Dysregulation of Synaptic Plasticity Markers in Schizophrenia.

Schizophrenia is a mental disorder characterized by cognitive impairment resulting in compromised quality of life. Since the regulation of synaptic plasticity has functional implications in various aspects of cognition such as learning, memory, and neural circuit maturation, the dysregulation of synaptic plasticity is considered as a pathobiological feature of schizophrenia. The findings from our recently concluded studies indicate that there is an alteration in levels of synaptic plasticity markers such as neural cell adhesion molecule-1 (NCAM-1), Neurotropin-3 (NT-3) and Matrix-mettaloproteinase-9 (MMP-9) in schizophrenia patients. The objective of the present article is to review the role of markers of synaptic plasticity in schizophrenia. PubMed database (http;//www.ncbi.nlm.nih.gov/pubmed) was used to perform an extensive literature search using the keywords schizophrenia and synaptic plasticity. We conclude that markers of synaptic plasticity are altered in schizophrenia and may lead to complications of schizophrenia including cognitive dysfunction.

Relationship of interleukin-23 with matrix metalloproteinase-9, pentraxin-3, sleep quality and prostate size in benign prostatic hyperplasia.

Benign prostatic hyperplasia (BPH) is known to be associated with sleep disturbance and inflammation. The objective of the study was to assess the levels of serum MMP-9 and its inhibitor (TIMP-1), interleukin-23 and pentraxin-3 and their association with sleep quality index and prostate size in BPH patients. Eighty-eight BPH patients were recruited based on clinical and ultrasound findings. MMP-9 and its inhibitor (TIMP-1), interleukin-23 and pentraxin-3 were estimated in all the subjects. Sleep quality was assessed using Pittsburgh Sleep Quality Index (PQSI). Interleukin-23 was significantly correlated with prostate size (p = 0.031), TIMP-1 (p = 0.035), MMP-9 (p = 0.004) and PSQI score (p = 0.020). TIMP-1 was significantly correlated with MMP-9 (p = 0.006) and prostate size (p = 0.016). Pentraxin-3 was positively correlated with PSQI score (p = 0.047). Multivariate analysis shows that interleukin -23 (p = 0.006) predicts prostate enlargement in BPH patients. Interleukin-23 was significantly increased in BPH patients with PSQI score >9 compared to those with PSQI <9. We conclude that poor sleep quality contributes to inflammation in BPH. Inflammation leads to prostate enlargement in patients with BPH.

Relationship Between Neural Cell Adhesion Molecule-1 and Cognitive Functioning in Schizophrenia Spectrum Disorder.

Abnormal synaptic plasticity leads to cognitive impairment in schizophrenia. Markers of synaptic plasticity are known to be altered in schizophrenia, but there are limited data available about neural cell adhesion molecule-1 (NCAM-1) levels and its association with cognitive functions in schizophrenia. The objective of the study was to analyze NCAM-1 levels and its association with various cognitive domains in schizophrenia. One hundred and seventy-six schizophrenia cases and 176 controls were recruited for the study. Serum NCAM-1 levels were analysed in both the groups. Cognitive examination was performed using Addenbrooke cognitive examination-III (ACE-III) and disease severity was assessed using Positive and negative symptoms scale (PANSS). Serum NCAM-1 levels were elevated in schizophrenia cases (p = 0.006) compared to controls. NCAM-1 was positively associated with attention (r = 0.196, p = 0.009), language (r = 0.192, p = 0.011), visuospatial abilities (r = 0.207, p = 0.006) and total ACE-III score (r = 0.189, p = 0.012). We conclude that elevated levels of NCAM-1 are associated with better cognitive functioning in schizophrenia.

Risperidone Reduces Matrix Metalloproteinase-9 and Increases Neurotrophin-3 in Schizophrenia Spectrum of Disorder.

