Miracle-dz/UniFAR-FTUs huggingface dataset:
Integrated healthy workplace model: An experience from North Indian industry

Background: Keeping in view of rapid industrialization and growing Indian economy, there has been a substantial increase in the workforce in India. Currently there is no organized workplace model for promoting health of industrial workers in India. Objective: To develop and implement a healthy workplace model in three industrial settings of North India. Materials and Methods: An operations research was conducted for 12 months in purposively selected three industries of Chandigarh. In phase I, a multi-stakeholder workshop was conducted to finalize the components and tools for the healthy workplace model. NCD risk factors were assessed in 947 employees in these three industries. In phase II, the healthy workplace model was implemented on pilot basis for a period of 12 months in these three industries to finalize the model. Findings: Healthy workplace committee with involvement of representatives of management, labor union and research organization was formed in three industries. Various tools like comprehensive and rapid healthy workplace assessment forms, NCD work-lite format for risk factors surveillance and monitoring and evaluation format were developed. The prevalence of tobacco use, ever alcoholics was found to be 17.8% and 47%, respectively. Around one-third (28%) of employees complained of back pain in the past 12 months. Healthy workplace model with focus on three key components (physical environment, psychosocial work environment, and promoting healthy habits) was developed, implemented on pilot basis, and finalized based on experience in participating industries. A stepwise approach for model with a core, expanded, and optional components were also suggested. An accreditation system is also required for promoting healthy workplace program. Conclusion: Integrated healthy workplace model is feasible, could be implemented in industrial setting in northern India and needs to be pilot tested in other parts of the country.
Regenerative properties of pyramidal cell dendrites in area CA1 of the rat hippocampus.

1. Intracellular recordings were obtained from 184 distal apical dendrites and twenty‐six somata of CA1 pyramidal neurones in the rat hippocampal slice preparation. In the presence of 3.25 mM K+ 200 ms suprathreshold current pulses evoked three different types of firing patterns in the apical dendrites, all of which were distinct from regular somatic firing. Fast tetrodotoxin (TTX)‐sensitive spiking was evoked in 38.8% of the dendrites. Compound spiking, consisting of an initial fast spike followed by one or more secondary slow spikes of variable amplitude and duration, was seen in 44.1% of dendrites. ‘Classical’ burst firing, resembling intrinsic somatic bursts, was evoked in 17.1% of the dendrites. 2. In fast spiking dendrites, the spikes evoked by long depolarizing pulses were rarely overshooting, showed prominent accommodation and declined progressively to about one‐third of the initial amplitude. The amplitude of single dendritic fast spikes (50.6 +/‐ 1.5 mV; mean +/‐ S.E.M.) was smaller than that of somatic spikes (82.2 +/‐ 1.9 mV) and their rate of rise (81.3 +/‐ 4.3 V s‐1) was markedly slower than that of somatic spikes (291.5 +/‐ 17.8 V s‐1). However, the thresholds were not significantly different (dendrites, ‐49.8 +/‐ 0.8 mV; somata, ‐50.8 +/‐ 1.3 mV). These results indicate that fast spikes in the distal parts of apical dendrites are generated by a local regenerative Na+ current. 3. 4‐Aminopyridine (4‐AP, 0.1‐0.5 mM) caused a dose‐dependent slowing of the repolarization of the fast spikes, while tetraethylammonium (TEA, 2 mM) and Co2+ (2 mM) induced a slowing of the late phase of the repolarization. These results indicate that the transient outward K+ current, IA, and the Ca(2+)‐activated K+ current, IC, are involved in the repolarization of dendritic Na(+)‐dependent spikes. 4. Compound spiking was completely blocked by TTX (0.5‐1 microM). The secondary slow spikes within the complex were blocked by Co2+ (2 mM), nifedipine (10 microM) and high concentrations (> 50 microM) of verapamil, while Ni2+ (100‐300 microM) had no effect. Thus, compound spiking consists of an initial Na(+)‐dependent spike followed by one or more slow Ca(2+)‐dependent spikes mediated by L‐type Ca2+ channels located in the apical dendrites. 5. In fast spiking dendrites, 4‐AP (0.5‐2.5 mM) changed the firing pattern from regular fast spiking to compound spiking. In the presence of 4‐AP (0.1‐0.5 mM), the single fast spike evoked by a short (20 ms), threshold current pulse, was followed by secondary slow spikes of variable amplitude and duration. (ABSTRACT TRUNCATED AT 400 WORDS)
Quantitative Determination of Morphometric Indices of the Total and Perfused Capillary Network of the Newborn Pig Brain

