Miracle-dz/UniFAR-FTUs huggingface dataset:
Chemotaxonomic differentiation of legionellae by detection and characterization of aminodideoxyhexoses and other unique sugars using gas chromatography-mass spectrometry

Legionellae have been differentiated previously by analyzing their carbohydrate contents by gas chromatography with flame ionization detection. In the present study, total ion mode gas chromatography-mass spectrometry (GC-MS) was used to detect a number of unusual sugars, including one that is structurally related to O-methyldideoxyheptoses. Increased sensitivity and selectivity for carbohydrate detection was achieved by selected ion-monitoring GC-MS. Two of the uncommon sugars previously discovered in the legionellae (X1 and X2) were identified as quinovosamine and fucosamine, respectively. Legionella pneumophila contained rhamnose and quinovosamine but not the quinovosamine isomer fucosamine. Tatlockia micdadei and Legionella maceachernii contained large amounts of rhamnose, fucose, and fucosamine but not quinovosamine. These two species were the only legionellae studied that contained another unusual sugar that is referred to as X3, pending determination of its structure. Fluoribacter dumoffi, Fluoribacter bozemanae, and Legionella anisa were varied in their carbohydrate contents, both within and between species, but could be distinguished from L. pneumophila and the T. micdadei and L. maceachernii group. Fluoribacter gormanii was unique among the legionellae in that it lacked both quinovosamine and fucosamine. Legionella jordanis contained other unusual carbohydrates in addition to quinovosamine. GC-MS may have wide application in the differentiation of bacterial species.
Sex cord‐stromal tumours of the ovary

The aim of this review is to give a reasonably concise resumé of our knowledge of the sex cord‐stromal tumours of the ovary. Lipoid cell tumours of the ovary are often included within this broad category but this poorly defined and heterogenous group of neoplasms will not be considered here. This review is a selective one and no attempt is made to cover all aspects of sex cord‐stromal tumours or to provide a complete bibliography. The histological features of many of the neoplasms in this group, particularly those which have been recently defined, are discussed but a consideration of differential histological diagnosis is excluded. The ultrastructural characteristics of the various neoplasms are considered only in terms of their relevance to histogenesis or metabolic activity.
HIV-1 Envelope Triggers Polyclonal Ig Class Switch Recombination through a CD40-Independent Mechanism Involving BAFF and C-Type Lectin Receptors1

Switching from IgM to IgG and IgA is essential for antiviral immunity and requires engagement of CD40 on B cells by CD40L on CD4+ T cells. HIV-1 is thought to impair CD40-dependent production of protective IgG and IgA by inducing progressive loss of CD4+ T cells. Paradoxically, this humoral immunodeficiency is associated with B cell hyperactivation and increased production of nonprotective IgG and IgA that are either nonspecific or specific for HIV-1 envelope glycoproteins, including gp120. Nonspecific and gp120-specific IgG and IgA are sensitive to antiretroviral therapy and remain sustained in infected individuals with very few CD4+ T cells. One interpretation is that some HIV-1 Ags elicit IgG and IgA class switch DNA recombination (CSR) in a CD40-independent fashion. We show that a subset of B cells binds gp120 through mannose C-type lectin receptors (MCLRs). In the presence of gp120, MCLR-expressing B cells up-regulate the CSR-inducing enzyme, activation-induced cytidine deaminase, and undergo CSR from IgM to IgG and IgA. CSR is further enhanced by IL-4 or IL-10, whereas Ab secretion requires a B cell-activating factor of the TNF family. This CD40L-related molecule is produced by monocytes upon CD4, CCR5, and CXCR4 engagement by gp120 and cooperates with IL-4 and IL-10 to up-regulate MCLRs on B cells. Thus, gp120 may elicit polyclonal IgG and IgA responses by linking the innate and adaptive immune systems through the B cell-activating factor of the TNF family. Chronic activation of B cells through this CD40-independent pathway could impair protective T cell-dependent Ab responses by inducing immune exhaustion.
Domain 3 of NS5A Protein from the Hepatitis C Virus Has Intrinsic α-Helical Propensity and Is a Substrate of Cyclophilin A*

