Miracle-dz/UniFAR-FTUs huggingface dataset:
Happiness among South African private sector physiotherapists

Background Happiness of people can affect their daily functioning and work performance. There is limited research assessing the happiness levels of various disciplines within the health care industry. This article is the first attempt to evaluate the happiness levels of private sector physiotherapists in South Africa. Objectives Research in happiness and physiotherapy studies are two research areas that are not associated with one another in a global perspective. The objective of this study was to assess the happiness levels of private sector physiotherapists in South Africa. Methods A hypothesised model was statistically tested using a quantitative questionnaire, which was completed online. The target population of this study were all private sector physiotherapists who are members of the South African Society of Physiotherapy. A total of 395 respondents participated in the study. Results This study confirmed that factors such as influence, social relations, life balance, optimism, work and leisure are all positively associated with the happiness levels of private sector physiotherapists in South Africa. These variables are recommended as key focus areas for physiotherapy practice owners to address, in order to positively affect the happiness levels of all people in their workplace. Conclusion The study concludes the following: if happiness becomes a priority, then owners of physiotherapy practices need to generate a workforce who are more productive, demonstrate greater collaboration with colleagues and patients, are more positively energised, are less absent and are more loyal to the practice. Clinical Implications The contribution of this study is that it highlights the importance of managing staff in private physiotherapy practices in a holistic manner.
Treatment of tuberculosis infection in children

ABSTRACT Introduction: Identifying and treating children with tuberculosis (TB) infection in both low and high-TB burden settings will decrease the incidence of TB disease worldwide. Areas covered: This review covers each of the available TB infection treatment options for children based on effectiveness, safety, tolerability and treatment completion rates. Six to 9 months of daily administered isoniazid is no longer the treatment of choice for many children with TB infection. Shorter, rifamycin based, TB infection treatment regimens are effective, safe and easier for children to complete. Fluroquinolone-based regimens are recommended for the treatment of children infected by a source case with drug-resistant TB. Directly observed therapy (DOT) programs improve childhood TB infection treatment completion rates. Expert commentary: As shorter, rifamycin-based, TB infection treatment regimens offer superior treatment success rate in both adults and children; the widespread use of these regimens has huge potential to decrease the burden of TB disease worldwide. The implementation of these programs will involve improving patient access to the medications, decreasing their cost to the patient, and the use of novel electronic methods to document patient treatment completion.
Change in mental health symptoms in families with nonresponding children referred to inpatient family units

Aims: To examine changes in child mental health symptoms following inpatient family unit treatment after long-term unsuccessful treatment in community and child psychiatry outpatient services. Follow-up from referral and admission to 3 and 12 months. Methods: Standardized questionnaires measuring the child mental health symptoms and parental anxiety and depression converted to standardized scores and compared to each child’s clinical diagnosis. Results: Significant group mean improvement on almost all problem scales at the 3-month follow-up (T2) remaining through 12-month follow-up (T3) relative to admission (T1). Aggression showed the highest levels and largest improvements. Statistically significant improvements were widespread, whereas clinically significant improvements were found for some diagnostic groups on diagnosis-related problems and secondary problems. Improvement in child symptoms were partly correlated with improvement in parental anxiety symptoms. Implications: Even previously nonresponding children may benefit from broad tailored interventions including parents and the wider system. Development of systematic component approaches is needed.
DNA topoisomerase 1 and 2A function as oncogenes in liver cancer and may be direct targets of nitidine chloride

The aim of the present study was to determine the role of topoisomerase 1 (TOP1) and topoisomerase 2A (TOP2A) in liver cancer (LC), and to investigate the inhibitory effect of nitidine chloride (NC) on these two topoisomerases. Immunohistochemistry (IHC) staining and microarray or RNA sequencing data mining showed markedly higher expression of TOP1 and TOP2A at the protein and mRNA levels in LC tissues compared with that in control non-tumor tissues. The prognostic values of TOP1 and TOP2A expression were also estimated based on data from The Cancer Genome Atlas. The elevated expression levels of TOP1 and TOP2A were closely associated with poorer overall survival and disease-free survival rates. When patients with LC were divided into high- and low-risk groups according to their prognostic index, TOP1 and TOP2A were highly expressed in the high-risk group. Bioinformatics analyses conducted on the co-expressed genes of TOP1 and TOP2A revealed that the topoisomerases were involved in several key cancer-related pathways, including the ‘p53 pathway’, ‘pathway in cancer’ and ‘apoptosis signaling pathway’. Reverse transcription-quantitative polymerase chain reaction and IHC performed on triplicate tumor tissue samples from LC xenografts in control or NC-treated nude mice showed that NC treatment markedly reduced the protein and mRNA expression of TOP1 and TOP2A in LC tissues. Molecular docking studies further confirmed the direct binding of NC to TOP1 and TOP2A. In conclusion, the present findings indicate that TOP1 and TOP2A are oncogenes in LC and could serve as potential biomarkers for the prediction of the prognosis of patients with LC and for identification of high-risk cases, thereby optimizing individual treatment management. More importantly, the findings support TOP1 and TOP2A as potential drug targets of NC for the treatment of LC.
Evaluate How Cyclomatic Complexity Changes in the Context of Software Evolution

