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Objective: This study examined whether there were significant changes (expectedly increase) in BMI (Body Mass Index), and relative subcutaneous body fat during the four years of study in a university and compared these changes between the students of different courses, viz., Computer science, Law and administration, Humanities and Physical education. Design: This was a prospective follow up study with measurements at two time points with gap of four years. Body mass index, Triceps, subscapular, mid-axillary, abdominal, supra-illiac and medial-calf skinfold thicknesses were measured at two points of time, just after entrance to university and again after completion of four years. Student’s T-test, one-way ANOVA, and repeated measures ANNOVA (two-way) were employed to assess significance of differences in anthropometric measures between groups of students. Setting: The study was conducted at the University of Rzeszów, Poland. Participants: 191 young men university students aged approximately 19.5 years and 24.0 years, at the beginning and after four years, respectively, during this study. Results: Students of all courses underwent increments in BMI, absolute- and relative skinfold thicknesses, except that the students of physical education course did not show change in skinfold thicknesses relative to BMI. Conclusions: It has been concluded that the change in the adiposity profile during the years of study at university varied according to the course types. Further, detailed studies on the nature and cause of such variation occurring between course types may lead to better understanding etiology of overweight and obesity before entering to adult life.

Diabetes mellitus is a chronic metabolic disorder resulting in an increased blood glucose level and prolonged hyperglycemia, causes long term health conse-quences. Chronic wound is frequently occurring in diabetes patients due to compromised wound healing capability. Management of wounds in diabetic patients remains a clinical challenge despite many advancements in the field of science and technology. Increasing evidence indicates that alteration of the biochemical milieu resulting from alteration in inflammatory cytokines and matrix metalloproteinase, decrease in fibroblast and keratinocyte functioning, neuropathy, altered leukocyte functioning, infection

Currently, research on natural products is facing challenging future in various aspects. A large group of natural polysaccharides such as β-glucan, cellulose, hemicellulose, chitin, pectin, agaropectin, heteroglycans, lignins, hydrocolloids, homopolysaccharides, heteropolysaccharides were studied extensively for their various therapeutical potential. Several research works have already demonstrated those polysaccharides has tremendous health benefits, and found to exhibit anticancer, antiviral, immunomodulatory, antimicrobial, anticoagulant, anti-inflammatory, antidiabetic, antioxidant and antitumor activities. Different mushroom, plant, fungus, algae, vegetables, microalgae etc. are some important source of several polysaccharide macromolecules such as glucans, ulvan A, ulvan B, fucoidan, rhamnan sulfate, laminarin sulfate, agar, alginate, heteroglycans. Earlier research work demonstrated that natural polysaccharides have the highest ability to carry biological properties along with some biopolymers like as proteins and nucleic acids due to their structural variability. The preventive effect of these biomacromolecules was extensively studied, especially their beneficial effect on chronic metabolic conditions like dyslipidemia and related disorders. Dyslipidemia is a serious metabolic disorder associated with coronary heart disease, coronary artery diseases, hypercholesterolemia, atherosclerosis, etc. Dietary natural polysaccharides could play an important role in the management and prevention of dyslipidemia. Polysaccharides from natural sources mainly sulfated polysaccharides exhibited predominant lipid-lowering and cholesterol-lowering activities through different mechanisms. Polysaccharides isolated from different edible plants, vegetables, plant, algae, mushroom with higher biological activities, particularly hypolipidemic activity were highlighted in this paper, in a way for their futuristic therapeutic application. This review aims to comprehensively discuss overall advances in hypolipidemic activity of polysaccharides, including their sources, structural characteristic and chemistry, biological activity and their probable mode of action.

Expression of a neuropilin-like protein, DCBLD2, is reduced in human calcific aortic valve disease (CAVD). DCBLD2-deficient mice develop bicuspid aortic valve (BAV) and CAVD, which is more severe in BAV mice compared with tricuspid littermates. In vivo and in vitro studies link this observation to up-regulated bone morphogenic protein (BMP)2 expression in the presence of DCBLD2 down-regulation, and enhanced BMP2 signaling in BAV, indicating that a combination of genetics and BAV promotes aortic valve calcification and stenosis. This pathway may be a therapeutic target to prevent CAVD progression in BAV.

