Miracle-dz/UniFAR-FTUs huggingface dataset:
Determinants of Household Education Expenditures: Do Poor Spend Less on Education?

Accumulation of human capital is proved to be crucial for economic growth and poverty alleviation. Education is counted as one of the basic services that allows individuals to gain better skills and knowledge which enhances economic growth and is also essential to combat poverty. Although investment in education is mostly financed by the government, most of the families privately contribute to their children’s education. Some of the researches argued that education expenditures depend on the income level of the households. From this point of view, private education can only be afforded by households who are at the higher income groups. Therefore, the focus of this study has twofold: One is to examine the determinants of education expenditure of Turkish households and the other is to reveal the impact of the different income groups on the education expenditures. Household Budget Survey (HBS) for the years 2002, 2010 and 2013 conducted by Turkish Statistic Institution (TurkStat) is utilized for Tobit model estimations. Findings show that higher Household income levels leads to higher educational expenditures. We also find that households with better human capital spend more on their children’s education. For 002, however, income elasticity of education expenditure is higher compare for poorer households compared to the richer ones, which means that poor are more sensitive to income changes with respect to education expenditures. We do not find this for the year 2013.
Cultured Human Fibroblasts Express Constitutive IL-16 mRNA: Cytokine Induction of Active IL-16 Protein Synthesis Through a Caspase-3-Dependent Mechanism1

Human fibroblasts can express numerous regulatory molecules that influence immune function. IL-16, a ligand for CD4, is a chemoattractant molecule expressed by lymphocytes, eosinophils, mast cells, and lung epithelium. It appears that the sole target for IL-16 is the CD4-bearing cell. Here we demonstrate that fibroblasts from several tissues can express IL-16 mRNA and protein as well as IL-16-dependent chemoattractant activity. The transcript is expressed abundantly under basal culture conditions as a 2.5-kb band on Northern analysis, similar to that observed in lymphocytes. IL-16 protein and activity are undetectable in fibroblast cultures under these same control conditions. However, when treated with proinflammatory cytokines such as IL-1β, they express very high levels of IL-16 protein and chemoattractant activity, a substantial component of which can be blocked with IL-16-neutralizing Abs. The amount of IL-16 protein released into the medium is 3- to 4-fold greater, on a per cell basis, than that observed in lymphocytes. The induction of IL-16 protein by IL-1β can be attenuated with specific inhibition of caspase-3, which could be detected in IL-1β-treated fibroblasts. IL-1β also induces RANTES mRNA, protein, and activity, and most of the chemoattractant activity released from fibroblasts not derived from IL-16 can be attributed to RANTES. Human fibroblasts appear to be an important source of IL-16 and through expression of this molecule may have key roles in the recruitment of CD4+ cells to sites of inflammation. IL-16 expression and the mechanism involved in its regulation appear to be cell type specific.
A kernel correlation filter based scale adaptive tracker: The full occlusion case

Although the existing correlation filter based on trackers has appeared to be more excellent in the visual tracking problem, there is still tremendous space for the improvement of the tracking performance, especially in the occlusion situation which is often ignored due to the difficulty in detection and processing. In this paper, a scale-adaptive tracker is proposed to handle the case of occlusion. We make full use of the response map to determine the occlusion degree of targets. Then, the global speeded up robust features (SURF) are extracted to train the supporters which help the tracker find the target once the complete occlusion occurs. Meanwhile, the target scale is estimated by utilizing the local features around the target. Finally, some experiments are implemented in the object tracking benchmark 2013 dataset (OTB2013). The experimental results demonstrate that the proposed tracker outperforms other existing trackers in terms of robustness, precision and accuracy.
Two methods of skin closure in abdominal operations: A controlled clinical trial

