Miracle-dz/UniFAR-FTUs huggingface dataset:
Oil Price Collapse and Firm Leverage in Resource-Dependent Countries

This study examines the financial channel between oil price volatility and the resource curse using firm-level data. A collapse in oil prices adversely affects firm borrowing in resource-dependent countries. However, unlike in non-resource-dependent countries where just the resource sector is harmed, both resource and non-resource firms are affected in resource-dependent countries in an oil price collapse. We also find evidence of a flight to quality in lending, implying that the decline in leverage can partly be attributed to a reduction in the credit supply. Our results suggest that oil price volatility operates via the financial channel to impede economic diversification in resource-dependent countries.
The Influence of Charter School Competition on Public School District Revenues across the U.S.

abstract:Since Minnesota passed the first charter school law in 1991, charter schools have become one of the most prominent school reforms in the U.S. While charter schools educate a small portion of public school enrollments, their existence has prompted various responses from traditional public school (TPS) districts. This paper explores education finance implications for charter schools and their encompassing TPS districts. Using a dataset comprised of U.S. TPS districts over seventeen years, I examine the average TPS district's revenue response to the establishment of a charter school. Using geographic information system software to map charter school locations, I estimate the TPS district's revenue response to various measures of charter school competition. Results from the estimation suggest that as a charter school moved closer to the TPS district, revenues from local and state sources decreased. The effect size of charter school competition was marginal, however, and may reflect the variation in policy environments across states.
DOES TUBERCULOSIS AFTER KIDNEY TRANSPLANTATION FOLLOW THE TREND OF TUBERCULOSIS IN GENERAL POPULATION?

Despite improvement in graft survival, infection continues to be an important cause of morbidity and mortality after kidney transplantation. We analyzed the clinical courses and outcomes of 16 transplanted patients with positive cultures for mycobacterium tuberculosis. In the course of a 20 year period, there were 13 cases of tuberculosis registered that developed in 456 patients who underwent kidney transplantation in our department, and in three refugees transplanted in other centers (a prevalence of 3.13%). Five of them developed tuberculous infections during 1997. Five patients had residual tuberculosis in preoperative chest X-ray, and specific pyelonephritis as an underlying kidney disease in two of them. All patients with treated with triple immunosuppressives. Before tuberculosis onset, 14 patients experienced one or more episodes of acute rejection and were treated with steroid pulses, ALG or OKT3. Tuberculosis was diagnosed after a period of 1.5 months to 10 years after transplantation. At the time of an infection, the graft function was normal in eight patients and chronic graft failure was evident in eight patients (sCr 210–700 μmol/L). The infection was pulmonary in 12 patients; urinary in two; disseminated in two; pulmonary and urinary, pulmonary and intestinal, and pancytopenia in one patient. All patients were treated with rifampicin and isoniazid in addition to ethambutol for the first two-month period. Treatment lasted from 1–22 months. With 14 patients favorable microbiological responses were registered. Two patients died within the first six months (both with disseminated disease), and the mortality rate was 14.3%. Throughout the followup period, the graft function remained stable and normal in eight patients who had normal graft function at the time of infection onset. Although six patients recovered, progressive graft failure developed and hemodialysis was restarted in one patient two months after antituberculous therapy introduction, and in two patients three years later. Four patients died 2–14 months after AT therapy withdrawal. The causes of death were severe liver failure, cerebrovascular insult and CMV.
Clinical Consequences of Antiphospholipid Antibodies: An Historic Cohort Study

Objective: To determine the risk of antiphospholipid antibody-related disorders in women with elevated levels of these antibodies. Methods: We used an historic cohort study design. Surveys of medical and obstetric histories for the interval from initial antibody testing to the time of patient interview were used to calculate age-adjusted rates for the development of medical disorders associated with antiphospholipid antibodies. The cohort included 130 women with lupus anticoagulant, medium to high levels of immunoglobulin G anticardiolipin antibodies, or both. Results: The median interval of study was 3.2 years (range 0.7-9.5, mean 3.7). Sixty-three subjects (48%) developed at least one new disorder during the study interval. The age-adjusted rates (per 1000 patient-years; ± standard error) for the development of the disorders studied were as follows: thrombosis (156.8 ± 30.0), cerebrovascular accident (93.8 ± 25.1), amaurosis fugax (57.1 ± 23.2), transient ischemic attack (170.4 ± 27.6), systemic lupus erythematosus (9.8 ± 3.8), and autoimmune thrombocytopenia (56.0 ± 22.2). Of the 34 thrombotic events that occurred during the study interval, eight were associated with pregnancy and eight occurred while the patients were taking anticoagulant medications. Conclusions: Our subjects developed complications associated with antiphospholipid antibodies at a substantial rate, and almost half suffered at least one new event during the study interval. The high rate of thrombosis in individuals with antiphospholipid antibodies, especially associated with pregnancy, underscores the need to evaluate long-term anticoagulation in these patients.
Epilepsy syndrome, focus location, and treatment choice affect testicular function in men with epilepsy