The purpose of this study was to determine if the newborn pig brain had a reserve of unperfused capillaries during normoxia. To accomplish this, a method was developed to determine the volume fraction, surface area, and number of both total and perfused capillaries in the newborn pig brain. Newborn pigs of either sex, 2–7 d old, were used. FITC-dextran, molecular weight 147 000, was used as a plasma marker to visualize the perfused capillaries. Alkaline phosphatase staining was used to stain the total capillary bed of the brain. Our results showed that FITC-dextran stayed within the vascular compartment, as it was not seen in areas that were not subsequently visualized with alkaline phosphatase staining. Eighty-four to 86% of the alkaline phosphatase-stained capillaries could be visualized with perfusion markers (india ink or FITC-dextran) in different brain regions. Similar results were obtained in two animals using a basement membrane stain, silver methenamine. The total volume fraction of capillaries (mm3/mm3) was cortex 0.055 ± 0.012, cerebellum 0.062 ± 0.011, and medulla 0.039 ± 0.012. Capillary surface area (mm2/mm3) of different brain regions averaged cortex 23.2 ± 1.8, cerebellum 24.8 ± 2.5, and medulla 15.8 ± 2.9. The total number of capillaries (per mm2) was cortex 375 ± 37, cerebellum 329 ± 37, and medulla 216 ± 32. The time course of filling of the capillaries indicated that approximately 50% were perfused at 6 s, which increased to over 80% at 12 s and remained unchanged thereafter. We found that FITC-dextran (molecular weight 147 000) was a suitable plasma marker to visualize the perfused capillaries, and alkaline phosphatase staining could mark the total capillary bed in the newborn pig brain. We conclude that the capillaries in the newborn pig brain fill rapidly and that this organ lacks a capillary reserve at rest.
Room temperature solid-state synthesis of a conductive polymer for applications in stable I₂-free dye-sensitized solar cells.

A solid-state polymerizable monomer, 2,5-dibromo-3,4-propylenedioxythiophene (DBProDOT), was synthesized at 25 °C to produce a conducting polymer, poly(3,4-propylenedioxythiophene) (PProDOT). Crystallographic studies revealed a short interplane distance between DBProDOT molecules, which was responsible for polymerization at low temperature with a lower activation energy and higher exothermic reaction than 2,5-dibromo-3,4-ethylenedioxythiophene (DBEDOT) or its derivatives. Upon solid-state polymerization (SSP) of DBProDOT at 25 °C, PProDOT was obtained in a self-doped state with tribromide ions and an electrical conductivity of 0.05 S cm⁻¹, which is considerably higher than that of chemically-polymerized PProDOT (2×10⁻⁶ S cm⁻¹). Solid-state ¹³C NMR spectroscopy and DFT calculations revealed polarons in PProDOT and a strong perturbation of carbon nuclei in thiophenes as a result of paramagnetic broadening. DBProDOT molecules deeply penetrated and polymerized to fill nanocrystalline TiO₂ pores with PProDOT, which functioned as a hole-transporting material (HTM) for I₂-free solid-state dye-sensitized solar cells (ssDSSCs). With the introduction of an organized mesoporous TiO₂ (OM-TiO₂) layer, the energy conversion efficiency reached 3.5 % at 100 mW cm⁻², which was quite stable up to at least 1500 h. The cell performance and stability was attributed to the high stability of PProDOT, with the high conductivity and improved interfacial contact of the electrode/HTM resulting in reduced interfacial resistance and enhanced electron lifetime.
‘It’s like a problem that doesn’t exist’: The emotional well-being of mothers caring for a child with brain injury

Abstract Background: Although research has shown that significant burden and adverse psychological impact are associated with caring for a child with brain injury, limited knowledge exists concerning the qualitative experience and impact of this burden. Objective: To provide an account of the experiences of mothers who care for a childhood survivor of brain injury. Research design: Postal survey. Methods and procedures: A self-report questionnaire was sent to a consecutive sample of mothers (n = 86) of children (aged 2–28) with acquired brain injury, registered with a UK children’s brain injury charity. Five essay style questions enabled mothers to reflect on and describe at length their caring experiences, with particular emphasis placed on the perceived impact on emotional well-being. Main outcomes and results: Thematic analysis identified five key themes: Perpetually Anxious, The Guilty Carer, The Labour of Caring, A Self-Conscious Apologist and Perpetually Grieving. Collectively, these themes highlight two core processes shaping mothers’ caring experiences and concomitant mental well-being. First, the collective and enduring nature of caregiver burden over time. Second, the crucial role played by socio-cultural values in perpetuating caregiver burden. Conclusions: Societal norms, particularly those relating to the nature and outcome of brain injury and motherhood, serve to marginalize mothers and increase feelings of isolation. Findings suggest the value of peer support programmes as an effective means of providing appropriate social support.
Crystal structure of a crustacean hyperglycemic hormone (CHH) precursor suggests structural variety in the C‐terminal regions of CHH superfamily members

