Synthesis and characterization of X (X = Ni or Fe) modified BaTiO3 for effective degradation of Reactive Red 120 dye under UV-A light and its biological activity.

For the sustainable advancement of industrial expansion that is environmentally conscious, harmful dyes must be removed from wastewater. Untreated effluents containing colors have the potential to harm the ecosystem and pose major health risks to people, animals, and aquatic life. Here, we have fabricated Ni or Fe modified with BaTiO3 materials and effectively utilized them for Reactive Red 120 (RR 120) dye degradation under UV-A light. The synthesized materials were characterized, and their structural, and photo-physical properties were reported. Phase segregation was not present in the XRD pattern, as evidenced by the absence of secondary phase peaks linked to iron, nickel, or oxides. Low metal ion concentrations may be the cause of this, and the presence of those elements was confirmed by XPS measurements. The Raman spectra of the BaTiO3/Ni and BaTiO3/Fe samples show a widened peak at 500 cm-1, which suggests that Ni or Fe are efficiently loaded onto the BaTiO3. RR 120 dye photodegradation under UV light conditions was effectively catalyzed by BaTiO3/Fe, as evidenced by its superior performance in the UV irradiation technique over both BaTiO3 and BaTiO3/Ni. Compared to bare BaTiO3, both metal-modified materials efficiently degraded the RR 120 dye. Acidic pH facilitated the degradation process, which makes sense given that the heterogeneous photo-Fenton reaction was the mechanism of degradation along with BaTiO3 sensitization. High-acidity sewage can be dangerous and carcinogenic, and conventional biological treatment methods are not appropriate for managing it. In the current investigation, it may be used to treat color effluents with extremely low pH levels. Additionally, the ability of the produced nanocomposites to inhibit the growth of twenty pathogens was examined, along with two fungi, fifteen Gram-negative Bacilli (GNB), one Gram-positive Bacilli (GPB), and two Gram-positive Cocci (GBC).

Serum CRP biomarker detection by using carbon nanotube field-effect transistor (CNT-FET) immunosensor.

C-reactive protein (CRP) is produced by the liver in response to systemic inflammation caused by bacterial infection, trauma and internal organ failures. CRP serves as a potential biomarker in the precise diagnosis of cardiovascular risk, type-2 diabetes, metabolic syndrome, hypertension and various types of cancers. The pathogenic conditions indicated above are diagnosed by an elevated CRP level in the serum. In this study, we successfully fabricated a highly sensitive and selective carbon nanotube field-effect transistor (CNT-FET) immunosensor for the detection of CRP. The CNTs were deposited on the Si/SiO2 surface, between source-drain electrodes, afterwards modified with well-known linker PBASE and then anti-CRP was immobilized. This anti-CRP functionalized CNT-FET immunosensor exhibits a wide dynamic detection range (0.01-1000 µg/mL) CRP detection, rapid response time (2-3 min) and low variation (<3 %) which can be delivered as a low-cost and rapid clinical detection technology for the early diagnosis of coronary heart disease (CHD). For the clinical applications, our sensor was tested using CRP fortified serum samples and sensing performance was validated using enzyme-linked immune-sorbent assay (ELISA). This CNT-FET immunosensor will be helpful in taking over the complex laboratory-based expensive traditional CRP diagnostic procedures practiced in the hospitals.

Correlation Between Maternal Age and Cytokine (IL-6 and TGF-Beta) Levels in Colostrum.

BACKGROUND: Cytokines are small proteins that play an important role in cell signaling, particularly in inflammatory pathways. There are both pro- as well as anti-inflammatory cytokines that regulate this pathway and modulate the immune responses. Advancing maternal age is associated with systemic inflammation. The present study intends to evaluate the effect of advancing maternal age on cytokine (IL-6 and TGF-ß) levels in colostrum, the first breast milk secreted by mothers. METHODOLOGY: A total of 77 term deliveries were enrolled in the study. Colostrum specimens were collected and evaluated for cytokine IL-6 and TGF-ß levels. Colostrum IL-6 and TGF-ß levels were correlated with maternal age and were assessed using the Spearman rank correlation coefficient. Multivariate analysis was done using a linear regression model comprising age, parity, and mode of delivery. RESULTS: Mean colostrum IL-6 and TGF-ß levels were 113.3±73.1 pg/ml and 20.9±23.6 pg/ml, respectively. No significant correlation between maternal age and colostrum IL-6 levels was observed (r=0.137; p=0.314). However, there was a significant positive correlation between maternal age and colostrum TGF-ß levels (r=0.452; p<0.001). CONCLUSIONS: The findings of the study show a significant association between maternal age and colostrum TGF-ß levels. The impact of colostrum cytokine levels on neonatal growth and development in context with advancing maternal age needs to be evaluated.

