Miracle-dz/UniFAR-FTUs huggingface dataset:
Human papillomavirus infection among Indian mothers and their infants.

OBJECTIVE Several studies have demonstrated that infants can acquire human papillomavirus (HPV) infection at birth from their mothers. The aim of the present investigation was to determine prevalence of HPV infection among pregnant women and evaluate the extent of perinatal transmission of HPVs to infants. METHODS The study included 135 pregnant women and their infants. The polymerase chain reaction (PCR) was performed to detect HPV DNA in cervical cells of the women and buccal cells of the infants. RESULTS HPVs detected were genotyped by PCR using type specific primers. HPV DNA was identified in 38 mothers (28.14%, 38/135) and 14 babies (10.37%, 14/135). The prevalence rate of HPV type 16 was highest both in HPV positive maternal (63.15%, 24/38) and baby samples (85.71%, 12/14). At birth, the frequency of HPV transmission from infected mothers to their infants was 18.42% (7/38). The proportion of infants with HPV infection delivered by cesarean section was 78.57% (11/14). CONCLUSION Cesarean section was not found protective for infants against perinatal HPV transmission. Infection in the infants was cleared within one year. This is the first report of its kind from India.
Subdural EEG Classification Into Seizure and Nonseizure Files Using Neural Networks in the Gamma Frequency Band

This study describes a new method for offline seizure detection using intracranial EEG (iEEG). The proposed method integrated two interrelated steps: (1) establishing a decisional space on the basis of the interelectrode mean of the spectral power in the gamma frequencies after a thorough evaluation of temporal and frequency-based features and (2) constructing an artificial neural network that operated on this decisional space to delineate EEG files that contained seizures from those that did not. The data were obtained from 14 patients who underwent two-stage epilepsy surgery with subdural recordings. Of the total 157 files considered, 35 (21 interictal and 14 ictal) iEEG data files or 22% were selected randomly and used initially in a training phase. The remaining 122 iEEG data files or 78% were then used in the testing phase to assess the merits in selecting gamma power as means to detect a seizure. The results obtained exhibited an accuracy of 95.90%, a sensitivity of 92.59%, and a specificity of 96.84%. Although this method had to contend with the complex nature of iEEG and the inherent heavy computational load, the constructed artificial neural networks together with the chosen decisional space yielded the best possible outcome. The proposed method was based on aggregating the power in the 36 to 44-Hz frequency range and analyzing its behavior in time, looking for patterns indicative of seizure evolution. It was shown that the power measurement in the gamma range contains the information needed to discriminate seizure files from nonseizure files. The algorithm consisted in establishing a decision space most suitable for iEEG data classification by relying on the power spectra in the gamma frequencies and constructing and implementing an artificial neural network that generates the highest classification accuracy possible. It was noted that although only 29% (35/122) of the files were used randomly for training the detector, high measures in sensitivity, specificity, and accuracy were still achieved in the remaining files, which were subsequently used in the testing phase. Seizures are known to occur intermittently and unpredictably, and massive amounts of EEG or iEEG data need to be analyzed offline to detect seizures. This is a challenge that can only be met through reliable and time-efficient seizure-detection paradigms, an affirmation this study attempted to prove.
The GRK4 Subfamily of G Protein-coupled Receptor Kinases

G protein-coupled receptor kinases (GRKs) desensitize G protein-coupled receptors by phosphorylating activated receptors. The six known GRKs have been classified into three subfamilies based on sequence and functional similarities. Examination of the mouse GRK4 subfamily (GRKs 4, 5, and 6) suggests that mouse GRK4 is not alternatively spliced in a manner analogous to human or rat GRK4, whereas GRK6 undergoes extensive alternative splicing to generate three variants with distinct carboxyl termini. Characterization of the mouse GRK 5 and 6 genes reveals that all members of the GRK4 subfamily share an identical gene structure, in which 15 introns interrupt the coding sequence at equivalent positions in all three genes. Surprisingly, none of the three GRK subgroups (GRK1, GRK2/3, and GRK4/5/6) shares even a single intron in common, indicating that these three subfamilies are distinct gene lineages that have been maintained since their divergence over 1 billion years ago. Comparison of the amino acid sequences of GRKs from various mammalian species indicates that GRK2, GRK5, and GRK6 exhibit a remarkably high degree of sequence conservation, whereas GRK1 and particularly GRK4 have accumulated amino acid changes at extremely rapid rates over the past 100 million years. The divergence of individual GRKs at vastly different rates reveals that strikingly different evolutionary pressures apply to the function of the individual GRKs.
Gut peptides and the regulation of appetite