The present investigation aimed to find the in vitro antioxidant and anti-inflammatory potential of fractions of methanol extract of Alangium chinense (Lour.) Harms leaves followed by isolation and identification bioactive molecule and evaluate its possible mechanism through in silico study. A methanol extract of Alangium chinense (Lour.) Harms leaves subjected for chromatographic fractionation and pure isolates (F1-F8) were evaluated for their in vitro anti-inflammatory activity using albumin denaturation inhibition assay and in vitro antioxidant activity. Fraction F4 showed highest in vitro anti-inflammatory activity (IC50 = 70.02 μg/mL), whereas fractions F3, F4, F7 showed better in vitro antioxidant activity compare to other fractions. F4 fraction was screened for its tentative structure using FTIR, 1H and 13C NMR. The spectral analysis showed that the fraction F4 has a tentative structure of olean 19-ene-1yl-acetate. The molecular docking studies showed that test ligand significantly interact with different key active sites of amino acids and thus confirm possible COX-2 inhibitory activity of fraction F4. In vitro and in silico study confirmed the isolation of possible anti-inflammatory from Alangium chinense (Lour.) Harms leaves, which may further used as lead to a development of a new therapeutic agent.

Medicinal plants always play a vital role by enhancing immunity and protecting us against different infections caused by microorganisms like fungi, bacteria, and viruses. The complex immune protection mechanism produces limitless cells or chemicals to control the spectrum of infectious agents and diseases caused by them. Medicinal plants contain different immunomodulatory constituents that amplify or inhibit the components present in the immune system. In India, people have used numerous medicinal plants and plant products since ancient times to boost the immune system and maintain its normal functioning capacity. Traditional herbaceuticals can boost body defense and improvise our health to survive better. In the last two years, the COVID-19 pandemic became a significant health concern. The healthcare system and scientists are fighting generously to save people. Existing medical facilities are not enough to beat the pandemic condition; therefore, the search for alternative remedies is gaining attention. Indeed, public health measures and the immune-boosting process are considered crucial approaches to dwindle the threat and mortality caused by infection. This chapter highlighted immune boosters from plant sources that can play an essential role as an alternative approaches to managing the current pandemic scenario.

Respiratory Tract Infection (RTI) may be caused by different microorganisms and resulting deadly diseases such as novel coronavirus (Covid-19), severe acute respiratory syndrome (SARS), Middle East Respiratory Syndrome (MERS), influenza and other viral infection, tuberculosis, pneumonia 8 other Bacterial RTI etc. Till now there is no recommended treatment strategy for COVID-19, as for this no specific pharmacologically proved drug till invented or identified. To identify/find out any new drug to treat particularly Covid-19 demands detailed attention in the characteristics of virus, so that the specific chemical approach in a short time can solve the health problem arouse worldwide. This paper is highlighting the comparative theoretical analysis of RTI caused by different microorganisms for the purpose of designing antiviral drugs to combat Covid-19.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections have posed a problematic healthcare situation worldwide since December 2019. Diabetes mellitus is associated with an increased risk and severity of coronavirus disease 2019 (COVID-19). While interacting with various other risk factors, high blood sugar was found to reduce immunity and increase the replication of SARS-CoV-2. Oxidative stress and the release of pro-inflammatory cytokines are greater in diabetic individuals than in healthy people, worsening the outcome of SARS-CoV-2 infection in diabetics. Increased expression of furin and angiotensin converting enzyme 2 (ACE-2) receptor in the hyperglycemic environment may promote the entry of SARS-CoV-2 in the host cell. COVID-19 infection primarily modulates immune and inflammatory responses, and may cause a cytokine storm, resulting in possible lethal outcomes in diabetics. An experimental report suggests that ACE expressed in the pancreas and the SARS-CoV-2 virus invariably destroy β-cells which contain ACE-2 receptors and results in acute diabetes. Moreover, COVID-19 also causes hyperglycemia in an individual with diabetes which may be related to insulin resistance and destruction of β-cells during SARS-CoV-2 infection. Early observations also suggest a correlation between oral hypoglycemic agents and the risk of COVID-19. This review focused on the possible cause and mechanism involved in SARS-CoV-2 infection in diabetics and the role of antidiabetic drugs in COVID-19.

