Social Withdrawal and Social Anxiety in Relation to Stylistic Parenting Dimensions in the Indian Cultural Context

Abstract The purpose of the study was to examine associations between composite parenting behaviors' (parenting styles and dimensions) and social withdrawal and social anxiety. Participants of the study were 227 girls in India with age ranging from 6-11 years. The parents completed the parenting styles and dimension questionnaire and girls completed Social anxiety scale for children while the parents/teachers completed the Teacher report syndrome scale for social withdrawal behavior in girls. Pearson's product moment correlations were done to study the associations between parenting behaviors' and social anxiety and social withdrawal respectively. A standard multiple regression analysis was used with social withdrawal and social anxiety as dependent variables. Correlational results indicated that authoritarian, uninvolved parenting styles and physical coercion, verbal hostility, non-reasoning and indifference parenting dimensions are positively correlated with social anxiety and socially withdrawn behaviors'. Authoritative style, and parental dimensions of connection, regulation and autonomy granting are inversely correlated with social anxiety and socially withdrawn behaviors' Results from multiple regression analyses indicated that uninvolved, non-reasoning, neglect and reject parenting dimensions positively predicted social anxiety and social withdrawal in girls, while authoritative style and connection parenting dimensions inversely predicted social withdrawal and social anxiety among girls. The present findings suggest the positive contribution of authoritative, connection stylistic dimensions in amelioration of social emotional problems among girls and inverse contribution of uninvolved, non-reasoning, neglect, reject parenting styles and dimensions in exacerbation of social anxiety and socially withdrawn behaviors' in girls in the Indian cultural context

Phylogeography and domestication of Indian river buffalo

<p>Abstract</p> <p>Background</p> <p>The water buffalo- <it>Bu</it><it>balus bubalis </it>holds tremendous potential in livestock sector in many Asian countries, particularly India. The origin, domestication and genetic structure of the Indian river buffalo are poorly understood. Therefore, to understand the relationship among the maternal lineages of Indian river buffalo breeds and their domestication process, we analysed mitochondrial D-loop region of 217 animals representing eight breeds from eight different locations in India along with published sequences of Mediterranean buffalo.</p> <p>Results</p> <p>The maximum parsimony tree showed one major clade with six internal branches. Reduced median network revealed expansion from more than one set of haplotypes indicating complex domestication events for this species. In addition, we found several singleton haplotypes. Using rho statistics, we obtained a time estimate of 6300 years BP for the expansion of one set of hapltoypes of the Indian domestic buffalo. A few breed specific branches in the network indicated an ancient time depth of differentiation of some of the maternal lineages of river buffalo breeds. The multidimensional display of breed pairwise F_STvalues showed significant breed differentiation.</p> <p>Conclusion</p> <p>Present day river buffalo is the result of complex domestication processes involving more than one maternal lineage and a significant maternal gene flow from the wild populations after the initial domestication events. Our data are consistent with the available archaeological information in supporting the proposition that the river buffalo was likely to be domesticated in the Western region of the Indian subcontinent, specifically the present day breeding tracts of the Mehsana, Surati and Pandharpuri breeds.</p

Meta-Analysis of 1,200 Transcriptomic Profiles Identifies a Prognostic Model for Pancreatic Ductal Adenocarcinoma

PURPOSE: With a dismal 8% median 5-year overall survival, pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy. Only 10% to 20% of patients are eligible for surgery, and more than 50% of these patients will die within 1 year of surgery. Building a molecular predictor of early death would enable the selection of patients with PDAC who are at high risk. MATERIALS AND METHODS: We developed the Pancreatic Cancer Overall Survival Predictor (PCOSP), a prognostic model built from a unique set of 89 PDAC tumors in which gene expression was profiled using both microarray and sequencing platforms. We used a meta-analysis framework that was based on the binary gene pair method to create gene expression barcodes that were robust to biases arising from heterogeneous profiling platforms and batch effects. Leveraging the largest compendium of PDAC transcriptomic data sets to date, we show that PCOSP is a robust single-sample predictor of early death—1 year or less—after surgery in a subset of 823 samples with available transcriptomics and survival data. RESULTS: The PCOSP model was strongly and significantly prognostic, with a meta-estimate of the area under the receiver operating curve of 0.70 (P = 2.6E−22) and d-index (robust hazard ratio) of 1.9 (range, 1.6 to 2.3; ( = 1.4E−04) for binary and survival predictions, respectively. The prognostic value of PCOSP was independent of clinicopathologic parameters and molecular subtypes. Over-representation analysis of the PCOSP 2,619 gene pairs—1,070 unique genes—unveiled pathways associated with Hedgehog signaling, epithelial–mesenchymal transition, and extracellular matrix signaling. CONCLUSION: PCOSP could improve treatment decisions by identifying patients who will not benefit from standard surgery/chemotherapy but who may benefit from a more aggressive treatment approach or enrollment in a clinical trial

