Tuberculosis-diabetes screening: how well are we doing? A mixed-methods study from North India.

SETTING: Public health care facilities in Sonipat District, Haryana State, India. OBJECTIVES: To assess 1) the proportion of tuberculosis (TB) patients screened for diabetes mellitus (DM) and vice versa, 2) factors associated with screening, and 3) the enablers, barriers and solutions related to screening. DESIGN: A mixed-methods study with quantitative (cohort study involving record reviews of patients registered between November 2016 and April 2017) and qualitative (interviews of patients, health care providers [HCPs] and key district-level staff) components. RESULTS: Screening for TB among DM patients was not implemented, despite documents indicating that it had been. Of 562 TB patients, only 137 (24%) were screened for DM. TB patients registered at tertiary and secondary health centres were more likely to be screened than primary health centres. Low patient awareness, poor knowledge of guidelines among HCPs, lack of staff and inadequate training were barriers to screening. Enablers were the positive attitude of HCPs and programme staff. The key solutions suggested were to improve awareness of HCPs and patients regarding the need for screening, training of HCPs and wider availability of DM testing facilities. CONCLUSION: The implementation of bidirectional screening was poor. Adequate staffing, regular training, continuous laboratory supplies for DM diagnosis and widespread publicity should be ensured.

Neurophysiological alterations following fluvalinate administration in mice.

Median lethal dose (LD50) of fluvalinate (Marvik 25EC) was 105 (94.6-116.5 mg/kg, ip) in albino mice. Gross observable signs were dose dependent and indicative of central and peripheral nervous system stimulation. Fluvalinate, at 10.5 and 21.0 mg/kg, ip doses in mice, facilitated maximal electroshock seizures, reduced reaction time in analgesic test and enhanced duration of ether anaesthesia. Acute and subacute (7 days) treatment at lower and higher doses enhanced pentobarbitone sleeping time. Acute and subacute treatment (7 days) with phenobarbitone (50 mg/kg, ip) prior to fluvalinate enhanced toxicity of fluvalinate.

Disposition of norepinephrine and epinephrine in jejunum of WLH chicken.

Disposition of (-)-norepinephrine and (-)-epinephrine in jejunum of WLH chicken was studied using oil-immersion technique. The relative rate of different routes of disposition of catecholamines was in the following order: for (-)-NE COMT greater than or equal to MAO greater than or equal to U2 greater than U1, for (-)-Epi U2 greater than or equal to COMT greater than MAO greater than U1. The role of enzymatic degradation is almost equal to that of uptake processes for (-)-Epi, but it was greater for (-)-NE.

Immunotoxic effects of imidacloprid following 28 days of oral exposure in BALB/c mice.

Imidacloprid, a neonicotinoid insecticide has been in use worldwide for several years in agriculture and veterinary medicine. It is possible that residue of this compound may be recycled in the food chain and thus information regarding effects from potential exposure to it is warranted. The objective of the present study was to evaluate immunotoxic effects of imidacloprid in female BALB/c mice. Imidacloprid was administered orally daily at 10, 5, or 2.5mg/kg over 28 days. Specific parameters of humoral and cellular immune response including hemagglutinating antibody (HA) titer to sheep red blood cells (SRBC; T-dependent antigen), delayed type hypersensitivity (DTH) response to SRBC, and T-lymphocyte proliferation in response to phytohemagglutinin (PHA) were evaluated. The results showed that imidacloprid at high dose, specifically suppressed cell-mediated immune response as was evident from decreased DTH response and decreased stimulation index of T-lymphocytes to PHA. At this dose, there were also prominent histopathological alterations in spleen and liver. Histopathological analysis of footpad sections of mice revealed dose-related suppression of DTH response. Imidacloprid at low dose of 2.5mg/kg/day did not produce any significant alterations in cellular and humoral immune response and it seemed to be an appropriate dose for assessment of 'no observable adverse effects level' for immunotoxicity in BALB/c mice. The results also indicated that imidacloprid has immunosuppressive effects at doses >5mg/kg, which could potentially be attributed to direct cytotoxic effects of IMD against T cells (particularly TH cells) and that long-term exposure could be detrimental to the immune system.

Studies on biochemical changes in subacute thiodicarb toxicity in rats.

Effect of thiodicarb was investigated on various biochemical parameters and blood enzymes in adult male Wistar rats following its intraperitoneal administration at rates of 2.9 and 5.8 mg/kg daily for 28 days. Rats did not exhibit any marked changes in their gross behavioral signs and symptoms. Thiodicarb caused hyperglycemia in rats; however, increase in plasma glucose level was nonsignificant. There was no effect on total plasma protein indicating no severe damage to vital organs and no interference with protein metabolism in rats. Thiodicarb did not cause significant change in blood urea and creatinine levels, thus indicating to have no toxic effect on kidneys in rats. It did not affect aspartate aminotransferase (AST) level except a significant increase in AST level only on 7th day of treatment. There was an increase in the levels of alanine aminotransferase (ALT), but this trend reversed on 14th and 28th day. Thiodicarb did not alter significantly the levels of alkaline phosphatase in rats. It caused inhibition of plasma and brain acetylcholinesterase (AChE) in rats throughout the entire period of 28 days of treatment, which was dose-dependent. The findings of this investigation indicated that thiodicarb did not effect or alter much the various biochemical profiles except inhibiting AChE following i.p. administration up to 28 days in adult male rats.

Pharmacokinetics and urinary excretion of sulphadimidine in buffalo calves.

Pharmacokinetics and urinary excretion of sulphadimidine (SDI) were determined in buffalo calves following single oral administration (150 mg/kg). The plasma levels of free sulphadimidine were above minimum effective therapeutic concentration (> 40 micrograms/ml) between 4 and 12 h and the N4-acetylated form of the drug was in the range of 7.2-19.3%. Kinetic evaluation of plasma levels was performed using a two-compartment open model. The absorption and elimination half-lives of SDI were 3.01 and 11.94 h, respectively. Based on this study, an optimal dosage regimen of sulphadimidine in buffalo calves would be 100 mg/kg, followed by 50 mg/kg at 12 h intervals. Sulphadimidine was mainly excreted in the urine as free amine. The percentage of N4-acetyl sulphadimidine in urine was comparatively higher than in plasma.