Miracle-dz/UniFAR-FTUs huggingface dataset:
Antimicrobial resistance of enteropathogenic Escherichia coli strains from a nosocomial outbreak in Kenya

The majority of the 78 enteropathogenic (EPEC) and the 151 non‐EPEC Escherichia coli strains isolated from preterm neonates during an outbreak of gastroenteritis in a hospital in Nairobi, Kenya, were resistant to trimethoprim‐sulfamethoxaxole, chloramphenicol, oxytetracycline and ampicillin, but only a few strains were resistant to cefazolin, cefamandole, cefotaxime, amikacin and nalidixic acid. Fourteen different antimicrobial resistance patterns were observed in the 229 strains of E. coli analysed. Eighty‐two percent of the EPEC strains belonged to two resistance patterns compared with 79% of non‐EPEC strains which exhibited three resistance patterns. There was no consistent relationship between plasmid profile group and antimicrobial resistance pattern, although one resistance pattern was more frequently observed in EAF‐positive strains belonging to the dominant plasmid profile group. Nine percent of the EPEC strains were resistant to gentamicin compared to 37% in the non‐EPEC group. No correlation was observed between administration of gentamicin and percentage of resistant strains isolated. None of the nine neonates receiving gentamicin died during the outbreak. Gentamicin resistance was observed in E. coli strains from six out of these nine neonates. Five out of fourteen neonates who received other antimicrobials, or no antibiotic treatment at all, died.
Effects of Environmental Changes on Expression of the Oligopeptide Permease (opp) Genes of Borrelia burgdorferi

ABSTRACT We analyzed expression of a putative oligopeptide permease (Opp) of Borrelia burgdorferi. Unlike the opp operons of other bacteria for which there is a single substrate binding protein, B. burgdorferi codes for three substrate binding proteins (OppA-I to -III) in its opp operon and an additional two homologs on plasmids (OppA-IV and -V). Instead of a single promoter region regulating transcription of the entire operon, as seen in other bacterial opp operons, it appears that among oppA-I, -II, and -III, as well as oppA-IV and -V, each has a potential upstream promoter region. We tested the function of these putative promoter sequences by fusion to a promoterless β-galactosidase reporter gene in pCB182. Each of the promoter regions was found to be active. The level of activity in the reporter constructs closely paralleled the level of expression of each gene in in vitro-grown B. burgdorferi. Changes in carbon and nitrogen availability differentially affected individual promoters, but no changes in promoter activity were seen when Escherichia coli bacteria (with the promoter constructs) were grown in various concentrations of phosphate and leucine and changes in pH. Expression of specific oppA genes with B. burgdorferi varied significantly between its mouse and fed and unfed tick hosts. Differences in regulation of opp gene expression suggest a potential role in environmental response by the organism.
Respiratory Syncytial Virus Infection in Recipients of Allogeneic Stem-Cell Transplantation: A Retrospective Study of the Incidence, Clinical Features, and Outcome

Background. Respiratory syncytial virus (RSV) is a common cause of serious respiratory infections in hematopoietic stem-cell transplant (HSCT) recipients. We aimed to determine the frequency, risk factors, and outcome of RSV infection in allo-HSCT recipients. Design and methods. Data were collected from 275 allo-HSCT recipients and identified 32 patients (11.6%, 26 adults and 6 children) RSV infection. A control group was selected matched for age, conditioning intensity and regimens, year of transplant. Results. Eighteen patients had upper and 14 had lower respiratory tract infection (LRTI). The duration of viral shedding was long (20 days; 7–84). Twenty-eight patients received ribavirin (6 received intravenously, 11 orally, 9 both, 1 oral +aerosolized, and 1 received all three forms). The median duration of therapy was 22.5 days (7–54 days). Three (1.1% of entire cohort, 9.4% of infected patients; 21.4% of patients with LRTI) patients died from the RSV (attributable mortality), whereas two patients died from other subsequent infections 38 days to 5 months after diagnosis of RSV. Seven patients died from progression of underlying disease. Long-term respiratory function was assessed in 14 patients. Two patients died from respiratory failure. Three of 14 patients developed marked respiratory dysfunction after SCT. Three of 16 patients in the RSV group had normal respiratory function compared with 18 of 26 in the control group (P<0.01). Conclusion. RSV infection results in a low overall attributable mortality after allo-HSCT, but progression of the infection to LRTI is associated with increased risk for death. Late respiratory dysfunction is more common among patients, experienced RSV infection compared with controls.
Mapping PrPSc Propagation in Experimental and Natural Scrapie in Sheep with Different PrP Genotypes

