Miracle-dz/UniFAR-FTUs huggingface dataset:
Rising standards of sustainability reporting in India

Purpose The increasing awareness among the stakeholders demands the companies to be more transparent in their annual reporting. In the absence of standardized reporting norms, companies are free to structure sustainability report as per their understanding, willingness and intent. Although some voluntary guidelines have been issued by the regulatory authorities in India, the norms are still not clear as to what to report and how to report. This paper aims to look in to sustainability reporting practices by top companies listed in Bombay stock exchange and its impact on financial performance. Design/methodology/approach Using this sample of 68 companies from top 100 in the list of ET500 for 2016, self-constructed sustainability reporting score has been computed for each company for the financial year 2012-2013 and 2015-2016. The two periods represent pre- and post-disclosure reform periods in India. A sustainability reporting scale has been constructed using 16 parameters of sustainable performance based on social, environment and governance aspects as reported in the annual report, sustainability report and business responsibility report. Findings It has been found that there is a significant improvement in sustainability reporting by Indian companies after the introduction of disclosure reforms. Different sectors show significant difference in the sustainability reporting during pre-reform period but as the sustainability reporting improves after the reforms, sector difference reduces. Sustainability reporting is a significant predictor of financial parameters of return on sales, return on equity and Tobin’s Q in pre-reform period, but in the post-reform period, no significant impact was found on financial performance. Practical implications Disclosure reforms have made a significant impact on sustainability reporting by Indian companies. Companies need to identify the core areas of social responsibility, to implement Indian model of mandatory 2 per cent spending on corporate social responsibility. Disclosure of carbon foot prints should be mandatory and more number of independent directors should be appointed for successful implementation of these reforms. Market regulators should be made more powerful and given a free hand to prosecute the companies involved in frauds and high penalties should be imposed for non-compliance. Originality/value Sustainability reporting has drawn increased strategic attention in India to make reporting more transparent and responsible toward society and environment. The structural changes and introduction of disclosure reforms make an interesting case to investigate their implications on Indian companies. Accordingly, this research studies the sustainability reporting by Indian companies before and after the introduction of disclosure reforms. No previous research has investigated the impact of these reforms considering two different periods.
Electrocardiographic markers of abnormal left ventricular wall motion in acute subarachnoid hemorrhage.

A reversible and presumably neurogenic form of myocardial dysfunction may occur following subarachnoid hemorrhage (SAH), but the relationship of this finding to electrocardiographic abnormalities remains unclear. To clarify this issue, serial electrocardiograms (ECGs, mean 6.2 per patient) and echocardiograms (mean 3.4 days after SAH) were obtained in 57 SAH patients without preexisting cardiac disease. The goal was to determine which specific electrocardiographic changes, if any, reflect abnormal left ventricular wall motion in acute SAH. Wall motion abnormalities were identified in five (8%) of 57 patients. Four of these affected patients experienced hypotension (systolic blood pressure < 100 mm Hg) and three exhibited pulmonary edema within 6 hours of SAH, compared to none of the 52 patients with normal wall motion (p < 0.0001). Patients with abnormal wall motion were more likely than patients with normal echocardiograms to have symmetrical T wave inversion (five of five vs. seven of 52, p < 0.001) and severe (> or = 500 msec) QTc segment prolongation (five of five vs. three of 52, p < 0.001) on serial ECGs. These associations maintained their significance with analysis limited to single ECGs performed on or near the day of echocardiography. Abnormal wall motion was also associated with borderline (2% to 5%) creatine kinase MB elevation (five of five vs. three of 52, p < 0.001) and poor neurological grade (p < 0.0001). Although no combination of findings on a single ECG resulted in 100% sensitivity for abnormal wall motion, the presence of either inverted T waves or severe QTc segment prolongation on serial ECGs was associated with 100% sensitivity and 81% specificity. These results demonstrate an association between reduced left ventricular systolic function, mild creatine kinase MB elevation, and electrocardiographic repolarization abnormalities in acute SAH. Symmetrical T wave inversion and severe QTc segment prolongation best identified patients at risk for myocardial dysfunction and may serve as useful criteria for echocardiographic screening following SAH.
Pattern and spectrum of morphology referrals in breast pathology consultation.