There is a growing worldwide epidemic of obesity. Obese people have a higher incidence of type 2 diabetes and cardiovascular disease, and hence present increasing social, financial and health burdens. Weight loss is always difficult to achieve through lifestyle changes alone, and currently licensed anti‐obesity drug treatments, such as orlistat and sibutramine, if tolerated, only achieve modest weight loss. Therefore, there is a need to identify more potent pharmacological targets. In the last 10 years, discoveries of new hormones such as leptin and ghrelin, together with greater understanding of previously described hormones such as cholecystokinin (CCK), pancreatic polypeptide (PP), peptide YY (PYY) and glucagon‐like peptide 1 (GLP‐1), have led to a rapid increase in our knowledge of the regulation of energy balance. Among the most important factors, controlling appetite and satiety are peptide hormones released from the gut. In this paper, we provide a full up‐to‐date overview of the current state of knowledge of this field, together with the potential of these peptides as drugs, or as other therapeutic targets, in the treatment of obesity. Finally, we propose an integrated model to describe the complex interplay of these hormones in the broader physiology of energy balance.
Ischaemic preconditioning limits infarct size in the rat heart.

OBJECTIVE One of the mechanisms by which ischaemic preconditioning is thought to protect against later prolonged ischaemia is via a reduction in ATP utilisation during ischaemia. The ATP "wastage" that occurs during ischaemia is thought to be due to mitochondrial ATPase activity, which may be prevented in ischaemic preconditioning by the binding of a specific inhibitor protein. As the rat is known to have less inhibitor protein than other species, this study was designed to determine whether the rat heart could be ischaemically preconditioned. METHODS Rats were anaesthetised with pentobarbitone, the chest opened and the hearts ischaemically preconditioned with a 5 min occlusion of the left main coronary artery followed by 10 min reperfusion. The hearts were then subjected to a 45 min occlusion followed by 3 h reperfusion. Control hearts were treated identically but without ischaemic preconditioning. Infarct size was measured using triphenyl tetrazolium and expressed as a percentage of the region at risk, measured with fluorescent particles. RESULTS Infarct size as a percent of the risk area in the ischaemically preconditioned group (n = 8) was 31.4(SEM 6.1)%, versus 61.0(4.8)% in control hearts (n = 8) (p < 0.005). CONCLUSIONS These results show that rat hearts can be ischaemically preconditioned and suggest that the protective mechanism involved in this phenomenon is not mediated through the endogenous inhibition of mitochondrial ATPase. An overall reduction in mitochondrial ATP "wastage" may not be the sole mechanism in the protection seen in ischaemic preconditioning.
Decrease of replicative capacity of HIV isolates after genotypic guided change of therapy

A longitudinal study of the replication capacity of HIV strains isolated from 18 patients failing highly active antiretroviral therapy (HAART) was undertaken at the time of genotypic guided change of therapy and after 12 months. Patients were divided in two groups according to the response to therapy: immune responders (12 patients with immune recovery defined as having more than 100 CD4 cells compared to baseline value), and failing patients (six patients without immune recovery). At enrolment no significant difference in terms of CD4 cell count and HIV plasma viremia was detected between the two groups. One year after change of therapy, all patients experienced a decrease in the replication capacity of HIV strains. The HIV replication capacity of the failing and of immune‐responder patients decreased from 60% (range 14–96%) to 26.4% (range 0.4–74.5) and from 46.8% (range 15–98%) to 3.6% (range 0.1–26.8%), respectively. At month 12, the difference of HIV replication capacity between the two groups reached a statistical significance (P < 0.03). After the change of therapy, an increase in the number of drug resistance mutations in the protease gene was detected in both groups with a higher prevalence of M36I mutation in immune responders. The HIV strains of patients failing HAART showed a progressive impaired replication capacity. The degree of the impairment in viral replication correlated with the viro‐immunological discordant response to HAART and with the acquisition of new drug resistant mutations in the protease gene. In patients failing HAART, the impaired replication capacity of HIV strains could justify the persistence of an immune recovery. J. Med. Virol. 72:511–516, 2004. © 2004 Wiley‐Liss, Inc.
Packaged Tunable Combline Bandpass Filters

