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):---------. 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.
The exposure to high risk strains of Human papilloma virus (16/18) in combination can be fabricotor of trouble (p<0.001, Adjusted odds ratio; 21.42) in OSCC.
Harlequin Ichthyosis (HI) is a dreadful skin disorder with steady rise of cases with prolonged survival. Harlequin fetus follows an autosomal recessive pattern with the incidence of 1in 300,000 live births. In the succeeding case report, a male child was born with keratinized and kaleidoscopic diamond pattern of skin suggestive of HI. He was born at 36th week of gestation from consanguineous marriage. The newborn remained under extensive intensive care in a tertiary care unit where he breathed his last on 11th day after birth. Prenatal diagnosis and genetic counseling is of vital importance due to the association of ABCA12 mutation with HI. doi: https://doi.org/10.12669/pjms.35.5.916 How to cite this:Devnani J, Kumari U, Zil-e-Rubab. Harlequin fetus born from Consanguinity: A deleterious case report. Pak J Med Sci. 2019;35(5):---------. doi: https://doi.org/10.12669/pjms.35.5.916 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.
Zinc, an important micronutrient for the storage, structural stabilization, secretion and action of insulin, is present in highest concentration in pancreas. The transport of zinc occurs through the zinc transporter-8 (ZnT8) to the insulin secretory vesicles. Zinc Transporter-8 Autoantibodies (ZnT8A) has been found to be associated with Type 2 Diabetes Mellitus. Recently it is recognized as a new autoantigen in Type 1 Diabetes Mellitus (T1DM) and its autoantibodies have been found in 50-60% of individuals with T1DM. Moreover, ZnT8A exhibit humoral auto reactivity which is not displayed by any of the other islet autoantigen like glutamine decarboxylase (GAD), insulin or tyrosine phosphate-related molecules (IA-2). Immunity against ZnT8 is dependent on clinical characteristics, which may provide evidence for early recognition highlighting the importance of this transporter in the pathogenesis of T1DM. Information regarding this article was retrieved through PubMed, Google Scholar and other search engines available in the University by using the keywords zinc, ZnT, ZnT8, SLC30A8 (Solute carrier 30 member 8) and Type 1 Diabetes Mellitus. Information was gathered through original researches, reviews and epidemiological studies published up to August 2019.The aim of this review is to summarize the emerging role of ZnT8A in diagnosis and understanding the genetic basis of Type 1 Diabetes Mellitus.
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