Operative bacterial contamination of surgical wounds is common. The ability of the host to eradicate these bacteria and prevent subsequent wound infection is affected by a number of factors; one of these has been shown experimentally to be the presence of suture material in the subcutaneous tissues. In a prospective randomized controlled clinical trial in 341 abdominal operations we compared the primary infection rates after two methods of skin closure: either vertical mattress monofilament nylon sutures (182 patients) or steel clips which penetrated only the dermis (159 patients). All patients received a single dose of a cephalosporin intravenously at induction of anaesthesia and neither sutures nor drains were placed in the subcutaneous plane. The overall wound infection rate in the sutured wounds was 17·0 per cent, compared with 6·3 per cent in those closed by clips (χ2 = 9·26, P < 0·01). We conclude that skin closure with clips reduces the incidence of wound infection in patients in whom operative parietal contamination has occurred.
Theory And Practice In Capital Budgeting: Evidence From Kuwait

Capital budgeting is an important tool in corporate finance, which is supported with numerous methods. Previous researches in this field shows that simple methods of capital budgeting are preferred over complex methods. With an objective to adopt relevant modification in the academic sector this paper evaluates the preferred capital budgeting practices in Kuwait, one of the strongest economy in the world, through a structured questionnaire distributed among 100 firms. The study also reveals the significance of demographic factors on real life capital budgeting practices as well as it probes in to the significance of the subjects; introductory finance, financial management and risk management. The results of the study are consistent with the previous researches in this field, that majority of the respondents use the NPV. Furthermore, age, educational qualification, managerial levels, years of experience, company size, among others all have significant effects on most capital budgeting methods.
GSK-3β inhibitors attenuate the organ injury/dysfunction caused by endotoxemia in the rat*

Objective:Serine-threonine protein kinase glycogen synthase kinase (GSK)-3 is involved in regulation of many cell functions, but its role in regulation of inflammatory response is unknown. Here we investigate the effects of GSK-3β inhibition on organ injury/dysfunction caused by lipopolysaccharide or coadministration of lipopolysaccharide and peptidoglycan in the rat. Design:Prospective, randomized study. Setting:University-based research laboratory. Subjects:Ninety-nine anesthetized male Wistar rats. Interventions:Study 1: Rats received either intravenous Escherichia coli lipopolysaccharide (6 mg/kg) or vehicle (1 mL/kg; saline). Study 2: Rats received either intravenous E. coli lipopolysaccharide (1 mg/kg) and Staphylococcus aureus peptidoglycan (0.3 mg/kg) or vehicle. The potent and selective GSK-3β inhibitors TDZD-8 (1 mg/kg intravenously), SB216763 (0.6 mg/kg intravenously), and SB415286 (1 mg/kg intravenously) or vehicle (10% dimethyl sulfoxide) was administered 30 mins before lipopolysaccharide or lipopolysaccharide and peptidoglycan. Measurements and Main Results:Endotoxemia resulted in increases in the serum levels of creatinine (indicator of renal dysfunction), aspartate aminotransferase, alanine aminotransferase (markers for hepatocellular injury), lipase (indicator of pancreatic injury), and creatine kinase (indicator of neuromuscular injury). Coadministration of lipopolysaccharide and peptidoglycan resulted in hepatocellular injury and renal dysfunction. All GSK-3β inhibitors attenuated the organ injury/dysfunction caused by lipopolysaccharide or lipopolysaccharide and peptidoglycan. GSK-3β inhibition reduced the Ser536 phosphorylation of nuclear factor-&kgr;B subunit p65 and the messenger RNA expression of nuclear factor-&kgr;B-dependent proinflammatory mediators but had no effect on the nuclear factor-&kgr;B/DNA binding activity in the lung. GSK-3β inhibition reduced the increase in nuclear factor-&kgr;B p65 activity caused by interleukin-1 in human embryonic kidney cells in vitro. Conclusions:The potent and selective GSK-3β inhibitors TDZD-8, SB216763, and SB415286 reduced the organ injury/dysfunction caused by lipopolysaccharide or lipopolysaccharide and peptidoglycan in the rat. We propose that GSK-3β inhibition may be useful in the therapy of the organ injury/dysfunction associated with sepsis, shock, and other diseases associated with local or systemic inflammation.
Circadian phase-shifting effects of repeated ramelteon administration in healthy adults.

