Miracle-dz/UniFAR-FTUs huggingface dataset:
The evolving science of detection of ‘blood doping’

Blood doping practices in sports have been around for at least half a century and will likely remain for several years to come. The main reason for the various forms of blood doping to be common is that they are easy to perform, and the effects on exercise performance are gigantic. Yet another reason for blood doping to be a popular illicit practice is that detection is difficult. For autologous blood transfusions, for example, no direct test exists, and the direct testing of misuse with recombinant human erythropoietin (rhEpo) has proven very difficult despite a test exists. Future blood doping practice will likely include the stabilization of the transcription factor hypoxia‐inducible factor which leads to an increased endogenous erythropoietin synthesis. It seems unrealistic to develop specific test against such drugs (and the copies hereof originating from illegal laboratories). In an attempt to detect and limit blood doping, the World Anti‐Doping Agency (WADA) has launched the Athlete Biological Passport where indirect markers for all types of blood doping are evaluated on an individual level. The approach seemed promising, but a recent publication demonstrates the system to be incapable of detecting even a single subject as ‘suspicious’ while treated with rhEpo for 10–12 weeks. Sad to say, the hope that the 2012 London Olympics should be cleaner in regard to blood doping seems faint. We propose that WADA strengthens the quality and capacities of the National Anti‐Doping Agencies and that they work more efficiently with the international sports federations in an attempt to limit blood doping.
Goodwill and Mandatory Disclosure Compliance: A Critical Review of the Literature

The aim of this paper is to critically analyse the literature published from 2002 to mid-2015 on disclosures of goodwill and their respective impairment tests; identify the main contributions of the literature, as well as its limitations; and suggest new approaches for future research. We also present a summary of the main determinants of disclosures on goodwill in the literature as well as the still scarce studies’ conclusions of those disclosures in the market. After a review of the literature, we discuss the need to reinforce enforcement mechanisms, so as to improve the level of compliance of disclosures on goodwill and their impairment tests. The majority of the analysed literature reveals that the information disclosed about goodwill is incomplete and largely heterogeneous, indicating a reduced level of compliance with the disclosures required by accounting standards. The paper may support the development of future empirical studies about goodwill's disclosures, which will bridge the identified gaps in the literature.
The relationship of patient reading ability to self-reported health and use of health services.

OBJECTIVES This study examined the relationship of functional health literacy to self-reported health and use of health services. METHODS Patients presenting to two large, urban public hospitals in Atlanta, Ga, and Torrance, Calif, were administered a health literacy test about their overall health and use of health care services during the 3 months preceding their visit. RESULTS Patients with inadequate functional health literacy were more likely than patients with adequate literacy to report their health as poor. Number of years of school completed was less strongly associated with self-reported health. Literacy was not related to regular source of care or physician visits, but patients in Atlanta with inadequate literacy were more likely than patients with adequate literacy to report a hospitalization in the previous year. CONCLUSIONS Low literacy is strongly associated with self-reported poor health and is more closely associated with self-reported health than number of years of school completed.
Distributed adaptive droop control for DC distribution systems

Summary form only given: A distributed-adaptive droop mechanism is proposed for secondary/primary control of dc microgrids. The conventional secondary control that adjusts the voltage set point for the local droop mechanism is replaced by a voltage regulator. A current regulator is also added to fine-tune the droop coefficient for different loading conditions. The voltage regulator uses an observer that processes neighbors' data to estimate the average voltage across the microgrid. This estimation is further used to generate a voltage correction term to adjust the local voltage set point. The current regulator compares the local per-unit current of each converter with the neighbors' on a communication graph and, accordingly, provides an impedance correction term. This term is then used to update the droop coefficient and synchronize per-unit currents or, equivalently, provide proportional load sharing. The proposed controller precisely accounts for the transmission/distribution line impedances. The controller on each converter exchanges data with only its neighbor converters on a sparse communication graph spanned across the microgrid. Global dynamic model of the microgrid is derived with the proposed controller engaged. A low-voltage dc microgrid prototype is used to verify the controller performance, link-failure resiliency, and the plug-and-play capability.
Extracellular regulated kinase5 is expressed in fetal mouse submandibular glands and is phosphorylated in response to epidermal growth factor and other ligands of the ErbB family of receptors