Generation and Characterisation of Novel Pancreatic Adenocarcinoma Xenograft Models and Corresponding Primary Cell Lines

<div><p>Pancreatic adenocarcinoma is one of the most lethal cancer types, currently lacking efficient treatment. The heterogeneous nature of these tumours are poorly represented by the classical pancreatic cell lines, which have been through strong clonal selection <i>in vitro</i>, and are often derived from metastases. Here, we describe the establishment of novel pancreatic adenocarcinoma models, xenografts and corresponding <i>in vitro</i> cell lines, from primary pancreatic tumours. The morphology, differentiation grade and gene expression pattern of the xenografts resemble the original tumours well. The cell lines were analysed for colony forming capacity, tumourigenicity and expression of known cancer cell surface markers and cancer stem-like characteristics. These primary cell models will be valuable tools for biological and preclinical studies for this devastating disease.</p></div

Molecular characterisation of TP53 mutated squamous cell carcinomas of the lung to identify putative targets for therapy

Personalised cancer treatment depends on identification of therapeutically relevant biological subgroups of patients for assessing effect of treatment and to discover new therapeutic options. By analyses in heterogeneous patient populations, the effects may be lost in noise. Squamous cell carcinoma of the lung is a major killer worldwide. Despite recent advances, mortality is high and response to therapies varies greatly from patient to patient. Target search in biologically relevant subgroups may identify treatment options not so far discovered. A total of 198 patients undergoing surgery for squamous cell carcinomas of the lung were included in the study. The tumours were analysed for copy number alterations (n = 152) and gene expression from tumour (n = 188) and normal lung (n = 21), with both data levels present in 140 patients. We studied alterations in tumours harbouring mutations in TP53 and in previously published gene expression subtypes. Genes with consistent alterations in both genomic levels were identified as putative biomarkers. Results were validated in TCGA. The most convincing biomarker in TP53 mutated squamous cell carcinomas of the lung was BIRC5 with amplification in 36% of mutated samples, 5% in wild‐type samples and a 17%‐fold change of expression between TP53 mutated tumours and normal lung tissue. BIRC5 was significantly altered in the classical and primitive subtypes. We suggest BIRC5 as a putative predictive biomarker and putative druggable target in squamous cell lung carcinomas harbouring TP53 mutation or classified as classical and primitive subtypes

Characterisation of tumour mutation status and xenograft tumours.

1<p>: p53 staining is scored as hot spots where 5 = 30–60% and 6 = 60–100%, and the staining intensity is given in brackets (1 = weak, 2 = medium and 3 = strong).</p>2<p>: S100A4 is scored as % positive cells where 1 = 1–4%, 2 = 5–9%, 3 = 10–14%, 4 = 15–49%, 5≥50%, and the staining intensities is given in brackets (1 = weak, 2 = medium and 3 = strong).</p>3<p>: Time in weeks required for the implanted patient material to reach 10 mm.</p>4<p>:Time in weeks required for the xenograft passage to reach 10 mm for F3 and forward.</p

Cell surface expression of known cancer and stem cell markers.

<p>Shown here is the average % positive cells out of single, live cells, n = at least 3, n.d = not done.</p><p>Cells were analysed in the following passage spans: PpaC1 p1–p10, PpaC2 p3–p14, PpaC6 p5–p9 and PpaC8 p4–p20.</p

<i>In vivo</i> tumourigenicity.

<p>Shown is the number of tumours growing/the number of injected sites in NSG mice for each cell lines, harvested at the following passages: PpaC1 p6, PpaC2 p12, PpaC6 p6, PpaC8 p13.</p