STUDY OBJECTIVES To assess the ability of repeated daily oral ramelteon to facilitate re-entrainment of human circadian rhythms after an imposed phase advance of the sleep-wake cycle. METHODS A total of 75 healthy adult volunteers aged 18-45 years remained in a sleep laboratory for 6 days and 5 nights; a 5-h phase advance in their sleep-wake cycle was imposed under dim-light conditions. Oral ramelteon (1,2, 4, or 8 mg once daily for 4 days) or placebo was administered 30 min before bedtime. The primary endpoint was the phase of the circadian rhythm as assessed by the time at which salivary melatonin concentrations declined below 3 pg/mL after morning awakening (dim-light melatonin offset [DLMoff]). RESULTS After 4 days of once-daily treatment, participants receiving 1, 2, or 4 mg ramelteon exhibited statistically significant phase shifts in DLMoff of -88.0 (16.6), -80.5 (14.8), and -90.5 (15.2) minutes respectively, versus -7.1 (18.6) minutes for placebo (least-squares mean(SEM), p = 0.002, p = 0.003, p = 0.001, respectively). Change in DLMoff for the 8 mg dose of ramelteon, -27.9 (16.4) minutes, was not significantly different than that for placebo (p = 0.392). CONCLUSIONS Ramelteon (1, 2, or 4 mg per day) administered before bedtime significantly advanced the phase of the circadian rhythm after a 5-h phase advance in the sleep-wake cycle. These findings suggest that ramelteon has potential as a specific therapy for circadian rhythm sleep disorders.
In Vivo Studies of the Evolution of Physical Properties of the Human Skin with Age

In vivo measurements taken by valid methods, help to interpret the phenomena associated with the aging process. The authors developed some routine techniques to measure physical properties of the skin both deep in the dermis-epidermis and at the surface (stratum corneum). Measurements on the forearm of 150 people yielded the following results regarding the dermis-epidermis level: (1) skin thickness begins to decrease at 45 years of age for men and women, when women's skin becomes thinner than men's skin; (2) torsion extensibility, normalized for a given skin thickness, sharply decreases after 35 years of age; (3) skin optical properties are modified, ie the photoplethysmographic signal, measured on the forehead, greatly increase after 60 years of age; (4) at the cutaneous surface level, the main modifications are increased shedding of stratum corneum after 60 years of age in parallel with a modification of the stratum corneum cohesivity, altered skin microrelief during the aging process, and slightly decreased transepidermal water loss while the corneocyte projected size increases. These findings allow consideration of the aging process at the skin level as a phased process. The alterations of the physical properties and their kinetics suggest a various process according to the different cutaneous sections.
Functional connectivity predictors and mechanisms of cognitive behavioural therapies: A systematic review with recommendations

Objective: While there is now strong evidence that psychological therapies can alter the activity of individual brain regions, their impact on the functional integration between regions has not yet been systematically evaluated. This area is important given that brain dysconnectivity has been implicated across almost all psychiatric disorders. Accordingly, we sought to establish connectivity predictors and mechanisms of effective psychological therapies. We further establish whether connectivity changes represent normalisation of disorder pathophysiology or compensatory changes. Method: We reviewed studies examining structural and functional connectivity longitudinally as either a predictor or outcome variable of successful psychological therapies across psychiatric disorders. Results: Fifteen studies met our inclusion criteria. All but three related to cognitive behavioural therapy. Of these, five assessed resting state, nine probed affective processing and one probed cognitive processing. Twelve studies reported evidence of functional connectivity as a significant predictor or outcome of cognitive behavioural therapy, with prefronto-limbic circuitry most commonly implicated. Only six studies included healthy participants, limiting direct inferences about normalisation as opposed to compensatory changes. Anxiety disorders were overrepresented, totalling 13 of the studies reviewed. No studies examined structural connectivity or utilised analyses allowing the directionality of functional connectivity to be inferred. Conclusion: While the evidence base is still in its infancy for other therapy approaches, there was clearer evidence that functional connectivity both predicts and is altered by cognitive behavioural therapy. Connections from prefrontal cortex appear especially key, perhaps given their role in cognitive appraisal of lower order affective, motivational and cognitive processes. A number of recommendations are made for this rapidly developing literature.
Increased long‐term cardiovascular morbidity among patients treated with radioactive iodine for hyperthyroidism