Twenty-one orally inoculated and seven naturally infected sheep with scrapie were examined for PrPSc in peripheral tissues and in the central nervous system (CNS), using immunohistochemistry. In the inoculated group, VRQ (valine at codon 136, arginine at codon 154 and glutamine at codon 171)/VRQ sheep generally had a greater accumulation of the pathologic form of prion protein (PrPSc) in peripheral tissues, as compared with VRQ/ARQ (alanine at codon 136, arginine at codon 154, and glutamine at codon 171) animals at corresponding time points after inoculation. PrPSc was not detected in the ileal Peyer's patch, the spleen, the superficial cervical lymph node, and peripheral nervous tissues of several inoculated VRQ/ARQ animals. All inoculated VRQ/VRQ sheep, but only one of eight inoculated VRQ/ARQ animals, were PrPSc-positive in the CNS. Thus, the propagation of PrPSc seemed slower and more limited in VRQ/ARQ animals. Tissue and cellular localization of PrPSc suggested that PrPSc was disseminated through three different routes. PrPSc-positive cells in lymph node sinuses and in lymphatics indicated spreading by lymph. The sequential appearance of PrPSc in the peripheral nervous system and the CNS, with satellite cells as early targets, suggested the periaxonal transportation of PrPSc through supportive cells. Focal areas of vascular amyloid-like PrPSc in the brain of five sheep, suggested the hematogenous dissemination of PrPSc. There was a poor correlation between the amount of PrPSc in the CNS and clinical signs. One subclinically affected sheep showed widespread PrPSc accumulation in the CNS, whereas three sheep had early clinical signs without detectable PrPSc in the CNS. A VV136 (homozygous for valine at codon 136) sheep inoculated with ARQ/ARR (alanine at codon 136, arginine at codon 154, and arginine at codon 171) tissue succumbed to disease, demonstrating successful heterologous transmission. Less susceptible sheep receiving VRQ/VRQ or ARQ/ARR material were PrPSc-negative by immunohistochemistry, enzyme-linked immunosorbent assay, and western blot.
Altered Expression of Aquaporins in Bullous Keratopathy and Fuchs' Dystrophy Corneas

Corneas with edema-related diseases lose transparency, which causes significant vision loss. This study analyzed seven aquaporins (AQPs) in normal corneas, pseudophakic/aphakic bullous keratopathy (PBK/ABK) corneas, Fuchs' dystrophy corneas, keratoconus corneas, post-cataract surgery (PCS) corneas, and normal organ-cultured corneas. RNA levels for AQP1, AQP4, and β2-microglobulin were measured by RT-PCR. AQP1 antibody localized to stromal cells of all corneas. PBK/ABK and Fuchs' dystrophy corneas had decreased endothelial cell staining compared with normal. AQP1 mRNA was found in whole corneas and cultured stromal fibroblasts but not in isolated epithelial cells. AQP3 staining was found in basal epithelial cells of the normal, Fuchs' dystrophy, and keratoconus corneas but throughout the entire epithelium of PBK/ABK corneas. AQP4 antibody localized to endothelial cells of all corneas and in stromal cells of PBK/ABK corneas. AQP4 mRNA was identified in whole human corneas. AQP5 was found in epithelial cells of all corneas. AQP0, AQP2, and AQP9 were not found in any corneas. Normal AQP distributions were found in PCS and organ-cultured corneas, although they showed signs of swelling. Our study demonstrates that AQP abnormalities are found in PBK/ABK corneas (decreased AQP1, increased AQP3 and AQP4) and Fuchs' dystrophy corneas (decreased AQP1). Although both have vision-disrupting corneal edema, the mechanisms of fluid accumulation may be different in each disease.
“It’s Back! My Remission Is Over”