Objective: To evaluate testicular function in men with epilepsy treated with different antiepileptic drugs (AED) vs no drugs. Methods: Two hundred men with epilepsy (mean age 36 years) were investigated. Inclusion criteria included one or no AED, no co-medication, and no endocrine co-morbidity. Findings were compared with those from 105 healthy men (mean age 33.9 years). Luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone (T), free testosterone (free T), and inhibin B were measured. Results: One hundred seventy-eight men had focal epilepsy (117 of these had temporal lobe epilepsy [TLE]) and 22 idiopathic generalized epilepsy (IGE). Thirty-three men were not on AED; 124 men received enzyme-inducing AED. Free T was lowered in all patient subgroups, and the T/LH ratio was lowered in all groups except patients with IGE and patients receiving valproate (VPA). T was lower in patients with temporal than extratemporal focal epilepsy. Compared with TLE patients on carbamazepine (CBZ), patients treated with VPA had higher total T and lower LH values, resulting in a significantly lower T/LH ratio with CBZ. Conclusions: Epilepsy, especially TLE, adversely affects testicular endocrine function. CBZ may increase the negative effects of epilepsy on serum levels of reproductive hormones.
Cost-Effectiveness Analysis of Percutaneous Vertebroplasty for Osteoporotic Compression Fractures

Study Design: Single-center, single-arm, prospective time-series study. Objective: To assess the cost-effectiveness and improvement in quality of life (QOL) of percutaneous vertebroplasty (PVP). Summary of Background Data: PVP is known to relieve back pain and increase QOL for osteoporotic compression fractures. However, the economic value of PVP has never been evaluated in Japan where universal health care system is adopted. Methods: We prospectively followed up 163 patients with acute vertebral osteoporotic compression fractures, 44 males aged 76.4±6.0 years and 119 females aged 76.8±7.1 years, who underwent PVP. To measure health-related QOL and pain during 52 weeks observation, we used the European Quality of Life–5 Dimensions (EQ-5D), the Rolland-Morris Disability Questionnaire (RMD), the 8-item Short-Form health survey (SF-8), and visual analogue scale (VAS). Quality-adjusted life years (QALY) were calculated using the change of health utility of EQ-5D. The direct medical cost was calculated by accounting system of the hospital and Japanese health insurance system. Cost-effectiveness was analyzed using incremental cost-effectiveness ratio (ICER): &Dgr; medical cost/&Dgr; QALY. Results: After PVP, improvement in EQ-5D, RMD, SF-8, and VAS scores were observed. The gain of QALY until 52 weeks was 0.162. The estimated lifetime gain of QALY reached 1.421. The direct medical cost for PVP was ¥286,740 (about 3061 US dollars). Cost-effectiveness analysis using ICER showed that lifetime medical cost for a gain of 1 QALY was ¥201,748 (about 2154 US dollars). Correlations between changes in EQ-5D scores and other parameters such as RMD, SF-8, and VAS were observed during most of the study period, which might support the reliability and applicability to measure health utilities by EQ-5D for osteoporotic compression fractures in Japan as well. Conclusions: PVP may improve QOL and ameliorate pain for acute osteoporotic compression fractures and be cost-effective in Japan.
The effect of tamoxifen on the pharmacokinetics of letrozole in female rats