Mid-upper arm circumference (MUAC) is an alternative anthropometric measurement to assess undernutrition but a universally accepted cut-off is yet to be established. The objectives of the present study are to determine whether the proposed sex-specific global cut-offs are suitable across several tribes in India. This cross-sectional study was conducted among nine tribal populations in India (1046 males, 1087 females). Weight, height and MUAC values were obtained, and body mass index (BMI) was calculated. The BMI cut-off (

Background: Coronary allograft vasculopathy (CAV) is a devastating sequela of heart transplant in which arterial intimal thickening limits coronary blood flow. There are currently no targeted therapies to prevent or reduce this pathology that leads to transplant failure. Vascular smooth muscle cell (VSMC) phenotypic plasticity is critical in CAV neointima formation. TET2 (TET methylcytosine dioxygenase 2) is an important epigenetic regulator of VSMC phenotype, but the role of TET2 in the progression of CAV is unknown. Methods: We assessed TET2 expression and activity in human CAV and renal transplant samples. We also used the sex-mismatched murine aortic graft model of graft arteriopathy (GA) in wild-type and inducible smooth muscle–specific Tet2 knockout mice; and in vitro studies in murine and human VSMCs using knockdown, overexpression, and transcriptomic approaches to assess the role of TET2 in VSMC responses to IFNγ (interferon γ), a cytokine elaborated by T cells that drives CAV progression. Results: In the present study, we found that TET2 expression and activity are negatively regulated in human CAV and renal transplant samples and in the murine aortic graft model of GA. IFNγ was sufficient to repress TET2 and induce an activated VSMC phenotype in vitro. TET2 depletion mimicked the effects of IFNγ, and TET2 overexpression rescued IFNγ-induced dedifferentiation. VSMC-specific TET2 depletion in aortic grafts, and in the femoral wire restenosis model, resulted in increased VSMC apoptosis and medial thinning. In GA, this apoptosis was tightly correlated with proliferation. In vitro, TET2-deficient VSMCs undergo apoptosis more readily in response to IFNγ and expressed a signature of increased susceptibility to extrinsic apoptotic signaling. Enhancing TET2 enzymatic activity with high-dose ascorbic acid rescued the effect of GA-induced VSMC apoptosis and intimal thickening in a TET2-dependent manner. Conclusions: TET2 is repressed in CAV and GA, likely mediated by IFNγ. TET2 serves to protect VSMCs from apoptosis in the context of transplant vasculopathy or IFNγ stimulation. Promoting TET2 activity in vivo with systemic ascorbic acid reduces VSMC apoptosis and intimal thickening. These data suggest that promoting TET2 activity in CAV may be an effective strategy for limiting CAV progression.

The current work was designed to study the starch's physicochemical attributes, tablet disintegration and dissolution efficiency and its derivatives obtained from the glutinous Assam bora rice (G-ABR) variety of Assam, Northeast India. Starch was isolated by a simple protein denaturation method, and a starch derivative was prepared through citric acid modification. G-ABRS and citrated G-ABRS were characterized through FTIR, DSC, XRD and SEM. The rate of consolidation, consolidation index, angle of internal friction, packing rearrangement and cohesive properties were determined to investigate their applications as functional excipients in pharmaceutical industries. G-ABRS and citrated G-ABRS exhibited better packing rearrangement and cohesive properties than standard corn starch. Furthermore, immediate release of API from the tablet compact was observed when the starch concentration increased from 1 to 5 %, indicating facilitation of the tablet compact disintegration. Therefore, G-ABRS and citrated G-ABRS are potentially functional and sustainable materials for pharmaceutical industries.