The crustacean hyperglycemic hormone (CHH) is one of the major hormones in crustaceans, and peptides belonging to the CHH superfamily have been found in diverse ecdysozoans. Although the basic function of CHH is to control energy metabolism, it also plays various roles in crustacean species, such as in molting and vitellogenesis. Here, we present the crystal structure of Pej‐SGP‐I‐Gly, a partially active precursor of CHH from the kuruma prawn Marsupenaeus japonicus, which has an additional Gly residue in place of the C‐terminal amide group of the mature Pej‐SGP‐I. The 1.6‐angstrom crystal structure showed not only the common CHH superfamily scaffold comprising three α‐helices, three disulfide bridges, and a hydrophobic core but also revealed that the C‐terminal part has a variant backbone fold that is specific to Pej‐SGP‐I‐Gly. The α‐helix 4 of Pej‐SGP‐I‐Gly was much longer than that of molt‐inhibiting hormone (Pej‐MIH) from the same species, and as a result, the following C‐terminal helix, corresponding to α‐helix 5 in MIH, was not formed. Unlike monomeric Pej‐MIH, Pej‐SGP‐I‐Gly forms a homodimer in the crystal structure via its unique α‐helix 4. The unexpected dissimilar folds between Pej‐SGP‐I‐Gly and Pej‐MIH appear to be the result of their distinct C‐terminal amino acid sequences. Variations in amino acid sequences and lengths and the resulting variety of backbone folds allow the C‐terminal and sterically adjoining regions to confer different hormonal activities in diverse CHH superfamily members.
Isolation of Histones and Nucleosome Cores from Mammalian Cells

In vitro analysis of DNA in chromatin is often important for understanding mechanisms of regulation of transcription and other processes that occur on DNA. The basic unit of chromatin is the nucleosome core, containing two copies each of the core histones H2A, H2B, H3, and H4 to form a histone octamer that wraps 145 base pairs of DNA in a left‐handed superhelix. In vivo, chromatin is associated with linker histones (such as H1), which facilitate the ordered packing of nucleosomes. This linker histone‐containing particle is properly termed the nucleosome (or chromatosome), while the linker histone‐free particle is the nucleosome core. Pure polynucleosome cores and histones can be readily isolated from mammalian tissue culture cells. This unit describes procedures for isolation and purification of nuclei, isolation of polynucleosomes lacking linker histones from these nuclei, isolation of pure populations of mono‐ and dinucleosome cores from oligonucleosome fractions, and isolation of core histones from purified nuclei. The methods presented here do not denature the histones, and may yield histones that are more active for in vitro assemblies.
Evaluation of the antimicrobial activity of ebselen: Role of the yeast plasma membrane H+‐ATPase

Ebselen (2‐phenyl‐1,2‐benzisoselenazol‐3(2H)‐one) is a selenium‐containing antioxidant demonstrating anti‐inflammatory and cytoprotective properties in mammalian cells and cytotoxicity in lower organisms. The mechanism underlying the antimicrobial activity of ebselen remains unclear. It has recently been proposed that, in lower organisms like yeast, the plasma membrane H+‐ATPase (Pma1p) could serve as a potential target for this synthetic organoselenium compound. Using yeast and bacteria, the present study found ebselen to inhibit microbial growth in a concentration‐ and time‐dependent manner, and yeast and Gram‐positive bacteria to be more sensitive to this action (IC50 ∼ 2–5 μM) than Gram‐negative bacteria (IC50 < 80 μM). Washout experiments and scanning electron microscopic analysis revealed ebselen to possess fungicidal activity. In addition, ebselen was found to inhibit medium acidification by PMA1‐proficient haploid yeast in a concentration‐dependent manner. Additional studies comparing PMA1 (+/−) and PMA1 (+/+) diploid yeast cells revealed the mutant to be more sensitive to treatment with ebselen than the wild type. Ebselen also inhibited the ATPase activity of Pma1p from S. cerevisae in a concentration‐dependent manner. The interaction of ebselen with the sulfhydryl‐containing compounds L‐cysteine and reduced glutathione resulted in the complete and partial prevention, respectively, of the inhibition of Pma1p ATPase activity by ebselen. Taken together, these results suggest that the fungicidal action of ebselen is due, at least in part, to interference with both the proton‐translocating function and the ATPase activity of the plasma membrane H+‐ATPase. © 2007 Wiley Periodicals, Inc. J Biochem Mol Toxicol 21:252–264, 2007; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20189
Effect of Patient Selection Method on Provider Group Performance Estimates