The effects of single doses of tamoxifen (TAM; 0.5–5 mg/kg, i.v.) and chronic pretreatment with TAM (0.1–5.0 mg/kg/day, i.p. for 7 consecutive days) on letrozole (0.5 mg/kg, i.v.) pharmacokinetics were evaluated in female Sprague‐Dawley rats. The plasma concentration‐time profiles of letrozole (0.1–2.0 mg/kg) after single i.v. doses were analysed by the non‐compartment model with terminal half‐lives (t1/2,λz) ranging from 34.3 to 37.5 h. The volume of distribution at the terminal phases (Vd(λz)) ranged from 1.9 to 2.1 l/kg and clearance (CL) varied from 0.036 to 0.042 l/(h·kg). After co‐administration of TAM and letrozole intravenously, the t1/2, Vd(λz) and CL of letrozole were not significantly altered. Chronic pretreatment with TAM significantly decreased the t1/2 of letrozole by about 33%, and increased its clearance by an average of 40%. However, TAM pretreatment did not significantly affect the Vd((λz) of letrozole in female rats. Co‐administration of letrozole and TAM orally increased the absorption half‐life of letrozole threefold although the absolute bioavailability remained unchanged. These observations suggest that single oral doses of TAM delay the absorption of letrozole while chronic pretreatment with TAM accelerates the elimination of letrozole, probably due to induction of cytochrome P450 enzymes in rats. Copyright © 2006 John Wiley & Sons, Ltd.
Effects of a 98% solution of glycerol or sterilization with ethylene oxide on FeLV in bone allografts and effects on bone incorporation of allografts in cats.

OBJECTIVES To compare virucidal effects and bone incorporation properties of cortical bone allografts transplanted into specific-pathogen-free (SPF) cats. Allografts consisted of untreated bone from a SPF cat (negative-control group) and bone from 5 FeLV-infected cats that was subjected to sterilization with ethylene oxide (ETO), preservation with glycerol, or no treatment (positive-control group). SAMPLE POPULATION Bones from the aforementioned groups and twenty 8-week-old SPF cats (5 cats/group) implanted with an allograft from 1 of the aforementioned groups. PROCEDURE After implantation, blood samples were collected weekly to monitor FeLV p27 antigen and antibody titers. Quantification of FeLV provirus was performed on blood samples at weeks 0, 4, and 8 and donor bone samples at time of implantation. Cats were euthanatized 8 weeks after transplantation, and graft sites were evaluated. RESULTS All results for negative-control cats were negative. All ETO group cats had negative results for antigen and provirus in blood, whereas 1 cat had a low antibody titer. Although 3 ETO-treated allografts were positive for provirus, the DNA appeared denatured. One cat in the glycerol group had positive results for all tests in blood samples. All glycerol-preserved allografts were positive when tested for provirus. All results for positive-control group cats were positive. Differences in incorporation of bone grafts were not observed. CONCLUSIONS AND CLINICAL RELEVANCE Glycerol preservation of FeLV-infected bone allografts did not eliminate transmission of retrovirus to recipients. In contrast, ETO sterilization appeared to denature DNA and prevent infection. Treatments did not affect incorporation of bone grafts in young cats.
Evolving Role of Serum Biomarkers in the Management of Ovarian Cancer

The availability of an ideal serum tumor marker would be of great clinical benefit for both the diagnosis and management of patients with epithelial ovarian cancer. Serum cancer antigen 125 assay significantly increases the diagnostic reliability of ultrasound in discriminating a malignant from a benign ovarian mass, especially in postmenopausal women, and it is the only well validated tumor marker for monitoring disease course. Several other tumor-associated antigens have been assessed, including glycoprotein antigens other than cancer antigen 125, soluble cytokeratin fragments, kallikreins, cytokines and cytokine receptors, vascular endothelial growth factor, D-dimer, and lisophosphatidic acid. This article assesses the potential diagnostic and prognostic role of these novel biomarkers, both alone and in combination with cancer antigen 125. The future for serum tumor marker research is represented by the emerging technology of proteomics, which may allow scientific advances comparable to those achieved with the introduction of monoclonal antibody technology.
Unique genome organization of non-mammalian papillomaviruses provides insights into the evolution of viral early proteins