Growth factors and their receptors regulate development of many organs through activation of multiple intracellular signaling cascades including a mitogen‐activated protein kinase (MAPK). Extracellular regulated kinases (ERK)1/2, classic MAPK family members, are expressed in fetal mouse submandibular glands (SMG), and stimulate branching morphogenesis. ERK5, also called big mitogen‐activated protein kinase 1, was recently found as a new member of MAPK super family, and its biological roles are still largely unknown. In this study, we investigated the expression and function of ERK5 in developing fetal mouse SMGs. Western blotting analysis showed that the expression pattern of ERK5 was different from the pattern of ERK1/2 in developing fetal SMGs. Both ERK1/2 and ERK5 were phosphorylated after exposure to ligands of the ErbB family of receptor tyrosine kinases (RTKs). Phosphorylation of ERK1/2 was strongly induced by epidermal growth factor (EGF) in SMG rudiments at embryonic day 14 (E14), E16 and E18. However, ERK5 phosphorylation induced by EGF was clearly observed at E14 and E16, but not at E18. Branching morphogenesis of cultured E13 SMG rudiments was strongly suppressed by administration of U0126, an inhibitor for ERK1/2 activation, whereas the phosphorylation of ERK5 was not inhibited by U0126. BIX02188, a specific inhibitor for ERK5 activation, also inhibited branching morphogenesis in cultured SMG rudiments. These results show that EGF‐responsive ERK5 is expressed in developing fetal mouse SMG, and suggest that both ERK1/2 and ERK5 signaling cascades might play an important role in the regulation of branching morphogenesis.
Discovery of hundreds of mirtrons in mouse and human small RNA data

Atypical miRNA substrates do not fit criteria often used to annotate canonical miRNAs, and can escape the notice of miRNA genefinders. Recent analyses expanded the catalogs of invertebrate splicing-derived miRNAs (“mirtrons”), but only a few tens of mammalian mirtrons have been recognized to date. We performed meta-analysis of 737 mouse and human small RNA data sets comprising 2.83 billion raw reads. Using strict and conservative criteria, we provide confident annotation for 237 mouse and 240 human splicing-derived miRNAs, the vast majority of which are novel genes. These comprise three classes of splicing-derived miRNAs in mammals: conventional mirtrons, 5′-tailed mirtrons, and 3′-tailed mirtrons. In addition, we segregated several hundred additional human and mouse loci with candidate (and often compelling) evidence. Most of these loci arose relatively recently in their respective lineages. Nevertheless, some members in each of the three mirtron classes are conserved, indicating their incorporation into beneficial regulatory networks. We also provide the first Northern validation for mammalian mirtrons, and demonstrate Dicer-dependent association of mature miRNAs from all three classes of mirtrons with Ago2. The recognition of hundreds of mammalian mirtrons provides a new foundation for understanding the scope and evolutionary dynamics of Dicer substrates in mammals.
Serodiagnosis of cystic echinococcosis in naturally infected camels

An ELISA was developed for serological detection of Echinococcus granulosus infection in dromedary camels. Antigen B (AgB) partially purified from hydatid cyst fluid of camels or sheep naturally infected with cystic echinococcosis (CE) due to E. granulosus, as well as a recombinant antigen B product (r-AgB) were used in an ELISA to screen panels of serum samples from slaughtered camels naturally infected with CE. Native hydatid cyst fluid antigen preparations were able to detect antibodies in sera from a significant proportion of camels with CE, as confirmed at post-mortem. Seroreactivity however, was variable. ELISA specificity for sera from naturally infected camels versus inspection-negative animals ranged from 90 to 99%. Native antigen B gave the highest sensitivity (97%) in ELISA for camel CE confirmed at slaughter. In contrast, r-AgB gave lower sensitivity for camel (84%) and sheep (28%) CE. The r-AgB-ELISA was, however, highly specific (90 and 95%) respectively for both camel and sheep natural CE infection. These results indicate that an ELISA based on serum antibody detection to AgB could be developed for immunodiagnosis of cystic echinococcosis in camels.
Genetic Mutations, Birth Lengths, Weights and Head Circumferences of Children with IGF-I Receptor Defects. Comparison with other Congenital Defects in the GH/IGF-I axis.

