To compare the levels of organochlorine pesticide (OCP) residues in sera and bone marrow of children with malignant and non-malignant hematological disorders (HDs) with those in healthy controls. This case–control study was conducted among children aged ≤ 12 years with malignant and non-malignant HDs and non-anemic healthy controls. Children with gross congenital malformations, neurodevelopmental disorders, and chronic systemic diseases were excluded. OCPs were estimated in sera and bone marrow aspirate using gas–liquid chromatography/63Ni electron capture detection. Thirty children, each, with malignant HDs, non-malignant HDs, and controls, were included. The median (Q1, Q3) serum total OCPs (ng/mL) were significantly higher in children with malignant and non-malignant HDs compared to controls [38.67 (33.64, 42.51); 32.72 (17.26, 41.60); and 14.11 (12.82, 16.40)]; levels were significantly higher in the malignant versus non-malignant HD group. The median (Q1, Q3) serum levels of total hexachlorocyclohexane [3.30 (2.23, 4.28) vs. 2.16 (1.31, 3.31) ng/mL] and β-hexachlorocyclohexane [0.98 (0.67, 1.68) vs. 0.54 (0.10, 0.77) ng/mL] levels were significantly higher in children with non-malignant HDs compared to malignant HD, respectively. The median (Q1, Q3) total bone marrow OCPs (ng/mL) were significantly higher in the malignant HD group [23.53 (20.83, 26.91)] compared to the non-malignant HD group [17.41 (0, 25.63)]; bone marrow endosulfan II (ng/mL) was significantly higher in the non-malignant HD group [1.56 (0.56, 3.89)] compared to malignant HD group [0.45 (0.35, 1.72)]. Children with HDs had significantly higher OCP residues in sera compared to controls. The cumulative OCP residues in sera and bone marrow were significantly higher in children with malignant versus non-malignant HDs.

Organochlorine pesticides (OCPs) were extensively used in India in agriculture as insecticides and in public health programs to control vector borne diseases like Malaria, and typhus. This rampant use led OCPs to persist in the environment due to their resistance to natural degradation and biotransformation, consequently, enter the human body through the food chain and bio-accumulate in adipose tissue as they are lipophillic. Exposure to OCPs have been linked to various diseases due to their endocrine disrupting properties, and lipophillic nature. The purpose of the study is to estimate the OCPs level in the breast cancer patients, and to compare the OCP levels within breast cancer patients based on their clinical features. A case control study was conducted on 100 breast cancer cases and 100 controls of benign breast disease patients. Quantification of OCPs was done by Gas Chromatography system equipped with 63 Ni Electron Capture Detector. Significantly higher levels of γHCH, Endosulfan-II, p'p'DDT, p'p' DDD and o'p'DDT were found in cases with respect to controls (p < 0.05). The odds ratios (ORs) show a significant association of Endosulfan-II (1.3) and p'p'DDT (2.7) levels with risk of breast cancer. Further, significantly higher levels of γHCH, p'p'DDT and Endosulfan-II were found in lymph node metastasis cases and γHCH and pp'DDD in advanced tumor stage cases as compared to the cases without lymph node involvement, and early tumor stage respectively. The findings of the present study support the contribution of OCPs in the pathophysiology of breast cancer. Further, OCPs like p'p'DDT, Endosulfan-II, and γHCH may promote the progression of breast cancer by influencing the metastatic ability through lymphatic pathway.

BackgroundOne of the common findings in systemic sclerosis (SSc) patients has been long-term exposure to environmental toxins such as pesticides. However, the data available shows an equivocal association between pesticide exposure and autoimmunity in SSc.MethodsWe investigated the levels of organochlorine pesticides (OCPs) in blood of 20 SSc patients and 17 healthy controls, and also studied their effect in-vitro on T lymphocytes and their functional responses.ResultsWe found higher levels of hexachlorocyclohexane (HCH- alpha-, beta-, and gamma) and o,p'-dichlorodiphenyltrichloroethane (DDT) metabolite (p,p '-DDE) in blood of SSc patients. In vitro treatment of SSc patient PBMCs with either of HCH (100 mM) or DDT (50 mu M) caused a significant increase merely in CD8+ memory (CD8+CD45RO+) T lymphocytes. We also observed reduced FoxP3 expression in CD4+CD25+ (regulatory T cells) of SSc patients. Neither HCH nor DDT exposure of SSc PBMCs altered significantly the secretion of IL-2, IL-10, or IFN-gamma, but both of these pesticides elevated their IL-4 (a pro-fibrotic cytokine) secretion.ConclusionTaken together, our findings indicate that persistent exposure to these OCPs results in decreased lymphoproliferative activity which promotes disease activity by producing pro-fibrotic cytokine(s). Thus, SSc patients are less able to initiate or augment an immune response to foreign antigens, when there is substantial suppression of lymphocyte function, which increases their susceptibility to infection. Strategies to prevent and control pesticide exposure may play an important role in reducing the morbidity and mortality associated with this disease.