AIMS We aimed to identify common reasons for second opinion breast pathology referrals at the Pathology Department, Singapore General Hospital, focusing on queries and diagnostic issues raised by referring clinicians and pathologists. METHODS Request forms for breast pathology consultations were retrieved from a specialist's correspondence files consisting of pathologists' referrals, and from centralised laboratory records, comprising clinician-initiated referrals. Clinical and histomorphological queries raised by the referrals were collated. RESULTS Of 299 cases evaluated, clinician-initiated referrals (n = 137, 46%) included requests for review of overall histopathology to confirm carcinoma subtype (n = 47), grade (n = 2), size (n = 4), lymphovascular invasion (n = 1) and confirm hormonal receptor and c-erbB-2 assays (n = 33). Also required were: comparison of recurrent with previous lesions (n = 8); settling discrepant diagnoses between two or more prior pathology reports (n = 4); verification of microinvasion (n = 6), in situ carcinomas (n = 6) or atypical ductal hyperplasias (n = 4); delineation of benign (n = 8) and spindle cell lesions (n = 3); to establish a breast origin of metastatic lesions (n = 5); and distinction of carcinoma from lymphoma (n = 2). Pathologist-initiated referrals (n = 162, 54%) sought arbitration between borderline proliferative lesions (n = 46) and papillary lesions (n = 34); verification of microinvasion (n = 23), stromal lesions (n = 16), and carcinoma subtype (n = 13), especially if the patient was young (n = 5); clarification of metaplastic changes (n = 4) and lobular neoplasia (n = 8); and comparison of fibroepithelial lesions (n = 11). CONCLUSIONS Clinicians sought a second opinion mainly to verify histological diagnoses and report important pathological details for staging and confirmation of hormonal receptor and c-erbB-2 status prior to therapy. Borderline breast lesions are worrisome for both clinicians and pathologists in view of implications for management.
mRNA and protein expression of dog liver cytochromes P450 in relation to the metabolism of human CYP2C substrates

1. Interpretation of novel drug exposure and toxicology data from the dog is tempered by our limited molecular and functional knowledge of dog cytochromes P450 (CYPs). The aim was to study the mRNA and protein expression of hepatic dog CYPs in relation to the metabolism of substrates of human CYP, particularly those of the CYP2C subfamily. 2. The rate of 7-hydroxylation of S -warfarin (CYP2C9 in humans) by dog liver microsomes (mean ± SD from 12 (six male and six female) dogs = 10.8 ± 1.9 fmol mg − 1 protein min − 1) was 1.5-2 orders of magnitude lower than that in humans. 3. The rate of 4'-hydroxylation of S -mephenytoin, catalysed in humans by CYP2C19, was also low in dog liver (4.6 ± 1.5 pmol mg − 1 protein min − 1) compared with human liver. In contrast, the rate of 4'-hydroxylation of the R -enantiomer of mephenytoin by dog liver was much higher. The kinetics of this reaction (range of K m or K 0.5 15-22 µM, V max 35-59 pmol mg − 1 protein min − 1, n = 4 livers) were consistent with the involvement of a single enzyme. 4. In contrast to our findings for S -mephenytoin, dog liver microsomes 5'-hydroxylated omeprazole (also catalysed by CYP2C19 in humans) at considerably higher rates (range of K m 42-64 µM, V max 22-46 pmol mg − 1 protein min − 1, n = 4 livers). 5. For all the substrates except omeprazole, a sex difference in their metabolism was observed in the dog (dextromethorphan N-demethylation: female range = 0.7-0.9, male = 0.4-0.8 nmol mg − 1 protein min − 1 (p < 0.02); S -warfarin 7-hydroxylation: female = 9-15.5, male = 8-12 fmol mg − 1 protein min − 1 (p < 0.02); R -mephenytoin 4'-hydroxylation: female = 16-35, male = 11.5-19 pmol mg − 1 protein min − 1 (p < 0.01); omeprazole 5'-hydroxylation: female = 15-20, male 13-22 pmol mg − 1 protein min − 1 (p < 0.2)). 6. All dog livers expressed mRNA and CYP3A12, CYP2B11, CYP2C21 proteins, with no sex differences being found. Expression of CYP2C41 mRNA was undetectable in the livers of six of 11 dogs. 7. Correlation analysis suggested that CYP2B11 catalyses the N-demethylation of dextromethorphan (mediated in humans by CYP3A) and the 4'-hydroxylation of mephenytoin (mediated in humans by CYP2C19) in the dog, and that this enzyme and CYP3A12 contribute to S -warfarin 7-hydroxylation (mediated in humans by CYP2C9). 8. In conclusion, we have identified a distinct pattern of hepatic expression of the CYP2C41 gene in the Alderley Park beagle dog. Furthermore, marked differences in the metabolism of human CYP2C substrates were observed in this dog strain compared with humans with respect to rate of reaction, stereoselectivity and CYP enzyme selectivity.
Dissemination of discharge summaries. Not reaching follow-up physicians.