Even though earlier studies have reported alteration in the markers of synaptic plasticity (Matrix metalloproteinase-9 [MMP-9] and Neurotrophin-3 [NT-3]), there are no reports about the effect of risperidone on the same. The present study was designed to assess the effect of risperidone on NT-3 and MMP-9 levels in patients with schizophrenia spectrum of disorder and to investigate whether these markers can be used to predict the treatment response in these patients. 62 schizophrenia spectrum of disorder patients were enrolled in the study and were treated with 4 mg of risperidone OD. Serum NT-3 and MMP-9 levels were compared at baseline and after 6 weeks following risperidone treatment. Severity of the disease was assessed using Positive and Negative Syndrome Scale (PANSS). MMP-9 was significantly reduced and NT-3 was significantly increased in schizophrenia spectrum of disorder after treatment with risperidone. We also found a significant reduction in MMP-9 levels in the non-responders group. At a cut off of 1225 ng/mL, MMP-9 can predict response to treatment with 64% sensitivity and 62% specificity and at a cut off of 957 pg/mL, NT-3 predicted the response to treatment with 60% sensitivity and 62% specificity. We conclude that risperidone decreases the serum levels of MMP-9 and increases the NT-3 levels in schizophrenia spectrum of disorder. MMP-9 and NT-3 can predict the response to treatment with risperidone.

Assessment of vascular function in complete glycaemic spectrum.

Purpose: The present study was conceived to delineate the point of vascular dysfunction along the glycemic spectrum (normoglycemic individuals with no family history of diabetes, normoglycemic individuals with family history of diabetes, prediabetic individuals, and diabetic individuals).Materials and Methods: In this cross-sectional comparative study, we enrolled 252 participants of both gender in the age group of 30-50 years. They were classified based on their family history of diabetes and glycemic status into four groups along the glycemic spectrum as mentioned above. We measured flow-mediated dilation (FMD) from brachial artery and vascular function biomarkers such as enthothelin-1 (ET-1), von Willbrand Factor (vWF), Vascular Endothelial Growth Factor (VEGF) to assess the vascular function. The comparison of data between groups were done using One Way ANOVA/Kruskal-Wallis followed by post-hoc analysis using LSD/Mann-Whitney U Test depending on the normality of the data. Spearman correlation was done between vascular function and plasma glucose levels to identify its relationship. Linear regression was carried out to identify the factors influencing the FMD across the glycemic spectrum.Results: We observed that vascular function negatively correlated with blood glucose levels. However, endothelin-1 and vWF derangement was there even in normoglycemic first degree relatives of diabetes (FDRD) and the derangement increased in prediabetes and diabetes. Physiological dysfunction in terms of decreased flow-mediated dilation starts from prediabetes only. VEGF derangement is found only in diabetic individuals.Conclusion: Vascular dysfunction is found even in normoglycemic FDRD and the derangement increased and compounded with the advancement of disease.

Matrix metalloproteinase-9 increases the risk of cognitive impairment in schizophrenia.

PURPOSE OF THE ARTICLE: Synaptic plasticity is known to play role in pathogenesis of schizophrenia. Cognitive impairment is one of the complications of schizophrenia, leading to poor quality of life. Matrix metalloprotease-9 (MMP-9) and neurotrophin-3 (NT-3) are markers of synaptic plasticity, widely investigated in neuropsychiatric disorders. The objective of the study was to investigate the levels of MMP-9 and NT-3 and their association with cognitive impairment in schizophrenia. MATERIAL AND METHODS: 124 schizophrenia patients and 124 controls were enrolled in the study. MMP-9 and NT-3 were estimated in both the groups using ELISA. Cognition was assessed using Addenbrooke cognitive examination-III (ACE-III) and disease severity was assessed using PANSS. RESULTS: MMP-9 (p = .003) and NT -3 (p < .001) were found to be elevated in schizophrenia cases compared to controls. There was significant association of MMP-9 with fluency (r = -0.195, p = .030), language (r = -0.196, p = .029) and total ACE-III scores (r = -0.197, p = .029). Also we observed that MMP-9 increases the risk of cognitive impairment in schizophrenia patients (OR = 2.509, CI= 1.215 - 5.18, p = .013). CONCLUSION: MMP-9 and NT-3 are elevated in schizophrenia. MMP-9 was associated with fluency and language component of cognition and increases the risk of cognitive impairment in schizophrenia.

Relationship of Brain-Derived Neurotrophic Factor with Interleukin-23, Testosterone and Disease Severity in Schizophrenia.

