Miracle-dz/UniFAR-FTUs huggingface dataset:
Developing social trust in IJVs: the characteristics of effective boundary spanners in Western-Chinese IJVs

IJVs are confronted by institutional, cultural and organizational diversity. Prior research has shown that the development of social trust is a significant factor in overcoming diversity and in ensuring IJV durability. Questions remain, nonetheless, as to how social trust can be effectively built and maintained. In this paper, we explore the characteristics of key individual boundary spanners in developing social trust. We do so the basis of a polar-sample: two 50/50 IJVs that involve the same MNE and two local enterprises. Despite the many commonalities of the two IJVs, our data indicate that while both are facing challenging market conditions the one IJV is characterized by social trust and the other by distrust. Employing a managerial level approach we identified a ‘mixed bundle of capabilities’ possessed by boundary spanners who were effective in the development of social trust.
Asymmetric localization of Numb:EGFP in dividing neuroepithelial cells during neurulation in Danio rerio

In the neural plate and tube of the zebrafish embryo, cells divide with their mitotic spindles oriented parallel to the plane of the neuroepithelium, whilst in the neural keel and rod, the spindle is oriented perpendicular to it. This change is achieved by a 90° rotation of the mitotic spindle. We cloned zebrafish homologues of the gene for the Drosophila cell fate determinant Numb, and analyzed the localization of EGFP fusion proteins in vivo in dividing neuroepithelial cells during neurulation. Whereas Numb isoform 3 and the related protein Numblike are localized in the cytoplasm, Numb isoform 1 is localized to the cell membrane. Time‐lapse analyses showed that Numb 1 is distributed uniformly around the cell cortex in dividing cells during plate and keel stages, but becomes localized at the basolateral membrane of some dividing cells during the transition from neural rod to tube. Using in vitro mutagenesis and Numb:EGFP deletion constructs, we showed that the first 196 amino acids of Numb are sufficient for this localization. Furthermore, we found that an 11–amino acid insertion in the PTB domain is essential for localization to the cortex, whereas amino acids 2–12 mediate the basolateral localization in the neural tube stage. Developmental Dynamics 235:934–948, 2006. © 2006 Wiley‐Liss, Inc.
Financial literacy of cocoa farmers in Ghana

Approximately 800,000 farm families are spread over six of ten regions of Ghana while empirical evidence on cocoa farmers' financial literacy remains sparse. This study examines the level of personal finance literacy among cocoa farmers. It also examines whether gender, age, level of education and farm size are related to cocoa farmers' financial literacy. A structured questionnaire is employed to collect data from randomly selected 569 cocoa farmers in the Assin Foso and Twifo Praso districts of the Central region. We use logistic regression analysis to estimate whether cocoa farmers' demographic variables are related to their level of financial literacy. We find that cocoa farmers have lower levels of financial knowledge. The level of financial literacy of cocoa farmers in Ghana is also related to their geographical location, age and education levels. This study provides stakeholders in the finance industry with vital information that will enhance decision making and policy directions. This study contributes to the literature of financial literacy from the perspective of cocoa farmers in Ghana, a Sub-Sahara Africa country.
Effect of bacterial density and substrate concentration on yield coefficients

Measurements were made of the yield coefficient during the aerobic metabolism of glucose by a heterogeneous bacterial mixture. Expressed in terms of carbon, the coefficient was approximately 0.48. The value did not vary with initial bacterial densities ranging from 0.4 pg to 40 micrograms of cell carbon per ml and with glucose concentrations ranging from 43 pg to 100 micrograms of carbon per ml. Under all these circumstances, about 44% of the glucose carbon was converted to CO2, and 7.4% was excreted as organic products. The significance of uncharacterized organic substrates contaminating the medium to the coefficients calculated for low glucose concentrations is discussed.
Pattern of admissions to neonatal unit.