Nonstructural protein 5A (NS5A) is essential for hepatitis C virus (HCV) replication and constitutes an attractive target for antiviral drug development. Although structural data for its in-plane membrane anchor and domain D1 are available, the structure of domains 2 (D2) and 3 (D3) remain poorly defined. We report here a comparative molecular characterization of the NS5A-D3 domains of the HCV JFH-1 (genotype 2a) and Con1 (genotype 1b) strains. Combining gel filtration, CD, and NMR spectroscopy analyses, we show that NS5A-D3 is natively unfolded. However, NS5A-D3 domains from both JFH-1 and Con1 strains exhibit a propensity to partially fold into an α-helix. NMR analysis identifies two putative α-helices, for which a molecular model could be obtained. The amphipathic nature of the first helix and its conservation in all genotypes suggest that it might correspond to a molecular recognition element and, as such, promote the interaction with relevant biological partner(s). Because mutations conferring resistance to cyclophilin inhibitors have been mapped into NS5A-D3, we also investigated the functional interaction between NS5A-D3 and cyclophilin A (CypA). CypA indeed interacts with NS5A-D3, and this interaction is completely abolished by cyclosporin A. NMR heteronuclear exchange experiments demonstrate that CypA has in vitro peptidyl-prolyl cis/trans-isomerase activity toward some, but not all, of the peptidyl-prolyl bonds in NS5A-D3. These studies lead to novel insights into the structural features of NS5A-D3 and its relationships with CypA.
Inhibition of in vitro Friend murine leukemia virus infection of lipopolysaccharide-activated B-cells with concanavalin A.

Stimulation with bacterial lipopolysaccharide (LPS) of splenic B-lymphocytes infected in vitro with Friend virus complex increased the number of cells with replicating murine leukemia virus (MuLV) [i.e., infectious centers (IC)] up to 100-fold. Concanavalin A (Con A) did not have such an effect. However, the addition of Con A to the LPS-stimulated cultures decreased the number of IC. The inhibitory concentration of Con A (2.5 microgram/ml) was eightfold less than that capable of neutralizing the in vitro infectivity of MuLV (20 microgram/ml). The effect of Con A was not mediated by T-cells; the inhibition of infection was comparable with use of whole spleen cell suspensions from normal BALB/c mice, with T-cell-depleted cell suspensions, or with spleen cells with congenitally athymic nude mice. However, specific removal of Con A from the surface of B-cells with alpha-methyl-D-mannopyranoside prior to the infection reversed the inhibitory effect entirely. It is suggested that the lectin interferes with MuLV on the membrane of B-cells.
Sphenoidal Mucoceles with Intracranial Extension

Two cases of sphenoid sinus mucocele with intracranial extension are presented. Multiplanar computed tomography scans delineated the extent of these lesions, facilitating both preoperative diagnosis and proper clinical management. One lesion was isodense and the other hyperdense (98 Hounsfield units: 1,000 scale). Neither demonstrated significant enhancement after the administration of contrast medium.
Rit-mediated Stress Resistance Involves a p38-Mitogen- and Stress-activated Protein Kinase 1 (MSK1)-dependent cAMP Response Element-binding Protein (CREB) Activation Cascade*

Background: Rit signaling promotes cell survival. Results: Rit controls stress-dependent p38-MSK1 signaling and CREB-mediated expression of anti-apoptotic Bcl-2 proteins. Conclusion: Rit regulates a p38-MSK1-CREB survival cascade in cells adapting to stress. Significance: Defining how diverse stimuli induce CREB-dependent gene expression is crucial to understanding complex cellular processes ranging from development to disease. The cAMP response element (CRE)-binding protein (CREB) is a key regulatory factor of gene transcription, and plays an essential role in development of the central nervous system and for neuroprotection. Multiple signaling pathways have been shown to contribute to the regulation of CREB-dependent transcription, including both ERK and p38 mitogen-activated protein (MAP) kinases cascades. Recent studies have identified the Ras-related small G-protein, Rit, as a central regulator of a p38-MK2-HSP27 signaling cascade that functions as a critical survival mechanism for cells adapting to stress. Here, we examine the contribution of Rit-p38 signaling to the control of stress-dependent gene transcription. Using a pheochromocytoma cell model, we find that a novel Rit-p38-MSK1/2 pathway plays a critical role in stress-mediated CREB activation. RNAi-mediated Rit silencing, or inhibition of p38 or MSK1/2 kinases, was found to disrupt stress-mediated CREB-dependent transcription, resulting in increased cell death. Furthermore, ectopic expression of active Rit stimulates CREB-Ser133 phosphorylation, induces expression of the anti-apoptotic Bcl-2 and BclXL proteins, and promotes cell survival. These data indicate that the Rit-p38-MSK1/2 signaling pathway may have an important role in the stress-dependent regulation of CREB-dependent gene expression.
Prevalence and factors associated with self-reported vaccination rates among US adults at high risk of vaccine-preventable hepatitis*

