Miracle-dz/UniFAR-FTUs huggingface dataset:
Gender differences in coping with functional disability in older married couples: The role of personality and social resources

The present study examines the impact of functional disability on subjective well-being (SWB) and the moderating effects of personal resources on a sample of 144 community-dwelling, older adult couples age 60–84 years, with emphasis on gender differences in both direct and moderating effects. Functional disability in self and in the spouse was associated with poorer well-being in both men and women, but differences were found by gender in the effects of coping resources. While high neuroticism was associated with poorer well-being for both husbands and wives, extraversion and social support had unique benefits in enhancing well-being only in husbands. Husbands were more introverted, and had fewer social resources, and individual differences in social resources may be more critical for older husbands. Results are interpreted in terms of gender differences in coping and their implications for interventions to enhance well-being in older adults.
Homing in hematopoietic stem cells: focus on regulatory role of CXCR7 on SDF1a/CXCR4 axis

Hematopoietic stem cells (HSCs) form a rare population of multipotent stem cells, which give rise to all hematopoietic lineages. HSCs home to bone marrow niches and circulate between blood and bone marrow. Many factors, especially SDF1a, affect the circulation of HSCs, but these have not been fully recognized. SDF1a has been shown to bind CXCR7 in addition to CXCR4 and can also function as SDF1a/CXCR4 modulator. CXCR7 plays a role in HSCs homing via SDF1a gradient and is a mediator of CXCR4/SDF1a axis. This review describes the current concepts and questions concerning CXCR7/CXCR4/SDF1a axis as an important key in hematopoietic stem cells homing with particular emphasis on CXCR7 receptor. Homing of HSCs is an essential step for successful hematopoietic stem cell transplantation.
Forward Integration by a Monopolist: Some Extensions

Vertical integration by imperfectly competitive firms poses both positive and normative economic questions. The positive questions concern the incentives of such firms to engage in forward or backward integration. On the other hand, the normative questions concern the impact of integration by such firms on social welfare. If the incentives of imperfectly competitive firms lead to a welfare gain, then there is no need for public intercession in the process, say, by antitrust authorities. However, if private incentives are at odds with social welfare, then public policy attention may be needed. These matters are considered in an extensive theoretical and empirical literature on vertical integration. A review of the central issues in this literature is provided by Machlup and Taber [5] and Warren-Boulton [12]. Here, I shall focus on the recent work by Schmalensee [8] and Warren-Boulton [11] on forward integration by a monopolist. The basic insight of their models is as follows. Suppose a monopolist is producing a product used as an input by a competitive downstream industry in variable proportions with another input. Monopoly pricing of the first input induces inefficient input utilization by the downstream industry in the production of the final good (the monopoly input price exceeds its marginal costs of production). The resulting efficiency loss represents an incentive for the monopolist to integrate forward. By producing the final product in an integrated firm, the monopolist "transfer" prices the otherwise monopolized input at marginal costs and thereby converts the efficiency loss into profit. This point was originally made by Burstein [3], but the recent work appears to have been motivated by the graphical formulation of Vernon and Graham [10]. After developing the case of a fixed proportions technology we present the Vernon and Graham illustration.
Serum and Urinary Concentrations of Type IV Collagen and Laminin as a Marker of Microangiopathy in Diabetes

Serum and urinary concentrations of type IV collagen and laminin were measured by enzyme‐linked immunosorbent assay (ELISA) in diabetic patients and compared with normal control subjects. In diabetic patients with proteinuria or with renal insufficiency, serum and urinary concentrations of type IV collagen were higher than those of control subjects (p < 0.005). Furthermore urinary concentrations of type IV collagen and laminin were significantly higher in diabetes, even in the absence of nephropathy, than in normal controls (p < 0.05). Urinary concentrations of type IV collagen in patients with diabetes and microalbuminuria (0.73 ± 0.11 mg mmol−1) were significantly higher than in diabetic patients without nephropathy (0.40 ± 0.060 mg mmol−1) (p < 0.025). Urinary concentrations of type IV collagen may have a role as an indicator of early diabetic nephropathy. Serum concentrations of type IV collagen in diabetic patients with retinopathy were significantly higher than in normal controls (p < 0.025). However, urinary concentrations of type IV collagen (p < 0.05) and serum concentrations of laminin (p < 0.025) were significantly higher in diabetic patients than normal controls and the difference between patients with and without retinopathy was not significant.
Durable Mucosal Simian Immunodeficiency Virus-Specific Effector Memory T Lymphocyte Responses Elicited by Recombinant Adenovirus Vectors in Rhesus Monkeys