OBJECTIVE To document the number, disease pattern and outcome of patients admitted to neonatal unit. DESIGN Descriptive study. PLACE AND DURATION OF STUDY The study was conducted in the Neonatal Unit of National Institute of Child Health, Karachi, Pakistan from 1st January 2001 to 31st December 2001. PATIENTS AND METHODS The data of all the admitted neonates was analyzed for age and weight at the time of admission, sex, duration of stay, cause of admission and outcome. RESULTS A total of 1984 neonates were admitted during study period. Among them 62.1% were males, 17.54% were admitted within 6 hours of their life, and 51.36% within 72 hours of birth. The low birth weight accounted for 55.4% admissions. Neonatal infection was the major cause of admission (45.21%) comprising 30.64% cases of septicemia, 9.82% of pneumonia and 4.73% of meningitis. Other causes of admission were birth asphyxia (18.85%), neonatal jaundice (13.15%), pre-term (6.87%), meconium aspiration syndrome (3.67%), hemorrhagic disease of newborn (2.21%), diarrhea (2.11%) and hyaline membrane disease (1.05%). 48.53% were discharged with satisfactory condition, 25.5% died and 25.85% left against medical advice (LAMA) and or discharged on request (DoR). CONCLUSION Low birth weight (LBW), infections and birth asphyxia were the major causes of neonatal admission.
The contribution of XRCC6/Ku70 to hepatocellular carcinoma in Taiwan.

BACKGROUND Hepatocellular carcinoma (HCC) is a neoplasm for which the prevalence and mortality rates are very high in Taiwan. The DNA non-homologous end-joining repair gene XRCC6/Ku70 plays an important role in the repair of DNA double-strand breaks (DSBs) induced by both exogenous and endogenous DNA-damaging agents. Defects in overall DSB repair capacity can lead to genomic instability and carcinogenesis. In this study, we investigated the contribution of variant XRCC6 in relation to the risk of HCC, from the levels of DNA, RNA and protein. MATERIALS AND METHODS In this hospital-based case-control study, we collected 298 patients with HCC and 298 cancer-free controls, with frequency matched by age and gender. Firstly, the associations of XRCC6 promoter T-991C (rs5751129), promoter G-57C (rs2267437), promoter A-31G (rs132770), and intron-3 (rs132774) polymorphisms with HCC risk in this Taiwanese population were evaluated. Secondly, 30 HCC tissue samples with variant genotypes were tested to estimate the XRCC6 mRNA expression by real-time quantitative reverse transcription. Finally, the HCC tissue samples of variant genotypes were examined by immunohistochemistry and western blotting to estimate their XRCC6 protein expression levels. RESULTS Compared with the TT genotype, the TC and CC genotypes conferred a significantly increased risk of HCC [adjusted odds ratio (aOR)=2.43 and 3.52, 95% confidence interval (CI)=1.52-4.03 and 1.18-13.36, p=0.0003 and 0.0385, respectively]. The mRNA and protein expression levels in HCC tissues revealed statistically significantly lower XRCC6 mRNA and protein expressions in the HCC samples with TC/CC genotypes compared with those with the TT genotype (p=0.0037 and 0.0003, respectively). CONCLUSION Our multi-approach findings at the DNA, RNA and protein levels suggested that XRCC6 may play an important role in HCC carcinogenesis in the Taiwanese population.
Insulin-mediated glucose disposal in type I diabetes: evidence for insulin resistance.