Hormonal imbalance, inflammation and alteration in synaptic plasticity are reported to play a crucial role in the pathogenesis of schizophrenia. The objective of the study was to assess the serum levels of brain derived neurotrophic factor (BDNF) and its association with interleukin-23 (IL-23), testosterone and disease severity in schizophrenia. 40 cases and 40 controls were included in the study. Serum levels of BDNF, IL-23 and testosterone were estimated in all the subjects. Disease severity was assessed using Positive and Negative Syndrome Scale (PANSS). The study was designed in Tertiary care hospital, South India. The results were compared between two groups using Mann-Whitney U test. Spearman Correlation analysis was used to assess the association between biochemical parameters and PANSS. Interleukin-23 and testosterone were significantly increased and BDNF was significantly reduced in schizophrenia cases when compared with controls. BDNF was negatively correlated with IL-23 (r = - 400, p = 0.011), positive symptom subscale (r = - 0.393, p = 0.012), general psychopathology score subscale (r = - 407, p = 0.009) and total symptom subscale (r = - 404, p = 0.010). There was no significant association of IL-23 and testosterone with disease severity in schizophrenia cases. BDNF was reduced in schizophrenia cases and negatively associated with interleukin-23 and disease severity scores.

Over expression of PI3K-AkT reduces apoptosis and increases prostate size in benign prostatic hyperplasia.

INTRODUCTION: Even though the role of the phosphatidylinositol 3-kinase (PI3K)/AKT pathways and apoptosis has been well established in prostate cancer, there are no studies regarding alteration in the gene expression of PI3K/AKT pathway and protein expression of apoptotic components and their association with prostate size in Benign prostatic hyperplasia (BPH). Hence the study was designed to analyze the expression pattern of PI3K/AKT and apoptotic components in patients with BPH. MATERIALS AND METHODS: A total of 27 BPH patients aged between 55 and 75 years were recruited in the study and prostatic tissues were obtained after transurethral resection of the prostate. Gene expression levels of PI3K and AKT were assessed by q-PCR. Apoptotic components like BcL-2, caspase-3, caspase-9, BAD, and p-BAD were analyzed by western blotting and immunohistochemistry. RESULTS: Gene expression of PI3K (p85-A) (p = .02), AKT1 (p < .01) and AKT2 (p < .01), and protein expression of BcL-2 (p < .01) and caspase-9 (p < .01) were significantly increased in BPH patients with larger prostate size compared to smaller prostate size. CONCLUSIONS: Overexpression of PI3K/AKT pathway and BcL-2 were associated with reduced apoptosis and increased prostate size in BPH.

Gene expression of insulin receptor, insulin-like growth factor increases and insulin-like growth factor-binding protein-3 reduces with increase in prostate size in benign prostatic hyperplasia.

INTRODUCTION: Although the role of insulin in the development of benign prostatic hyperplasia (BPH) is well established, there are no studies regarding alteration in the gene expression of components of insulin-signaling pathway and their association with prostate size in BPH. Hence, the study was designed to analyze the gene and protein expression of insulin receptor and its related components in patients with BPH. MATERIALS AND METHODS: Twenty-seven BPH patients aged between 55 and 75 years were recruited in the study and prostatic tissues were obtained after transurethral resection of the prostate. Gene expression levels of Insulin receptor (IR), insulin receptor substrate (IRS), insulin-like growth factor (IGF) and insulin-like growth factor-binding protein-3 (IGFBP-3) were assessed by q-PCR. RESULTS: Insulin receptor (IR-A and B) and insulin-like growth factors (IGF-1 and IGF-2) gene expression were significantly increased and IGFBP-3 gene expression was reduced in BPH patients with larger prostate size. Also, serum insulin was significantly increased and IGFBP-3 was significantly reduced in patients with larger prostate size. CONCLUSION: Increased expression of IR-A, B and IGF-1, 2 genes and reduced IGFBP-3 gene expression was associated with larger prostate size in BPH.

Association of elevated interleukin-17 and angiopoietin-2 with prostate size in benign prostatic hyperplasia.