Cancer in adolescence presents unique challenges to patients and families due to the dramatic physical and psychological vulnerabilities that occur during a time of identity development. Additionally, adolescents who experience progression of their cancer, or failure of first-line therapies, represent an understudied group within pediatric oncology. Illness blogs offer a unique opportunity to understand the experience of a chronic or serious illness through a naturalistic and longitudinal perspective that is inherently patient centered. The purpose of this exploratory qualitative study was to describe the experiences of adolescents with cancer who experienced disease progression through analysis of their online illness blogs. Seven illness blogs written by adolescents with cancer diagnosed between the ages of 13 and 18 years were analyzed using thematic analysis. Several key themes were described among the adolescents, including normalizing the news, facing treatment failure, and reconciling chronos—the finite concept of time. These findings provide vital descriptive evidence for the experience of disease progression as described by adolescents, as well as identifying key points of further study and intervention development for nurse researchers and nurses who care for this vulnerable patient population.
A Single-Nucleotide-Polymorphism-Based Multilocus Genotyping Assay for Subtyping Lineage I Isolates of Listeria monocytogenes

ABSTRACT Listeria monocytogenes is a facultative intracellular pathogen responsible for food-borne disease with high mortality rates in humans and is the leading microbiological cause of food recalls. Lineage I isolates of L. monocytogenes are a particular public health concern because they are responsible for most sporadic cases of listeriosis and the vast majority of epidemic outbreaks. Rapid, reproducible, and sensitive methods for differentiating pathogens below the species level are required for effective pathogen control programs, and the CDC PulseNet Task Force has called for the development and validation of DNA sequence-based methods for subtyping food-borne pathogens. Therefore, we developed a multilocus genotyping (MLGT) assay for L. monocytogenes lineage I isolates based on nucleotide variation identified by sequencing 23,251 bp of DNA from 22 genes distributed across seven genomic regions in 65 L. monocytogenes isolates. This single-well assay of 60 allele-specific probes captured 100% of the haplotype information contained in approximately 1.5 Mb of comparative DNA sequence and was used to reproducibly type a total of 241 lineage I isolates. The MLGT assay provided high discriminatory power (Simpson's index value, 0.91), uniquely identified isolates from the eight listeriosis outbreaks examined, and differentiated serotypes 1/2b and 4b as well as epidemic clone I (ECI), ECIa, and ECII. In addition, the assay included probes for a previously characterized truncation mutation in inlA, providing for the identification of a specific virulence-attenuated subtype. These results demonstrate that MLGT represents a significant new tool for use in pathogen surveillance, outbreak detection, risk assessment, population analyses, and epidemiological investigations.
Inhibition of Src with AZD0530 reveals the Src-Focal Adhesion kinase complex as a novel therapeutic target in papillary and anaplastic thyroid cancer.

CONTEXT Focal adhesion kinase (FAK) and Src are overexpressed and activated in many cancers and have been associated with tumor progression. The role of the Src-FAK complex has not been characterized in papillary and anaplastic thyroid cancer (PTC and ATC). OBJECTIVE The goal of this study was to determine the role of Src and FAK in the growth and invasion of PTC and ATC. DESIGN PTC and ATC cells were treated with the oral Src inhibitor, AZD0530, to determine the consequences of Src inhibition using growth and invasion assays. FAK and phospho-FAK levels were analyzed in cell lines as well as in PTC tumor samples. RESULTS AZD0530 treatment inhibited the growth and invasion in four of five thyroid cancer cell lines, and inhibition did not correlate with basal levels of phospho-Src. Instead, we show for the first time that FAK, a critical substrate and effector of Src, is phosphorylated at tyrosine residue 861 (pY861) in PTC and ATC cells, and high levels of phospho-FAK correlate with AZD0530 sensitivity. We further showed that pY861-FAK phosphorylation is Src-dependent. Sensitivity to AZD0530 was confirmed using a preclinical three-dimensional culture model. Phospho-ERK1/2 was not affected by AZD0530, indicating that Src signaling does not require MAPK. Finally, FAK and pY861-FAK were expressed in 10 of 10 and five of 10 PTC tumors, respectively. CONCLUSIONS Inhibition of the Src-FAK complex represents a promising therapeutic strategy for patients with advanced thyroid cancer, and phospho-FAK represents a potential biomarker for response.
Factors Associated with the Excessive CD-13 Undervote in the 2006 General Election in Sarasota County, Florida