Cyclomatic complexity (CC) is often used as a factor to evaluate the quality of source code. Many researchers have studied the relationships between CC and LOC, between CC and basic testing paths, and between CC and code maintainability etc. However, few researchers studied how software evolution affects CC. In this paper, we propose a methodology based on source code change analysis and develop a supporting tool, called CCEvaluator, to evaluate CC variation during software evolution. By empirical studies on six pieces of typical open source projects, a series of interesting findings including six commonness and five differences have been obtained. To explain why these commonness and differences are produced during software evolution, code change information among successive versions are captured and used in this paper.
Computer-assisted handwriting style identification system for questioned document examination

Handwriting originates from a particular copybook style such as Palmer or Zaner-Bloser that one learns in childhood. Since questioned document examination plays an important investigative and forensic role in many types of crime, it is important to develop a system that helps objectively identify a questioned document’s handwriting style. Here, we propose a computer vision system that can assist a document examiner in the identification of a writer’s handwriting style and therefore the origin or nationality of an unknown writer of a questioned document. We collected 33 Roman alphabet copybook styles from 18 countries. Each character in a questioned document is segmented and matched against all of the 33 handwriting copybook styles. The more characters present in the questioned document, the higher the accuracy observed.
Krukovine Suppresses KRAS-Mutated Lung Cancer Cell Growth and Proliferation by Inhibiting the RAF-ERK Pathway and Inactivating AKT Pathway

Oncogenic activation of the KRAS gene via point mutations occurs in 20–30% of patients with non-small cell lung cancer (NSCLC). The RAS-RAF-ERK and RAS-PI3K-AKT pathways are the major hyper-activated downstream pathways in RAS mutation, which promotes the unlimited lifecycle of cancer cells and their metastasis in humans. However, the success of targeted therapy is restricted by many factors. Herein, we show a new pharmacological KRAS signaling inhibitor krukovine, which is a small molecular bisbenzylisoquinoline alkaloid, isolated from the bark of Abuta grandifolia (Mart.) Sandw. (Menispermaceae). This alkaloid targets the KRAS downstream signaling pathways in different NSCLC cell lines, such as H460 and A549, which are established by KRAS mutations. In the present study, we initially investigated the anti-cancer activities of krukovine in KRAS-mutated NSCLC cell lines, as well as KRAS wild type cancer cell line and normal lung cell. Results indicated that krukovine can inhibit the growth and dose-dependently inhibit the colony formation capacity and wound healing ability of H460 and A549. This cytotoxic effect is associated with the induction of cell apoptosis and G1 arrest in those cell lines. Krukovine treatment also suppressed the C-RAF, ERK, AKT, PI3K, p70s6k, and mTOR phosphorylation in H460 and A549. This finding suggests that krukovine represses the growth and proliferation of KRAS-mutated cells by inactivating AKT signaling pathway and downregulating the RAF-ERK signaling pathway. This study provides detailed insights into the novel cytotoxic mechanism of an anti-cancer compound from an herbal plant and promotes the anti-cancer potential of krukovine in NSCLC with KRAS mutation.
The Voronoi-Quadtree: construction and visualization

We deﬁne a quadtree-based planar Voronoi diagram codiﬁcation, the Voronoi-Quadtree, valid for generalized sites (points, line-segments, curve-arc segments, .) and for different distance functions (Euclidean metrics, convex distance functions, .). We present an algorithm for constructing, at a preﬁxed level of detail, the Voronoi-Quadtree associated to a Voronoi diagram determined by a set of sites and a given distance function. A second algorithm that, taking as input a Voronoi-Quadtree, visualizes a polygonal approximation of the boundary of the Voronoi diagram is also described
Skin color constancy for illumination invariant skin segmentation

Accuracy of skin segmentation algorithms is highly sensitive to changes in lighting conditions. When the lighting condition in a scene is different from that in the training examples, miss-classification rate of the skin segmentation algorithms is high. Using color constancy approach we aim to compensate for skin color variations to achieve accurate skin color segmentation. Skin color constancy is realized in an unsupervised manner by using the color changes observed on face regions under different illuminations to drive the model. By training on a few faces of different ethnicities, our model is able to generalize the color mapping for any unseen ethnicity. The color changes observed are used to learn the color mapping from one lighting condition to the other. We show the proof of concept of unsupervised skin color constancy on faces from the PIE database. Skin segmentation with and without color compensation was performed on the PIE database. Results are presented which show improved skin segmentation accuracy after performing color compensation.
Non-aversive photographic measurement method for subcutaneous tumours in nude mice