OBJECTIVE To discover how often hospital discharge summaries were available to physicians seeing patients for follow-up visits after hospitalization. DESIGN Cohort study. SETTING Teaching hospital in Ottawa, Ont. PARTICIPANTS We studied 792 patients discharged from an internal medicine service after treatment for acute illness. We determined when and by which physician each patient was seen during the first 6 months after discharge. We also determined the date each patient's discharge summary was printed and the physicians to whom it was sent. We confirmed that summaries were received by means of a survey or by telephoning physicians' offices. Patients were observed for 6 months or until they were readmitted to hospital. MAIN OUTCOME MEASURES Proportion of follow-up visits to physicians for which discharge summaries were available. RESULTS During the observation period, patients made 6619 visits (median six per patient, interquartile range [IQR] 2 to 9) to 914 different physicians (median three per patient, IQR 2 to 4). Discharge summaries were available for only 996 (15%) visits. Summaries were available for only 65 initial visits (8.2%); no summaries were available for any visit for 542 (68.4%) patients. Summaries were most commonly unavailable because they were not generated in time for follow-up visits (20.0%) or were not sent to follow-up physicians (50.8%). CONCLUSION At our institution, discharge summaries often did not get to physicians seeing patients after discharge from hospital.
The Rootes group: From growth to take-over

Abstract This article focuses on how a disparate group of firms was put together by the Rootes brothers in the late 1920s and early 1930s through a series of takeovers and mergers, catapulting the brothers from being simply car dealers to becoming major manufacturers in less than a decade. The article considers the wartime and post-war experiences of the firm, before proceeding to examine why, within a relatively short time, the firm, despite further merger activity, declined in terms of product development, investment and profitability, and was saved from extinction only by being taken over by the American firm, Chrysler.
Triple-Helix Formation Induces Recombination in Mammalian Cells via a Nucleotide Excision Repair-Dependent Pathway

ABSTRACT The ability to stimulate recombination in a site-specific manner in mammalian cells may provide a useful tool for gene knockout and a valuable strategy for gene therapy. We previously demonstrated that psoralen adducts targeted by triple-helix-forming oligonucleotides (TFOs) could induce recombination between tandem repeats of asupF reporter gene in a simian virus 40 vector in monkey COS cells. Based on work showing that triple helices, even in the absence of associated psoralen adducts, are able to provoke DNA repair and cause mutations, we asked whether intermolecular triplexes could stimulate recombination. Here, we report that triple-helix formation itself is capable of promoting recombination and that this effect is dependent on a functional nucleotide excision repair (NER) pathway. Transfection of COS cells carrying the dual supF vector with a purine-rich TFO, AG30, designed to bind as a third strand to a region between the two mutant supF genes yielded recombinants at a frequency of 0.37%, fivefold above background, whereas a scrambled sequence control oligomer was ineffective. In human cells deficient in the NER factor XPA, the ability of AG30 to induce recombination was eliminated, but it was restored in a corrected subline expressing the XPA cDNA. In comparison, the ability of triplex-directed psoralen cross-links to induce recombination was only partially reduced in XPA-deficient cells, suggesting that NER is not the only pathway that can metabolize targeted psoralen photoadducts into recombinagenic intermediates. Interestingly, the triplex-induced recombination was unaffected in cells deficient in DNA mismatch repair, challenging our previous model of a heteroduplex intermediate and supporting a model based on end joining. This work demonstrates that oligonucleotide-mediated triplex formation can be recombinagenic, providing the basis for a potential strategy to direct genome modification by using high-affinity DNA binding ligands.
NeuroD Factors Discriminate Mineralocorticoid From Glucocorticoid Receptor DNA Binding in the Male Rat Brain