ABSTRACT The induction of potent and durable cellular immune responses in both peripheral and mucosal tissues may be important for the development of effective vaccines against human immunodeficiency virus type 1 and other pathogens. In particular, effector responses at mucosal surfaces may be critical to respond rapidly to incoming mucosal pathogens. Here we report that intramuscular injection of nonreplicating recombinant adenovirus (rAd) vectors into rhesus monkeys induced remarkably durable simian immunodeficiency virus (SIV)-specific T lymphocyte responses that persisted for over 2 years in both peripheral blood and multiple mucosal tissues, including colorectal, duodenal, and vaginal biopsy specimens, as well as bronchoalveolar lavage fluid. In peripheral blood, SIV-specific T lymphocytes underwent the expected phenotypic evolution from effector memory T cells (TEM) to central memory T cells (TCM) following vaccination. In contrast, mucosal SIV-specific T lymphocytes exhibited a persistent and durable TEM phenotype that did not evolve over time. These data demonstrate that nonreplicating rAd vectors induce durable and widely distributed effector memory mucosal T lymphocyte responses that are phenotypically distinct from peripheral T lymphocyte responses. Vaccine-elicited TEM responses at mucosal surfaces may prove critical for affording protection against invading pathogens at the mucosal portals of entry.
Susceptibility of stromelysin 1-deficient mice to collagen-induced arthritis and cartilage destruction.

OBJECTIVE It has long been proposed that stromelysin is one of the major degradative matrix metalloproteinases responsible for the loss of cartilage in rheumatoid arthritis (RA) and osteoarthritis (OA). This hypothesis was tested by examining the arthritic paws of stromelysin 1 (SLN1)-deficient mice for loss of cartilage and for generation of neoepitopes that would be indicative of aggrecan cleavage. METHODS The SLN1 gene was inactivated in murine embryonic stem cells, and knockout mice deficient in SLN1 activity were bred onto the B10.RIII background. The incidence and severity of collagen-induced arthritis (CIA) were compared in wild-type and knockout mice. Paws from mice with CIA were examined for loss of cartilage and for proteoglycan staining, as well as for the generation of the neoepitope FVDIPEN341. RESULTS SLN1-deficient mice developed CIA, as did the wild-type N2 mice. Histologic analyses demonstrated no significant differences among the B10.RIII, wild-type, and knockout mice in loss of articular cartilage and proteoglycan staining. No decrease in the FVDIPEN341 epitope was observed in the SLN1-deficient mice. CONCLUSION Disruption of the SLN1 gene neither prevents nor reduces the cartilage destruction associated with CIA. Moreover, SLN1 depletion does not prevent the cleavage of the aggrecan Asn341-Phe342 bond.
CUDA-MAFFT: Accelerating MAFFT on CUDA-enabled graphics hardware

Multiple sequence alignment (MSA) constitutes an extremely powerful tool for many biological applications including phylogenetic tree estimation, secondary structure prediction, and critical residue identification. However, aligning large biological sequences with popular tools such as MAFFT requires long runtimes on sequential architectures. Due to the ever increasing sizes of sequence databases, there is increasing demand to accelerate this task. In this paper, we demonstrate how Graphic Processing Units (GPUs), powered by the Compute Unified Device Architecture (CUDA), can be used as an efficient computational platform to accelerate the MAFFT algorithm. To fully exploit the GPU's capabilities for accelerating MAFFT, we have optimized the sequence data organization to eliminate the bandwidth bottleneck of memory access, and designed a memory allocation and reuse strategy to make full use of limited memory of GPUs. Our implementation achieves speedup up to 19.58 and 4.14 on an NVIDIA Tesla C2050 GPU compared to the sequential and multi-thread MAFFT 7.017, respectively.
Longitudinal evaluation of adrenocorticotrophin and β‐lipotrophin plasma levels following bilateral adrenalectomy in patients with Cushing's disease