Severe COVID-19-associated hyperinflammatory syndrome versus classic hemophagocytic lymphohistiocytosis: similarities, differences, and the way forward.

The hyperinflammatory immune response in severe COVID-19 infection shares features with secondary hemophagocytic lymphohistiocytosis (sHLH) in the form of fever, cytopenia, elevated inflammatory markers, and high mortality. There are contrasting opinions regarding utility of HLH 2004 or HScore in the diagnosis of severe COVID-19-related hyperinflammatory syndrome (COVID-HIS). This was a retrospective study of 47 patients of severe COVID-19 infection, suspected to have COVID-HIS and 22 patients of sHLH to other illnesses, to evaluate the diagnostic utility and limitations of HLH 2004 and/or HScore in context to COVID-HIS and to also evaluate the utility of Temple criteria for predicting severity and outcome in COVID-HIS. Clinical findings, hematological, and biochemical parameters along with the predictor of mortality were compared between two groups. Only 6.4% (3/47) of cases fulfilled ≥5/8 HLH 2004 criteria and only 40.52% (19/47) of patients showed HScore >169 in COVID-HIS group. 65.9% (31/47) satisfied the Temple criteria in COVID-HIS as compared with 40.9% (9/22) in the non-COVID group (p = 0.04). Serum ferritin (p = 0.02), lactate dehydrogenase (p = 0.02), direct bilirubin (p = 0.02), and C-reactive protein (p = 0.03) were associated with mortality in COVID-HIS. Both HScore and HLH-2004 criteria perform poorly for identifying COVID-HIS. Presence of bone marrow hemophagocytosis may help to identify about one-third of COVID-HIS missed by the Temple Criteria.

Diagnostic Accuracy of Plasma Cystatin C and Renal Resistive Index for Acute Kidney Injury in Critically Ill Patients: A Prospective Observational Study.

Background: Acute kidney injury (AKI) is a quite common problem in critically ill patients. Serum cystatin C has emerged as a marker of AKI. This study was aimed to evaluate the diagnostic ability of serum Cystatin-C and Renal Resistive Index in prediction of AKI among critically ill patients. Methodology: This prospective observational study was carried out in the department of Medicine, over a period of one year. After informed consent and ethical clearance total 120 critically ill patients suffering from sepsis were enrolled, out of which 70 patients developed AKI while 50 did not develop AKI during treatment in Intensive care unit (ICU). Serum cystatin C was measured on day 1 by particle-enhanced immune nephelometric assay, Renal resistive index (RRI) calculated by ratio of the velocities of arterial perfusion throughout the cardiac phase and glomerular filtration rate was measured on days 1, 3, and 7 respectively. Results: S. cystatin C value was significantly higher(>3times) in AKI patients (14.07±4.8 mcg/ml) as compared to those who did not develop AKI (4.28±3.27 mcg/ml) (p<0.001). After ROC analysis it was found that day1, S. cystatin C, at cut off value of ≥9.29 mcg/ml had diagnostic accuracy 90% with sensitivity 91%, specificity89% and PPV 95.5%. While RRI value on day 7, at cut-off value of ≥0.72, had diagnostic accuracy 98%, sensitivity (98.6%) and specificity (96.7%) for AKI with 98.6% PPV, 96.7% NPV. Conclusion: Serum cystatin C appears to be a promising bio- markers for early diagnosis of AKI in critically ill patients. Whereas, RRI although non-invasive had good diagnostic accuracy but it diagnosed AKI after few days thus diagnosis of kidney injury delayed.

Lipid Profile and Small Dense Low-Density Lipoprotein in Acute Coronary Syndrome Patients: Relationships to Demographic, Clinical, Angiographic, and Therapeutic Variables.