∗We thank Martha Mahoney for helpful discussion and Herbie Ziskend for assistance. This material is based in part upon work supported by the National Science Foundation under Grant No. CNS-0524155. Any opinions, findings, and conclusions or recommendations expressed in this material are those of the author(s) and do not necessarily reflect the views of the National Science Foundation. †Professor, Department of Government, Cornell University. 217 White Hall, Ithaca, NY 14853– 7901 (Phone: 607-255-3868; Fax: 607-255-4530; E-mail: wrm1@cornell.edu). ‡Professor, Department of Computer Science, Stanford University. Gates Building 3A, Stanford, CA 94305-9030 (Phone: 650-725-3642; Fax: 650-725-6949; E-mail: dill@cs.stanford.edu).
A SU-8-Based Microfabricated Implantable Inductively Coupled Passive RF Wireless Intraocular Pressure Sensor

With the growing demand in noncontact detection of human diseases, this paper presents an implantable passive wireless pressure sensor using an inductively coupled wireless sensing technique, particularly designed to monitor the intraocular pressure (IOP) of glaucoma patients. The microfabricated IOP sensor consists of a planar spiral gold coil inductor, a two-parallel-gold-plate (metal-insulator-metal) capacitor, and a SU-8 pressure-sensitive diaphragm. The IOP sensor is fully encapsulated inside biocompatible SU-8 stacking layers to isolate the IOP sensor from the biological tissue medium environment. By measuring the impedance phase dip frequency shift from the external coil, the IOP signal can be obtained through the implanted IOP sensor. The optimized size of the manually wound external coil was investigated. The readout distance is up to 6 mm from the implanted sensor. Characterization results show that the microfabricated IOP sensor has relatively high sensitivities-7035 ppm/mmHg in air and 3770 ppm/mmHg in saline medium-with pressure resolution lower than 1 mmHg, which is adequate for IOP monitoring application.
Expression of the proto-oncogene, trk, receptors in the developing rat retina

Abstract The neurotrophins, including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) and NT-4/5 are important in a variety of developmental processes in the peripheral and central nervous systems. These molecules bind to a low-affinity receptor and to distinct high-affinity receptors. The high-affinity receptor for NGF is the proto-oncogene product, p140trkA(trkA). Isoforms of p140trkA, p145trkB(trkB), and p140trkC(trkC), are the primary high-affinity receptors for BDNF and NT-3, respectively. We evaluated the developmental regulation of the high-affinity neurotrophin receptors in the rat retina using polyclonal antibodies directed to a highly conserved region of the C-terminus of the p140trkA isoforms (pantrk) and antibodies directed to unique amino-acid sequences of p140trkA, p145trkB, and p140trkC. Immunoreactivities for trkA and trkB, as well as pantrk, were detected in the developing retina and showed similar distributions. At similar antibody concentrations, trkC immunoreactivity was not detected. In the embryo, immunoreactivities were present in cells located throughout the neuroblastic retina, especially in the inner retinal layers, and in fibers in the nerve fiber layer and optic nerve. In the newborn retina, immunoreactivities for these two receptor isoforms were localized to numerous somata in the inner nuclear layer (INL), as well as to cells in the ganglion cell layer (GCL) and axons in the nerve fiber layer and optic nerve. A similar pattern of immunostaining persisted throughout the first postnatal week. By postnatal day-10, immunostaining was confined to large-diameter cells in the GCL, both heavily stained and lightly stained cells in the INL and a plexus of processes in the inner plexiform layer (IPL). In the adult retina, specific immunoreactivity was present in sparsely distributed, lightly and moderately stained, large cells in the GCL, numerous lightly and moderately stained cells throughout the INL and in plexuses of processes in the IPL and outer plexiform layer. Specific immunostaining of photoreceptor cells was not observed. These observations indicate that high-affinity receptors for the neurotrophins are expressed in cells of the inner retina, including ganglion cells, during the period of retinal development. This is congruent with roles for neurotrophins in such processes as survival, differentiation and synapse formation of cells in the developing visual system.
Discharge Counseling for Patients with Heart Failure or Myocardial Infarction: A Best Practices Model Developed by Members of the American College of Clinical Pharmacy's Cardiology Practice and Research Network Based on the Hospital to Home (H2H) Initiative