Objectives: This study aimed to compare the efficacy of yoga combined with an integrated multimodal approach on the incidence and severity of post-mastectomy pain syndrome (PMPS) and the role of miR-133B expressions in patients undergoing breast cancer surgery. Methods: With approval from the institutional ethics committee and informed consent obtained from each participant, forty patients of ASA grade I - II, aged 20 - 65 years, undergoing breast cancer surgery were included. Patients received a thoracic paravertebral block for up to 72 hours and pregabalin until the end of the fourth postoperative week. Patients were randomly allocated into two groups: “Control” and “yoga.” Patients in the Yoga group practiced the yogic exercise “Anulom-vilom" from the third day until the 90th day postoperatively. The delta-CT of miRNA-133B expression of genes on the 90th postoperative day was compared to the baseline, along with various pain intensity and quality of life parameters. Results: In the Yoga group, a significant up-regulation in miR-133B expression was observed on days 30 and 90 postoperatively. Patients with PMPS in the Yoga group showed a decreased ΔCT of miR-133B, indicating an up-regulation of gene expression, compared to the control group. A lower incidence of PMPS (10% vs. 30%) was observed in the experimental group, along with a significant enhancement of quality of life in post-mastectomy patients and decreased mean Visual Analogue Scale )VAS( pain scores, Pain Detect Questionnaire )PDQ( ، and Neuropathic Pain Symptom Inventory )NPSI( scores in the Yoga group; however, these were not statistically significant. Conclusions: The study demonstrated the feasibility of integrating yoga with a multimodal pain management approach and highlighted the role of miR-133B in the pathogenesis of PMPS.

Aim: Diabetic peripheral neuropathy (DPN) induces chronic neuropathic pain in diabetic patients. Current treatments like pregabalin and duloxetine offer limited efficacy. This study evaluates combining pregabalin and duloxetine versus pregabalin alone for DPN pain relief, and explores gene modulation (PPAR gamma and Akt) to understand neuropathic pain's molecular basis. Materials & methods: Diabetic patients with DPN were randomized into groups receiving combination therapy or pregabalin alone for 4 weeks. Pain intensity, gene expression and quality of life were assessed. Results: Combination therapy significantly reduced pain, improved quality of life and upregulated PPAR gamma and Akt genes compared with monotherapy. Conclusion: Pregabalin and duloxetine combination therapy in DPN led to PPAR gamma mRNA upregulation and negative correlation of Akt gene expression with pain scores. This combination therapy effectively reduced pain and improved quality of life.

The list of environmental factors that trigger autoimmune diseases in genetically susceptible individuals has grown in the recent years and is far from complete. The possible intervention of the environment in triggering these diseases is ever more perceived by the clinicians. This study investigated the effect of environmental factors like organochlorine pesticides (OCPs) on proportions of different T lymphocyte subsets and their cytokine secretion in-vitro among pemphigus patients, before and after specific immunosuppressive therapy. Higher levels of OCPs like β-HCH (isoform of hexachlorohexane), α-endosulfan (a form of endosulfan) and p,p΄-DDE (a metabolite of o,p’-dichlorodiphenyltrichloroethane) were observed in the blood of pemphigus patients as compared to healthy controls. HCH and DDT exposure caused specific reduction in CD8+CD45RA+ and CD4+CD25+ T lymphocyte subpopulations in these patient PBMCs. A strong reduction in Th1 (IL-2 and IFN-γ) cytokines upon exposure to these OCPs in-vitro was also observed. These findings indicate that HCH and DDT have a significant impact on Th1 lymphocytes. Impaired production of these cytokines might favor infections and production of autoantibodies. We therefore speculate that the systemic absorption of the pesticide after the topical contact may be one of the factors triggering the immunological mechanism among pemphigus patients.