Background: Several lines of evidence have supported small dense low-density lipoproteins (sd-LDL) as a marker of cardiovascular disease. The present study assessed the relationship between lipid profile and sd-LDL levels with demographic, clinical, angiographic, and therapeutic variables in acute coronary syndrome (ACS) patients. Methods: This was a single-centre, prospective, cross-sectional study conducted from September 2014 to September 2015. Patients with a diagnosis of ACS were included in this study. High-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) were determined by direct homogenous assay and sd-LDL levels were calculated using an earlier described equation by Srisawadi et al. Results: A total of 200 patients with a diagnosis of ACS were studied. Males constituted 78% of the population cohort and almost 45% of participants were aged <45 years. Patients aged ≤45 years displayed higher mean sd-LDL levels of 30.40 ± 14.18 mg/dL versus patients aged >45 years with mean sd-LDL levels of 28.01 ± 11.58 mg/dL, but the difference was not statistically significant (p = 0.19). Females also displayed higher mean sd-LDL levels, but the difference also failed to achieve statistical significance (30.95 ± 13.44 mg/dL and 28.54 ± 12.64, respectively; p = 0.185). Diabetics had higher mean sd-LDL levels (33.64 ± 13.01 mg/dL and 28.07 ± 12.60 mg/dL; p = 0.273) whilst smokers had lower mean levels (27.21 ± 12.12 mg/dL and 30.51 ± 13.21 mg/dL, respectively; p = 0.071). However, the ratio of sd-LDL/lb-LDL (large buoyant LDL) was significantly higher in diabetics (0.48 vs. 0.39; p = 0.023). In the angiography cohort (n = 88), single-vessel disease was the most predominant overall while among patients aged >45 years, triple-vessel disease was significantly higher (p = 0.005). Similarly, the sd-LDL levels were 33.12 ± 11.13 mg/dL, 27.68 ± 9.80 mg/dL, and 31.65 ± 15.26 mg/dL among patients with single, double, and triple-vessel disease and did not differ significantly (p = 0.262). Prior statin users had significantly lower mean sd-LDL levels of 24.79 ± 12.23 mg/dL compared to statin-naïve patients with a mean sd-LDL of 30.01 ± 12.79 mg/dL (p = 0.027). Non-HDL levels were also significantly lower in prior statin users (112.83 mg/dL vs. 128.9 mg/dL; p = 0.017). Conclusion: In this cohort of ACS patients, age, sex, diabetes, smoking, and the angiographic severity of coronary artery disease had no significant impact on sd-LDL levels, while prior statin usage led to significantly lower sd-LDL levels. Diabetic patients, however, did have significantly higher sd-LDL/lb-LDL ratios.

Serum Tumor Necrosis Factor-Alpha Levels in Acute Leukemia and Its Prognostic Significance.

Introduction Tumor necrosis factor-alpha (TNF-α) is a pleiotropic cytokine that facilitates malignant cells in immune evasion, survival, and treatment resistance by generating a favorable milieu for them. It is shown to be ectopically produced by malignant/leukemic and immune cells in the tumor microenvironment, providing a tumor-supportive environment and playing an important part in the establishment and progression of malignant cells. It is linked to hyperleukocytosis, high blast count, and poor clinical outcomes in acute leukemia (AL). Considering the varied role and different expression patterns of tumor necrosis factor-alpha in acute leukemia and its clinical relevance, the present study was planned to monitor the level of tumor necrosis factor-alpha in patients with acute leukemia and its correlation with disease outcome. The aim of this study was to monitor the level of tumor necrosis factor-alpha in patients with acute leukemia at the time of diagnosis and after induction chemotherapy. Material and methods The study included cases classified as acute leukemia based on morphological examination, bone marrow analysis, and flow cytometry. In all patients with acute leukemia (n = 90) and controls (n = 10), the serum tumor necrosis factor-alpha level was measured using a Diaclone Human ELISA kit (Diaclone, Besancon, France) (solid phase sandwich ELISA) at diagnosis and after induction chemotherapy. Results Tumor necrosis factor-alpha levels were substantially higher in T-acute lymphoblastic leukemia (T-ALL) cases, followed by acute myeloid leukemia (AML) and B-acute lymphoblastic leukemia (B-ALL), at the time of diagnosis, compared to the control. A significant reduction in serum tumor necrosis factor-alpha level was seen in patients with acute leukemia after induction phase chemotherapy (P < 0.05). Tumor necrosis factor-alpha levels were considerably reduced (P < 0.001) in the majority of acute leukemia cases after the induction phase, while high tumor necrosis factor-alpha levels were positively correlated with incomplete remission status in the remaining cases. Conclusion Tumor necrosis factor-alpha is involved in the progression of acute leukemia and its relapse. High levels of tumor necrosis factor-alpha are linked to leukocytosis, high blast counts, and worse survival in patients with acute leukemia. Monitoring of tumor necrosis factor-alpha may be helpful in patients with acute leukemia in view of available antitumor necrosis factor-alpha therapy.