We have developed a new method for the measurement of subcutaneous tumour volume which consists in taking photographs of mice in their home cages, to refine the standard method of measurement with calipers. We consider this new method to be non-aversive, as it may be more compatible with mice behavioural preferences and, therefore, improve their welfare. Photographs are captured when mice voluntarily go into an acrylic tube containing graph paper that is later used as a scale. Tumour volumes measured with the caliper and the non-aversive photographic method were compared to those obtained by water displacement volume and weight. Behavioural and physiological changes were evaluated to assess animal welfare. Significant differences were found between measurements obtained with the caliper and the non-aversive photographic method, v. the reference volume acquired by water displacement (P < 0.001). Nevertheless, there was good consistency for these measurements when tumours were measured repeatedly, with all Intra-Class Correlation Coefficients above 0.95. Mice on which the non-aversive photographic method was employed were significantly less reluctant to establish contact with the experimenter (P < 0.001) and behaved less anxiously in a modified-Novelty Suppressed Feeding test. Particularly, statistically significant differences were found in connection with the latency to eat an almond piece (P < 0.05), the frequency of grooming (P < 0.001) and the frequency of defecation (P < 0.001). Corticosterone concentration in faeces and blood glucose were determined and no significant changes were found. Therefore, we propose the non-aversive photographic method to measure subcutaneous tumours as a way to refine methodologies in the field of experimental oncology.
Amnion‐Analogous Medical Device for Fetal Membrane Healing: A Preclinical Long‐Term Study

Although recent invasive fetal surgeries have improved fetal outcomes, fetal membrane rupture remains a major complication, leading to premature delivery, thus undermining the complete benefits of such procedures. A biocompatible amnion‐analogous medical device (AMED) consisting of polycaprolactone framework and decellularized amniotic membrane (dAM)–derived hydrogel for restoration of amniotic membrane defect is developed using 3D printing technology. Its efficacy on healing iatrogenic fetal membrane defects in vitro is evaluated, showing that the dAM gel contains migratory and proliferative properties. The fetoscope feasibility of the developed AMED is assessed using a pregnant swine model. All animals had successfully recovered from anesthesia and the fetoscopic procedure and maintained a healthy condition until the end of the pregnancy. AMED exhibits superior surgical handling characteristics and is easy to manufacture, nonimmunogenic, biocompatible, and suitable for storage and transport for off‐the‐shelf use; hence, it can be used in successfully sealing defect sites, thus improving the preservation of the amniotic fluid, which in turn improves fetal survival and development.
DistGear: A Lightweight Event-Driven Framework for Developing Distributed Applications

The emergence of cloud computing makes it easier for enterprises and individual users to obtain distributed computing resources. At the same time, developing distributed systems is still complex and difficult. In order to reduce the complexity in distributed application development, a series of techniques such as RPC, message-oriented middleware have been proposed and widely used. These techniques hide the underlying communicating details but require developers to take control of coordination among different machines for complex distributed tasks. This paper proposes a lightweight event-driven framework called DistGear to simplify the development of complex task processing in distributed applications. DistGear is a layer of software built on top of communication facilities for providing developers with a programming abstraction to easily handle distributed tasks and control machine coordination in tasks. We implement DistGear based on coroutines and message communication. Experience with DistGear in a simplified real-world system suggests it is effective. Performance evaluation also demonstrates DistGear's good concurrency and low resources consumption.
MMP‐9 gene rs3918242 polymorphism increases risk of stroke: A meta‐analysis

The association between matrix metalloproteinase‐9 (MMP‐9) gene rs3918242 polymorphism and the risk of stroke has been investigated, but the findings have been found to be contradictory. Thus, this association was assessed by meta‐analysis. Potential studies were searched throughout PubMed, Embase, and CNKI. Pooled odds ratios and 95% confidence intervals were calculated. Sixteen original studies analyzing this association were included, involving 3647 stroke patients and 3685 unrelated controls. It was confirmed that MMP‐9 gene rs3918242 polymorphism increased the risk of stroke. Stratification analysis of ethnicity revealed an increased risk of stroke among Asians, but not among Caucasians. Subgroup analysis by the type of stroke showed that MMP‐9 gene rs3918242 polymorphism increased the risk of ischemic stroke. Sensitivity analysis did not draw different findings. In conclusion, MMP‐9 gene rs3918242 polymorphism increases the risk of stroke.
NDFMF: An Author Name Disambiguation Algorithm Based on the Fusion of Multiple Features