BackgroundPerformance measurement at the provider group level is increasingly advocated, but different methods for selecting patients when calculating provider group performance have received little evaluation. ObjectiveWe compared 2 currently used methods according to characteristics of the patients selected and impact on performance estimates. Research Design, Subjects, and MeasuresWe analyzed Medicare claims data for fee-for-service beneficiaries with diabetes ever seen at an academic multispeciality physician group in 2003 to 2004. We examined sample size, sociodemographics, clinical characteristics, and receipt of recommended diabetes monitoring in 2004 for the groups of patients selected using 2 methods implemented in large-scale performance initiatives: the Plurality Provider Algorithm and the Diabetes Care Home method. We examined differences among discordantly assigned patients to determine evidence for differential selection regarding these measures. ResultsFewer patients were selected under the Diabetes Care Home method (n=3558) than the Plurality Provider Algorithm (n=4859). Compared with the Plurality Provider Algorithm, the Diabetes Care Home method preferentially selected patients who were female, not entitled because of disability, older, more likely to have hypertension, and less likely to have kidney disease and peripheral vascular disease, and had lower levels of predicted utilization. Diabetes performance was higher under Diabetes Care Home method, with 67% versus 58% receiving >1 A1c tests, 70% versus 65% receiving ≥1 low-density lipoprotein (LDL) test, and 38% versus 37% receiving an eye examination. ConclusionsThe method used to select patients when calculating provider group performance may affect patient case mix and estimated performance levels, and warrants careful consideration when comparing performance estimates.
Solute Carrier Family 26 Member a2 (Slc26a2) Protein Functions as an Electroneutral SO42−/OH−/Cl− Exchanger Regulated by Extracellular Cl−*

Background: Slc26a2 is an SO42− transporter, mutations in which cause diastrophic dysplasia. How Slc26a2 transports SO42− is unknown. Results: We found that Slc26a2 exchanges SO42− for 2OH− or 2Cl− and is regulated by a promiscuous extracellular anion site. Conclusion: Slc26a2 functions as SO42−/2OH− or SO42−/2Cl− exchanger, regulated by extracellular Cl−o. Significance: The findings should help in understanding aberrant SLC26A2 function in diastrophic dysplasia. Slc26a2 is a ubiquitously expressed SO42− transporter with high expression levels in cartilage and several epithelia. Mutations in SLC26A2 are associated with diastrophic dysplasia. The mechanism by which Slc26a2 transports SO42− and the ion gradients that mediate SO42− uptake are poorly understood. We report here that Slc26a2 functions as an SO42−/2OH−, SO42−/2Cl−, and SO42−/OH−/Cl− exchanger, depending on the Cl− and OH− gradients. At inward Cl− and outward pH gradients (high Cl−o and low pHo) Slc26a2 functions primarily as an SO42−o/2OH−i exchanger. At low Cl−o and high pHo Slc26a2 functions increasingly as an SO42−o/2Cl−i exchanger. The reverse is observed for SO42−i/2OH−o and SO42−i/2Cl−o exchange. Slc26a2 also exchanges Cl− for I−, Br−, and NO3− and Cl−o competes with SO42− on the transport site. Interestingly, Slc26a2 is regulated by an extracellular anion site, required to activate SO42−i/2OH−o exchange. Slc26a2 can transport oxalate in exchange for OH− and/or Cl− with properties similar to SO42− transport. Modeling of the Slc26a2 transmembrane domain (TMD) structure identified a conserved extracellular sequence 367GFXXP371 between TMD7 and TMD8 close to the conserved Glu417 in the permeation pathway. Mutation of Glu417 eliminated transport by Slc26a2, whereas mutation of Phe368 increased the affinity for SO42−o 8-fold while reducing the affinity for Cl−o 2 fold, but without affecting regulation by Cl−o. These findings clarify the mechanism of net SO42− transport and describe a novel regulation of Slc26a2 by an extracellular anion binding site and should help in further understanding aberrant SLC26A2 function in diastrophic dysplasia.
Ang-(1-7) might prevent the development of monocrotaline induced pulmonary arterial hypertension in rats.