Bleeding Versus Thrombotic Tendency in Young Children With Beta-Thalassemia Major.

Introduction Bleeding and thrombotic events are known to occur in beta-thalassemia major (BTM) patients and have been attributed to hepatic iron overload associated with multiple blood transfusions. We evaluated hemostatic parameters in children with BTM who had no previous history of bleeding or thrombotic episodes. Materials and Methods Hemostatic parameters including prothrombin time (PT), activated partial thromboplastin time (APTT), platelet aggregation, protein C and S, iron profile, and liver function tests were evaluated in 54 children (median age = 12 months, age range = 4-144 months) with BTM and 15 age and sex-matched controls. Results The mean PT and APTT of patients were significantly higher (P=0.016 and P <.001) than that of controls. Mean protein C, protein S activity and platelet aggregability with adenosine 5-diphosphate (ADP) as an agonist in patients were significantly lower (P <.001, P <.001 and P=0.007, respectively) than that in controls. Mean serum ferritin in BTM children was not significantly elevated to be associated with hepatic dysfunction. Conclusion Deranged hemostatic parameters indicative of bleeding and thrombotic tendencies are observed in BTM children from an early age and may not be solely due to hyperferritinemia-associated hepatic dysfunction. Despite the presence of deranged hemostatic parameters, a state of balance exists between bleeding and thrombosis, and an imbalance may lead to bleeding or thrombotic events at a later age.

Diagnostic significance of serum and salivary lipid levels in oral precancer and oral cancer.

INTRODUCTION: Lipids are one of the major constituents of the cell. Variations in the serum lipids have been considered a cofactor of carcinogenesis, as lipids play a crucial role in cell integrity. Saliva is an ultrafiltrate of plasma and correlates with the serum, which may be used as an alternate method of serum lipid level estimation. The study was conducted to find any correlation between serum and salivary lipid levels and to evaluate the changes in serum and salivary lipid levels in oral precancer and cancer patients. AIMS AND OBJECTIVES: This study aimed to evaluate the changes in serum and salivary lipid levels in oral precancer and cancer patients and to correlate salivary lipid levels with serum lipid levels. MATERIALS AND METHODS: The study was an in vivo study conducted on randomly selected 129 patients with oral cancer and oral precancer. The selected subjects were divided into four groups as Group 1 - healthy control, Group 2 - oral submucous fibrosis, Group 3 - leukoplakia, and Group 4 - oral cancer. Serum and salivary lipid levels were estimated biochemically and statistically analyzed for any correlation with oral precancer and cancer. RESULTS: Lipid level estimation showed no statistically significant difference on comparison of intergroup serum and saliva total cholesterol level and high-density lipoproteins among all four groups, whereas intergroup comparison of serum and saliva triglycerides (TG) levels among the four groups showed a statistically significant difference in saliva TG level. The correlation of serum and salivary lipid levels showed a significant positive correlation. CONCLUSION: In the present study association between serum/salivary lipid levels and oral precancer and oral cancer could not be established. A positive association was there in serum and salivary lipids hence salivary lipid levels may be used as a noninvasive technique for serum lipid level estimation.

Evaluation of Effect of Propranolol on Serum Vascular Endothelial Growth Factor and Tissue Inhibitor of Metalloproteinase-2 Levels in Infantile Hemangioma.