ABSTRACT Background: Despite a routine vaccination for preventing HAV and HBV in young age groups during the past decade, adults at high risk of hepatitis are not reached effectively by vaccination programs. This study sought to estimate the prevalence of adults at higher risk of vaccinepreventable hepatitis (hepatitis A virus (HAV) and hepatitis B virus (HBV)) in the US and their vaccination rates. Also, the association between vaccination rates and selected demographic, socioeconomic characteristics and comorbidities was investigated. Methods: Four years, 1999–2002, of publicly available National Health and Nutrition Examination Survey (NHANES) data were utilized. Survey participants aged 20–59 years were selected. A survey participant was considered at higher risk when their situation and/or behavior placed them at a greater risk of contracting hepatitis as identified by the Centers for Disease Control and Prevention. All prevalence estimates were weighted to represent the total US population using 4-year interview and examination weights. Logistic regression was utilized to identify factors associated with vaccination rates. Results: The study included 6237 survey participants who represent over 153 million adults age 20–59 years. Of these adults, 8.0%, 12.3% and 1.4% were at higher risk of HAV, HBV or both respectively. The self-reported vaccination rates among the higher risk population groups were 13%, 23.6% and 13.4% respectively. The most prevalent risk groups were persons with sexually transmitted diseases and persons using noninjection illegal drugs. Within the higher risk population, being single, male, aged 50–59 years and uninsured were all significantly (p < 0.05) less likely to be vaccinated than their counterparts. Limitations: The results of this study should be interpreted within the context of the following limitations: (1) the potential biases associated with participants' self-reported vaccination rates; (2) institutionalized US population with high prevalence rates of hepatitis infection are not included in the NHANES data. Conclusions: Among the population identified at higher risk of vaccine-preventable hepatitis (HAV, HBV or both), only a small proportion of this group had evidence of hepatitis vaccination.
Downlink Spectrum Sharing for Cognitive Radio Femtocell Networks

Femtocell is envisioned as a highly promising solution for indoor wireless communications. The spectrum allocated to femtocells is traditionally from the same licensed spectrum bands of macrocells. In this case, the capacity of femtocell networks is highly limited due to the finite number of licensed spectrum bands and also the interference with macrocells and other femtocells. In this paper, we propose a radically new communication paradigm by incorporating cognitive radio in femtocell networks. The cognitive radio enabled femtocells are able to access spectrum bands not only from macrocells but also from other licensed systems (e.g. TV systems) provided the interference from femtocells to the existing systems is not harmful. It results in more channel opportunities for femtocells. Thus, the co-channel interference in femtocells can be greatly reduced and the network capacity can be significantly improved. Because of the difference from other traditional wireless networks, we argue the traditional spectrum sharing schemes such as coloring methods are not efficient to femtocell networks especially for dense deployment scenarios. We formulate the downlink spectrum sharing problem in cognitive radio femtocell networks, and employ decomposition theories to solve the problem. Simulation results indicate that cognitive radio enabled femtocells could achieve much higher capacity than the femtocell networks which do not employ agile spectrum access. Simulation results also show that our proposed scheme without any iteration can achieve almost twice of the average capacity by coloring method when the number of available channels is less than five. Moreover, our proposed scheme can converge very fast with a typical value of only five iterations, and it can achieve around two percent extra average capacity than the fixed power control scheme.
Apoptosis and proliferation as predictors of chemotherapy response in patients with breast carcinoma

