Publications by authors named "Sudhansu Sekhar Nishank"

Epithelial-mesenchymal plasticity (EMP) is a process in which epithelial cells lose their characteristics and acquire mesenchymal properties, leading to increased motility and invasiveness, which are key factors in cancer metastasis. Targeting EMP has emerged as a promising therapeutic approach to combat cancer metastasis. Various strategies have been developed to target EMP, including inhibition of key signaling pathways, such as TGF-β, Wnt/β-catenin, and Notch, that regulate EMP, as well as targeting specific transcription factors, such as Snail, Slug, and Twist, that promote EMP.

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Earthworms have remarkable ability to regenerate its tail and head region. However the list of genes expressed in this regeneration process has been less explored baring a few species. The current study involves the transcriptome sequencing of intact tail and regenerating tail (15 day post amputation) of earthworms belonging to two different genera (Kinberg, 1867) and (Gates, 1945).

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Background: Oxidative stress constitutes one of the significant cause of vaso-occlusive clinical episodes in sickle cell disease (SCD) patients. It brings about the generation of reactive oxygen species and consequent damage to DNA. DNA damage repair genes such as hOGG1, XRCC1 and p53 play an important role in the repair of DNA damage during oxidative stress.

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Patients with sickle cell disease (SCD) produce significantly low levels of plasma nitric oxide (NO) during acute vaso-occlusive crisis. In transgenic sickle cell mice, NO synthesized by endothelial nitric oxide synthase (eNOS) enzyme of vascular endothelial cells has been found to protect the mice from vaso-occlusive events. Therefore, the present study aims to explore possible association of eNOS gene polymorphism as a potential genetic modifier in SCD patients.

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Background: It is known that patients with sickle cell disease (SCD) present activation of the blood coagulation and fibrinolytic systems, especially during vaso-occlusive crises and also during the steady state of the disease. We determined whether the presence of the factor prothrombin gene G20210A variant, factor V gene G1691A mutation (factor V Leiden), and methylenetetrahydrofolate reductase (MTHFR) C677T polymorphisms may be risk factors for vascular complications in individuals with SCD.

Methods: The study involved 150 patients with sickle cell anemia and 150 healthy controls of Central India.

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Background And Objective: Females with sickle cell disease (SCD) often show late onset of menarche. In transgenic sickle cell mouse, deficiency of gene encoding endothelial nitric oxide synthase (eNOS) has been reported to be associated with late onset of menarche. Thus to explore the possible association of eNOS gene polymorphism with age of onset of menarche in SCD females, 3 important eNOS gene polymorphisms- eNOS 4a/b, eNOS 894G>T (rs1799983) and eNOS-786 T>C (rs2070744) and plasma nitrite levels were tested among three groups of females- SCD late menarche, SCD early menarche and control females.

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Prevention of beta thalassaemia implies knowledge of the molecular spectrum occurring in the population at risk. This knowledge is necessary, especially when a prevention protocol is applied to a multiethnic population. For this purpose, we carried out molecular analysis of 431 beta thalassaemia subjects belonging to tribal (aboriginal) and non-tribal communities of Orissa, a part of peninsular India and found six types of mutation (four previously unreported and two reported).

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Prevention of beta thalassemia requires knowledge of the molecular spectrum occurring in the population at risk. This knowledge is particularly necessary when prevention control is applied to a multiethnic population. For this purpose, we are analyzing different populations of Orissa (India).

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