BACKGROUND: Infantile hemangioma is the most common tumor of infancy. Currently, propranolol is a preferred drug for treating hemangioma. The exact mechanism of action of propranolol is not known. In this study, we attempted to assess whether propranolol has any effect on vascular endothelial growth factor (VEGF) and tissue inhibitor of metalloproteinase-2 (TIMP-2) over a period of time, and if it is there, how long it affects it. MATERIALS AND METHODS: Propranolol was administered in the dosage of 2-3 mg/kg. The first serum sample was collected before starting the propranolol treatment. Thereafter, samples were collected at monthly intervals up to a total of six samples. The samples were assessed for TIMP-2 and VEGF using enzyme-linked immunosorbent assay kit. RESULTS: The duration of this study was from June 2016 to November 2017. The total number of patients in this study was 15. Thirteen patients responded to treatment. The mean age of patients was 7.1 months. The mean value of baseline VEGF was 0.234 ± 0.059 and that of TIMP-2 was 1.338 ± 0.679. As compared to baseline value, the P value was statistically not significant in any of sequential values. In category-wise analysis, apart from statistically significant value in the 6th month in excellent category and good response category in the 1st month, all other values did not reveal any significant change in VEGF analysis. The analysis of TIMP-2 revealed a significant change in the levels from Sample 2 to Sample 6 in the excellent response group; however, the levels did not show a specific trend either increasing or decreasing. CONCLUSION: Despite its beneficial action in regression of hemangioma, the exact mechanism is yet to be identified. The exact duration of treatment needs further evaluation.

A case control study on HDL associated PON1 enzyme level in Northern Indian type 2 diabetes mellitus patients.

AIM: To evaluate the serum paraoxonase 1 activity and determine its association with duration in type 2 Diabetes mellitus patients. METHODS: A total of 80 cases from type 2 diabetes mellitus and healthy controls were enrolled in the present case control study. Human serum PON1 concentration was measured by ELISA and western blotting and it activity was determined spectrophotometrically using 4-nitrophenyle acetate. Diagnostic accuracy of serum PON1 to identify type 2 Diabetes mellitus was calculated with ROC analysis. RESULT: Serum concentration of LDL, VLDL, TG, A1C, FBS and TC levels showed significantly higher levels in type 2 diabetes patients as compared to healthy controls, however there were no significant differences found in the level of HDL. Serum PON1 concentration and activity monitored in patients with >1 year diabetes showed higher level (75.1 ±â€¯6.8 ng/mL) as compared to patients with >3 years diabetes (65.24 ±â€¯1.6 ng/mL), its level was further decreased in patients with >5 (53.8 ±â€¯2.6 ng/mL) and >7 years (48.1 ±â€¯2.7 ng/mL) of diabetes. PON1 concentration decreased as the duration of diabetes increased. PON1 level was further decreased due to habits like smoking and alcohol consumption. CONCLUSION: Serum PON1 levels decrease in states of high oxidative stress like metabolic syndrome, obesity, uncontrolled diabetes, and dyslipidemia. It can be used as diagnostic marker for diabetes mellitus along with increased TG, LDL, VLDL and FBG.

Protective effects of lupeol against mancozeb-induced genotoxicity in cultured human lymphocytes.