Hospital to Home is a quality‐based initiative led by the American College of Cardiology and the Institute for Healthcare Improvement, aimed at reducing 30‐day hospital readmission rates for patients with heart failure or myocardial infarction. Several factors have been shown to attribute to early readmission for these conditions including comorbidities, environmental factors, insufficient discharge planning, lack of health literacy, and nonadherence to drug therapy. Pharmacists play a significant role in reducing readmissions by ensuring that appropriate evidence‐based pharmacotherapy regimens have been prescribed during hospitalization; monitoring for drug duplications, medication errors, and adverse reactions; and performing medication reconciliation. Studies have demonstrated the role of pharmacists in reducing medication‐related visits to the emergency department as well as hospital readmissions, solely by preventing adverse drug events. Although all of these factors impact early readmissions, providing quality counseling to the patient as well as the patients' caregiver(s) at discharge is critical in order to optimize adherence as well as outcomes. In order to accomplish the goal of reducing readmissions, health care providers must partner together across the continuum of care and include pharmacists as pivotal members of the health care team. In this best practice statement, we summarize key components of discharge counseling for patients with heart failure or myocardial infarction including medication use, medication dose and frequency, drug interactions, medications to avoid, common adverse effects, role of the medication in the disease state, signs and symptoms of the disease, diet, the patient's role in self‐care (lifestyle modifications), and when patients should seek medical advice.
Management of the Cardinal Features of Andropause

There are several problems facing aging men, especially sexual dysfunction, hypogonadism, and psychologic changes. This constellation of changes is sometimes referred to as “manopause” or “andropause. ” Unlike the dramatic changes in the hormonal milieu occurring during menopause in women, the age-related changes in reproductive hormones of men are subtle and occur gradually throughout the years of mature life. It has been estimated that circulating testosterone (T) declines longitudinally from age 19 at an average rate of 1% per year. The free or dialyzable fraction of serum T and the bioavailable (the sum of free fraction and loosely bound to albumin fraction) T decline more rapidly with age. Although the essential role of androgens in reproductive tissue development and emergence of secondary sex characteristics is well known, their role in adult sexual function seems to be primarily facultative. The effect of T on the central nervous system extends beyond sexual behavior. T has been shown to alter mood, memory, ability to concentrate, and the overall sense of vigor and well being that may interact with a host of other psychologic changes associated with aging. Disordered erectile function is not generally an endocrine problem but rather vascular, neurologic, and psychogenic in origin. It also may be the first sign of systemic vascular disease. The clinical management of andropause requires an individualized approach. In some men, the main problem may be psychologic, whereas in others, hypogonadism may play an important role. Many with erectile failure, suffer silently regardless of its etiology. In this review, we suggest some practical guidelines for the management of these conditions.
Optimising microservice-based reliable NFV management & orchestration architectures

A highly reliable set up of Management and Orchestration (MANO) functionality is crucial for telecom operators in order to support demanding NFV-powered telecom services such as elastic emergency or security services, or other applications requiring fast, dynamic and reliable (re-) provisioning processes. NFV MANO functionality controls the entire life cycle of such services, from instantiation and configuration to monitoring, migrating, scaling and terminating them. In this paper, we introduce tunable and scalable mechanisms that provide MANO with high availability and fault recovery, two reliability facets that are barely covered in the data plane dominated state-of-the-art. The mechanisms use state sharing and distributed load balancing in the context of both a centralised and distributed microservice-based architecture. The proposed mechanisms are unique as they are able to quantitatively characterise the trade-offs between both the degree of reliability and the associated cost in terms of bandwidth and computing power. This feature allows us to introduce a cost function to determine which configuration of the mechanism is optimal with respect to an operator's needs.