Miracle-dz/UniFAR-FTUs huggingface dataset:
The Respiratory Responses of Subjects With Allergic Rhinitis To Ozone Exposure and Their Relationship To Nonspecific Airway Reactivity

Ozone exposure in man produces changes in respiratory function and symptoms. There is a large degree of unexplained intersubject variability in the magnitude of these responses. There is concern that individuals with chronic respiratory diseases may also be more responsive to ozone than normal individuals. The purpose of this study was to describe the responses of subjects with allergic rhinitis to ozone exposure and to compare these responses to those pre viously observed in normal individuals. A further purpose was to measure the association of baseline nonspecific airway reactivity with changes in lung function and respiratory symptoms following ozone exposure. A group of 26 nonasthmatic subjects with allergic rhinitis performed a bronchial inhalation challenge with histamine and subsequently underwent two hour exposures to both clean air and to 0.18 part per million ozone with alternating periods of rest and heavy exercise. The airway reactivity of this group of subjects was no greater than that of a comparable group of subjects without allergic rhinitis. The respiratory responses of these subjects to ozone exposure were similar to those previously reported for sub jects without allergic rhinitis with the exception that the allergic rhinitis subjects appeared to have a modestly increased broncho constrictor response compared to normals. Furthermore, we observed no significant relationships between nonspecific airway reactivity and response to ozone as measured by changes in lung function or the induction of symptoms.
CD48 controls T-cell and antigen-presenting cell functions in experimental colitis.

BACKGROUND & AIMS The cell-surface receptor CD48 is a lipid-anchored protein expressed on all antigen-presenting cells and T cells. CD2 and 2B4 are known ligands for CD48, which themselves are expressed on the surface of hematopoietic cells. Here we examine the effect of CD48 in the development of chronic experimental colitis and how CD48 affects adaptive and innate immune functions. METHODS The role of CD48 in experimental colitis was first assessed by transferring CD4(+)CD45RB(hi) cells isolated from either wild-type or CD48(-/-) mice into either Rag-2(-/-) or CD48(-/-) x Rag-2(-/-) mice. Development of chronic colitis in these adoptively transferred mice was assessed by disease activity index, histology, and production of interferon-gamma in mesenteric lymph nodes. Relevant functions of CD48(-/-)CD4(+) T cells and CD48(-/-) macrophages were examined using in vitro assays. In a second set of experiments, the efficacy of anti-CD48 in prevention or treatment of chronic colitis was determined. RESULTS CD48(-/-)CD4(+) cells induced colitis when transferred into Rag-2(-/-) mice, but not when introduced into CD48(-/-) x Rag-2(-/-) recipients. However, both recipient mouse strains developed colitis upon adoptive transfer of wild-type CD4(+) cells. Consistent with a CD4(+) T-cell defect was the observation that in vitro proliferation of CD48(-/-)CD4(+) T cells was impaired upon stimulation with CD48(-/-) macrophages. In vitro evidence for a modest macrophage functional defect was apparent because CD48(-/-) macrophages produced less tumor necrosis factor alpha and interleukin 12 than wild-type cells upon stimulation with lipopolysaccharide. Peritoneal macrophages also showed a defect in clearance of gram-negative bacteria in vitro. Treatment of the CD4(+)CD45RB(hi)-->Rag-2(-/-) mice or the wild-type BM-->tg26 mice with anti-CD48 (HM48-1) ameliorated development of colitis, even after its induction. CONCLUSIONS Both CD48-dependent activation of macrophages and CD48-controlled activation of T cells contribute to maintaining the inflammatory response. Consequently, T cell-induced experimental colitis is ameliorated only when CD48 is absent from both T cells and antigen-presenting cells. Because anti-CD48 interferes with these processes, anti-human CD48 antibody treatment may represent a novel therapy for inflammatory bowel disease patients.
Short-term effect of soy consumption on thyroid hormone levels and correlation with phytoestrogen level in healthy subjects.