Laboratory evidence suggests that many anticancer agents exert their effect by altering the ratio between apoptosis and cellular proliferation. The objective of this clinical study was to examine in vivo changes in apoptotic index (AI), Bcl‐2 expression, proliferation (Ki‐67 and S‐phase fraction [SPF]), and ploidy as potential indicators of chemoresponsiveness.
EVALUATION OF THE FINANCIAL PERFORMANCE OF PENSION

The aim of this paper is to evaluate the financial performance of pension funds in Croatia. Although there are other factors which are important in the pension funds overall performance, this paper focuses on investment accomplishments. The purpose of measuring portfolio performance is to determine whether portfolio managers add value compared to passive investment strategies. The traditional approach to pension funds’ performance evaluation underlines standard measures of financial performance (e.g. ratios such as Sharpe’s, Sortino’s, Treynor’s, etc.) which quantify the ability of pension fund managers to deliver an active management risk premium, with respect to benchmarks. In this paper, the previously mentioned traditional measures of risk-adjusted performance are applied to Croatian pension funds. Due to recent changes in pension systems in other Eastern European countries once again emphasis is put on this issue in Croatia. The analysis furthermore includes evaluation of pension funds’ asset allocation. The period of analysis covers twelve years, from the establishment of pension funds in Croatia in 2002 until 2013. The main hypothesis of the paper states that Croatian pension funds underperform with respect to benchmark comparisons, set as return on the combined CROBEX/CROBIS portfolio. Results show that the main hypothesis does not hold. The financial performance of pension funds directly influences their competitiveness, derived from the possibility of measuring their success in active portfolio management. In addition, pension funds are expected to support the national economy. By investing their accumulating assets, they can protect jobs and enhance economic growth. However, they can achieve that only if they are competitive in means of financial performance.
Monte Carlo analysis of single fiber reflectance spectroscopy: photon path length and sampling depth

Single fiber reflectance spectroscopy is a method to noninvasively quantitate tissue absorption and scattering properties. This study utilizes a Monte Carlo (MC) model to investigate the effect that optical properties have on the propagation of photons that are collected during the single fiber reflectance measurement. MC model estimates of the single fiber photon path length (⟨LSF⟩) show excellent agreement with experimental measurements and predictions of a mathematical model over a wide range of optical properties and fiber diameters. Simulation results show that ⟨LSF⟩ is unaffected by changes in anisotropy (g ∊ [0.8, 0.9, 0.95]), but is sensitive to changes in phase function (Henyey–Greenstein versus modified Henyey–Greenstein). A 20% decrease in ⟨LSF⟩ was observed for the modified Henyey–Greenstein compared with the Henyey–Greenstein phase function; an effect that is independent of optical properties and fiber diameter and is approximated with a simple linear offset. The MC model also returns depth-resolved absorption profiles that are used to estimate the mean sampling depth (⟨ZSF⟩) of the single fiber reflectance measurement. Simulated data are used to define a novel mathematical expression for ⟨ZSF⟩ that is expressed in terms of optical properties, fiber diameter and ⟨LSF⟩. The model of sampling depth indicates that the single fiber reflectance measurement is dominated by shallow scattering events, even for large fibers; a result that suggests that the utility of single fiber reflectance measurements of tissue in vivo will be in the quantification of the optical properties of superficial tissues.
Pyloric Gland Adenoma: An Entity Distinct From Gastric Foveolar Type Adenoma