INTRODUCTION: Inflammation and angiogenesis are known to play a role in the development prostate tumors. The present study was designed to assess the levels of markers of inflammation and angiogenesis like interleukin-17 (IL-17) and angiopoietin-2 (ANGPT2) levels and their association with prostate size in patients with benign prostatic hyperplasia (BPH). MATERIALS AND METHODS: 42 BPH cases and 42 controls were enrolled in the study. IL-17 and ANGPT2 were estimated in both the groups. RESULTS: IL-17 and ANGPT2 were significantly increased in BPH cases when compared with controls. Multivariate analysis showed that ANGPT2 predicts the prostate size in patients with BPH (R2 = 0.203, beta = 0.355, p = 0.028). Linear regression analysis showed that IL-17 was significantly associated with ANGPT2 in BPH cases (R2 = 0.129, beta - 0.359, p = 0.020). CONCLUSIONS: We conclude that IL-17 and ANGPT2 are elevated in BPH cases and ANGPT2 was associated with IL-17 and prostate size.

Relationship between matrix metalloproteinase-9 and oxidative stress in drug-free male schizophrenia: a case control study.

BACKGROUND: Deregulation of synaptic plasticity and oxidative stress are reported to play a crucial role in the pathogenesis of schizophrenia. Matrix metalloproteinase-9 (MMP-9) is an extracellular protease involved in regulation of synaptic plasticity. Malondialdehyde (MDA) is a marker of lipid peroxidation which is elevated in schizophrenia. Earlier studies have reported polymorphism of MMP-9 and its association with schizophrenia. The present study was designed to assess the serum levels of MMP-9, MDA and total antioxidant status (TAS) and their association in schizophrenia. METHODS: A total of 40 cases and 40 controls were included in the study. Serum MMP-9, MDA and TAS were estimated in all the subjects. Disease severity was assessed using Positive and Negative Syndrome Scale (PANSS). RESULTS: MMP-9 and MDA were significantly increased and TAS were significantly reduced in schizophrenia cases compared to controls. MMP-9 was positively correlated with MDA (r=0.353, p=0.025) and negatively correlated with TAS (r=-0.461, p=0.003). TAS was significantly correlated with total (r=0.322, p=0.043) and negative symptom scores (r=0.336, p=0.034). Higher MMP-9 levels were associated with previous exposure to antipsychotics (p=0.032). CONCLUSIONS: MMP-9 and oxidative stress were increased and correlate well with each other in schizophrenia cases. Though total oxidant status showed positive association with disease severity, MMP-9 and MDA were not associated with the severity of the disease.

Carbohydrate Deficient Transferrin and Interleukin-6 as Predictors of Fibrosis in Alcohol Cirrhosis.

The severity of alcoholic cirrhosis depends on the presence of liver inflammation and fibrogenesis. Previous studies have hypothesized that carbohydrate deficient transferrin can be used as marker of liver impairment in alcoholic liver disease patients. The present study was designed to assess whether carbohydrate deficient transferrin is associated with procollagen III peptide and predict fibrosis in alcohol cirrhosis patients. We enrolled 48 patients with alcoholic cirrhosis and 38 healthy controls. Serum carbohydrate deficient transferrin, procollagen III peptide and interleukin-6 levels were estimated in both groups. Serum carbohydrate deficient transferrin, procollagen III peptide and interleukin-6 were significantly increased in alcoholic cirrhosis patients compared to controls. Stepwise regression analysis showed that carbohydrate deficient transferrin (adjusted R(2) = 0.313, ß = 0.362, p = 0.003) and interleukin-6 (adjusted R(2) = 0.194, ß = 0.459, p = 0.001) were positively associated with procollagen III peptide when age, duration and amount of alcohol consumption were considered as covariates. We conclude that elevated carbohydrate deficient transferrin and interleukin-6 act as predictors of fibrosis in alcoholic cirrhosis.

Prognostic Impact of Proteinuria at Manifestation in Adult Nephrotic Syndrome Patients: Insights from a Prospective Cohort Study.