Abstract The family Papillomaviridae contains more than 320 papillomavirus types, with most having been identified as infecting skin and mucosal epithelium in mammalian hosts. To date, only nine non-mammalian papillomaviruses have been described from birds (n = 5), a fish (n = 1), a snake (n = 1), and turtles (n = 2). The identification of papillomaviruses in sauropsids and a sparid fish suggests that early ancestors of papillomaviruses were already infecting the earliest Euteleostomi. The Euteleostomi clade includes more than 90 per cent of the living vertebrate species, and progeny virus could have been passed on to all members of this clade, inhabiting virtually every habitat on the planet. As part of this study, we isolated a novel papillomavirus from a 16-year-old female Adélie penguin (Pygoscelis adeliae) from Cape Crozier, Ross Island (Antarctica). The new papillomavirus shares ∼64 per cent genome-wide identity to a previously described Adélie penguin papillomavirus. Phylogenetic analyses show that the non-mammalian viruses (expect the python, Morelia spilota, associated papillomavirus) cluster near the base of the papillomavirus evolutionary tree. A papillomavirus isolated from an avian host (Northern fulmar; Fulmarus glacialis), like the two turtle papillomaviruses, lacks a putative E9 protein that is found in all other avian papillomaviruses. Furthermore, the Northern fulmar papillomavirus has an E7 more similar to the mammalian viruses than the other avian papillomaviruses. Typical E6 proteins of mammalian papillomaviruses have two Zinc finger motifs, whereas the sauropsid papillomaviruses only have one such motif. Furthermore, this motif is absent in the fish papillomavirus. Thus, it is highly likely that the most recent common ancestor of the mammalian and sauropsid papillomaviruses had a single motif E6. It appears that a motif duplication resulted in mammalian papillomaviruses having a double Zinc finger motif in E6. We estimated the divergence time between Northern fulmar-associated papillomavirus and the other Sauropsid papillomaviruses be to around 250 million years ago, during the Paleozoic-Mesozoic transition and our analysis dates the root of the papillomavirus tree between 400 and 600 million years ago. Our analysis shows evidence for niche adaptation and that these non-mammalian viruses have highly divergent E6 and E7 proteins, providing insights into the evolution of the early viral (onco-)proteins.
Human-derived gut microbiota modulates colonic secretion in mice by regulating 5-HT3 receptor expression via acetate production.

Serotonin [5-hydroxytryptamine (5-HT)], an important neurotransmitter and a paracrine messenger in the gastrointestinal tract, regulates intestinal secretion by its action primarily on 5-HT3 and 5-HT4 receptors. Recent studies highlight the role of gut microbiota in 5-HT biosynthesis. In this study, we determine whether human-derived gut microbiota affects host secretory response to 5-HT and 5-HT receptor expression. We used proximal colonic mucosa-submucosa preparation from age-matched Swiss Webster germ-free (GF) and humanized (HM; ex-GF colonized with human gut microbiota) mice. 5-HT evoked a significantly greater increase in short-circuit current (ΔIsc) in GF compared with HM mice. Additionally, 5-HT3 receptor mRNA and protein expression was significantly higher in GF compared with HM mice. Ondansetron, a 5-HT3 receptor antagonist, inhibited 5-HT-evoked ΔIsc in GF mice but not in HM mice. Furthermore, a 5-HT3 receptor-selective agonist, 2-methyl-5-hydroxytryptamine hydrochloride, evoked a significantly higher ΔIsc in GF compared with HM mice. Immunohistochemistry in 5-HT3A-green fluorescent protein mice localized 5-HT3 receptor expression to enterochromaffin cells in addition to nerve fibers. The significant difference in 5-HT-evoked ΔIsc between GF and HM mice persisted in the presence of tetrodotoxin (TTX) but was lost after ondansetron application in the presence of TTX. Application of acetate (10 mM) significantly lowered 5-HT3 receptor mRNA in GF mouse colonoids. We conclude that host secretory response to 5-HT may be modulated by gut microbiota regulation of 5-HT3 receptor expression via acetate production. Epithelial 5-HT3 receptor may function as a mediator of gut microbiota-driven change in intestinal secretion.NEW & NOTEWORTHY We found that gut microbiota alters serotonin (5-HT)-evoked intestinal secretion in a 5-HT3 receptor-dependent mechanism and gut microbiota metabolite acetate alters 5-HT3 receptor expression in colonoids.View this article's corresponding video summary at https://www.youtube. com/watch? v=aOMYJMuLTcw&feature=youtu.be.
Be13, a human T-leukemia cell line highly sensitive to dexamethasone-induced cytolysis.