OBJECTIVES To investigate whether Angiotensin-(1-7) [Ang-(1-7)] could prevent the development of monocrotaline (MCT) induced pulmonary arterial hypertension and vascular remodeling. MATERIALS AND METHODS 30 Sprgue-Dawely rats were randomly assigned into three groups: control group, pulmonary arterial hypertension (PAH) group and PAH +Ang-(1-7) group. Rats in PAH group and PAH +Ang-(1-7) group received 60 mg/kg monocrotaline (MCT) injection subcutaneously and after 24 hours received either saline or 24 microg/kg/h of Ang-(1-7) injection via osmotic minipumps for 4 weeks. Those rats in control group were firstly injected saline subcutaneously and then received saline injection via osmotic minipumps. RESULTS After four weeks, in PAH group, right ventricular systolic pressure (RVSP), right ventricular hypertrophy index (RVHI), percentage of wall thickness (WT%) and percentage of wall area (WA%) were significantly increased, and the level of endothelial nitric oxide synthase (eNOS) protein, eNOS ser 1177-phosphorylati, Akt-phosphorylation were significantly decreased compared with control group. However, RVSP, RVHI, WT%, WA% were dramatically decreased in PAH+Ang-(1-7) group and the level of eNOS protein, eNOS ser 1177-phosphorylation, Akt-phosphorylation were significantly increased compared with PAH group. CONCLUSION Those results suggest that Ang-(1-7) could prevent the development of monocrotaline induced pulmonary arterial hypertension and vascular remodeling, which appears to be associated with up-regulation of eNOS activation via Akt pathway.
Description of a method for inducing fetal growth restriction in the spiny mouse

Intrauterine or fetal growth restriction (IUGR) is a major complication of pregnancy and leads to significant perinatal morbidities and mortality. Typically, induction of IUGR in animals involves the complete occlusion or ablation of vessels to the uterus or placenta, acutely impairing blood flow and fetal growth, usually with high fetal loss. We aimed to produce a model of reduced fetal growth in the spiny mouse with minimal fetal loss. At 27 days gestational age (term is 38–39 days), a piece of silastic tubing was placed around the left uterine artery to prevent the further increase of uterine blood flow with advancing gestation to induce IUGR (occluded). Controls were generated from sham surgeries without placement of the tubing. Dams were humanely euthanized at 37 days gestational age and all fetuses and placentas were weighed and collected. Of the 17 dams that underwent surgery, 15 carried their pregnancies to 37 days gestational age and 95% of fetuses survived to this time. The difference in fetal body weight between occluded and control was ~21% for fetuses in the left uterus side: there were no differences for fetuses in the right uterus side. Offspring from the occluded group had significantly lower brain, liver, lung, kidney and carcass weights compared with shams. Preventing the gestation-related increase of uterine blood flow induced significant growth restriction in the fetal spiny mouse, with minimal fetal loss. This technique could be readily adapted for other small animal.
Skeletal muscle and bone marrow derived stromal cells: A comparison of tenocyte differentiation capabilities

This study investigated the comparative ability of bone marrow and skeletal muscle derived stromal cells (BMSCs and SMSCs) to express a tenocyte phenotype, and whether this expression could be augmented by growth and differentiation factor‐5 (GDF‐5). Tissue harvest was performed on the hind limbs of seven dogs. Stromal cells were isolated via serial expansion in culture. After four passages, tenogenesis was induced using either ascorbic acid alone or in conjunction with GDF‐5. CD44, tenomodulin, collagen I, and collagen III expression levels were compared for each culture condition at 7 and 14 days following induction. Immunohistochemistry (IHC) was performed to evaluate cell morphology and production of tenomodulin and collagen I. SMSCs and BMSCs were successfully isolated in culture. Following tenocytic induction, SMSCs demonstrated an increased mean relative expression of tenomodulin, collagen I, and collagen III at 14 days. BMSCs only showed increased mean relative expression of collagen I, and collagen III at 14 days. IHC revealed positive staining for tenomodulin and collagen I at 14 days for both cell types. The morphology of skeletal muscle derived stromal cells at 14 days had an organized appearance in contrast to the haphazard arrangement of the bone marrow derived cells. GDF‐5 did not affect gene expression, cell staining, or cell morphology significantly. Stromal cells from either bone marrow or skeletal muscle can be induced to increase expression of matrix genes; however, based on expression of tenomodulin and cell culture morphology SMSCs may be a more ideal candidate for tenocytic differentiation. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 30:1710–1718, 2012