Background and objective Nephrotic syndrome is a significant worldwide health concern impacting millions of people and is marked by heavy proteinuria, edema, and decreased serum levels of albumin. Albuminuria arises from abnormal glomerular permeability and impaired tubular reabsorption, contributing to declining kidney function and a heightened risk of cardiovascular complications. The objective of this study was to investigate the prognostic role of proteinuria on the persistent decline in estimated glomerular filtration rate (eGFR) (<30 ml/minute/1.73m2) during follow-up and the dynamics of remission and relapse in various subtypes of nephrotic syndrome. Methods A total of 134 adult patients, diagnosed with various histopathological categories of nephrotic syndrome, were prospectively studied. Urine protein levels were assessed using the pyrogallol red-molybdate (PRM) method. The Kaplan-Meier analysis and log-rank test were utilized to assess the prognostic role of proteinuria at manifestation on persistent decline in estimated glomerular filtration rate (eGFR) (<30 ml/minute/1.73m2) and to evaluate remission and relapse based on proteinuria levels over an 18-month follow-up period. Results Patients with sub-nephrotic levels of proteinuria at manifestation did not progress to end-stage renal disease on follow-up. Patients with sub-nephrotic levels of albuminuria at manifestation were significantly associated with remission on follow-up. The Kaplan-Meier analysis indicated a significant probability of persistent eGFR decline (p < 0.001) in adult nephrotics with higher levels of albuminuria. Furthermore, patients with sub-nephrotic range proteinuria had earlier remission (p < 0.001) compared to those with relapse (p = 0.001) during the follow-up, as demonstrated by log-rank tests. Conclusion This study highlights that sub-nephrotic albuminuria at manifestation is linked to a reduced risk of renal progression and persistent eGFR decline compared to adult nephrotics with higher levels of albuminuria. Early detection and effective management of proteinuria, are crucial for preventing renal function decline and improving patient outcomes.

Soluble Tumor Necrosis Factor Receptor 2: A Promising Predictive Biomarker for Renal Dysfunction in Membranous Glomerulonephritis.

Background and objective Membranous glomerulonephritis (MGN) is a common cause of adult nephrotic syndrome. Tumor necrosis factor-α (TNF-α) is a proinflammatory cytokine that signals by attaching to TNF receptors. TNF-α plays a pivotal role in the development and progression of different forms of glomerulonephritis. Several research findings suggest that TNF-α receptors (TNFR1 and TNFR2) are predictors of estimated glomerular filtration rate (eGFR) decline. In light of this, this study aimed to explore the relationship between TNFR2 and eGFR, as well as the predictive role of TNFR2 in eGFR decline in MGN. Methods A total of 50 consecutive patients with a diagnosis of primary MGN based on renal biopsies and clinical workups were included in the study. TNFR2 levels in serum, urine, and gene expression were evaluated at baseline and after three months of follow-up by using enzyme-linked immunosorbent assay (ELISA) kits for TNFR2 (KTE60215, Abbkine, Wuhan, China). Cox regression was employed to determine the predictive significance of TNFR2 in persistent eGFR decline. Additionally, an ROC curve analysis was conducted to assess the prognostic value of TNFR2 in predicting persistent eGFR decline among MGN patients. Results We assessed the levels of inflammatory markers TNF-α and TNFR2, examined their correlation with eGFR and renal injury, and investigated their potential in predicting persistent eGFR. Patients with MGN exhibited elevated levels of TNFR2 in their serum, urine, and gene expression compared to healthy individuals. Additionally, there was a positive correlation between serum TNFR2 and TNF-α, urine protein-creatinine ratio (UPCR), uric acid, and total cholesterol. Conversely, there was a negative correlation with eGFR, serum albumin, and calcium. Serum TNFR2 showed statistical significance in a univariate Cox regression analysis (HR: 1.010, 95% CI: 1.00-1.01, p = 0.045) for predicting a persistent decline in eGFR. However, it did not show significance concerning relapse and remission. An ROC curve was created to assess TNFR2's prognostic potential as a biomarker, demonstrating an AUC of 0.683, with a sensitivity of 68% and specificity of 64%. Conclusions Based on our findings, TNFR2 is a predictive biomarker for eGFR decline in MGN, correlating with renal inflammation and predicting deterioration in renal function. TNFR2 emerges as a promising biomarker for early identification in patients at risk of renal function decline.