OBJECTIVES Bilateral adrenalectomy may be indicated in patients with Cushing's disease in whom hypercortlsolism is not resolved after pituitary microsurgery. However, Nelson's syndrome is a major long‐term complication of such therapy. We have carried out a longitudinal study on patients with Cushing's disease who underwent bilateral adrenalectomy comparing plasma /Mipotrophin (β‐LPH) with ACTH levels.
Finding the Pitch of the Missing Fundamental in Infants

Pitch perception is critical for the perception of speech and music, for object identification, and for auditory scene analysis, whereby representations are derived for each sounding object in the environment from the complex sound wave that reaches the ears. The perceived pitch of a complex sound corresponds to its fundamental frequency. However, removal of energy at the fundamental does not alter the pitch because adults use the harmonics to derive the pitch (Bendor and Wang, 2005; Trainor, 2008). Although sound frequency is represented subcortically, the integration of harmonics into a representation of pitch does not occur until auditory cortex (Bendor and Wang, 2005). Given that auditory cortex is immature in young infants, we examined the development of cortical representations for pitch by measuring electrophysiological (EEG) responses to pitch changes that required processing the pitch of the missing fundamental. Adults and infants 4 months and older showed a mismatch negativity response to these pitch changes, but 3-month-old infants did not. Thus, cortical representations of the pitch of the missing fundamental emerge between 3 and 4 months of age, indicating that there is a profound change in auditory perception for pitch in early infancy.
Neuronal necrosis is regulated by a conserved chromatin-modifying cascade

Significance Neuronal necrosis widely occurs in devastating neurodegenerative diseases, such as stroke, traumatic brain injury, and Alzheimer’s disease. However, it has long been considered a stochastic process lacking genetic regulations. Our inadequate understanding of its molecular mechanism has hindered pharmacological design to suppress this type of cell death. Through construction and studying of a Drosophila model of neuronal necrosis, we identified a chromatin-modifying cascade to play a key role in execution of neuronal necrosis. Our results indicate that neuronal necrosis is a stereotypically regulated process in both insect and mammalian neurons. This discovery provides previously unidentified biomarkers and potential therapeutic targets for neuronal necrosis. Neuronal necrosis induced by calcium overload causes devastating brain dysfunction in diseases such as stroke and brain trauma. It has been considered a stochastic event lacking genetic regulation, and pharmacological means to suppress neuronal necrosis are lacking. Using a Drosophila model of calcium overloading, we found JIL-1/mitogen- and stress-activated protein kinase 1/2 is a regulator of neuronal necrosis through phosphorylation of histone H3 serine 28 (H3S28ph). Further, we identified its downstream events including displacement of polycomb repressive complex 1 (PRC1) and activation of Trithorax (Trx). To test the role of JIL-1/PRC1/Trx cascade in mammals, we studied the necrosis induced by glutamate in rat cortical neuron cultures and rodent models of brain ischemia and found the cascade is activated in these conditions and inhibition of the cascade suppresses necrosis in vitro and in vivo. Together, our research demonstrates that neuronal necrosis is regulated by a chromatin-modifying cascade, and this discovery may provide potential therapeutic targets and biomarkers for neuronal necrosis.
Prevalence of Urogenital Mycoplasmas and Ureaplasmas in Women After Kidney Transplantation

Background. The prevalence of urogenital mycoplasmas and ureaplasmas in kidney transplant and hemodialyzed patients was studied. Methods. Vaginal and cervical swabs taken from 40 women of the study group and 40 women of the control group were investigated. Identification of ureaplasmas, Mycoplasma genitalium, and human papillomavirus was performed by polymerase chain reaction. Each vaginal slide was evaluated for bacterial vaginosis. Results. Urogenital mycoplasmas and ureaplasmas were significantly more common in patients from the study group (40%) compared with the control group (27.5%). Mycoplasma hominis and M. genitalium were demonstrated only in a few cases. Ureaplasma parvum was isolated predominantly, but Ureaplasma urealyticum was more common in patients from study group (10%) compared with control group (2.5%). In all U. urealyticum-positive women from the study group, human papillomavirus DNA was detected. Conclusion. Our observation showed the necessity of careful examination of possible atypical pathogens in diagnostic materials from hemodialyzed and kidney transplant patients.
Antigenic characterization of respiratory syncytial virus associated with acute respiratory infections in Uruguayan children from 1985 to 1987