The phenotypic plasticity of vascular smooth muscle cells (VSMCs) is central to growth and remodeling processes, but also contributes to the pathology of atherosclerosis, restenosis, and other cardiovascular diseases. This ability of VSMCs to reversibly differentiate and de-differentiate is incompletely understood. SUV39H1, a histone methyltransferase, specifically trimethylates Lys-9 of histone H3 (H3K9me3), resulting in epigenetic transcriptional repression. We hypothesized that SUV39H1 plays a role in VSMC phenotypic switching. Using knockdown, qPCR, western blot, chromatin immunoprecipitation (ChIP), RNA-Seq, and murine vascular injury to determine the role of SUV39H1 in VSMC plasticity. A qPCR array screen of epigenetic regulators revealed that SUV39H1 is upregulated with PDGF-induced dedifferentiation but downregulated with rapamycin-induced differentiation in hCASMCs. SUV39H1 knockdown promoted differentiation measured by increased contractile gene, protein expression, enhanced contractility, decreased migration, proliferation, and de-differentiation-associated gene expression. RNA-seq trasncriptomics confirmed changes in multiple pathways consistent with a role for SUV39H1 in promoting hCASMC dedifferentiation. Mechanistically, SUV39H1 knockdown suppressed expression of KLF4, the master transcriptional regulator of VSMC dedifferentiation, decreasing KLF4 mRNA stability and upregulating miRNA143, a known repressor of KLF4. siSUV39H1 also increased expression of KDM4a, a JMJD family lysine demethylase that targets H3K9me3. ChIP assays at contractile gene promoters showed significant decrease in the H3K9me3 mark and increase in H3K27Ac after SUV39H1 knockdown. In vivo, we noted a significant increase in SUV39H1 and H3K9me3 expression in murine carotid artery ligation induced intimal hyperplasia. We identify SUV39H1 as an epigenetic regulator of VSMC phenotype whose expression and activity increase with dedifferentiation in vitro and in vivo . PDGF promotes H3K9me3 repressive marks at contractile genes by promoting expression of SUV39H1, which also inhibits the KDM4a. Understanding the role of SUV39H1 in VSMC plasticity may reveal new therapeutic strategies for treating vascular diseases.

Vascular smooth muscle cell (VSMC) phenotypic switching contributes to cardiovascular diseases. Epigenetic regulation is emerging as a key regulatory mechanism, with the methyl cytosine dioxygenase TET2 acting as a master regulator of SMC phenotype. The histone acetyltransferases (HATs) p300 and CBP are highly homologous and often considered to be interchangeable, and their roles in SMC phenotypic regulation are not known. We assessed the roles of p300 and CBP in human VSMC with knockdown, in inducible smooth muscle-specific knockout mice ( p300 iKO or CBP iKO ), and in human intimal hyperplasia. P300, CBP, and histone acetylation were differently regulated in VSMCs undergoing phenotypic switching and in injury-induced vessel remodeling. Knockdown experiments revealed opposing effects of p300 and CBP in VSMC phenotype: p300 promoted contractile protein expression and inhibited migration, but CBP inhibited contractile genes and enhanced migration. p300 iKO mice exhibited severe intimal hyperplasia following arterial injury while CBP iKO mice were entirely protected. In normal aorta, p300 iKO reduced, but CBP iKO enhanced, contractile proteins and contractility. Mechanistically, we found that these HATs oppositely regulate histone acetylation, DNA hydroxy methylation, and RNA PolII binding to promoters of differentiation-specific contractile genes. We report p300 and TET2 function together, as p300 was required for TET2-dependent hydroxy methylation of contractile promoters, and TET2 was required for p300-dependent acetylation of these loci. TET2 co-immunoprecipitated with p300 and this interaction was enhanced by rapamycin but repressed by PDGF, with p300 promoting TET2 protein stability. CBP did not associate with TET2, instead facilitated recruitment of histone deacetylases (HDAC2, HDAC5) to contractile gene promoters. Immunostaining revealed, p300 expression is repressed but CBP is induced in human intimal hyperplasia. This work reveals that p300 and CBP serve non-redundant and opposing functions in VSMC phenotypic switching and coordinately regulate chromatin modifications through distinct functional interactions with TET2 or HDACs. Targeting specific HATs may hold therapeutic promise for cardiovascular diseases.

Natural disasters (NDs) experienced by women and their children during prenatal and infant growth may have long-lasting effects on offspring’s development. Handgrip strength (HGS) is one of the measures of muscular strength and an indicator of health status. This study compared HGS in children exposed to cyclone Aila in India during their prenatal and infant growth compared to a control group from a non-affected, adjacent area. The total sample involved 444 boys and 423 girls aged 7–9 years, categorised into 3 groups: prenatally exposed to Aila, exposed to Aila in infancy, and the control group, non-exposed to Aila. Results revealed that prenatally exposed children of both sexes had significantly lower HGS than the controls (at least, p