To clarify whether type I diabetes is characterized by insulin resistance, insulin-mediated glucose metabolism (M; milligrams per kg/min) was estimated by means of the glucose clamp technique in five insulin-dependent diabetic patients and six normal subjects. Three glucose clamps were carried out under different metabolic conditions. Free insulin plateaux were similar during each clamp in both groups. The first clamp was performed in normal subjects after an overnight fast [blood glucose, 80 +/- 3 mg/dl (mean +/- SEM)] and in diabetic patients 18 h after insulin withdrawal (blood glucose, 366 +/- 47 mg/dl). Diabetic patients had a M value (4.25 +/- 0.74) not different from normals (5.38 +/- 0.63; P = NS). The second clamp was done with the same glycemic values (approximately 125 mg/dl) in both groups. M increased to 8.07 +/- 1.06 (P less than 0.01) in the normal subjects and decreased to 2.87 +/- 0.50 (P = NS) in the diabetic patients. The M value in the diabetic patients was lower than that in the normal subjects (P less than 0.05). The third clamp was performed in three diabetic patients after 1 month of treatment with continuous sc insulin infusion. The mean blood glucose level was 88 +/- 6 mg/dl, and M was 3.23 +/- 0.38, significantly lower than that of the normal subjects in the basal state (P less than 0.05). No differences were found in insulin binding to erythrocytes. The mean plasma clearance rate (milliliters per m2/min) of free insulin was the same in both groups (428 +/- 113 in normal subjects and 354 +/- 83 in diabetic patients). Basal endogenous glucose production was higher in the diabetics (3.13 +/- 0.48 mg/kg X min) than in the normal subjects (1.71 +/- 0.57). During the clamp, however, endogenous glucose production was similarly inhibited (approximately 95%) in both groups. Multiple glucose clamp studies were also performed at three different insulin infusion rates (21, 73, and 760 mU/m2 X min, respectively) to generate an insulin-dose response curve for glucose disposal in six diabetic patients treated with continuous sc insulin infusion for at least 6 months. This allowed investigation of the effect of chronic strict insulin therapy leading to normal glucose and intermediary metabolite levels and identification of the cellular mechanism of insulin resistance. A significant reduction of the maximal glucose disposal rate (10.7 +/- 0.5 mg/kg X min) was found in these diabetic patients compared to that in normal subjects (14.9 +/- 1.0; P less than 0.05). (ABSTRACT TRUNCATED AT 400 WORDS)
How does the brain sustain a visual percept?

Perception involves the processing of sensory stimuli and their translation into conscious experience. A novel percept can, once synthesized, be maintained or discarded from awareness. We used event–related funtional magnetic resonance imaging to separate the neural responses associated with the maintenance of a percept, produced by single–image, random–dot stereograms, from the response evoked at the onset of the percept. The latter was associated with distributed bilateral activation in the posterior thalamus and regions in the occipito–temporal, parietal and frontal cortices. In contrast, sustained perception was associated with activation of the pre–frontal cortex and hippocampus. This observation suggests that sustaining a visual percept involves neuroanatomical systems which are implicated in memory function and which are distinct from those engaged during perceptual synthesis.
Cancer-Related Microangiopathic Hemolytic Anemia: Clinical and Laboratory Features in 168 Reported Cases

AbstractCancer-related microangiopathic hemolytic anemia (CR-MAHA) is a paraneoplastic syndrome characterized by Coombs-negative hemolytic anemia with schistocytes and thrombocytopenia. We reviewed and analyzed all cases of CR-MAHA reported since 1979 (the time of the last published review on this topic) according to predefined criteria. We found 154 cases associated with solid cancer and 14 with lymphoma. Among the solid cancers, gastric, breast, prostate, lung, and cancer of unknown primary (CUP) were most common; 91.8% of cancers were metastatic, and in 19.4% of solid cancers CR-MAHA did not occur until recurrence of cancer. Lymphoma cases included Hodgkin disease, angiotropic lymphoma, diffuse large cell lymphoma, and myeloma. Evaluation of the clinical and laboratory findings revealed that only a minority of cases presented with the features of thrombotic thrombocytopenic purpura (TTP) or atypical hemolytic uremic syndrome (aHUS), with the exception of prostate cancer, where aHUS was a common presentation. Compared to hereditary or immune TTP or aHUS, disseminated intravascular coagulation and pulmonary symptoms were more common in CR-MAHA. Plasma exchange or fresh frozen plasma was rarely effective except in prostate cancer patients with aHUS. CR-MAHA responded to antitumor therapy in many patients with gastric, breast, lung, and CUP cancers. These patients had a superior survival compared to patients without chemotherapy. Compared to the prognosis of patients with metastatic cancer without CR-MAHA, the prognosis of CR-MAHA patients was greatly inferior. There is evidence that some cases of CR-MAHA in lymphoma are immune mediated.
Infant satiety depends on transient expression of cholecystokinin‐1 receptors on ependymal cells lining the third ventricle in mice