OBJECTIVE Since soy isoflavones may influence the thyroid hormone feedback system by interference with their biosynthesis, secretion and metabolism, we tested whether their controlled shortterm consumption affects thyroid function. METHODS Eighty six volunteers--university students (32 males and 54 females) were eating unprocessed boiled natural soybeans (2 g/kg body weight/day) for 7 consecutive days. Thyrotropin, free thyroid hormones, antibodies to thyroid peroxidase and to thyroglobulin, and actual levels of unconjugated major soy phytoestrogens, daidzein and genistein, were measured in sera collected before, at the end and one week after finishing soy meal consumption. RESULTS Both phytoestrogens increased significantly (p<0.0001) at the end of soy-diet and fell down after its termination nearly back to the initial values. No significant changes were found in female group, while in males a significant transitory increase of thyrotropin (p<0.0001) was recorded. When actual levels of phytoestrogens were related to thyroid parameters, the only significant correlations were found between basal levels of daidzein and thyrotropin, daidzein and antithyroglobulin at the end of soy consumption in males, and between daidzein and free thyroxine at the end of the soy ingestion in females. CONCLUSION Though only modest and transitory effects on thyroid parameters occurred after controlled short-term soy consumption, some actual thyroid hormone parameters do correlate with actual isoflavone levels.
Childhood obesity and elevated blood pressure in a rural population of northern Greece.

INTRODUCTION The objective of this study was to determine the prevalence of childhood obesity and elevated blood pressure (BP) in a rural population of northern Greece. METHODS In total, 572 schoolchildren between the age of 4 and 10 years were examined. Obesity was defined using three different standards: (1) body mass index (BMI) charts of the French society of Paediatrics (FR), selected because of the low cardiovascular risk profile and low prevalence of obesity in France; (2) United States BMI CDC charts (US), selected because of the high prevalence of childhood obesity in the USA; and the reference curves of the International Obesity Task Force (IOTF). Children with elevated BP were defined as BP > or = 95th percentile for age, gender and height, according to the Greek national charts. RESULTS The prevalence of obesity for boys was 13.6% (IOTF), 23.7% (US) and 31.7% (FR); for girls 14.4% (IOTF), 21.1% (US) and 35.1% (FR). The prevalence of elevated BP was 7.9% (45 children). It was 5 to 6 times more common for obese than non-obese children to have elevated BP (relative risk of 5.2 to 6.2 and odds ratio 6.3 to 7.7). CONCLUSIONS The results confirm the high prevalence of childhood obesity in Greece, in this study found to be more prevalent in rural than urban Greece. The IOTF criteria tend to underestimate obesity and may not be optimal for use in a primary clinical care setting where the approach is for health education and patient treatment, rather than purely epidemiological. The study also confirms a strong relationship between high BP and increased BMI.
The Role of Patient Activation in Improving Blood Pressure Outcomes in Black Patients Receiving Home Care

Variations in patients’ self-management knowledge, skills, and confidence as measured by the Patient Activation Measure (PAM) have been linked to variations in health behavior and outcomes. In a randomized trial, we tested two blood pressure (BP) control interventions, one grounded in activation principles. Study participants were Black home care patients (N = 587) with uncontrolled hypertension. This article examines intervention impacts on 12-month PAM score change, other predictors of PAM change, and associations between PAM change and BP outcomes. In multivariate models, the interventions did not significantly affect PAM change. Baseline characteristics associated with increased PAM were lower PAM score, higher income, higher health literacy, younger age, lower systolic BP, diabetes, and fewer medications. PAM increase was associated with a modest reduction in diastolic BP but not with improved systolic BP or BP control. Although studies suggest that increasing activation may lead to improved patient outcomes, this study did not find it to be so.
Randomized open-label phase II study of decitabine in patients with low- or intermediate-risk myelodysplastic syndromes.