Objective The phenotypic plasticity of vascular smooth muscle cells (VSMCs) is central to vessel growth and remodeling, but also contributes to cardiovascular pathologies. New technologies including fate mapping, single cell transcriptomics, and genetic and pharmacologic inhibitors have provided fundamental new insights into the biology of VSMC. The goal of this review is to summarize the mechanisms underlying VSMC phenotypic modulation and how these might be targeted for therapeutic benefit. Methods We summarize findings from extensive literature searches to highlight recent discoveries in the mechanisms underlying VSMC phenotypic switching with particular relevance to intimal hyperplasia. PubMed was searched for publications between January 2001 and December 2020. Search terms included VSMCs, restenosis, intimal hyperplasia, phenotypic switching or modulation, and drug-eluting stents. We sought to highlight druggable pathways as well as recent landmark studies in phenotypic modulation. Results Lineage tracing methods have determined that a small number of mature VSMCs dedifferentiate to give rise to oligoclonal lesions in intimal hyperplasia and atherosclerosis. In atherosclerosis and aneurysm, single cell transcriptomics reveal a striking diversity of phenotypes that can arise from these VSMCs. Mechanistic studies continue to identify new pathways that influence VSMC phenotypic plasticity. We review the mechanisms by which the current drug-eluting stent agents prevent restenosis and note remaining challenges in peripheral and diabetic revascularization for which new approaches would be beneficial. We summarize findings on new epigenetic (DNA methylation/TET methylcytosine dioxygenase 2, histone deacetylation, bromodomain proteins), transcriptional (Hippo/Yes-associated protein, peroxisome proliferator-activity receptor-gamma, Notch), and β3-integrin-mediated mechanisms that influence VSMC phenotypic modulation. Pharmacologic and genetic targeting of these pathways with agents including ascorbic acid, histone deacetylase or bromodomain inhibitors, thiazolidinediones, and integrin inhibitors suggests potential therapeutic value in the setting of intimal hyperplasia. Conclusions Understanding the molecular mechanisms that underlie the remarkable plasticity of VSMCs may lead to novel approaches to treat and prevent cardiovascular disease and restenosis.

Fetal life and infancy are critical periods when adverse environmental conditions, such as natural disasters, may alter a developing organism, leading to life-lasting unfavorable health outcomes, such as central body fat distribution. Therefore, the aim of this study was to assess the effect of the exposure to cyclone Aila in utero or during infancy on the relative subcutaneous adiposity distribution in preadolescent Indian children. The study included children prenatally (N = 336) or postnatally (during infancy, N = 212) exposed to Aila and a non-affected group (N = 284). Anthropometric indices involved, i.e., subscapular, suprailiac, triceps, and biceps skinfolds. The relative adiposity distribution (PC1) and socioeconomic status (SES) were assessed using principal component analysis. An analysis of covariance and Tukey’s post hoc test for unequal samples were performed to assess the effect of exposure to a natural disaster on the PC1, controlling for age, sex, Z-BMI, and SES. Prenatally and postnatally Aila-exposed children revealed a significantly more central-oriented pattern of relative subcutaneous fat distribution compared to the controls (p < 0.05). Early-life exposure to a natural disaster was related to an adverse pattern of relative adipose tissue distribution in preadolescent children.

Smooth muscle cells (SMC) can undergo distinct fate transitions that influence atherosclerotic plaque phenotype: SMC make up the protective fibrous cap that prevents plaque rupture, but can also transdifferentiate to a destabilizing pro-inflammatory phenotype. We found that LMO7, a scaffolding protein that modulates SMC phenotype, is induced in atherosclerosis. SMC LMO7 deletion produced a paradoxical phenotype with enhanced indices of plaque stability despite greater lipid content. We determined that LMO7 promotes SOAT1 ubiquitination and degradation. LMO7 depletion thus favored cholesterol esterification and “safe” storage, relieving ER stress and subsequent induction of KLF4 and SMC transdifferentiation. Immunostaining and single cell sequencing confirmed that SMC LMO7 depletion enhanced cap stabilizing fate transitions while substantially reducing inflammatory transdifferentiation. Similarly, LMO7 was induced in human atherosclerosis, but at lower levels in stable versus ruptured plaques. These findings reveal that SMC cholesterol esterification, rather than total cholesterol content, influences plaque composition and stability.