The occurrence of subgroup A and B strains of respiratory syncytial virus (RSV) was studied during three epidemic years, 1985 to 1987, in Uruguay. A set of monoclonal antibodies was selected according to their reactivity with local RSV isolates and used for the typing of RSV directly in nasopharyngeal cells by indirect immunofluorescence. Of 77 specimens, 69 could be typed as belonging to subgroup A or B, 5 could not be typed with the restricted set of monoclonal antibodies employed, and 3 reacted with both subgroup-specific antibodies. In 1985 and 1986 subgroup A predominated, accounting for 65.7% of all typed specimens, but in 1987 subgroup B surpassed subgroup A, accounting for 82.4% of the samples.
Histological alterations in the structure of the testis in tench (Tinca tinca) after exposure to 17 alpha‐ethynylestradiol

Environmental pollution with synthetic estrogens may pose a serious threat to reproduction of aquatic wildlife species. The current study describes the effects of 17α‐ethynylestradiol (EE2) on the structure of the testis in tench (Tinca tinca). Adult male tench were exposed to sublethal doses of EE2 (50, 100, and 500 μg/Kg t.w.) under semistatic conditions for a period of 30 days. The condition factor (CF), testicular somatic index (TSI), and histology (including a morphometric analysis) of the testis were examined. No consistent differences were observed in the CF of EE2‐exposed tench when compared with nonexposed fish. A significant decrease in TSI could only be observed at a 50 μg/Kg t.w. EE2 dose (p < 0.05) when compared with the control group. The histopathology of the testis was associated with loss of normal tubular structure with increased doses of exposure, decrease of tubule number, degeneration in Sertoli and Leydig cells, increase in necrotic testicular cells including formation of syncytia structures and, finally, a high incidence of fish with early primary oocytes at 100 and 500 μg/Kg t.w. EE2. These results indicate that long‐term exposure to EE2 may produce clear negative effects on testicular structure in tench. © 2013 Wiley Periodicals, Inc. Environ Toxicol 29: 1182–1192, 2014.
Neonatal sepsis and infection control policies in Australia

The pattern of neonatal bacterial infection, its management and the types of infection control policy were ascertained in 20 neonatal intensive care units (NICU) in Australia by questionnaire survey. Group B Streptococcus and Escherichia coli were the predominant organisms responsible for perinatally acquired infection for which the most common antibiotic combination used was Penicillin and Gentamicin. Staphylococcus epidermidis and aureus (majority Methicillin resistant) were the predominant organisms responsible for nosocomial infection for which the most common antibiotic combination used was Vancomycin and Cefotaxime. A Serratia epidemic was experienced in four NICU. Lumbar and suprapubic punctures were frequently done as part of the diagnostic workup in nosocomial infections but not with perinatally acquired infections. Haematological indices considered useful as a diagnostic aid varied between NICU and acute phase reactants were rarely relied upon for diagnosis or for monitoring treatment response. Granulocyte transfusion and intravenous immunoglobulins were infrequently used in therapy. No consensus was found on infection control policies. Eight NICU required routine gowning on entry, two restricted sibling visiting and four restricted visiting by relatives and friends. Although routine bacteriological surveillance on staff or equipment was uncommon, serial cultures were carried out in infants from the body surface in six NICU and from the endotracheal aspirate in 17 NICU. Antiseptics used with technical procedures included iodine, chlorhexidine and alcohol used singly or in combination. Skin and umbilical cord care also varied between NICU. The literature was reviewed to determine the effectiveness or otherwise of some of the existing policies in the prevention or management of neonatal infection to encourage consensus towards a more rational approach to neonatal infection in Australia.
Cloning and sequencing of the bovine flavocytochrome b subunit proteins, gp91‐phox and p22‐phox: comparison with other known flavocytochrome b sequences