Pyloric gland adenoma (PGA) is a rare neoplasm demonstrating gastric epithelial differentiation. In this series, we studied 41 PGAs from 36 patients. We compared them to 28 gastric foveolar type gastric adenomas (GTAs) from 25 patients. PGAs occurred in an older population with a mean age of 73 compared with 48 in GTAs (P<0.001). There was a significant female predominance, particularly for gastric PGAs. Morphologically, PGAs were characterized by closely packed pyloric gland-type tubules with a monolayer of cuboidal to low columnar epithelial cells containing round nuclei and pale to eosinophilic cytoplasm with a ground glass appearance. The cells lacked an apical mucin cap, a feature distinct from GTAs. An immunohistochemical panel of mucin core peptides (MUCs) and CDX2 was performed on a subset of the lesions. All PGAs expressed MUC6 with coexpression of MUC5AC, whereas GTAs expressed predominantly MUC5AC without MUC6. Both lesions lacked CDX2 and MUC2 except in areas of intestinal metaplasia (IM) found in some PGAs. Histologic features consistent with conventional dysplasia were found in 26 (63.4%) PGAs. Using a 2-tier grading system, 5 (12.2%) cases demonstrated low-grade dysplasia whereas 21 (51.2%) cases showed high-grade dysplasia including 5 (12.2%) cases with an associated intramucosal or more deeply invasive adenocarcinoma. This was significantly different from GTAs; all cases showed only low-grade dysplasia (P<0.001). In addition, 60% of gastric PGAs were associated with IM in the surrounding mucosa and 40% of lesions arose in a background of autoimmune gastritis, whereas these 2 conditions were only associated with 1 case (3%) of GTA. In summary, PGA is a distinct entity. Despite its bland histologic appearance, it is much more likely to be accompanied by background IM and autoimmune gastritis and can evolve into invasive adenocarcinoma displaying pyloric gland differentiation.
Hypoperfusion of Wernicke's area predicts severity of semantic deficit in acute stroke

Based on earlier findings that the presence of word comprehension impairment (a deficit in the meaning of words, or lexical semantics) in acute stroke was strongly associated with the presence of hypoperfusion or infarct in Wernicke's area, we tested the hypothesis that the severity of word comprehension impairment was correlated with the magnitude of delay in perfusion of Wernicke's area on magnetic resonance perfusion‐weighted imaging. Eighty patients were prospectively studied within 24 hours of onset or progression of acute left hemisphere stroke symptoms, with diffusion‐weighted imaging, perfusion‐weighted imaging, and detailed language tests. For 50 patients without infarct in Wernicke's area, we found a strong Pearson correlation between the rate of errors on a word comprehension test and the mean number of seconds of delay in time‐to‐peak concentration of contrast in Wernicke's area, relative to the homologous region on the right. These results add further evidence for the crucial role of Wernicke's area (Brodmann's area 22) in word comprehension and indicate that the magnitude of delay on PWI may be a gross indicator of tissue dysfunction.
Stretch of the Vascular Wall Induces Smooth Muscle Differentiation by Promoting Actin Polymerization*

Stretch of the vascular wall by the intraluminal blood pressure stimulates protein synthesis and contributes to the maintenance of the smooth muscle contractile phenotype. The expression of most smooth muscle specific genes has been shown to be regulated by serum response factor and stimulated by increased actin polymerization. Hence we hypothesized that stretch-induced differentiation is promoted by actin polymerization. Intact mouse portal veins were cultured under longitudinal stress and compared with unstretched controls. In unstretched veins the rates of synthesis of several proteins associated with the contractile/cytoskeletal system (α-actin, calponin, SM22α, tropomyosin, and desmin) were dramatically lower than in stretched veins, whereas other proteins (β-actin and heat shock proteins) were synthesized at similar rates. The cytoskeletal proteins γ-actin and vimentin were weakly stretch-sensitive. Inhibition of Rho-associated kinase by culture of stretched veins with Y-27632 produced similar but weaker effects compared with the absence of mechanical stress. Induction of actin polymerization by jasplakinolide increased SM22α synthesis in unstretched veins to the level in stretched veins. Stretch stimulated Rho activity and phosphorylation of the actin-severing protein cofilin-2, although both effects were slow in onset (Rho-GTP, >15 min; cofilin-P, >1 h). Cofilin-2 phosphorylation of stretched veins was inhibited by Y-27632. The F/G-actin ratio after 24 h of culture was significantly greater in stretched than in unstretched veins, as shown by both ultracentrifugation and confocal imaging with phalloidin/DNase I labeling. The results show that stretch of the vascular wall stimulates increased actin polymerization, activating synthesis of smooth muscle-specific proteins. The effect is partially, but probably not completely, mediated via Rho-associated kinase and cofilin downstream of Rho.