Author name disambiguation is a very important and complex research topic. During the retrieval and research of literature the quality of the investigation results has been reduced because of the high probability of different authors sharing the same name, which lengthens the whole cycle of the scientific research. Therefore, it is necessary to find a reasonable and efficient method to distinguish the different authors who share the same name. In this paper, an author name disambiguation algorithm based on the fusion of multiple features (NDFMF) is proposed. First we proposed a single feature similarity detection algorithm (SFSD). SFSD is used to compute the degree of similarity between two features of a paper and to assess the threshold value. Then, SFSD is used to realize the preliminary SFSD-based disambiguation algorithm (SFSDD). Furthermore, different features are evaluated according to the disambiguation results of author names and the evaluation metrics, including precision, recall and F-measure with SFSDD. The evaluation parameter of weight (W) is introduced to express each feature's influence in disambiguation. NDFMF can disambiguate author names more efficiently based on the fusion of multiple features. Experiments were implemented to test the performance of NDFMF. Experimental results show that NDFMF was effective in the disambiguation precision, recall and F-measure.
MAPK15 is part of the ULK complex and controls its activity to regulate early phases of the autophagic process

Autophagy, a pathway for bulk protein degradation and removal of damaged organelles, represents one of the major responses of cells to stress, thereby exerting a strict control on their correct functioning. Consequently, this process has been involved in the pathogenesis and therapeutic responses of several human diseases. Mitogen-activated protein (MAP) kinase 15 (MAPK15) is an atypical member of the MAP kinase family that recently emerged as a key modulator of autophagy and, through this, of cell transformation. Still, no information is available about signaling pathways mediating the effect of MAPK15 on this process, nor is it known which phase of autophagosome biogenesis is affected by this MAP kinase. Here, we demonstrate that MAPK15 stimulated 5′-AMP–activated protein kinase–dependent activity of UNC-51-like kinase 1 (ULK1), the only protein kinase among the ATG-related proteins, toward downstream substrates and signaling intermediates. Importantly, MAPK15 directly interacted with the ULK1 complex and mediated ULK1 activation induced by starvation, a classical stimulus for the autophagic process. In turn, ULK1 and its highly homologous protein ULK2 are able to transduce MAPK15 signals stimulating early phases of autophagosomal biogenesis in a multikinase cascade that offers numerous potential targets for future therapeutic intervention in cancer and other autophagy-related human diseases.
G protein–coupled receptor kinases (GRKs) orchestrate biased agonism at the β2-adrenergic receptor

A mutant GPCR exhibits G protein–biased signaling because of defective phosphorylation by GRK, not because of an inability to bind to β-arrestin. Determining bias Biased signaling by GPCRs results in their preferential use of either G proteins or β-arrestins to transduce signals. Drugs that selectively activate one of these pathways provide effective treatment without side effects. Noting that GPCRs must undergo GRK-mediated phosphorylation to recruit β-arrestins, Choi et al. characterized a mutant GPCR that exhibits G protein–biased signaling and found that it could not be phosphorylated by GRKs. When a phosphorylated peptide was fused to the C-terminal region of the mutant receptor, mimicking GRK-mediated phosphorylation, β-arrestin protein recruitment and biased signaling were recovered. These data suggest that G protein–biased signaling is driven more by an inability to recruit GRKs than by an inability to couple to β-arrestins, which may have implications for the design of biased drugs. Biased agonists of G protein–coupled receptors (GPCRs), which selectively activate either G protein– or β-arrestin–mediated signaling pathways, are of major therapeutic interest because they have the potential to show improved efficacy and specificity as drugs. Efforts to understand the mechanistic basis of this phenomenon have focused on the hypothesis that G proteins and β-arrestins preferentially couple to distinct GPCR conformations. However, because GPCR kinase (GRK)–dependent receptor phosphorylation is a critical prerequisite for the recruitment of β-arrestins to most GPCRs, GRKs themselves may play an important role in establishing biased signaling. We showed that an alanine mutant of the highly conserved residue tyrosine 219 (Y219A) in transmembrane domain five of the β2-adrenergic receptor (β2AR) was incapable of β-arrestin recruitment, receptor internalization, and β-arrestin–mediated activation of extracellular signal–regulated kinase (ERK), whereas it retained the ability to signal through G protein. We found that the impaired β-arrestin recruitment in cells was due to reduced GRK-mediated phosphorylation of the β2AR Y219A C terminus, which was recapitulated in vitro with purified components. Furthermore, in vitro ligation of a synthetically phosphorylated peptide onto the C terminus of β2AR Y219A rescued both the initial recruitment of β-arrestin and its engagement with the intracellular core of the receptor. These data suggest that the Y219A mutation generates a G protein–biased state primarily by conformational selection against GRK coupling, rather than against β-arrestin. Together, these findings highlight the importance of GRKs in modulating the biased agonism of GPCRs.