BACKGROUND In recent years more and more genetic defects along the GHRH-GH-IGF-I axis have been reported. Mutations of the IGF-I receptor (R) are a rare abnormality of whom only the heterozygote progenies survive. OBJECTIVES To summarize, from the literature, data on birth length, weight and head circumference of neonates with IGF-I-R mutations, and to correlate the data with that of other types of mutations in the GH/IGF-I axis. SUBJECTS Sixty seven neonates from 24 published articles were included and forty seven different mutations of the IGF-I (R) located on chromosome 15 have been identified. RESULTS Mean (±SD) birth length (BL), available for 26, (10 M, 16F) neonates with a gestational age of 34-41weeks, was 44.2±4cm; one was premature (30cm at 31 weeks). There was a significant correlation between birth length and gestational age (GA) r=0.71 (p>.001). Mean birth weight (BW) of 41 neonates (18M, 23F) was 2388±743gr. Two premature neonates weighed 650gr and 950gr respectively. The BW correlated significantly with gestational age, (males: r=0.68; p=0.007, females: r=0.49; p=0.024). The BMI of 25 neonates ranged from 6 to 13. In 22 records marked microcephaly was ascertained or stated. Nine of 16 mothers were short (133 -148cm), m±SD = 150.5±7.3cm.
Adherence to Human Vaginal Epithelial Cells Signals for Increased Expression of Trichomonas vaginalis Genes

ABSTRACT Host parasitism by Trichomonas vaginalis is complex, and the adhesion to vaginal epithelial cells (VECs) by trichomonads is preparatory to colonization of the vagina. Since we showed increased synthesis of adhesins after contact with VECs (A. F. Garcia, et al., Mol. Microbiol. 47:1207-1224, 2003) and more recently demonstrated up-regulated gene expression in VECs after parasite attachment (A. S. Kucknoor, et al., Cell. Microbiol. 7:887-897, 2005), we hypothesized that enhanced expression of adhesin and other genes would result from signaling of trichomonads following adherence. In order to identify the genes that are up-regulated, we constructed a subtraction cDNA library enriched for differentially expressed genes from the parasites that were in contact with the host cells. Thirty randomly selected cDNA clones representing the differentially regulated genes upon initial contact of parasites with host cells were sequenced. Several genes encoded functional proteins with specific functions known to be associated with colonization, such as adherence, change in morphology, and gene transcription and translation. Interestingly, genes unique to trichomonads with unknown functions were also up-regulated. Semiquantitative reverse transcription-PCR (RT-PCR) confirmed expression of select genes. An increased amount of protein was demonstrated by immunoblotting with monoclonal antibody. Finally, we showed the transcriptional regulation of some genes by iron by using RT-PCR. To our knowledge, this is the first report addressing the differential regulation of T. vaginalis genes immediately upon contact with VECs.
Intermittent ischaemia of skin flaps shortens time taken to divide pedicles: An experimental study in rats

Ischaemic preconditioning increases the survival of flaps. Random–pattern McFarlane dorsal flaps were raised in 30 female Wistar rats, which were divided into three groups. An ischaemic conditioning protocol with clamping of the pedicle was used. No clamping was used in the control group, and the pedicle was clamped for 15 minutes in the second group and 20 minutes in the third group daily to see if the duration of ischaemia had any effects on the viability of the flaps. The pedicles were divided earlier in the clamped groups than in the control group. The size of necrotic areas of the flaps in the clamped groups was smaller than on the control group. Daily postoperative intermittent ischaemic conditioning in the pedicles of the flaps had a protective effect on their survival and led to earlier division of the pedicles.
Successful Treatment of Fosinopril-Induced Severe Cholestatic Jaundice with Plasma Exchange