BACKGROUND: Lup-20(29)-en-3H-ol (Lupeol), a dietary pentacyclic triterpenoid has been shown to possess multiple medicinal activities including anti-inflammatory, anti-oxidant and anti-carcinogenic effects. Mancozeb is a widely used broad-spectrum fungicide with well-known carcinogenic hazards in rodents. PURPOSE: The present study has been designed to investigate the protective effects of lupeol against mancozeb-induced genotoxicity and apoptosis in cultured human lymphocytes (CHLs). METHODS: The genotoxic effect of mancozeb was evaluated by chromosomal aberration and micronucleus assays. The cell cycle kinetics and intracellular reactive oxygen species (ROS) generation was measured by flow cytometry. The levels of anti-oxidant enzymes and lipid peroxidation (LPO) were estimated by enzymatic assays. The localization of p65NF-κB was measured by immunocytochemical analysis. The differential expression of genes associated with genotoxicity was measured by qRT-PCR. RESULTS: Mancozeb exposure (5µg/ml) for 24h caused significant induction of chromosomal aberrations (CAs) and micronuclei (MN) formation in CHLs. Pre-and post-treatment (25 and 50µg/ml) of lupeol for 24h significantly (p<0.05) reduced the frequency of CAs and MN induction, in a dose-dependent manner in mancozeb treated CHLs. Concomitantly, lupeol pre-treatment for 24h significantly increased the levels of anti-oxidant enzymes, superoxide dismutase (SOD) and catalase and decreased ROS generation and LPO. Additionally, lupeol pre-treatment significantly reduced mancozeb-induced apoptosis as shown by Sub-G1 peak analysis and annexin V-PI assay, in a dose dependent manner. Moreover, pre-treatment with lupeol attenuated mancozeb-induced NF-κB activation in CHLs. Furthermore, the results of qRT-PCR showed that lupeol pre-treatment significantly (p<0.05) decreased mancozeb-induced expression of DNA damage (p53, MDM2, COX-2, GADD45α and p21) and increased expression of DNA repair responsive genes (hOGG1 and XRCC1) in CHLs. CONCLUSION: Taken together, our findings suggest that lupeol could attenuate mancozeb-induced oxidative stress, which in turn could inhibit NF-κB activation and thus provide protection against mancozeb-induced genotoxicity and apoptosis. So, lupeol could be used as a potent anti-oxidant regimen against pesticide induced genotoxicity in agricultural farm workers.

Leptin augments protective immune responses in murine macrophages and enhances potential of miltefosine against experimental visceral leishmaniasis.

Adverse side effects and drug resistance issues are the two most important drawbacks which influence the widespread use of existing antileishmanial drugs. Use of immune stimulating agent with standard antileishmanial might be helpful to minimize the toxic effect of drug, shorten the dose regimen and delay the emergence of resistance. In the present study, we explored the in vitro immunomodulatory potential of an immunomodulator, leptin with lower concentration of standard drug, miltefosine. The level of Th1/Th2 cytokines, production of nitric oxide and reactive oxygen species and phagocytic activity was assessed by ELISA, Griess reaction and flow cytometric analysis, respectively. Leptin at a concentration of 15µg/mL showed heightened level of Th1 cytokines and nitric oxide generation from murine macrophages (J-774A.1 cells). Leptin (15µg/mL) also reduces the effective concentration of miltefosine by 2-folds from 7.5µM to 3.7µM. When given in conjunction with lower concentration of miltefosine (4µM), leptin (15µg/mL) significantly (***p<0.001) elevated the level of IL-12 (7.7 fold), TNF-α (8.1 fold) and nitric oxide (6.6 fold) along with markedly (***p<0.001) suppressed level of IL-10 and TGF-ß when compared with untreated infected macrophages. Leptin plus miltefosine also induces the phagocytic ability (**p<0.01) of macrophages in comparison to leptin alone and miltefosine alone treated groups. These finding illustrate that leptin activates host macrophages to generate protective immune response for the successful elimination of Leishmania parasite at lower concentration of miltefosine and has potential for further exploration in experimental animal model of visceral leishmaniasis (VL).

L-Plastin S-glutathionylation promotes reduced binding to ß-actin and affects neutrophil functions.

Posttranslational modifications (PTMs) of cytoskeleton proteins due to oxidative stress associated with several pathological conditions often lead to alterations in cell function. The current study evaluates the effect of nitric oxide (DETA-NO)-induced oxidative stress-related S-glutathionylation of cytoskeleton proteins in human PMNs. By using in vitro and genetic approaches, we showed that S-glutathionylation of L-plastin (LPL) and ß-actin promotes reduced chemotaxis, polarization, bactericidal activity, and phagocytosis. We identified Cys-206, Cys-283, and Cys-460as S-thiolated residues in the ß-actin-binding domain of LPL, where cys-460 had the maximum score. Site-directed mutagenesis of LPL Cys-460 further confirmed the role in the redox regulation of LPL. S-Thiolation diminished binding as well as the bundling activity of LPL. The presence of S-thiolated LPL was detected in neutrophils from both diabetic patients and db/db mice with impaired PMN functions. Thus, enhanced nitroxidative stress may results in LPL S-glutathionylation leading to impaired chemotaxis, polarization, and bactericidal activity of human PMNs, providing a mechanistic basis for their impaired functions in diabetes mellitus.

Factors affecting response to medical management in patients of filarial chyluria: A prospective study.