Background The diverse manifestations of urolithiasis provide very interesting epidemiological data. This has prompted various studies to look into the etiopathogenesis of renal stones, which is believed to be multifactorial, both exogenous and endogenous. VDR Fok1 is a risk factor for renal stone formation and could cause the formation of renal stones through the mechanism of crystal induction and crystallization in the urine. While a few recent studies have shown the role of heavy metals like cadmium and lead in the formation of renal stones, the current knowledge is still insufficient. Methods This case-control prospective study was conducted in Guru Teg Bahadur (GTB) Hospital, a tertiary care facility in Delhi with 30 cases and 30 controls. Patients visiting the department of surgery between November 2011 and April 2013 were enrolled in the study. Cases were defined as patients with renal stones diagnosed on the basis of history and radiological investigations. Controls were selected from the patients admitted to the department of surgery for reasons other than renal stones. The study protocol was approved by the Institutional Ethical Committee of the University College of Medical Sciences, GTB Hospital, Delhi. Written informed consent was obtained from all patients. A structured questionnaire was used to collect data. Metal levels were analyzed by an atomic absorption spectrophotometer (Shimadzu Flame AA-680, Shimadzu Corp., Kyoto, Japan) at Delhi University. The vitamin D receptor gene was measured using genomic DNA. Horizontal agarose gel electrophoresis was used for the quantification of the genomic DNA. Results There were 30 cases and 30 controls in the study. Stress was more prevalent among cases (63%) compared to controls (36%). Nearly 83% of cases had the ff allele of the Vitamin D receptor gene compared to 46% of controls. The median arsenic and lead levels were higher among cases compared to controls. In the unadjusted model of logistic regression, we found stressed patients had three times higher odds of developing renal stones compared to non-stressed patients (OR (95% CI): 2.98 (1.04-8.52); p=0.04). Similarly, patients with higher blood concentrations of arsenic and lead had higher odds of developing renal stones compared to those with lower concentrations. Conclusions There was a definitive role of heavy metals, including lead, cadmium, and arsenic, seen with renal stones. A significant association was seen between the ff allele of VDR polymorphism (Fok1 enzymes) and patients with renal stones. Other parameters, including male and stress factors, seem to have an important role in renal stone formation.

The loss of balance between regulatory T (Treg) and T helper 17 (Th17) causes loss of tolerance against desmoglein (Dsg)-3 leading to pemphigus vulgaris (PV), an autoimmune bullous skin disorder associated with autoantibodies against Dsg-3. We aimed to elucidate the complex relationship of Th17 and Treg cells, their molecules, and the underlying mechanism in the development of PV disease. Using cytokine secretion assays, Th17 and Treg cells were sorted by FACS Aria-III within Dsg-3-responsive PBMC population and homogeneous T cell clones were generated in-vitro. Different cell surface molecules like CD25, GITR, CD122, CD152, CD45RO, IL-23R, STAT3, STAT5, CD127, HLA-DR, CCR4, CCR5, CCR6 and CCR7 were studied. The functional response of Th17 and Treg cells were elucidated by measuring the levels of various cytokines released by IL-10 and IL-17 T cells. The mRNA expression of transcription factors (FoxP3 and RORγt) was also analyzed. IL-17 secreting (Th17) cells with phenotype CD4+IL-17+ were greatly increased and IL-10 secreting (Treg) cells with phenotype CD4+IL-10+ were reduced in PV cases than healthy controls. The qPCR analysis showing high expression of retinoic acid receptor-related orphan receptor gamma (RORγt) mRNA in comparison to forkhead box P3 (FoxP3) mRNA confirmed the development of pro-inflammatory Th17 response in PV. Further, the cytokine profile of pro-inflammatory and anti-inflammatory cytokines suggested defective suppressive functions in Treg cells with high inflammatory response. Our findings indicate that autoantigen Dsg-3 specifically allows the proliferation of IL-17 secreting T cells though has a negative effect on IL-10 secreting T cells leading to dysregulation of immunity in PV patients. This antagonistic relationship between Dsg-3-specific Th17 and Treg cells may be critical for the onset and persistence of inflammation in PV cases.

