Objective To evaluate the anxiety and depression amid novel coronavirus disease-19 (COVID-19) pandemic in health sciences students around the globe.Materials and Methods This cross-sectional observational study comprised 523 health science students. A well-structured online questionnaire consisting of closed-ended questions based on student’s general information, Patient Heath Questionnaire (PHQ)-9 and Generalized Anxiety Disorder (GAD)-7 scales were used to assess the psychological impact of COVID-19.Statistical Analysis SPSS-25 was used to analyze the outcome of this study. Multiple linear regression analysis test was used to assess variables which had impact on PHQ-9 and GAD-7 scores among the participants. A p-value of ≤ 0.05 was considered as statistically significant.Results Among the 523 participants, 365 (69.55%) students were from developing countries and 158 (30.21%) from developed countries; 424 (81.1%) students were tested negative for COVID-19 and 99 (18.9%) had suffered from severe acute respiratory syndrome coronavirus 2 infection during pandemic. The mean GAD-7 and PHQ-9 scores were 7.16 ± 5.755 and 7.30 ± 6.166, respectively. Significant impact on anxiety levels was associated with age, gender, education status, and COVID-19 positive patient, while depression was not significantly associated with gender, COVID-19, and its reported symptoms in participants.Conclusion As the world is trying to contain the health effects of COVID-19, the psychological effects might take a longer time to be addressed. Our study highlights the dire need to identify mental well-being of health science students as this may have a direct impact on their professional commitments and future responsibilities.

Objectives: The aim of this study was to assess the impact of smoking on the whole salivary flow rate (SFR), IgA levels and clinical oral dryness (COD) among active and passive smokers. Material and Methods: The participants were categorized as active smokers (N = 54) or passive smokers (N =...

Objective: This study aims to determine expression of Glial Fibrillary Acidic Protein and of Alpha Smooth Muscle Actin (?-SMA) in hepatic stellate cells of CHC cases and their association with stage of fibrosis.Methods: The study was conducted at Ziauddin University, Clifton Campus during the year 2010-2012. Sixty Chronic Hepatitis C cases were immmunostained using anti ?-SMA antibody and anti-GFAP antibody. Semi quantitative scoring in pericentral, periportal and perisinusoidal area of each case was done to assess immunoexpression of each marker.Results: Immunoexpression of GFAP showed significant association with ?-SMA. GFAP expression was inversely correlated with progression of fibrosis.Conclusion: GFAP could represent a useful marker for early hepatic stellate cells activation. Follow up biopsies showing decline in GFAP levels may help identify the target group requiring aggressive therapy.doi: http://dx.doi.org/10.12669/pjms.305.5534How to cite this:Hassan S, Syed S, Kehar SI. Glial Fibrillary Acidic Protein (GFAP) as a mesenchymal marker of early hepatic stellate cells activation in liver fibrosis in Chronic Hepatitis C infection. Pak J Med Sci 2014;30(5):1027-1032.

Objective: Viral hepatitis is associated with high morbidity and mortality. Identification of biological pathways involved in hepatic fibrosis resulting from chronic hepatitis C are essential for better management of patients. Constructing the HCV-human protein interaction network through bioinformatics may enable us to discover diagnostic biological pathways. We investigated to identify dysregulated pathways and gene enrichment based on actin alpha 2 (ACTA2) and glial fibrillar acidic protein (GFAP) interaction network analysis in hepatic fibrosis. Methods: This is an in-silico study conducted at Ziauddin University from March,2019 to September 2019. Enrichment and protein–protein interaction (PPI) network analysis of the identified proteins: GFAP and ACTA2 along with their mapped gene data sets was performed using FunRich version 3.1.3. Results: Biological pathway grouping showed enrichment of proteins (85.7%) in signalling pathway by epidermal growth factor receptor (EGFR) and Tumor growth factor (TGF)-beta Receptor followed by signaling by PDGF, FGFR and NGF (71.4%) (p < 0.001). SRC, PRKACA, PRKCA and PRKCD were enriched in both EGFR and TGF-beta Signalling pathways. Conclusion: EGFR and TGF-beta signalling pathways were enriched in liver fibrosis. SRC, PRKACA, PRKCA and PRKCD were enriched and differentially expressed in both EGFR and TGF-beta signalling pathways doi: https://doi.org/10.12669/pjms.36.4.1845 How to cite this:Hassan S, Zil-e-Rubab, Shah H, Shawana S. Dysregulated epidermal growth factor and tumor growth factor-beta receptor signaling through GFAP-ACTA2 protein interaction in liver fibrosis. Pak J Med Sci. 2020;36(4):782-787. doi: https://doi.org/10.12669/pjms.36.4.1845 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Background: Identification of gene targets and biological pathways involved in colorectal carcinoma (CRC) is essential for better management of patients. Our study aims to highlight common somatic mutations in colorectal carcinoma and to identify dysregulated pathways and gene enrichment based on KRAS and BRAF interaction network analysis. Methods: By using cancer browser tool in COSMIC database, mutation frequencies of the top 20 mutated genes listed for colorectal adenocarcinoma were identified. The most frequent variants of selected genes were explored with ClinVar database which led to identification of protein change along with its cytogenic location, variant type, variant length and the associated single nucleotide polymorphism (SNP). These identified SNPs were searched in Pakistani database using 1000genome in an attempt to identify common polymorphisms. Using the database ClinicalTrial.gov the number of clinical trials based upon these selected mutations was explored. Enrichment and protein interaction (PI) analysis of KRAS and BRAF was carried out to reveal significant biological pathways associated with these genes. Results: In cumulative data, among all variants about 57% of substitution mutations are observed to be G>A including mutations in KRAS, Tp53, SMAD4, PI3K and NRAS. The mutations of KRAS (c.35G>A), TP53 (c.524G>A) and APC (c.4348C>T) were found to be pathogenic with single nucleotide variation and variant length of 1bp. Searching 1000genome database revealed that 100 % of alleles found in East Asian population studied are ‘C’(frequency=1). Significant biological pathways (<0.05) identified by our search include Trk receptor signalling mediated by the MAPK pathway, signalling to p38 via RIT and RIN, signalling to ERKs, Frs2-mediated activation, ARMS-mediated activation and prolonged ERK activation events. Conclusion: Our study highlights the role of genetic profiling in CRC, with emphasis on mutations which may define treatment outcome. Targeting several collateral pathways simultaneously may be further explored to improve colorectal cancer therapeutics.