This article describes the design of a packaged tunable bandpass filter used for the Student Filter Design Competition held during the 2014 International Microwave Symposium (IMS2014) in Tampa, Florida. The focus of the 2014 competition was to demonstrate a tunable bandpass filter between two wide separated bands. The first band is 4.25-4.4 GHz, and the second band is 6.25-6.4 GHz. The tunable filter must be realized on a printed circuit board with planar and lumped surface-mounted components and required to be assembled in an open-tooled FP118118-1 package [1] securely sealed with a copper tape lid. The entire package was mounted on an evaluation board, with 50-X traces connecting the radio-frequency (RF) input and output pins to 50-X female subminiature version A (SMA) connectors. The evaluation board also had a trace that connects the dc control pin of the package to a pad on the perimeter of the evaluation board. The filter performance was measured at the SMA interfaces with a dc voltage level from 0 to 20 V to shift the passbands of the tunable bandpass filter using a varactor [Microwave Associates (M/A) Com 46H202].
The Akin procedure: an analysis of results.

This paper reports the initial and long-term results of 45 Akin procedures done at the Hospital for Joint Diseases/Orthopaedic Institute from 1966 to 1985. Indications for 36 of the 45 operated feet were for an essentially asymptomatic great toe valgus deformity which caused symptoms to develop in the second toe and in 9 of 45 feet for residual hallux valgus after previous hallux valgus surgery. Excellent and good results were reported in 89% of the patients. The most common technical problem reported in 22% of the patients was plantar angulation at the osteotomy site. The only technical problem that was associated with long-term complications was bone apposition of less than 50% which may have lead to a nonunion in one case and recurrence of deformity in another. Shortening of the hallux was observed in all cases secondary to the closing wedge osteotomy. Shortening can be limited if a minimum of bone is removed from the proximal phalanx. A mathematical analysis is presented in this paper which can be used to provide guidelines to osteotomy size so that a minimum of bone necessary for correction can be removed. The Akin procedure should be performed within certain guidelines. Rarely is an Akin procedure alone indicated for the correction of a hallux valgus deformity. In most patients the proximal phalangeal osteotomy needs to be performed in combination with some other procedure to correct all components of the hallux valgus deformity. Furthermore the procedure can be used with success in those patients who present with an essentially asymptomatic great toe valgus deformity at the metatarsophalangeal joint or the interphalangeal joint which causes symptoms and/or deformity to develop in the second toe. (ABSTRACT TRUNCATED AT 250 WORDS)
[Effect of cyclosporin A on the growth of human first trimester cytotrophoblasts in vitro].

OBJECTIVE To investigate effect of cyclosporin A (CsA) on the growth of first trimester human cytotrophoblast in vitro. METHODS To isolate and purificate first trimester human cytotrophoblasts by way of percoll density gradient centrifugation; to evaluate the effect of CsA on in vitro proliferation of cytotrophoblasts using (3)H-thymidine incorporation assay; to analyze of cell cycle of cytotrophoblasts with flow cytometric assay; and to survey morphology of the cells by scanning electro-microscope respectively. RESULTS CsA could increase in vitro proliferation of first trimester human cytotrophoblasts when concentration of CsA ranged from 1 x 10(-4) micromol/L to 1 micromol/L, but decrease in vitro proliferation of the cells if the concentration reached to 10 micromol/L. G(2)-M phase increased from (2.8 +/- 0.5)% to (6.7 +/- 1.3)% when the cytotrophoblasts were incubated with culture medium containing 1 micromol/L CsA for 24 hours, while S phase increased from (14 +/- 5)% to (28 +/- 8)% and apoptosis decreased from (8.7 +/- 2.2)% to (3.6 +/- 1.0)% when the culture in the same incubating condition lasted for 48 hours. Pseudopodia of the trophoblasts increased in number and length when they were incubated in culture medium containing 1 micromol/L of CsA for 48 hours, but decreased if the concentration reached to 10 micromol/L with the same incubating duration. CONCLUSION CsA is able to promote growth of first trimester human cytotrophoblasts and change their morphology, which appears to increase in invasive ability.
Species Distribution of the Mycobacterium tuberculosis Complex in Clinical Isolates from 2007 to 2010 in Turkey: a Prospective Study