The unregulated use of organochlorine pesticides (OCPs) has been linked to spread of breast cancer (BC), but the underlying biomolecular interactions are unknown. Using a case-control study, we compared OCP blood levels and protein signatures among BC patients. Five pesticides were found in significantly higher concentrations in breast cancer patients than in healthy controls: p',p' dichloro diphenyl trichloroethane (DDT), p'p' dichloro diphenyl dichloroethane (DDD), endosulfan II, delta-hexachlorocyclohexane (dHCH), and heptachlor epoxide A (HTEA). According to the odds ratio analysis, these OCPs, which have been banned for decades, continue to raise the risk of cancer in Indian women. Proteomic analysis of plasma from estrogen receptor-positive breast cancer patients revealed 17 dysregulated proteins, but transthyretin (TTR) was three times higher than in healthy controls, which is further validated by enzyme-linked immunosorbent assays (ELISA). Molecular docking and molecular dynamics studies revealed a competitive affinity between endosulfan II and the thyroxine-binding site of TTR, pointing towards the significance of the competition between thyroxin and endosulfan, resulting in endocrine disruption leading to breast cancer. Our study sheds light on the putative role of TTR in OCP-mediated BC, but more research is needed to decipher the underlying mechanisms that can be used to prevent the carcinogenic effects of these pesticides on women's health.

In the modern times, insecticides have grown to be an essential part of the atmosphere. Their full-size use in public health packages and agriculture has ended in capability environmental pollution and health risks, which relies upon their residual quantity and toxicity. The widespread uses cause general population to low dose of continual exposure of insecticides through meals and environment. The residue evaluation of human specimen suggests an increasing trend within the ranges of insecticides in serum, adipose tissue, breast milk, urine and others. Implications of pesticides residues on human fitness following subchronic publicity are but to be comprehensively answered. Subjection to insecticides can be closely associated with neurotoxicity, hepatotoxicity, immunotoxicity, genotoxicity and injurious reproductive effects. Pesticides leads to Reactive Oxygen Species (ROS) generation in significant quantities, resulting in oxidative stress and cellular damages. Findings of research have discovered a concomitant genotoxic and apoptotic effect of the pesticides in Peripheral Blood Mononuclear Cells (PBMCs). Since genotoxic consequences of pesticides on humans cannot be overlooked, therefore identification and implication of protective measures are urgently needed. This have been tested that PBMCs go through dose-structured apoptotic cell demise following pesticide exposure and additionally highlights the effectiveness of various antioxidants in counteracting pesticide-precipitated cytotoxicity. Heat Shock Proteins (HSPs) have emerged as an antiapoptotic molecules which counteract cytotoxicity. The inducible expression analysis of HSPs ought to make contributions to the human PBMCs to get over the toxic results of subchronic pesticide exposure. Though the linkage between cellular events of apoptosis is thought, the molecular mechanism highlighting the precise function of HSP in pesticidemediated cytotoxicity yet stays to be comprehensively replied. To better understand this mechanism, different antioxidant and HSP inducers have been employed, and also highlighted their attenuating effects towards the apoptotic capacity of such pesticides. This review article therefore, focuses on the fact that antioxidants and HSP inducers efficiently protect cells, emphasizing their role in pesticide-induced toxicity at molecular and cellular level as well as their possible use as therapeutic intervention.

Background Organochlorine pesticides (OCPs) have been long linked to type 2 diabetes mellitus (T2DM); however, this relation at the molecular level has not been explored yet. Endoplasmic reticulum (ER) stress and pro-inflammatory pathways are considered vital ones in the pathogenesis of T2DM. We aimed to investigate the existence of any association between OCPs, ER stress, and pro-inflammatory pathways in subjects with known T2DM. Methods Seventy subjects each with T2DM and normal glucose tolerance were recruited from the surgery department. Their visceral adipose tissue was collected intraoperatively. OCP concentration, ER stress, and pro-inflammatory markers were analyzed and compared between two study groups. Results We found 18 OCPs and their metabolites in visceral adipose tissue samples of study participants. The levels of δ-HCH, heptachlor, endrin, and p,p′DDT were significantly higher in the T2DM group and were also positively correlated with fasting and postprandial plasma glucose levels (p < 0.01). We observed a positive association of δ-HCH (p < 0.01), heptachlor (p < 0.05), and endrin (p < 0.05) with central adiposity and ER stress markers. However, we failed to establish the correlation of OCPs with any of the pro-inflammatory markers. Conclusion The existence and simultaneous complex correlation of OCPs with ER stress may explain their role in the pathogenesis of T2DM, revealing the persistence of the gene–environment interaction in the etiology of T2DM.