PURPOSE This open-label, randomized phase II trial assessed efficacy and tolerability of two low-dose regimens of subcutaneous (SC) decitabine in patients with low- or intermediate-1-risk myelodysplastic syndrome (MDS). PATIENTS AND METHODS Patients received decitabine 20 mg/m(2) SC per day for 3 consecutive days on days 1, 2, and 3 every 28 days (schedule A) or 20 mg/m(2) SC per day once every 7 days on days 1, 8, and 15 every 28 days (schedule B) for up to 1 year. Primary efficacy end point was overall improvement rate (OIR: complete remission [CR], partial remission [PR], marrow CR [mCR], or hematologic improvement [HI]). Secondary end points were HI, transfusion independence, cytogenetic response, overall survival (OS), and time to acute myeloid leukemia or death. RESULTS Efficacy and safety populations were identical: schedule A, n = 43; schedule B, n = 22. Median time from MDS diagnosis to treatment was 3.6 months; 89% had de novo MDS. The trial was terminated early on achievement of protocol-defined OIR superiority of schedule A over schedule B; OIR was 23% for schedule A (seven CRs, three HIs) and 23% for schedule B (one mCR, one PR, three HIs). No differences were observed in secondary end points. Median OS was not reached; approximately 70% of patients were alive at 500 days. Patients in schedule A (67%) and schedule B (59%) were RBC/platelet independent on study. The most frequent drug-related adverse events overall were neutropenia (28% v 36%), anemia (23% v 18%), and thrombocytopenia (16% v 32%). CONCLUSION In this phase II study, low-dose decitabine showed promising results in patients with low- or intermediate-1-risk MDS.
A new player in a deadly game: influenza viruses and the PI3K/Akt signalling pathway

Upon influenza A virus infection of cells, a wide variety of antiviral and virus‐supportive signalling pathways are induced. Phosphatidylinositol‐3‐kinase (PI3K) is a recent addition to the growing list of signalling mediators that are activated by these viruses. Several studies have addressed the role of PI3K and the downstream effector protein kinase Akt in influenza A virus‐infected cells. PI3K/Akt signalling is activated by diverse mechanisms in a biphasic manner and is required for multiple functions during infection. While the kinase supports activation of the interferon regulatory factor‐3 during antiviral interferon induction, it also exhibits virus supportive functions. In fact, PI3K not only regulates a very early step during viral entry but also results in suppression of premature apoptosis at later stages of infection. The latter function is dependent on the expression of the viral non‐structural protein‐1 (A/NS1). It has been shown that PI3K activation occurs by direct interaction of A/NS1 with the p85 regulatory subunit and interaction sites of A/NS1 and p85 have now been mapped in detail. Here, we summarize the current knowledge on influenza virus‐induced PI3K signalling and how this pathway supports viral propagation.
Cost-efficient decimal adder design in Quantum-dot cellular automata

Applications that cannot tolerate the loss of accuracy that results from binary arithmetic demand hardware decimal arithmetic designs. Binary arithmetic in Quantum-dot cellular automata (QCA) technology has been extensively investigated in recent years. However, only limited attention has been paid to QCA decimal arithmetic. In this paper, two cost-efficient binary-coded decimal (BCD) adders are presented. One is based on the carry flow adder (CFA) using a conventional correction method. The other uses the carry look ahead (CLA) algorithm which is the first QCA CLA decimal adder proposed to date. Compared with previous designs, both decimal adders achieve better performance in terms of latency and overall cost. The proposed CFA-based BCD adder has the smallest area with the least number of cells. The proposed CLA-based BCD adder is the fastest with an increase in speed of over 60% when compared with the previous fastest decimal QCA adder. It also has the lowest overall cost with a reduction of over 90% when compared with the previous most cost-efficient design.
Pathogenic mechanisms in proliferative vitreoretinopathy.

Landmarks in the development of treatment of retinal detachment include the recognition of the significance of retinal breaks that resulted in the distinction between rhegmatogenous retinal detachment (RRD) and exudative retinal detachment, the development of indirect ophthalmoscopy and scleral depression that allow better visualization of the peripheral area of the retina and better identification of retinal breaks, the recognition of the need to seal all retinal breaks, and the realization that vitreous traction is the major underlying cause of retinal tears and RRD. Scleral buckling procedures combine retinopexy to provide a scar around retinal breaks to seal them and scleral indentation to neutralize vitreous traction; they provided the first effective treatment of RRD. As surgeons gained experience with scleral buckling, they became aware that some RRDs, particularly those with fixed folds and/or a funnel configuration, often could not be repaired using this approach. It was thought that excessive vitreous traction was at fault, and the condition was called "massive vitreous retraction. "
“Conservation biased” distribution Volt/Var/(kW) management