Objective: To describe a case of fosinopril-induced severe cholestatic jaundice successfully treated with plasma exchange. Case Summary: A 78-year-old Taiwanese male presented with yellowish skin and generalized itching one month after starting fosinopril 10 mg once a day. Other drugs taken by the patient were excluded as the probable cause of jaundice. Diagnostic modalities, including abdominal ultrasound, computed tomography, and endoscopic retrograde cholangiopancreatography, revealed no evidence of biliary tract obstruction or intraabdominal tumor. According to the Council for International Organizations of Medical Science (CIOMS) scale, fosinopril was a highly probable cause of the patient's jaundice. Liver biopsy showed cholestasis without bile duct damage. Based on results of the CIOMS scale assessment and pathological characteristics of the liver, the diagnosis was highly probable that fosinopril had induced cholestatic jaundice in our patient. During hospitalization, the patient developed severe jaundice and liver failure, despite conservative treatment and withdrawal of fosinopril. He underwent a 5-day course of plasma exchange therapy, and the serum bilirubin level declined rapidly after treatment. His liver function returned to normal 2 months after treatment. Discussion: Angiotensin-converting enzyme (ACE) inhibitor–induced hepatotoxicity is rare and only a few cases, with most involving captopril, have been reported in the English-language literature. Hepatotoxicity caused by fosinopril is extremely rare. Most ACE inhibitor–induced hepatotoxicity is mild and transient, but it can be fatal. Although orthotopic liver transplantation (OLT) is the standard method for treating drug-induced liver failure, plasma exchange therapy is an alternative therapeutic method or a bridge to OLT for treating liver failure. Conclusions: Plasma exchange therapy may play a valuable role in the treatment of fosinopril-induced cholestatic jaundice and liver failure. This intervention can be considered for temporary liver support until recovery or OLT.
A very high-sensitivity CMOS power detector for high data rate biotelemetry applications

This paper presents a microwave power detector for an on-off keying (OOK) receiver for biotelemetry. The detector is designed using 130 nm CMOS technology and it consists of a high-gain inverting amplifier biased at the edge of turn-on and a low-frequency comparator circuit. The detector is designed to operate at 7.6 GHz and simulation results show that it has a sensitivity of -55 dBm while drawing just 9.3 μA from a 1 V supply. Furthermore, the detector can operate at bit rates of up to 100 Mbps.
Dysregulation of CXCR3 Signaling due to CXCL10 Deficiency Impairs the Antiviral Response to Herpes Simplex Virus 1 Infection1

The chemokine, CXCL10, chemotactic for NK cells, activated T cells, and dendritic cells is highly expressed during viral infections, including HSV-1. The importance of this chemokine to the control of HSV-1 infection was tested using mice deficient in CXCL10 (CXCL10−/−). Following corneal infection, HSV-1 viral titers were elevated in the nervous system of CXCL10−/− mice, which correlated with defects in leukocyte recruitment including dendritic cells, NK cells, and HSV-1-specific CD8+ T cells to the brain stem. In the absence of NK cells and HSV-1-specific CD8+ T cells in wild-type (WT) or CXCL10−/− mice, similar levels of virus were recovered in the nervous system, suggesting these cells are responsible for the observed defects in the control of viral replication in CXCL10−/− mice. Leukocyte mobilization was also compared between WT, CXCL10−/−, and mice deficient in the only known receptor for CXCL10, CXCR3 (CXCR3 −/−). NK cell mobilization was comparably reduced in both CXCL10−/− and CXCR3−/− mice relative to WT animals. However, the reduction in mobilization of HSV-1-specific CD8+ T cells in CXCL10−/− was not observed in CXCR3−/− mice following HSV-1 infection. The defect was not the result of an alternative receptor for CXCL10, as Ag-specific CD8+ T cell recruitment was not reduced in mice which were deficient in both CXCL10 and CXCR3. Thus, CXCL10 deficiency results in reduced mobilization of HSV-1-specific CD8+ T cells as a result of dysregulation of CXCR3 signaling.
Androgen Receptor Mediates Non-genomic Activation of Phosphatidylinositol 3-OH Kinase in Androgen-sensitive Epithelial Cells*