In mammals, satiety‐controlling mechanisms develop before the switch from ingestive behaviour from milk suckling to regular food intake; however, the underlying mechanisms are currently unknown. We show that absence of the cholecystokinin‐1 (CCK‐1) receptor gene significantly increases suckling pup weight, regardless of maternal genotype in mice. CCK‐1 receptor expression was observed in satiety‐controlling regions such as the hypothalamus, caudal brainstem, nodose ganglion and pylorus, which is consistent with suggested receptor function in adults, whereas corresponding receptor expression was low to non‐existent at pre‐weanling stages. Third ventricle ependymal tanycyte‐like cells transiently expressed CCK‐1 receptors at critical developmental stages, and gastrointestinal milk filling upregulated cFos expression in these cells. Localized blocking of ependymal CCK‐1 receptors was sufficient to produce overweight pups, suggesting that the ependymal CCK‐1 receptor is an infant‐specific satiety controller.
Absence of tissue inhibitor of metalloproteinases 3 disrupts alveologenesis in the mouse

Tissue inhibitors of metalloproteinases (TIMPs) regulate extracellular matrix (ECM) degradation by matrix metalloproteinases (MMPs) throughout lung development. We examined lungs from TIMP3 null mice and found significant air space enlargement compared with wild type (WT) animals during a time course spanning early alveologenesis (post‐partum days 1, 5, 9 and 14). Trichrome staining revealed a similar pattern of collagen distribution in the walls of nascent alveoli; however, the alveolar walls of TIMP3 mutant mice appeared to be thinner than controls. Assessment of MMP2 and MMP9 activities by gelatin zymography demonstrated a significant elevation in the active form of MMP2 at post‐partum days 1 and 5. Treatment of null pregnant dams with a broad spectrum synthetic metalloproteinase inhibitor, GM6001, on embryonic day 16.5 enhanced the formation of primitive alveoli during the saccular stage of lung development as evidenced by a partial, but significant, rescue of alveolar size in post‐partum day 1 animals. We propose that increased MMP activity in the absence of TIMP3 enhances ECM proteolysis, upsetting proper formation of primitive alveolar septa during the saccular stage of alveologenesis. Therefore, TIMP3 indirectly regulates alveolar formation in the mouse. To our knowledge, ours is the first study to demonstrate that in utero manipulation of the TIMP/MMP proteolytic axis, to specifically inhibit proteolysis, significantly affects lung development.
Leading improvement.

PURPOSE To provide research-informed guidance to leaders of quality and safety improvement and evidence-based materials for education programmes for leaders DESIGN/METHODOLOGY/APPROACH Search of databases and hard copy literature since 1985 into managers' and leaders' role in quality and safety improvement. Classification into "eA": Empirical research strong evidence, "eB": Empirical research, weak evidence and, "eC": Conceptual discussion, not based on systematic empirical research. Summary, and synthesis of the best available evidence for a guidance checklist for leaders. FINDINGS Although most literature emphasises the importance of committed leadership for successful quality and safety improvement, research evidence supporting this is scarce and often scientifically limited. The research shows evidence of the limitations and scope of leader actions for improving health care provision, the need to engage clinicians in this work and ways to do so, as well as the leadership role played by others apart from senior leaders. The ability of managers and other leaders skilfully to tailor Q&SI to the situation may be important but descriptions of how leaders do this and evidence supporting this proposition are lacking. RESEARCH LIMITATIONS/IMPLICATIONS More research is needed about whether or how the leader role is different according to the stage of quality and safety development of the organisation, the type of organisation, the type of context, the level and type of leader and the type of improvement and improvement method. PRACTICAL IMPLICATIONS Implications for leaders' actions are provided in a "best evidence guidance" checklist. This provides more tangible and research-informed guidance than the inspirational literature or studies from single organisations. ORIGINALITY/VALUE This paper provides the first overview and synthesis of a wide range of studies which can be used as a basis for future research and materials for educational programmes. It provides the first detailed guidance for leaders about specific actions which research suggests they need to take to improve quality and safety.
Estrogen receptor‐β gene disruption potentiates estrogen‐inducible aggression but not sexual behaviour in male mice