Although studies have suggested organochlorine pesticides (OCPs) exposure increased the risk of epithelial ovarian cancer, the mechanisms underlying its potential tumorigenic effects in the human ovary are not well understood. In this study, we investigated the impact of dichlorodiphenyldichloroethylene (DDE), endosulfan, and heptachlor exposure on epithelial cadherin (E‐cadherin) and proinflammatory mediators in human ovary surface epithelial (HOSE) cells. We found that DDE, endosulfan, and heptachlor exposure resulted in epithelial differentiation accompanied by upregulation of E‐cadherin expression and overexpression of proinflammatory cytokines (TNFα, IL‐1β, and IL‐6) in HOSE cells. The epithelial differentiation may accelerate HOSE cells to inclusion body formation, a common site for ovarian cancer initiation and persistent exposure to OCPs creates a chronic inflammatory microenvironment that may promote the neoplastic transformation of HOSE cells within the inclusion cyst.

DNA methylation of paired box-1 (PAX-1) gene has been shown to be a potential biomarker for the detection of high-grade cervical intra-epithelial neoplasia (CIN) and invasive cervical cancer. The objective of this pilot study was to quantify and compare methylation percentage of PAX1 gene in benign cervical lesion, pre-invasive and invasive cervical cancer. A total of 200 screen positive women (VIA, VILI and Pap test) underwent colposcopy. Cervical scrapes taken were taken and stored for DNA analysis and PAX 1 methylation status. Women with Swede score of 5 or more (n = 98) were biopsied. Cervical scrapes and biopsy were taken from women with obvious cervical growth (n = 14), without prior colposcopy. Sixty women were recruited to the study and allocated into three groups on the basis of histopathology, i.e., benign cervix (Group 1; n = 20), CIN 2/3 (Group 2; n = 20) and invasive cervical carcinoma (Group; n = 20). PAX 1 methylation percentage was calculated from the DNA extracted from the cervical scrapes of the women recruited. The mean PAX1 methylation percentage in benign lesions, CIN 2/3 and invasive cancer was 9.58

Aim: To determine the association of HOXA13 gene expression in vaginal wall tissue with the severity of pelvic organ prolapse (POP) among premenopausal women.Materials and methods: A cross-sectional study was conducted on a total of 60 premenopausal women.Subjects with ≥stage II POP were enrolled as cases, while those with benign gynecological conditions other than prolapse were taken as controls.Vaginal tissues were obtained during surgical procedures and HOXA13 gene analysis was done using real-time polymerase chain reaction.Spearman rank correlation coefficient was used for the correlation of true fold change of HOXA13 gene with other parameters.Results: Overall, HOXA13 gene was observed 1.21-fold downregulated in women with POP (p = 0.38).The gene was diminished in higher stages (stage III and stage IV) of POP (p = 0.007).It was found downregulated in most (84.21%) of the females above 40 years (p = 0.01).Conclusion: Downregulation of HOXA13 gene was seen in the majority of the women with POP, though not statistically significant.The gene expression was significantly diminished in women with advanced stages of prolapse (stage III and stage IV) as well as in women with age above 40 years.Clinical significance: Downregulation of HOXA13 gene can be one of the etiological factors of POP.Hence, preventive strategies may be developed using its gene expression analysis in future.

Background: India is one of the nation’s leading in number of preterm births (PTB), as reported by WHO. Despite extensive research the exact cause of PTB remains elusive. The present study was designed to study the effect of inflammatory genes (proinflammatory IL-6 and anti-inflammatory IL-10) in etiopathogenesis of idiopathic PTB.Methods: Maternal blood and placental tissue samples of PTB cases (n=263) and equal number of term delivery controls (n=263) were collected at the time of delivery. mRNA expression of IL-6 and IL-10 gene was analysed using Real-time PCR.Results: mRNA expression of IL-6 gene (pro-inflammatory) was 11.73 folds high in maternal blood and 2.60 folds higher in placental tissue in PTB compared to term birth cases. mRNA expression of IL-10 gene (anti-inflammatory) was 25 folds lower in maternal blood and 10 folds lower in placental tissue of PTB compared to term deliveries.Conclusions: Interleukins have been identified to have a major role in etiopathogenesis of idiopathic preterm birth.

