Browsing by Author "Shruti R. Hansda"

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Comprehensive property combination for biomedical application achieved in a Ti35Zr35Nb15Mo5Fe5Cr5 complex concentrated alloy
(Elsevier Ltd, 2024) Dharmendra K. Yadav; Anand K. Patel; Shruti R. Hansda; Arbind Acharya; Lakhindra Marandi; Surya D. Yadav; Subhasis Sinha
A novel Ti35Zr35Nb15Mo5Fe5Cr5 complex concentrated alloy (CCA) with potential for biomedical application was developed by vacuum arc melting and its microstructural evolution, mechanical properties, corrosion and wear behavior, and cytocompatibility were systematically evaluated. The alloy has an experimentally measured density of 6.37 g/cm³, suitable to fulfill the requirement of light weight. XRD analysis revealed that the as-cast and annealed specimens contain two BCC solid solution phases and a TiCr2 type Laves phase. The average microhardness (H) and elastic modulus (E) of the as-cast CCA are 618.39 ± 9.26 HV and 97.32 ± 3.58 GPa, respectively. Moreover, the yield strength (YS) of the as-cast alloy, estimated from elastoplastic analysis of the microindentation data, is 1203.94 ± 30.28 MPa. However, the CCA annealed at 1100˚C exhibits a microhardness of 833.08 ± 7.58 HV and a YS of 1669.65 ± 24.79 MPa, with the elastoplastic stress-strain response revealing no significant loss of plasticity due to the increased hard Laves phase. Corrosion and wear tests conducted in simulated body fluid confirmed the alloy's excellent corrosion and wear resistance. Cell culture experiments with MG-63 and HEK-293 cells demonstrated superior cell viability and proliferation compared to CP-Ti and 316 L SS. Moreover, confocal fluorescence images of MG-63 cells stained with AO/EtBr, Rh-123, and DCFH-DA revealed that the present CCA exhibits good biocompatibility. Thus, a comprehensive combination of low density, compatible elastic modulus, good strength with adequate plasticity, and sufficient corrosion resistance and biocompatibility were successfully achieved, unraveling significant potential of the alloy for biomedical applications. © 2024 Elsevier Ltd
Environmental toxicant compromised reproductive health: Rescue by melatonin
(Nova Science Publishers, Inc., 2020) Jitendra Kumar; Sriparna Pal; Shruti R. Hansda; Chandana Haldar; Rakesh Verma
Several factors are responsible for declined male and female reproductive potential such as altered lifestyle, nutritional deficiency, global industrialization and increased exposure to environmental toxicants. The World Health Organization documents that around 15% couples face the problems of infertility but its underlying aetiology and treatment still need to be explored. Increased exposure to environmental toxins impair testicular and ovarian physiology through modulation of metabolic status (IR-GLUTs), redox (SIRT-1/Nrf-2/HO-1), inflammatory (NF-κB/COX-2) and apoptotic (Bax/Bcl-2 ratio, caspase-3) proteins and thus compromises reproductive health. Moreover, environmental contaminants have been reported in human blood, urine and milk. Melatonin, a pineal hormone, controls numerous physiological functions and act as an antioxidant, antiapoptotic, anti-inflammatory molecule in various organisms including human. Extra pineal organs such as retina, cerebellum, gastrointestinal tract and reproductive organs are also the source of melatonin. Within gonads, presence of Aralkylamine N-acetyltransferase (AANAT) and N-acetylserotonin O-methyltransferase (ASMT) convinced the intra gonadal synthesis of melatonin. Further, melatonin receptor (MT-1/2) has been reported in testicular Leydig cells, Sertoli cells, sperm and ovarian granulosa cells of mammals including humans that altogether reinforced its autocrine and paracrine role in regulation of reproductive physiology. Recently, melatonin has been reported to modulate various transcription factors and proteins that controls metabolic status and survival factors such as SIRT-1/Nrf-2 and its downstream signalling pathway in various organs including gonads. Therefore, advancement in melatonin research suggests that it could be use for the treatment of fertility related problems and improve the reproductive health. © 2021 Nova Science Publishers, Inc.