INTRODUCTION: Filarial chyluria is a common problem in filarial endemic countries. Its management begins with medical therapy but some patients progress to require surgery. The present study aimed to determine factors affecting response to medical management in patients of filarial chyluria. MATERIALS AND METHODS: This prospective study conducted between August 2008 and November 2012, included conservatively managed patients of chyluria. Demographic profile, clinical presentation, treatment history and urinary triglycerides (TGs) and cholesterol levels at baseline were compared between the responders and non-responders. Apart from the clinical grade of chyluria, hematuria was evaluated as an independent risk factor. RESULTS: Out of the 222 patients (mean age, 37.99 ± 13.29 years, 129 males), 31 patients failed to respond while 35 had a recurrence after initial response; the overall success rate being 70.3% at a mean follow-up of 25 months. No difference was observed in demographics, clinical presentation, presence of hematuria, disease duration and mean urinary TGs loss between responders and non-responders. On multivariate analysis, patients with treatment failure were found to have a higher-grade disease (14.3% Grade-I, 36.6% Grades-II and 60% Grade-III), higher number of pretreatment courses (1.59 ± 1.08 vs. 1.02 ± 0.79) and heavier cholesterol (26.54 ± 23.46 vs. 8.81 ± 8.55 mg/dl) loss at baseline compared with responders (P < 0.05). CONCLUSION: Conservative management has a success rate in excess of 70%, not affected by the disease chronicity, previous episodes and recurrent nature. However, higher-grade disease, extensive pre-treatment with drugs and higher urinary cholesterol loss at baseline are the predictors of poor response. Hematuria is not an independent poor risk factor for conservative management.

Mancozeb-induced genotoxicity and apoptosis in cultured human lymphocytes.

AIMS: Mancozeb is a dithiocarbamate fungicide known to be genotoxic and induces tumors in rodents at various sites. There is no report in the literature about its genotoxicity in humans. Here, we investigated the association between mancozeb exposure and induction of genotoxic and proapoptotic changes in cultured human lymphocytes (CHLs). MAIN METHODS: Lymphocytes were isolated from peripheral blood of healthy non-smoking donors. Induction of micronuclei and chromosomal aberrations was recorded both by conventional and flow cytometric methods. Annexin-V FITC was used for the differentiation of apoptotic and necrotic cells by flow cytometry. KEY FINDINGS: Mancozeb exposure (0.5, 2 and 5 µg/ml) to CHLs leads to significant induction in the frequency of chromosomal aberrations (CAs) and micronuclei (MN), in a dose-dependent manner. Concomitantly, pro-oxidant potential of mancozeb was also recorded, by increase in the levels of reactive oxygen species (ROS) generation. Our results demonstrated that ROS plays a critical role in the initiation of mancozeb induced apoptosis in CHLs through two ways, primarily through mitochondria-mediated pathway including induction of ROS, decrease in mitochondrial membrane potential (ΔΨm), along with cytochrome c release from mitochondria, and activation of the caspase cascade. The other pathway includes increase in ROS, which resulted in activation of NF-κB, expression of FasL and triggered FasL-dependent pathway, which also involves caspase-8. Therefore, exposure to mancozeb can lead to induction of apoptosis in CHLs through both mechanisms. SIGNIFICANCE: The results of study confirm that mancozeb exposure can induce genotoxicity and apoptosis in CHLs, thus pose a potential risk to exposed human population.

Back from the brink: a personal account of the illness Guillain-Barre Syndrome

Dr. Wahid Ali has spent a long and useful life, almost two decades of which were dedicated to public service. This book is a further contribution to that life of public service in that it gives a detailed account of the symptoms and effects of Guillain-Barre Syndrome, a disease which so few of us know about. This account is also, sadly, a reflection of the inadequacy of health care in our society. That Dr. Ali was able to emerge alive and well after the attack seems surely the result of his position in the society, and his ability to afford health care at the best institutions. He makes constant reference to this inequality. This autobiography demonstrates quite clearly the close link between the spirit and the physical being. It shows how positive thinking can affect the physical well-being of our human persons. The book recommends itself as a serious reflection of the condition of our lives in this place as we seek to create a new culture out of the diverse elements of this New World (Dr. Brinsley Samaroo-back cover)