The advanced capabilities of modern LTC transformer and regulator tapchanger controls, distribution capacitor bank controls and communications equipment allows for an unprecedented ability to control the voltage profile from distribution substation to the ultimate customer. The use and coordination of these capabilities can result in immediate CVC programs that can affect the average electric power consumer voltage level. The implementation of proposed SG (SMART GRID) system features will further increase the accuracy and effectiveness of such programs. Recent studies have shown that the single act of reducing the average consumer voltage levels within the acceptable voltage range (114–126 volts) results in significant positive changes on the power system. These system benefits will be shared by the consumer with lower power bills and by the utility in lower losses, reduced fuel costs, increased equipment capability, reduced need for power factor correction equipment, delayed new generation requirements, and more. A loss of revenue for the utility will occur, as it does for any power efficiency or conservation activity.
Manipulation of Endogenous Neural Stem Cells Following Ischemic Brain Injury

The use of cell-based therapy is a valid therapeutic approach to ischemic brain injury. Endogenous neural stem cells (NSCs) have been identified in the central nervous system where they reside largely in the subventricular zone and in the subgranular zone of the hippocampus. Endogenous NSCs are capable of self-renewal and differentiation into functional brain cells. This paper summarizes the evidence recently gathered in support of a therapeutic role for endogenous NSCs in acute experimental stroke.
Failure of prostaglandins to modulate the time course of blood flow during dynamic forearm exercise in humans.

The time course and magnitude of increases in brachial artery mean blood velocity (MBV; pulsed Doppler), diameter (D; echo Doppler), mean perfusion pressure (MPP; Finapres), shear rate (gamma = 8.MBV/D), and forearm blood flow (FBF = MBV.pi r2) were assessed to investigate the effect that prostaglandins (PGs) have on the hyperemic response on going from rest to rhythmic exercise in humans. While supine, eight healthy men performed 5 min of dynamic handgrip exercise by alternately raising and lowering a 4.4-kg weight (approximately 10% maximal voluntary contraction) with a work-to-rest cycle of 1:1 (s/s). When the exercise was performed with the arm positioned below the heart, the rate of increase in MBV and gamma was faster compared with the same exercise performed above the heart. Ibuprofen (Ibu; 1,200 mg/day, to reduce PG-induced vasodilation) and placebo were administered orally for 2 days before two separate testing sessions in a double-blind manner. Resting heart rate was reduced in Ibu (52 +/- 3 beats/min) compared with placebo (57 +/- 3 beats/min) (P < 0.05) without change to MPP. With placebo, D increased in both arm positions from approximately 4.3 mm at rest to approximately 4.5 mm at 5 min of exercise (P < 0.05). This response was not altered with Ibu (P > 0.05). Ibu did not alter the time course of MBV or forearm blood flow (P > 0.05) in either arm position. The gamma was significantly greater in Ibu vs. placebo at 30 and 40 s of above the heart exercise and for all time points after 25 s of below the heart exercise (P < 0.05). Because PG inhibition altered the time course of gamma at the brachial artery, but not FBF, it was concluded that PGs are not essential in regulating the blood flow responses to dynamic exercise in humans.
Early hepatic stages of Plasmodium berghei: release of circumsporozoite protein and host cellular inflammatory response

After injection of Plasmodium berghei sporozoites into Norway-Brown rats, we were able to localize these sporozoites and the early hepatic trophozoites developing from them in histological sections of the liver stained with a sensitive immunogold-silver procedure. Sporozoites invading hepatocytes released substantial quantities of circumsporozoite protein into the hepatocyte cytoplasm. This intrahepatic cytoplasmic distribution reached a maximal level at about 4 h post-sporozoite injection. As the hepatic parasites continued to differentiate, circumsporozoite protein became undetectable within the cytoplasm of the hepatocytes and became localized around the periphery of each parasite. There was generalized cellular inflammation within the liver of the host, which first became evident at around 4 h post-sporozoite injection and progressed to the formation of well-defined granulomas by 24 h. Such histopathological changes were not seen in rats injected with killed sporozoites, indicating that the cellular inflammation was induced by viable, infective sporozoites. We did not observe cellular infiltration specifically associated with any of the developing hepatic stages that we observed, even up to 28 h post-sporozoite inoculation. These results indicate that viable sporozoites induced rapid and generalized hepatic inflammation in host rats. However, sporozoites that successfully invaded hepatocytes and then proceeded to develop further did not appear to be the target of inflammatory cells until a period beginning at around 40 h post-sporozoite inoculation.
[The urban world and rural-urban migration in Galicia from the sixteenth to the nineteenth century].