In the limbic brain, mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs) both function as receptors for the naturally occurring glucocorticoids (corticosterone/cortisol) but mediate distinct effects on cellular physiology via transcriptional mechanisms. The transcriptional basis for specificity of these MR- vs GR-mediated effects is unknown. To address this conundrum, we have identified the extent of MR/GR DNA-binding selectivity in the rat hippocampus using chromatin immunoprecipitation followed by sequencing. We found 918 and 1450 nonoverlapping binding sites for MR and GR, respectively. Furthermore, 475 loci were co-occupied by MR and GR. De novo motif analysis resulted in a similar binding motif for both receptors at 100% of the target loci, which matched the known glucocorticoid response element (GRE). In addition, the Atoh/NeuroD consensus sequence was found in co-occurrence with all MR-specific binding sites but was absent for GR-specific or MR-GR overlapping sites. Basic helix-loop-helix family members Neurod1, Neurod2, and Neurod6 showed hippocampal expression and were hypothesized to bind the Atoh motif. Neurod2 was detected at rat hippocampal MR binding sites but not at GR-exclusive sites. All three NeuroD transcription factors acted as DNA-binding-dependent coactivators for both MR and GR in reporter assays in heterologous HEK293 cells, likely via indirect interactions with the receptors. In conclusion, a NeuroD family member binding to an additional motif near the GRE seems to drive specificity for MR over GR binding at hippocampal binding sites.
Lymphocytes in Sweet syndrome: A potential diagnostic pitfall

Patients with Sweet syndrome (SS) have acute onset of cutaneous lesions with characteristic histopathology (dense and diffuse neutrophilic infiltrate, dermal edema, leukocytoclasis and no vasculitis) accompanied by systemic symptoms. Sometimes, only skin lesions with classic histopathologic features are seen. Although SS is considered to be a “neutrophilic dermatosis,” lymphocytes are also seen on histological examination.
Single dose intravenous ondansetron for the 24‐hour treatment of postoperative nausea and vomiting

Postoperative nausea and vomiting is a major concern for patients undergoing outpatient surgery under general anaesthesia, and may complicate and delay discharge from hospital. This paper evaluates the safety and efficacy of ondansetron, a 5‐HT3 receptor antagonist, in the treatment of postoperative nausea and vomiting. One thousand patients in 30 centres in the United States who received general anaesthesia and developed postoperative nausea and vomiting were studied. In a randomised, double‐blind, stratified and parallel designed protocol, patients received either ondansetron 1, 4, 8mg or placebo for nausea or vomiting occurring within 2 h of entry into the Post Anaesthesia Care Unit. Subsequent episodes of vomiting, nausea scores, laboratory and clinical safety data and adverse events were evaluated during the 24‐h study period. In a separate study, pharmacokinetic data were compared for intramuscularly and intravenously administered ondansetron. Each dose of ondansetron was significantly better than placebo in reducing nausea from control values during the initial 2‐h study period, and in preventing further emesis over 24 h. There were no significant differences in the incidence of adverse events, changes in laboratory values or measures of vital signs in the ondansetron groups compared to the placebo group. Dose comparisons between the three treatment groups showed that ondansetron 4 mg is the optimal dose to treat postoperative nausea and vomiting. Ondansetron is a well tolerated, efficacious antiemetic which has a similar side effect profile to placebo. Intramuscular administration has the same systemic availability as intravenous administration. Ondansetron 4mg appears to be the optimal dose for the treatment of postoperative nausea and vomiting in patients with or without a positive history.
Enumeration and characterization of Aeromonas hydrophila and Aeromonas caviae isolated from grocery store produce