Maternal education plays a central role in children’s health and nutrition. Living conditions and socioeconomic status are linked with mother’s education, which in turn determines the health and development of a child. The Composite Index of Anthropometric Failure (CIAF) is a single indicator that reflects overall rate of three conventional indices of undernutrition: underweight, stunting and wasting. The study was undertaken among 621 rural Bengalee children (308 boys and 313 girls) aged 3–12 years from the Purba Medinipur district of West Bengal, India. Height (cm) and weight (kg) were recorded and NCHS standard values used to calculate z-scores (

Background Rice (Oryza sativa L.) is the most popular staple food grain and an important source of fibre, energy, minerals, vitamins, and other biomolecules. Rice parts exhibited a number of health beneficial effect in pre-clinical/clinical studies. Rice constituents are getting popularity in preparation of pharmaceutical adjuvant, food additives and supplements. Scope & approach In this paper, we summarized the available literature on health-promoting and therapeutic activity of rice and rice biomolecules, and biomolecules, along with the scope of rice in pharmaceutical and food industry. In addition, we discussed the possible molecular mechanisms of action of the rice/rice part/biomolecules. Key findings Vitamin E, γ-oryzanol, phenolic acids (i.e. ferulic acid, gallic acid, syringic acid), anthocyanin and proanthocyanidin (i.e. epicatechin, cyanidin-3-O-glucoside), flavonoids (i.e. quercetin, apigenin, kaempferol, tricin), carotenoids (i.e. lutein, zeaxanthin, β-carotene) and phytosterol (i.e. stigmasterol, β-sitosterol) are some key rice biomolecules. Promoting endogenous antioxidants, scavenging free radicals, suppression of inflammatory/pro-inflammatory cytokinins (i.e. interleukin 6, cyclooxygenase, tumor necrosis factor, NOS) are some key antioxidant, anti-inflammatory mechanism of rice biomolecules. Rice bran cause apoptosis, inhibit DNA synthesis of cancer cell. Rice bran and biomolecules found effective against diabetes by enhancing insulin release and glucose uptake, inhibiting β-cell destruction, insulin resistance, carbohydrate metabolizing enzyme and AGE formation. Rice bran/rice bran oil enhanced LDL receptor, CYP7A1, SREBP-2 and excretion of faecal cholesterol and bile acid, while reduced cholesterol absorption, HMG-CoA reductase, fatty acid synthase. Rice and its biomolecules also exhibited nephroprotective, neuroprotective, GIT protective activity. Rice starch is getting importance in the pharmaceutical industry as an adjuvant.

SUMMARYAging is the predominant risk factor for atherosclerosis, the leading cause of death. Rare smooth muscle cell (SMC) progenitors clonally expand giving rise to up to ∼70% of atherosclerotic plaque cells; however, the effect of age on SMC clonality is not known. Our results indicate that aged bone marrow (BM)-derived cells non-cell autonomously induce SMC polyclonality and worsen atherosclerosis. Indeed, in myeloid cells from aged mice and humans, TET2 levels are reduced which epigenetically silences integrin β3 resulting in increased tumor necrosis factor [TNF]-α signaling. In turn, TNFα signals through TNF receptor 1 on SMCs to promote proliferation and induces recruitment and expansion of multiple SMC progenitors into the atherosclerotic plaque. Notably, integrin β3 overexpression in aged BM preserves dominance of the lineage of a single SMC progenitor and attenuates plaque burden. Our results demonstrate a molecular mechanism of aged macrophage-induced SMC polyclonality and atherogenesis and suggest novel therapeutic strategies.Graphical abstractAge of BM-derived monocytes/macrophages determines clonality of SMC lineage in the atherosclerotic plaque. Atherogenesis is depicted in a young (a) or aged (b) host. Aged monocytes/macrophages have decreased levels of the epigenetic regulator TET2, leading to reduction of the 5-hydroxymethylcytosine (5hmC) mark on the Itgb3 promoter. The resulting low integrin β3 levels in aged monocytes/macrophages induces high TNF-α levels, facilitating recruitment and expansion of multiple SMC progenitors (polyclonality) in the atherosclerotic plaque and worse disease burden. In contrast, the young control is characterized by mono/oligoclonal SMC expansion in a smaller plaque.

Utilization of native starch is increasing globally because of its wide distribution and natural occurrence. Starch is mainly abundant in tubers and food grains. Scientific research on starch is increasing in recent years due to its unique physiochemical and biomedical properties. Native starch is an emerging biopolymer and copolymer in the biomedical and pharmaceutical areas due to its renewability, biocompatibility, biodegradability, and relative inexpensiveness. Today, there is an increasing interest in natural starches to design and produce diverse products due to their pertinent structural properties and non-toxicity. Due to these attributes, these natural polymers are becoming functional core materials in the biomedical industry, construction materials, medicine industry, food industry, food packaging, and carrier for active drugs. In this paper, we mainly attempt to analyze the physicochemical attributions and the biomedical applications on native or non-conventional starches obtained from the natural botanical sources.