ABSTRACT The Mycobacterium tuberculosis complex (MTBC) consists of a group of closely related species that differ in their epidemiological profiles, host ranges, pathogenicities, geographic distributions, and drug resistances. Identification of members in the MTBC is essential for monitoring the epidemiology of tuberculosis (TB) and implementing appropriate public health control measures. In this study, 188 consecutive MTBC clinical isolates from 2007 to 2010 were evaluated to determine the prevalence of MTBC species in Turkey. PCR and restriction fragment length polymorphism analysis (PCR-RFLP) of the gyrB gene were used, and results for species other than M. tuberculosis were confirmed using the GenoType MTBC assay (Hain Lifescience, Nehren, Germany). Most of the strains were found to be M. tuberculosis (94.1%). The prevalences of M. bovis and M. caprae were 4.3% and 1.6%, respectively. Only one M. bovis BCG strain was identified. Overall, the frequency of bovine tuberculosis in humans was 5.3%. We had assumed that bovine TB infection was under control in animal herds, but primary M. bovis infections in humans caused by transmission from infected animals are still an issue in Turkey. Our results indicate that the frequent identification of M. bovis in routine mycobacteriological laboratory work has further importance due to the well-known resistance of this species to pyrazinamide.
Genetic factors for choroidal neovascularization associated with high myopia.

PURPOSE Nonsyndromic high myopia, defined by a refractive error greater than -6 diopters (D), is associated with an increased risk of macular choroidal neovascularization (CNV), a vision-threatening complication. The aim of this study was to investigate whether genetic factors associated with age-related macular degeneration (AMD) are related to myopic CNV. METHODS We conducted a case-control study, including 71 cases with myopic CNV and 196 myopic controls without CNV, from Creteil and Toulouse, France, and Boston, MA. Single nucleotide polymorphisms (SNPs) from 15 genes reported to be related to AMD were selected for association testing in this study. RESULTS In univariate analysis, the rs10033900 SNP located in CFI was associated with myopic CNV (P = 0.0011), and a SNP in APOE was also related (P = 0.041). After adjustment for age, sex, and degree of myopia, SNPs in three genes were significantly associated, including CFI (odds ratio [OR] 2.1, 95% confidence interval [CI] 1.3-3.37, P = 0.0023), COL8A1 (OR 1.88, 95% CI 1.18-2.98, P = 0.0076), and CFH (OR 1.65, 95% CI 1.02-2.66, P = 0.04). After correction for multiple testing, only CFI remained significantly related to high myopic CNV (P = 0.045). CONCLUSIONS We report the first genetic associations with choroidal neovascularization (CNV) in a high myopic Caucasian population. One SNP (rs10033900) in the CFI gene, which encodes a protein involved in the inflammatory pathway, was significantly associated with myopic CNV in multivariate analysis after correction for multiple testing. This SNP is a plausible biological marker associated with CNV outgrowth among high myopic patients. Results generate hypotheses about potential loci related to CNV in high myopia, and larger studies are needed to expand on these findings.
MITOCHONDRIAL KINETICS DURING AMPHIBIAN ERYTHROPOIESIS RELATED TO HAEME SYNTHESIS

Flow cytometry, light and epifluorescence microscopies and transmission electron microscopy were used to follow the mitochondrial kinetics during amphibian erythropoiesis. A similar behaviour in response to the induction of anaemia was observed in the diploid Bufo ictericus and the tetraploid Odontophrynus americanus. A high cellular activity was observed ten days after haemolytic anaemia induced by phenylhydrazine, based on the higher Rhodamine 123 uptake by the erythroid cells. In addition, the more intense expression of the mitochondrial enzyme cytochrome oxidase, isocitrate and succinic dehydrogenases were cytochemically detected at this stage. This suggests that erythroid cell mitochondria, at this time, could be in a more active functional state than at other stages. In both species, mitochondrial plasticity was observed during cell maturation. A progressive loss of oxidation—reduction enzyme expression seemed to follow changes at the mitochondrial cristae morphology, from transverse to longitudinal form, mainly at the 20th day of recovery from anaemia, possibly related to a natural loss of function. The presence of these mitochondrial enzymes in mitochondrion‐like organelles also favours their participation in the haeme synthesis, although with a reduced expression, since this suggests the presence of a complete and active enzymatic complex in these modified organelles. This also supports the idea that all these organelles are mitochondria in distinct metabolic stages, and not mitochondrion‐like organelles or haemosomes, as proposed by some authors.
In vitro infection of lymphocytes with Marek's disease virus.