Objective Previous studies suggest that hyperthyroid patients remain at increased risk of cardiovascular morbidity after restoring euthyroidism. The aim of this study was to compare the rate and causes of hospitalization of hyperthyroid patients treated with radioactive iodine (RAI) with those of an age‐ and gender‐matched reference population in a long‐term follow‐up study.
New Aspects of Graft-induced Central Plasticity and Neuroregeneration at T 10 in a Rat Model

Objective: Retest Brunelli’s graft induced glutamate neurotransmitter switch at the neuromuscular junction in rat for the translation of new aspects of central plasticity concepts for human reconstructive surgery in spinal cord lesions. Methods: Randomized double blind controlled study in rat, which was limited to 30 animals (Charles River, 220 to 280 g). Ethical research approval was obtained from the Animal Research Committee of the University Hospital Schleswig Holstein, UK-SH, Lubeck, D, and legitimated by the Governmental Department of Agriculture, Natural Environments and Agriculture Kiel, D, in compliance with the European Commission Recommendation to retest and review of graft-induced glutamatergic regeneration and /or cholinergic co-transmission at the neuromuscular junction for reinnervation of the skeletal obliquus abdominis internus muscle fibers. Assessments were performed to demonstrate pharmacological neuromodulation after attaching the lateral corticospinal tract at T10 to the bisected skeletal motor nerve. Medication was administered for 14 days postoperatively–a) verum Cerebrolysin® IP=12–b) shams NaCl 0.9% IP=11, and c) 7 controls (nil). 2nd Op at day 90 (16 surviving rats) for open proof of reinnervation and its type by a) CMAP, b)Vecuronium® application. Fast Blue® labeling were performed. 10 days later, on the 3rd Op N=15, euthanasia and organ fixation were performed. Extensive histology-morphology examinations were performed in Cluj. Results: Eight rats showed positive CMAPs. Reinnervation and neuromodulation were demonstrated by counting and comparison of the grafted muscle fibers diameter. Four CAMP- positive- rats received Vecuronium®: 1 CERE and 1 NaCl each demonstrated a loss of amplitude respectively two an incomplete muscle blockage due to the coexistence of glutamatergic and cholinergic neurotransmission. Confirmation of the VGluT2 in axons was observed by immunofluorescence. FB+ neurons were observed in many Rexed laminae in grafted spinal cord, but not in the brain. Conclusion: The coexistence of graft-induced cholinergic and glutamatergic neurotransmission and a great capacity of lower motor neurons and other types of spinal neurons to regenerate were observed. Because of limited animals, pharmacological neuromodulation requires further investigation.
A Functional Soluble Form of the Murine Mannose Receptor Is Produced by Macrophages in Vitro and Is Present in Mouse Serum*

A soluble form of the mannose receptor (sMR) has been found in conditioned medium of primary macrophages in vitro and in mouse serum. sMR was released as a single species, had a smaller size than the cell-associated form, and accumulated in macrophage-conditioned medium, in a cytokine-regulated manner, to levels comparable with those found for cell-associated mannose receptor. Pulse-chase experiments showed that sMR production in culture occurred by constitutive cleavage of pre-existing full-length protein. A binding assay was developed to determine the sugar specificity of sMR and its ability to interact with pathogens and particulate antigens (i.e. Candida albicans and zymosan). Protease inhibitor studies suggested that sMR was produced by cleavage of an intact mannose receptor by a matrix metalloprotease or ADAM metalloprotease. A role for sMR in the immune response is proposed based on its binding properties, regulation by cytokines, and the previous discovery of putative ligands for the cysteine-rich domain of the mannose receptor in lymph nodes and spleen.
Does AMP-activated Protein Kinase Couple Inhibition of Mitochondrial Oxidative Phosphorylation by Hypoxia to Calcium Signaling in O2-sensing Cells?*