Elevated glutathione peroxidase in newly diagnosed hypertension: its relation to insulin resistance.

Several studies have reported that insulin resistance and compensatory hyperinsulinemia often coexist with hypertension. Increased activity of glutathione peroxidase has been reported in patients with essential hypertension. Recently, overexpression of glutathione peroxidase has also been linked to the etiology of insulin resistance. The aim of this study was to determine the possible relation between the activity of glutathione peroxidase and insulin resistance status in essential hypertensive patients. A case-control study was performed on 35 hypertensive patients and 30 control subjects. The levels of insulin and insulin resistance as measured by the homeostasis model assessment insulin resistance index (HOMA-IR) and glutathione peroxidase were significantly increased in hypertensive patients compared with control subjects. In this study, a direct association was observed between glutathione peroxidase with HOMA-IR and insulin levels in essential hypertensive subjects. In conclusion, our results suggest that increased glutathione peroxidase can be one of the detrimental factors in contributing to insulin resistance in essential hypertensive subjects.

Association of hyperglycaemia and hyperlipidaemia with cognitive dysfunction in schizophrenia spectrum disorder.

The objective of the study was to investigate the association of blood glucose and lipid profile parameters with cognitive impairment in schizophrenia. A total of 200 schizophrenia patients and 169 controls were enrolled in the study. Blood glucose and lipid profile were estimated in all the subjects. Cognition was assessed using Addenbrooke cognitive examination-III (ACE-III). Fasting glucose (p ≤ .001) and triacylglycerol (p = .018) were increased and HDL-Cholesterol (p ≤ .001), was reduced in schizophrenia. Glucose (r = -0.158, p = .026), total cholesterol (r = -0.249, p = .0001) and triacylglycerol (r = -0.168, p = .018) was negatively correlated with total ACE III score. Triacylglycerol (p = .041) was elevated in cases with mild cognitive impairment. Plasma glucose, total cholesterol and triacylglycerol were associated with various cognitive domains suggesting that hyperglycaemia and hyperlipidaemia might increase the risk of cognitive impairment in schizophrenia.

Neurotrophin-3 gene polymorphism in schizophrenia and its relation with diseases severity and cognitive dysfunction.

Objectives: Synaptic plasticity markers are known to alter in schizophrenia. The objective of the study was to investigate the genotype and allele frequency of neurotrophin-3 (NT-3) gene polymorphism (rs6489630, rs6332, and rs11063714) and plasma NT-3 levels in schizophrenia and their relation with cognitive status. Materials and Methods: The study was conducted on 216 Schizophrenia patients and 216 controls. Single-nucleotide polymorphism (SNP) of NT-3 and its plasma levels were assessed in both groups. Cognitive status was evaluated using Addenbrooke Cognitive examination-III scores. Results: The rs6489630 polymorphism was found to be significantly associated with the severity of schizophrenia (P = 0.004). The CT genotype (P = 0.02, OR = 1.631 [1.10-2.43]) and minor allele T (P = 0.004, OR = 1.58 [1.16-2.16]) of rs6489630 conferred an increased susceptibility to develop schizophrenia. The rs6332 variant was found to affect cognitive status significantly in schizophrenia (P = 0.040), and memory dysfunction was seen in individuals with AG (P < 0.01) and AA variant (P = 0.03) of rs6332. Conclusion: We conclude that SNPs of NT-3 enhance the risk of schizophrenia and are related to cognitive dysfunction.

Comparison of cardiac autonomic function across complete glycaemic spectrum.