Suspension cultures of splenic lymphocytes, incubated at 41 degrees C, became infected with Marek's disease virus (MDV) following exposure to a) other infected lymphocytes, b) infected chicken kidney monolayer cultures, or c) cell-free MDV. Both viral antigen expression and virus isolation could be demonstrated after more than 40 passages made by the addition of fresh spleen cells at 2- to 3-day intervals. Susceptibility of spleen cells from bursectomized chickens was markedly lower than that of cells from intact birds. Furthermore, when spleen cell suspensions were depleted of cells having characteristics of bursa-derived cells, e.g., those with surface IgM, Fc receptors, or ability to adhere to nylon wool, the susceptibility of the cell suspension was diminished. Enrichment of the suspension with cells having those features enhanced overall susceptibility. The target cells for virus infection in vitro also were shown to be nonphagocytic, to be of low or medium density, and to bear Ia-like antigen. In vitro susceptibility to infection of spleen cells did not correlate with the genetic susceptibility of the donor to Marek's disease.
Oxidized LDL Modulates Bax/Bcl-2 Through the Lectinlike Ox-LDL Receptor-1 in Vascular Smooth Muscle Cells

Oxidized low density lipoprotein (Ox-LDL) induces apoptosis in vascular smooth muscle cells (VSMCs), which may increase atherosclerotic plaque instability. In this study, we examined the molecular mechanisms causing the Ox-LDL–induced apoptosis in VSMCs, especially focusing on the involvement of Bax/Bcl-2 and the lectinlike Ox-LDL receptor-1 (LOX-1). In cultured bovine aortic smooth muscle cells (BASMCs), Ox-LDL at high concentrations (>60 &mgr;g/mL) induced cell death as demonstrated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. DNA fragmentation was increased in BASMCs treated with high concentrations of Ox-LDL, indicating that the Ox-LDL–induced cell death in VSMCs was apoptosis. Ox-LDL upregulated LOX-1 expression through phosphorylation of extracellular signal–regulated kinase in BASMCs, and a neutralizing anti–LOX-1 monoclonal antibody, which can block LOX-1–mediated cellular uptake of Ox-LDL, prevented the Ox-LDL–induced apoptosis in BASMCs. This antibody also suppressed the increase in the Bax to Bcl-2 ratio induced by Ox-LDL in BASMCs. Furthermore, LOX-1 expression was well colocalized with Bax expression in the rupture-prone shoulder areas of human atherosclerotic plaques in vivo. LOX-1 may play an important role in Ox-LDL–induced apoptosis in VSMCs by modulating the Bax to Bcl-2 ratio. These molecular mechanisms may be involved in destabilization and rupture of atherosclerotic plaques.
MUC1 Mucin Core Protein Binds to the Domain 1 of ICAM-1

Background: MUC1 is aberrantly expressed on a variety of epithelial tumors. We have reported that MUC1 plays important roles in separation from primary site, invasion into the stromal tissue, and protection from immune responses. The aim of this study is to determine the precise binding of MUC1 to intercellular adhesion molecule 1 (ICAM-1) that accelerates the cancer metastasis. Methods: A cell aggregation assay between MUC1 cDNA transfectants and ICAM-1 expressing cells was employed. An anti-MUC1 antibody, anti-ICAM-1 antibody or synthetic peptide of MUC1 core protein was added to the assay to inhibit the cell aggregation. Results: MUC1 transfectants showed a significantly higher aggregation rate compared to the control cells. This aggregation was further enhanced by the inhibition of O-glycan biosynthesis. It was inhibited by either an anti-MUC1 antibody recognizing the tandem repeat domain of MUC1 core protein or an anti-ICAM-1 antibody identifying domain 1. It was also inhibited by a synthetic MUC1 peptide of 40 amino acids corresponding to two tandem repeats. Conclusions: The results revealed that a tandem repeat domain of MUC1 mucin core protein binds to domain 1 of ICAM-1, suggesting a potential role of MUC1- ICAM-1 interaction in the metastasis of epithelial tumors.