"In this paper an attempt has been made to identify the different migratory patterns from country to city which were generated in urban areas in Galicia [Spain] between the XVIth and XXth centuries. A classification has been drawn up which, in practice, revolves around the link which each urban area had with the surrounding countryside. This has allowed us to identify the existence of a genuine ¿culture of mobility' and in a similar way to what happened in the interior of Spain this culture developed in a clearly pre-industrial context until well into the XXth century. " (EXCERPT)
Effects of pressure on the activity and spectroscopic properties of carboxyl proteinases. Apparent correlation of pepstatin-insensitivity and pressure response.

The pressure dependence of the activity and spectroscopic properties of four carboxyl proteinases were investigated. Two were pepstatin-sensitive carboxyl proteinases (porcine pepsin and proteinase A from baker's yeast) and two were pepstatin-insensitive carboxyl proteinases (from Pseudomonas sp. 101 (pseudomonapepsin; PCP) and Xanthomonas sp. T-22 (xanthomonapepsin; XCP)). The specificity constant [k(cat)/K(m(app))] of PCP and XCP for a synthetic peptide substrate showed only a slight decrease with increasing pressure, whereas pepsin and proteinase A showed substantial disactivation at higher pressures. The calculated apparent activation volume (Delta V((k(cat)/(K(m)) was about 1, 3, 13, and 14 mL.mol(-1) for PCP, XCP, pepsin, and proteinase A, respectively. The hydrolysis of acid-denatured myoglobin by the four carboxyl proteinases was only slightly affected by high pressure (except for proteinase A at 400 MPa), in contrast to the results for the peptide hydrolysis. In fact, PCP, XCP, and proteinase A actually showed slightly higher degradations of acid-denatured myoglobin at higher pressures. The residual activities of these enzymes after the incubation at high pressures implied a pressure-induced stabilization towards autolysis. The changes in the fourth derivative near-UV absorbance spectrum of the four enzymes in aqueous solution were measured at various pressures from 0.1 to 400 MPa. Upon an increase in pressure, the peaks from PCP and XCP red-shifted slightly, whereas pepsin and proteinase A blue-shifted substantially, thus indicating a more polar environment. The intrinsic fluorescence also decreased upon increasing pressure. However, the change for XCP was rather small, but the change for the other three was very large. The changes in the peak wavelength for pepsin and proteinase A were characteristic, and also indicated a more polar environment under high pressure. An analysis by the center of spectra mass (CSM) gave the Delta G and Delta V of transition as 9.8 kJ x mol(-1) and -24 mL x mol(-1) (pepsin) and 11.7 kJ x mol(-1) and -43 mL x mol(-1) (proteinase A), respectively, by assuming a simple two-state transition. The circular dichroism (CD) showed relatively small changes after 1-h incubations at 400 MPa, indicating that the secondary structures were largely maintained.
Muscleblind‐like 2 (Mbnl2) ‐deficient mice as a model for myotonic dystrophy

Myotonic dystrophy (DM), the most common adult‐onset muscular dystrophy, is caused by CTG or CCTG microsatellite repeat expansions. Expanded DM mRNA microsatellite repeats are thought to accumulate in the nucleus, sequester Muscleblind proteins, and interfere with alternative mRNA splicing. Muscleblind2 (Mbnl2) is a member of the family of Muscleblind RNA binding proteins (that also include Mbnl1 and Mbnl3) that are known to bind CTG/CCTG RNA repeats. Recently, it was demonstrated that Mbnl1‐deficient mice have characteristic features of human DM, including myotonia and defective chloride channel expression. Here, we demonstrate that Mbnl2‐deficient mice also develop myotonia and have skeletal muscle pathology consistent with human DM. We also find defective expression and mRNA splicing of the chloride channel (Clcn1) in skeletal muscle that likely contributes to the myotonia phenotype. Our results support the hypothesis that Muscleblind proteins and specifically MBNL2 contribute to the pathogenesis of human DM. Developmental Dynamics 237:403–410, 2008. © 2008 Wiley‐Liss, Inc.