Neutrophils play an essential role in the cellular defense of the bovine mammary gland and compromised leukocyte function has been linked to the development of bovine mastitis. During mastitis, large numbers of leukocytes migrate into the mammary tissues where they become activated, resulting in the assembly of neutrophil membrane and cytosolic proteins to form a superoxide aniongenerating complex known as the NADPH oxidase. The key membrane‐associated component of the NADPH oxidase is flavocytochrome b, which is a heterodimer of p22‐phox and gp91‐phox. Currently, only the human, porcine, murine, and rattus p22‐phox and the human, porcine, and murine gp91‐phox gene sequences are known. Because of the important role neutrophils play in bovine host defense, we carried out studies to clone, sequence, and analyze expression of bovine flavocytochrome b. Using polymerase chain reaction cloning techniques and a bovine spleen cDNA library we have cloned both of the bovine flavocytochrome b subunits, p22‐phox and gp91‐phox. Comparison of the bovine sequences with those of other species also revealed important information regarding key structural features of gp91‐phox and p22‐phox, including location of putative glycosylation sites. This study greatly contributes to our understanding of the potential functional sites of the flavocytochrome b subunits as well as providing information that can be used to study the role of neutrophils in bovine inflammatory diseases such as mastitis. J. Leukoc. Biol. 64: 114–123; 1998.
Factors that contribute to the transneuronal spread of herpes simplex virus

In viral encephalitis and retinal necrosis, different herpes simplex virus (HSV) strains spread between neurons in the central nervous system (CNS) by distinctly different routes. The steps of viral infection and spread in a single neuron type and nearby glial cells in vivo have been determined for three different strains of HSV (F, H129, and McIntyre‐B). The corneas of mice were inoculated with equivalent titers of the strains. Two to 5 days later, the animals were killed. The spread of viral proteins within trigeminal cells was examined using immuno‐ and electron microscopy and Western blots with anti‐HSV polyclonal antiserum. McIntyre‐B virus infection resulted in fewer labeled ganglion cells, possibly as a result of reduced viral production in the corneal epithelium or trigeminal ganglion cells. Although the McIntyre‐B strain was at least as, if not more efficient, at retrograde transport than the other strains, the amount of McIntyre‐B virus that was transported in the trigeminal roots in an anterograde direction was significantly less than the other strains. Uptake by ganglionic satellite cells was qualitatively similar for the three strains, but maturation and release of virus from satellite cells to other neurons were reduced in the McIntyre‐B strain. These characteristics may account for the preferential retrograde transneuronal spread of McIntyre‐B strain. J. Neurosci. Res. 49:485–496, 1997. © 1997 Wiley‐Liss, Inc.
Ginkgo biloba extract (EGb 761) attenuates lung injury induced by intestinal ischemia/reperfusion in rats: roles of oxidative stress and nitric oxide.

AIM To investigate the effect of ginkgo biloba extract (EGb 761) on lung injury induced by intestinal ischemia/reperfusion (II/R). METHODS The rat model of II/R injury was produced by clamping the superior mesenteric artery for 60 min followed by reperfusion for 180 min. The rats were randomly allocated into sham, II/R, and EGb + II/R groups. In EGb + II/R group, EGb 761 (100 mg/kg per day) was given via a gastric tube for 7 consecutive days prior to surgery. Rats in II/R and sham groups were treated with equal volumes of the vehicle of EGb 761. Lung injury was assessed by light microscopy, wet-to-dry lung weight ratio (W/D) and pulmonary permeability index (PPI). The levels of malondialdehyde (MDA) and nitrite/nitrate (NO2(-)/NO3(-)), as well as the activities of superoxide dismutase (SOD) and myeloperoxidase (MPO) were examined. Western blot was used to determine the expression of inducible nitric oxide synthase (iNOS). RESULTS EGb 761 markedly improved mean arterial pressure and attenuated lung injury, manifested by the improvement of histological changes and significant decreases of pulmonary W/D and PPI (P < 0.05 or 0.01). Moreover, EGb 761 markedly increased SOD activity, reduced MDA levels and MPO activity, and suppressed NO generation accompanied by down-regulation of iNOS expression (P < 0.05 or 0.01). CONCLUSION The results indicate that EGb 761 has a protective effect on lung injury induced by II/R, which may be related to its antioxidant property and suppressions of neutrophil accumulation and iNOS-induced NO generation. EGb 761 seems to be an effective therapeutic agent for critically ill patients with respiratory failure related to II/R.