Aggressive behaviour of gonadally intact male mice is increased by estrogen receptor (ER)‐β gene disruption, whereas sexual behaviour remains unchanged. The elevated aggression levels following ER‐β gene disruption is pronounced during repeated aggression tests in young animals and the first aggression test in adults. In the present study, the roles of ER‐β activation in the regulation of aggressive and sexual behaviour were investigated in gonadectomized ER‐β knockout (βERKO) and wild‐type (WT) male mice treated with various doses of estrogen. Overall, estradiol benzoate (EB) treatment induced higher levels of aggression in βERKO mice than in WT mice. In WT mice, the levels of aggression induced by EB were highest in the lowest‐dose (2.5 µg/day) group and gradually decreased in higher‐dosage groups. On the other hand, equally high levels of aggressive behaviour were induced by all three doses of EB in βERKO mice. A marked genotype difference in dose responses is inferred, such that the ER‐α‐mediated facilitatory action of estrogen is more pronounced at lower and physiological doses and the ER‐β‐mediated inhibitory action is only unveiled at higher doses of estrogen. In contrast to aggression, the levels of sexual behaviour induced by EB were not different between βERKO and WT at either dose of EB (2.5 and 12.5 µg/day) examined. These findings support the notion that ER‐β activation may exert an attenuating action on male aggression induced by estrogen through ER‐α‐mediated brain mechanisms, whereas its effect on male sexual behaviour is relatively small.
Commonality in Analyst Coverage and Information Diffusion

I show that information diffusion emerges endogenously in the equity market due to strategic complementarities in analysts’ information production. I construct an information network of the equity market by connecting firms with commonalities in analyst coverage. Using the friendship paradox phenomenon, I identify stocks for which equilibrium information production is higher, and find that returns of these stocks lead other stocks. This effect is not completely explained by ex-ante firm characteristics and industry effects.
Corporate restructuring, work intensification and perceptual politics: Exploring the ambiguity of managerial job insecurity

Whereas social theorists, qualitative investigators and survey-based analysts suggest advanced economies are increasingly characterized by managerial job insecurity, database and questionnaire researchers propose relatively stable tenure rates for managers. This article aims to make sense of this ambiguity. First, following interviews with managers in Japan, the UK and the USA, the authors offer support for the ‘global convergence’ thesis, through data reflecting greater job insecurity generated by comparable and recurrent corporate restructuring. Second, considering research suggesting relative stability in managerial tenure rates, the authors argue that their findings – signifying increased insecurity – can be explained in terms of the ‘perceptual politics’ of US-style shareholder capitalism impinging, hegemonically, upon occupational sensibilities. Third, in conclusion, they suggest that everyday managerial experience can be understood in light of corporations purposively instilling a perceptual ‘insecurity message’ in managers, essentially as part of a tangible control strategy directed at the inexorable ratcheting-up of management productivity demands globally.
MAP kinase mediates silica‐induced fibrotic nodule formation and collagen accumulation in fibroblasts

It is well known that silica generates fibrosis around them in animals and human. However, the pathogenesis and mechanism of silica‐induced fibrosis are still poorly understood. Here, we established a new strategy through which the effects of silica on fibrotic nodule formation, key extracellular matrix accumulation, and the mechanism involved were explored. To achieve this, human dermal fibroblasts were directly exposed to silica gel for various durations. Fibrotic nodule formation was evaluated by their microscopic appearance, type‐1 procollagen, and fibronection expression in cell lysate and MMP‐1 and‐3 in conditioned media were analyzed by Western blotting. The results show an easily formation of nodule‐like structures around silica gel in an in vitro‐cultured system. The findings further revealed that silica gel stimulates collagen and fibronectin expression, while down‐regulates matrix metalloproteinase‐1 and ‐3 (MMP‐1 and MMP‐3) released in conditioned medium. To explore the mechanism involved, P38 and ERK1/2 Mitogen‐Activated Protein Kinase (MAPK) signaling pathways were evaluated. Result showed that silica inhibits P38 and extracellular signal‐regulated kinases (ERK1/2) MAP kinase phosphorylation. The addition of ERK1/2 inhibitor increases silica‐stimulated type‐1 collagen expression, reduces MMP‐1 release and further enhances silica‐induced nodule formation in dermal fibroblasts. These findings indicate that the inhibition of ERK1/2 MAPK signaling pathway may contribute to silica‐caused fibrosis. In summary, our findings suggest that silica can directly cause fibrotic phenotype when fibroblasts contact with silica particles independent of any inflammation and other factors may exist in an in vivo condition. J. Cell. Physiol. 227: 328–338, 2012. © 2011 Wiley Periodicals, Inc.