OBJECTIVES: Autonomic imbalance is attributed as key mechanism altering metabolic regulation in diabetes mellitus. In view of controversial reports on autonomic function in FDRD and prediabetes, we aimed to assess and compare the autonomic function across the complete glycaemic spectrum in Indian population. METHODS: Short term heart rate variability and cardiac autonomic reactivity tests - blood pressure and heart rate response to orthostatic tolerance and deep breathing exercise, and diastolic response to isometric handgrip exercise were recorded in normoglycemic apparently healthy individual, normoglycemic first degree relatives of diabetes, prediabetes and diabetes individuals. RESULTS: Resting heart rate is significantly higher in FDRD, prediabetes and diabetes as compared to controls (control < FDRD = prediabetes = diabetes). Total power, LF power (control < FDRD < prediabetes = diabetes) and HF power (control < FDRD < prediabetes < diabetes) decreased along the glycaemic spectrum. Time-domain variables of HRV (SDNN, RMSSD, NN50, pNN50) were reduced as we move along the glycaemic spectrum (control < FDRD < prediabetes = diabetes). Cardiac autonomic function reactivity parameters such as 30:15 ratio and E:I ratio are decreased in prediabetes and diabetes group as compared to control and FDRD group (control = FDRD < prediabetes = diabetes). Diastolic response to isometric hand grip increases along the glycaemic spectrum starting from FDRD (control < FDRD < prediabetes = diabetes). CONCLUSIONS: Autonomic dysfunction is observed even in first degree relatives of diabetes. Autonomic dysfunction increases as we move along the glycaemic spectrum (control < FDRD < prediabetes < diabetes).

Assessment of metabolic syndrome in infertile women with polycystic ovary syndrome in a rural population of South India: A cross-sectional study.

Background: Polycystic ovary syndrome (PCOS) is known to be associated with metabolic syndrome (MS). It is characterised by insulin resistance, hyperinsulinemia, dyslipidemia, obesity and hypertension. Data related to MS in infertile women with PCOS are limited in Indian populations. Objective: This study aims to compare the prevalence of MS in infertile women with and without PCOS in a rural population in South India. Materials and Methods: 130 women with PCOS and 130 women without PCOS were enrolled in this cross-sectional study. A detailed history was taken and a physical examination was done for all women. Anthropometric parameters, a glucose tolerance test, fasting glucose / insulin levels, trigylcerides, high-density lipoprotein cholesterol and blood pressure were assessed in all participants. The International Diabetes Federation criteria were applied for assessment of MS. Results: MS was more prevalent in infertile women with PCOS (42.3%) compared to women without PCOS (19.3%). 56.9% of women with PCOS had low high-density lipoprotein cholesterol levels, 46.2% had high triglycerides, 71.5% had a high waist circumference, 31.5% had high blood pressure and 37.7% had high blood glucose levels. 26.0% of the women with PCOS had a healthy weight, and MS was seen in 6.9% of these women. Conclusion: The prevalence of MS was higher in women with PCOS in comparison to women without PCOS. Among the women with PCOS, the prevalence of MS increased with age ( > 27 yr), body mass index and waist circumference (71.5%), and even healthy women with PCOS contributed to 7% of MS. Hence it becomes necessary to screen all women with PCOS for metabolic profile risk factors at young age itself to prevent long term cardiovascular complications.

Matrixmetalloproteinase-9 gene polymorphism (rs 17576) increases the risk of depressive symptoms in bipolar disorder.

Objectives: Plasticity of neural synapses is known to be involved in the complications in bipolar disorder (BD) patients. Matrix metalloproteinases (MMPs) play a role in synaptic plasticity and memory. Even though elevated MMP-9 levels are reported in neuropsychiatric disorders, there is limited data about MMP-9 gene polymorphism in BD. The objectives of the study was to investigate genotype frequency and allele frequency of MMP-9 genetic variant (rs 17576) in BD and its association with disease severity. Materials and Methods: Eighty BD cases and 80 controls were recruited in the study. MMP-9 genotyping and allele frequency and plasma MMP-9 levels were analyzed in both the groups. Hamilton depression rating scale and Young's Mania Rating Scale (YMRS) were used to evaluate severity of BD. Results: The genotype and minor allele (G allele) frequency were not significant between BD and controls. MMP-9 levels were significantly increased in BD patients with AG (P < 0.001) and GG (P = 0.022) genotypes compared to controls. BD patients with GG genotype (P = 0.038, OR: 3.26 (1.16-9.09), and G (mutant) allele (P = 0.013, OR 2.03(1.18-3.48) confer increased risk of depressive symptoms. MMP-9 was positively correlated with YMRS scale (r = 0.227, P = 0.043) in BD. Conclusion: MMP-9 gene polymorphism (rs 17576) is linked with depressive symptoms in BD.