Androgens are known to modulate many cellular processes such as cell growth and survival by binding to the androgen receptor (AR) and activating the transcription of target genes. Recent data suggested that AR can also mediate non-transcriptional actions outside the nucleus in addition to its ligand-inducible transcription factor function. Here, we describe a transcription-independent activation of the phosphatidylinositol 3-OH kinase (PI3-K) signaling pathway by androgens. Using non-transformed androgen-sensitive epithelial cells, we show that androgens enhance the PI3-K activity by promoting accumulation of phosphoinositide-3-P phospholipids in vitro. This activation is found in conjunction with an increased time-dependent phosphorylation of the downstream kinase AKT/protein kinase B on both Ser473 and Thr308 residues. Hormone-stimulated phosphorylation of AKT requires AR since incubation with the anti-androgen bicalutamide completely abolishes the androgen-stimulated AKT phosphorylation. Accordingly, we show that androgens increase AKT phosphorylation level in prostatic carcinoma PC3 cells only once they have been transfected with AR. Downstream, androgens enhance phosphorylation of transcription factor FKHR (Forkhead in rhabdomyosarcoma)-L1 and proapoptotic Bad protein and promote cell survival as they can counteract an apoptotic process. We also report that non-genomic effects of androgens are based on direct interaction between AR and the p85α regulatory subunit of class I(A) PI3-K. Together, these novel findings point out an important and physiologically relevant link between androgens and the PI3-K/AKT signaling pathway in governing cell survival.
Social Work’s Response to Poverty: From Benefits Dependence to Economic Self-Sufficiency

ABSTRACT Welfare reform in the 1990s represented a fundamental policy shift in the United States’ response to poverty from supporting benefits dependency to promoting economic self-sufficiency. Social work’s capacity to integrate this policy shift into practice is central to meeting its mission to alleviate poverty. This study looked at the preparation of future social workers as a way to gauge the extent of the profession’s integration of this shift. Findings showed that about half of social work education programs do not include skills and knowledge related to economic self-sufficiency in their curricula, and there is considerable variability among those that do. Most program administrators are interested in expanding their curricula but are hampered by a lack of resources and faculty and student resistance.
Effects of furosemide versus isolated ultrafiltration on extravascular lung water in oleic acid‐induced pulmonary edema

We studied the effects of no treatment, furosemide treatment, and isolated ultrafiltration on extravascular lung water (ETV1.) in mongrel dogs in whom pulmonary edema was induced with oleic acid. In all treatment groups, ETV1. was significantly elevated 90 min after oleic acid infusion. At 270 min, we found no difference between nontreatment and furosemide. There was, however, a significant difference between no treatment and ultrafiltration but not between furosemide and ultrafiltration. In spite of observations which suggest that ultrafiltration is of benefit in reducing ETVL, we could not demonstrate superiority of one therapy over another.
A PCM translation layer for integrated memory and storage management

Phase change memory (PCM) is known for its potentials as main memory and as storage. In contrast to the past work, this work presents a PCM translation layer that considers how the main memory is used by the operating system together with the usage patterns of storage by trading their performance and reliability. In particular, a joint management scheme is proposed to improve the capability of PCM as both main memory and storage so as to enhance the performance of the entire system. The endurance issue of PCM for main memory is resolved by utilizing the potentially large capacity of the PCM storage space with limited modifications to the existing operating system implementations. Moreover, three commands are proposed to help operating system engineers to take advantage of PCM as main memory and storage by reducing I/O overheads and speeding up both the initialization and termination of program executions. The experimental results show that the performance of PCM as both main memory and storage can be significantly improved with reasonable lifetime, while the system overhead is very limited under coarse-grained wear leveling.