in hopes of encouraging other researchers to use survey approaches to fill other, similarly important gaps in our knowledge. To illustrate the value of the survey project, we present a surprising empirical finding from our data, one that raises questions about existing scholarship and theories about why employers use noncompetes: We find little evidence that the incidence of noncompetition agreements in a state (after controlling for potentially confounding factors) has any relationship to the level of enforcement of such agreements in that state. In other words, an employee in California (where noncompetes are prohibited) appears to be just as likely to labor under a noncompete as an employee in Florida (where noncompetes are much more likely to be enforced).
Genetic Screen Yields Mutations in Genes Encoding All Known Components of the Escherichia coli Signal Recognition Particle Pathway

ABSTRACT We describe the further utilization of a genetic screen that identifies mutations defective in the assembly of proteins into the Escherichia coli cytoplasmic membrane. The screen yielded mutations in each of the known genes encoding components of the E. coli signal recognition particle pathway: ffh, ffs, and ftsY, which encode Ffh, 4.5S RNA, and FtsY, respectively. In addition, the screen yielded mutations in secM, which is involved in regulating levels of the SecA component of the bacterium’s protein export pathway. We used a sensitive assay involving biotinylation to show that all of the mutations caused defects in the membrane insertions of three topologically distinct membrane proteins, AcrB, MalF, and FtsQ. Among the mutations that resulted in membrane protein insertion defects, only the secM mutations also showed defects in the translocation of proteins into the E. coli periplasm. Genetic evidence suggests that the S382T alteration of Ffh affects the interaction between Ffh and 4.5S RNA.
Increased osteocyte death and mineralization inside bone after parathyroidectomy in patients with secondary hyperparathyroidism

In order to gain insight into the mechanisms underlying the dynamic changes in bone metabolism and bone quality after parathyroidectomy (PTX) in secondary hyperparathyroid patients with high levels of parathyroid hormone (PTH), we performed bone histomorphometric analysis with tetracycline labeling in iliac bone biopsy specimens taken before and after PTX, with special attention paid to osteocytes. At 2 to 4 weeks after PTX, PTH concentrations decreased markedly with evident reductions in bone turnover markers. Histomorphometry revealed that at 2 to 4 weeks following PTX, the osteoclast surface decreased to nearly 0%, with a substantial increase in osteoid volume and a reduction in fibrosis volume. Labeling with tetracycline was observed not only at the mineralization front on the bone surface but also around the osteocyte lacunar walls and canaliculi within both the basic multicellular units (BMUs) and bone structural units (BSUs), suggesting that mineralization was taking place along the lacunocanalicular system after PTX. The tetracycline‐labeled area was much greater in the BSUs than in the BMUs and at the mineralization front, and the tetracycline labeling in the BSUs was markedly increased after PTX compared with that in the low‐ and high‐PTH control groups without PTX. The osteocyte number was decreased significantly after PTX, concomitant with an increase in the number of empty lacunae and a reduction of lacunar volume. Thus the increased osteocyte death and mineralization around the lacunocanalicular system in association with a rapid decline in PTH may underlie the changes in bone metabolism and quality that occur following PTX. © 2010 American Society for Bone and Mineral Research.
Stem Cell Research, Regulatory Regimes, and the "Calculus of Consent" in the European Union: A Test of Three Hypotheses

What factors affect the decisions of Europeans either to support or oppose the development of human embryonic stem cell (hESC) research? This study tests the validity of three major hypotheses from the biotechnology literature that have significant implications for the strategies and tactics of regulatory agencies: the “risk assessment discourse,” “institutional context,” and “information” hypotheses. Ordered logit analysis of the responses of Europeans to a 2005 Eurobarometer survey on biotechnology supports and refines the risk assessment discourse hypothesis: respondents reporting higher levels of religiosity (more so than denomination) were a key determinant of European attitudes, and concern for the moral status of the fetus was even more powerful. It also offers support for the institutional context hypothesis: respondents with greater trust in the European Union and national hESC regulatory systems reported greater support for hESC research. Untangling the information hypothesis, analysis suggests Europeans who value the more cognitively driven print media over the less in-depth and more emotion-inspiring electronic media (TV and radio) as a source for their information offer substantially more support for hESC research. Analysis also indicates that Europeans who are more interested in politics, as well as the more highly educated (both indicators of “chronic” information”), are for the most part more supportive of research, while those who report that they “keep up-to-date” on biotechnology (“domain-specific” information) are strongly supportive of hESC research. Nevertheless, those who are objectively more knowledgeable about the subject actually exhibit less consistency in their support. The implications of these findings are significant for biotechnology regulatory agencies and theory building in Europe and beyond.
Epstein-Barr virus antibodies and vitamin D in prospective multiple sclerosis biobank samples

Background: The antibody reactivity against Epstein-Barr nuclear antigen-1 (EBNA-1), and 25-hydroxyvitamin D (25(OH)D) status have been associated with multiple sclerosis (MS) risk. Interaction between these two factors has been proposed. Objectives: The objective of this paper is to examine the association between antibody reactivity against EBNA-1 and five EBNA-1 domains, and the risk of MS, and to examine if these antibodies and 25(OH)D status interact regarding MS risk in prospectively collected blood samples. Methods: Antibody reactivity and 25(OH)D levels were measured using ELISAs in n = 192 MS cases and n = 384 matched controls. The risk of MS was analysed using matched logistic regression. Interaction on the additive scale was assessed. Results: The risk of MS increased across tertiles of antibody reactivity against EBNA-1, domain EBNA-1402–502, and domain EBNA-1385–420; p trends < 0.001. In young individuals (below median age at sampling, < 26.4 years), these associations were stronger, and 25(OH)D levels correlated inversely to antibody reactivity against EBNA-1 and the EBNA-1 domains. No statistical interaction was found. Conclusions: We confirm that increased antibody reactivity against EBNA-1 is a risk factor of MS. 25(OH)D status might influence the immune response towards Epstein-Barr virus in young subjects, and thereby modulate MS risk.