A unique human T-leukemia cell line highly sensitive to dexamethasone-induced lysis is described. The cell line designated Be13 is killed readily within 24 hr by 10(-9) M dexamethasone. No lysis is induced by nonglucocorticoid steroids. The lysis is mediated via specific cytoplasmic receptors and is efficiently blocked by the antagonist cortexolone. The inhibiting effect of actinomycin D and cycloheximide on the lytic process suggests the involvement of gene activation and destruction of the cells by an "autolytic protein. " Kinetic studies imply that the lytic process is induced during a distinct phase of the cell cycle. Dexamethasone, however, does not cause an arrest in a distinct phase of the cell cycle. The Be13 cell is a unique human cell line killed directly by glucocorticoids, and it may serve as a suitable in vitro model for studying the lytic effect of glucocorticoids on the proliferating compartment of human leukemias.
Comparison of developmental toxicology of aspirin (acetylsalicylic acid) in rats using selected dosing paradigms.

BACKGROUND Analysis of the literature for nonsteroidal anti-inflammatory drugs (NSAIDs) suggests that a low incidence of developmental anomalies occurs in rats given NSAIDs on specific days during organogenesis. Aspirin (acetylsalicylic acid [ASA]), an irreversible cyclooxygenase 1 and 2 inhibitor, induces developmental anomalies when administered to Wistar rats on gestational day (GD) 9, 10, or 11 (Kimmel CA, Wilson JG, Schumacher HJ. Teratology 4:15-24, 1971). There are no published ASA studies using the multiple dosing paradigm of GDs 6 to 17. Objectives of the current study were to compare results between Sprague-Dawley (SD) and Wistar strains when ASA is administered on GD 9, 10, or 11; to compare the malformation patterns following single and multiple dosings during organogenesis in SD rats; and to test the hypothesis that maternal gastrointestinal toxicity confounds the detection of low incidence malformations with ASA when a multiple dosing paradigm is used. METHODS ASA was administered as a single dose on GD 9 (0, 250, 500, or 625 mg/kg), 10 (0, 500, 625, or 750 mg/kg), or 11 (0, 500, 750, or 1000 mg/kg) and from GD 6 to GD 17 (0, 50, 125, or 250 mg/kg a day) in the multiple dose study to SD rats. Animals were killed on GD 21, and fetuses were examined viscerally. RESULTS The literature evaluation suggested that NSAIDs induce ventricular septal defects (VSDs) and midline defects (MDs) in rats and diaphragmatic hernia (DH), MDs, and VSDs in rabbits (Cook JC et al., 2003); hence, the present study focused on these malformations, even though ASA induces several other low-incidence malformations. In single dose studies, DH, MD, and VSD were induced on GDs 9 and 10. VSD also was noted following treatment on GD 11. In contrast, DH and MD were noted in the multiple dose study design only in the high-dose group, and VSD was noted across all dose groups. CONCLUSIONS High concordance in major developmental anomalies between Wistar and SD rats were noted with the exception of VSD in the SD rats and hydrocephalus in the Wistar rats. Variations and malformations were similar when ASA was administered as a single dose or during the period of organogenesis (GDs 6 to 17). It was also evident that, by titrating the dose to achieve a maximum tolerated dose, malformations that normally occur at low incidence, as reported from previous single dose studies, could also be induced with ASA given at multiple doses.
Interpretation of phenotype in genetically engineered mice.

BACKGROUND AND PURPOSE In mice, genetic engineering involves two general approaches-addition of an exogenous gene, resulting in transgenic mice, and use of knockout mice, which have a targeted mutation of an endogenous gene. The advantages of these approaches is that questions can be asked about the function of a particular gene in a living mammalian organism, taking into account interactions among cells, tissues, and organs under normal, disease, injury, and stress situations. METHODS Review of the literature concentrating principally on knockout mice and questions of unexpected phenotypes, lack of phenotype, redundancy, and effect of genetic background on phenotype will be discussed. CONCLUSION There is little gene redundancy in mammals; knockout phenotypes exist even if none are immediately apparent; and investigating phenotypes in colonies of mixed genetic background may reveal not only more phenotypes, but also may lead to better understanding of the molecular or cellular mechanism underlying the phenotype and to discovery of modifier gene(s).