Specialized O2-sensing cells exhibit a particularly low threshold to regulation by O2 supply and function to maintain arterial pO2 within physiological limits. For example, hypoxic pulmonary vasoconstriction optimizes ventilation-perfusion matching in the lung, whereas carotid body excitation elicits corrective cardio-respiratory reflexes. It is generally accepted that relatively mild hypoxia inhibits mitochondrial oxidative phosphorylation in O2-sensing cells, thereby mediating, in part, cell activation. However, the mechanism by which this process couples to Ca2+ signaling mechanisms remains elusive, and investigation of previous hypotheses has generated contrary data and failed to unite the field. We propose that a rise in the cellular AMP/ATP ratio activates AMP-activated protein kinase and thereby evokes Ca2+ signals in O2-sensing cells. Co-immunoprecipitation identified three possible AMP-activated protein kinase subunit isoform combinations in pulmonary arterial myocytes, with α1β2γ1 predominant. Furthermore, their tissue-specific distribution suggested that the AMP-activated protein kinase-α1 catalytic isoform may contribute, via amplification of the metabolic signal, to the pulmonary selectivity required for hypoxic pulmonary vasoconstriction. Immunocytochemistry showed AMP-activated protein kinase-α1 to be located throughout the cytoplasm of pulmonary arterial myocytes. In contrast, it was targeted to the plasma membrane in carotid body glomus cells. Consistent with these observations and the effects of hypoxia, stimulation of AMP-activated protein kinase by phenformin or 5-aminoimidazole-4-carboxamide-riboside elicited discrete Ca2+ signaling mechanisms in each cell type, namely cyclic ADP-ribose-dependent Ca2+ mobilization from the sarcoplasmic reticulum via ryanodine receptors in pulmonary arterial myocytes and transmembrane Ca2+ influx into carotid body glomus cells. Thus, metabolic sensing by AMP-activated protein kinase may mediate chemotransduction by hypoxia.
Resilience as an Underexplored Outcome of Workplace Bullying

The problem of workplace bullying appears to be especially common in the hospitality industry and in health, education, and social services. Bullying results in negative effects on the psychological and physical health and well-being of targets, bystanders, and those accused of bullying. I undertook a qualitative research project to investigate the experiences of 17 New Zealand social workers who identified themselves as having been targets of workplace bullying. All participants had experienced negative physical and psychological health impacts. I also found, however, that in the aftermath of their difficult experiences, most considered that they had eventually developed greater resilience. Resilience was enhanced when participants’ sense of control over their situation improved and when they received support from witnesses and managers. I make recommendations to indicate how these resilience-promoting conditions can be achieved in the organizational setting.
Mitochondrial dynamics and Parkinson's disease: focus on parkin.

SIGNIFICANCE Parkinson's disease (PD) is a prevalent neurodegenerative disease affecting millions of individuals worldwide. Despite intensive efforts devoted to drug discovery, the disease remains incurable. To provide more effective medical therapy for PD, better understanding of the underlying causes of the disease is clearly necessary. RECENT ADVANCES A broad range of studies conducted over the past few decades have collectively implicated aberrant mitochondrial homeostasis as a key contributor to the development of PD. Supporting this, mutations in several PD-linked genes are directly or indirectly linked to mitochondrial dysfunction. In particular, recent discoveries have identified parkin, whose mutations are causative of recessive parkinsonism, as a key regulator of mitochondrial homeostasis. CRITICAL ISSUES Parkin appears to be involved in the entire spectrum of mitochondrial dynamics, including organelle biogenesis, fusion/fission, and clearance via mitophagy. How a single protein can regulate such diverse mitochondrial events is as intriguing as it is amazing; the mechanism underlying this is currently under intense research. Here, we provide an overview of mitochondrial dynamics and its relationship with neurodegenerative diseases and discuss current evidence and controversies surrounding the role of parkin in mitochondrial quality control and its relevance to PD pathogenesis. FUTURE DIRECTIONS Although the emerging field of parkin-mediated mitochondrial quality control has proven to be exciting, it is important to recognize that PD pathogenesis is likely to involve an intricate network of interacting pathways. Elucidating the reciprocity of pathways, particularly how other PD-related pathways potentially influence mitochondrial homeostasis, may hold the key to therapeutic development.