HOXA10-TWIST2 antagonism drives partial epithelial-to-mesenchymal transition for embryo implantation
(Springer Nature, 2025) Nancy Ashary; Sanjana Suresh; Anshul Bhide; Sharmishtha Shyamal; Pranya N; Saee Patil; Anuradha Mishra; Anuradha A; Shruti R. Hansda; Harshavardhan BV; Mohit Kumar Jolly; Deepak Narhari Modi
In mammalian reproduction, a significant proportion of embryos fail to implant despite a receptive uterus, suggesting that defects in epithelial remodeling at the embryo–uterine interface contribute to implantation failure. The molecular programs enabling such remodeling remain incompletely understood. Here, we identify a conserved transcriptional circuit involving HOXA10 and TWIST2 that regulates epithelial plasticity in the endometrium via partial epithelial-to-mesenchymal transition (pEMT). HOXA10, a transcription factor essential for uterine receptivity, is specifically downregulated in the luminal epithelium at implantation in mice, hamsters, and monkeys. Integrated CUT&RUN and transcriptomic profiling in human endometrial epithelial cells reveal that HOXA10 directly activates epithelial gene networks and represses mesenchymal programs. HOXA10 loss, both in vitro and in vivo, induces a pEMT state with increased cell motility. Mechanistically, HOXA10 represses TWIST2, a core EMT regulator; its derepression promotes mesenchymal gene expression and epithelial cell migration. TWIST2 knockdown restores epithelial identity and impairs implantation. These findings establish a mutually antagonistic HOXA10-TWIST2 circuit as a key regulator of pEMT and epithelial remodeling during implantation. (Figure presented.) © The Author(s) 2025.
Uterine anomalies in cell proliferation, energy homeostasis and oxidative stress in PCOS hamsters, M. auratus: Therapeutic potentials of melatonin
(Elsevier Inc., 2021) Shruti R. Hansda; Chandana Haldar
Aims: Polycystic ovarian syndrome (PCOS) is a reproductive, endocrine and metabolic disorder. Less is known about the mechanism of its effect on uterine function and therapeutic potential of melatonin. Our aim was to evaluate uterine dysfunction(s) in letrozole induced PCOS and its possible rectification by melatonin. Main methods: Adult female golden hamsters were divided into groups of Control (C), Melatonin (M; 1 mg/kg b.w.), Letrozole (L; 3 mg/kg b.w.) and combination of Letrozole+Melatonin (L + M; 3 mg/kg b.w. + 1 mg/kg b.w.) which were treated for 40 days. Analysis of serum testosterone/estradiol/progesterone/leptin/insulin, uterine histomorphometry, immunohistochemistry for proliferation cell nuclear antigen (PCNA), homeostatic assessment model of insulin resistance (HOMA-IR), western blotting for PCNA, androgen receptor (AR), insulin receptor (InsR), glucose tansporter-4 (GLUT-4), nuclear factor-kappa B (NFκB), cyclooxygenase-2 (COX-2) and biochemical analysis of superoxide dismutase (SOD)/catalase/lipid peroxidation (LPO) were done. Key findings: Serum testosterone, leptin and insulin increased while uterine InsR/GLUT-4 expression decreased in L group indicating metabolic abnormalities. Endometrial hyperplasia, increased expression of PCNA and AR indicated abnormal proliferation in L compared to C. Increased uterine oxidative load (SOD/catalase/LPO) and inflammatory markers NFκB/COX-2 expression in L was responsible for high tissue oxidative stress and inflammation. M administration normalized all the above parameters suggesting its ameliorative effect in L + M group. Significance: We report PCOS induced uterine dysfunction in Mesocricetus auratus for the first time. M administration restores uterine functions modulating cellular dynamicity, metabolic status, decreased oxidative and inflammatory load in PCOS hamsters. Therefore, we suggest the therapeutic potential of M against PCOS led uterine abnormalities to restore female fertility. © 2021