The perinatal period is very critical as the embryo or the new born is more susceptible to Cd toxicity. This study was done to measure Cd levels in brain tissue of F1 and F2 generation mice whose mothers were exposed to Cd during lactation or during the entire period of gestation and lactation and also to investigate whether quercetin could modulate this effect. Dams were exposed to cadmium during lactation and during the entire perinatal period. F1 and F2 generations were reared till 100 days of age. After being sacrificed, their brains were extracted, and cadmium levels were estimated using Atomic absorption spectrophotometer. It was found that Cd levels in brain tissue were significantly higher in the F1 generation when animals were exposed in lactation. There was slight increase in Cd in brain tissue of animals exposed during gestation as well as lactation, but the change was not statistically significant. Quercetin reduced the Cd levels significantly in a dose dependent manner in lactation group. In the other two groups it reduced the Cd levels even lower than the controls. This study shows that Cd is passed on to the next generation more efficiently when exposed during lactation. Lesser transmission is seen when exposure is during gestation followed by lactation. Quercetin effectively reduces Cd levels in brain tissue irrespective of the type of exposure.

Background: Dipentyl phthalate (DPeP) is a plasticizer compound commonly used in polyvinylchloride plastic to enhance softness and flexibility. They are not bound covalently to plastic polymers; therefore, they can dissolve into the environment and adversely affect the health of humans and animals. Objectives: The aim of this study was to investigate the effect of DPeP on cognition and protective effects of N-acetylcysteine (NAC) on DPeP induced alteration in cognitive behaviour and oxidative stress markers in mice. Methods: Mice were orally treated with 2 doses (33 mg/kg and 100 mg/kg) of DPeP for 28 days. Cognitive functions were assessed using spatial navigation tasks on the Morris water maze and the step-down latency in the passive avoidance apparatus. Oxidative stress was assessed by examining the levels of malondialdehyde, glutathione, ferric reducing antioxidant power, and 8-hydroxy-deoxyguanosine levels in the whole brain of mice. Results: There was a significant increase in latency in spatial navigation tasks and a significant decline in the step-down latency in passive avoidance apparatus in the DPeP-treated group compared to the control groups. There was also a significant increase in the levels of oxidative stress following DPeP administration as seen with the rise in the levels of malondialdehyde, 8-hydroxy-deoxyguanosine, and a fall in glutathione and ferric reducing antioxidant power levels. Conclusion: The present study demonstrated that DPeP adversely affects learning and memory functions in mice by oxidative stress-mediated neuronal damage. These effects were attenuated by pretreatment with N-acetylcysteine.

Diabetes has affected nearly half a billion people worldwide. According to current guidelines, glycemic control is essential to mitigate diabetic complications. The antihyperglycemic effects of various chemically synthesized nanoparticles have been reported in animal models. However, their impact on humans has not been previously reported. This study was conducted to biosynthesize and assess the antihyperglycemic property of silica nanoparticles (SiO2-NPs) since they are non-toxic and biocompatible. SiO2-NPs biosynthesized using the endophytic fungus Fusarium oxysporum. In this collaborative study, 26 people, either hyperglycemic or euglycemic, diagnosed at the Endocrinology Outpatients, according to the American Diabetes Association, USA, were recruited. Silica nanoparticles were characterized and assessed for in vitro antihyperglycemic property using blood samples. Particle size distribution based on TEM images confirms that the average size of silica nanoparticle is 25 nm and is monodispersed in nature. The XRD pattern shows that only one broad peak at 2θ = 220 corresponds to the plane (101) of silica nanoparticles. UV Visible spectra show the λmax at 270 nm, peaks in FTIR at 1536 cm−1, 1640 cm−1, and 3420 cm−1 for the protein cap. The mean blood glucose was 120.2 mg/dL in the ‘SiO2-NP untreated’ group and decreased to 97.24 mg/dL in the ‘SiO2-NP treated’ group. A paired t-test (P-value < 0.0001) indicates a strong relationship between antihyperglycemia and silica NP. In our study, it has been observed that the biosynthesized silica nanoparticles using the endophytic fungus Fusarium oxysporum show antihyperglycemic property in vitro.