Starch-ampicillin agar was used to quantitatively isolate Aeromonas sp. from retail grocery store produce. All produce sampled, including parsley, spinach, celery, alfalfa sprouts, broccoli, and lettuce, contained Aeromonas sp. In most instances, the count of Aeromonas sp. increased 10- to 1,000-fold during 2 weeks of storage at 5 degrees C. Eleven (92%) of 12 kinds of produce yielded cytotoxic Aeromonas sp. Identification as Aeromonas hydrophila was the strongest indicator of cytotoxicity, and all 29 (100%) A. hydrophila isolates and 1 (6%) of 16 A. caviae isolates were cytotoxic. Twenty-seven (90%) of 30 cytotoxic Aeromonas sp. strains produced hemolysins. Strong correlations were also noted between ability to produce cytotoxin and positive Voges-Proskauer, lysine decarboxylase, and sorbitol fermentation reactions. It appears that grocery store produce is a potentially significant source of cytotoxic Aeromonas sp. and should be considered in the epidemiology of A. hydrophila gastroenteritis.
Concurrent down-regulation of Egr-1 and gelsolin in the majority of human breast cancer cells.

UNLABELLED A growing body of evidence suggests that early growth response-1 (Egr-1), a transcription factor, may function as a tumor suppressor. The aim of this study was to gain more evidence to support the role of Egr-1 in the suppression of cancer cell growth and to examine the potential correlation between Egr-1 and gelsolin. MATERIALS AND METHODS Histochemical staining coupled with breast cancer tissue arrays were used to examine the expression levels of Egr-1 and gelsolin. Reporter assays and gel shift were used to study the transcriptional activity of Egr-1 on the regulation of gelsolin. RESULTS Our data showed that most normal mammary tissues expressed high levels of Egr-1, while the majority of breast cancer tissues expressed very small amounts of Egr-1. The expression pattern of Egr-1 in human breast cancer tissues was highly correlated with gelsolin expression. Induction of Egr-1 by serum stimulation accompanied the increase of gelsolin expression. In cells lacking the induction of Egr-1 in response to serum stimulation, gelsolin expression remained unchanged. Furthermore, gelsolin promoter activity was profoundly reduced in Egr-1 null mouse embryonic fibroblasts compared to Egr-1 wild-type mouse embryonic fibroblasts. Gel shift experiments indicated that Egr-1 can directly bind to the gelsolin promoter. CONCLUSION Our results suggest that Egr-1 may be an important breast cancer marker and that an as yet uncharacterized pathway involved in Egr-1 and gelsolin expression exists which leads to breast cancer cell development.
VITAMIN D-BINDING PROTEIN IN HEALTHY PRE- AND POSTMENOPAUSAL WOMEN: RELATIONSHIP WITH ESTRADIOL CONCENTRATIONS.

OBJECTIVE To examine the relationship between endogenous serum estradiol and vitamin D-binding protein (DBP) and total, free, and bioavailable 25-hydroxyvitamin D (25OHD) concentrations in pre- and postmenopausal women. METHODS In 165 healthy women (ages, 26 to 75 years) not taking any form of exogenous estrogen, the serum concentrations of estradiol, 25OHD, DBP, parathyroid hormone, and albumin were measured. Free and bioavailable 25OHD (free + albumin-bound) levels were calculated from total 25OHD, DBP, and serum albumin levels. RESULTS Premenopausal women had higher serum 25OHD (31.5 ± 7.9 ng/mL), DBP (45.3 ± 6.2 mg/dL), and estradiol (52.8 ± 35.0 pg/mL) levels than postmenopausal women (26.5 ± 4.9 ng/mL, 41.7 ± 5.7 mg/dL, and 12.9 ± 4.9 pg/mL), respectively. In addition, the calculated free and bioavailable 25OHD levels were higher in pre- than postmenopausal women (P<.05). Serum estradiol correlated with DBP (r = 0.22; P<.01) and total 25OHD (r = 0.27; P<.01). In multivariate regression models (with or without serum 25OHD), estradiol was independently associated with DBP (P<.05). CONCLUSION Lower estradiol level is one of the factors that contribute to lower DBP levels in older women. Our data indicate that besides well-known factors such as age, gender, and race, serum estradiol concentrations are also a physiologic predictor of DBP concentration.