No presente trabalho, objetivou-se avaliar a época de colheita e a qualidade fisiológica de sementes de coentro produzidas no Norte de Minas Gerais. A primeira época de colheita das sementes foi realizada aos 15 dias após o florescimento pleno, quando aproximadamente 50% das plantas apresentavam flores. As demais colheitas foram realizadas de 7 em 7 dias, até as sementes atingirem 14,0% de umidade, fato que ocorreu na 6ª colheita. Imediatamente após cada colheita, as sementes foram avaliadas quanto ao teor de água, à germinação e ao vigor (testes de primeira contagem, emergência de plântulas e índice de velocidade de emergência). A maturidade fisiológica das sementes de coentro, cultivar Verdão, ocorre entre 42 a 44 dias após o florescimento, quando as sementes apresentam umidade em torno de 28,0%, podendo a colheita ser realizada até 50 dias após o florescimento, quando as sementes apresentavam 14,0% de umidade.

The present study aimed to evaluate the harvest season and physiological quality of coriander seeds produced in the North of Minas Gerais. The first season of harvest of the seeds was performed 15 days after full bloom, when approximately 50% of plants had flowers. The other crops were carried out 7 in 7 days, until the seeds reach 14,0% moisture, a fact that occurred in the 6th harvest. Immediately after each harvest, the seeds were evaluated for water content, germination and vigor tests (first count, seedling emergence and emergence speed index). The physiological maturity of coriander seeds, cultivate Verdão, occurs between 42 to 44 days after flowering, when the seeds had humidity around 28,0% at physiological maturity, the harvest may be held until 50 days after flowering, when seeds had 14,0% humidity.

Fifty-seven type 2 diabetic patients with metabolic syndrome and on insulin were assessed by a paired analysis before and 6 months after addition of metformin as combination therapy to evaluate the impact of the association on glycemic control, blood pressure, and lipid profile. This was a historical cohort study in which the files of type 2 diabetic patients with metabolic syndrome on insulin were reviewed. The body mass index (BMI), waist circumference, lipid profile, A1C level, fasting blood glucose level, daily dose of NPH insulin, systolic blood pressure, and diastolic blood pressure were assessed in each patient before the start of metformin and 6 months after the initiation of combination therapy. Glycemic control significantly improved (P < 0.001) after the addition of metformin (1404.4 ± 565.5 mg/day), with 14% of the 57 patients reaching A1C levels up to 7%, and 53% reaching values up to 8%. There was a statistically significant reduction (P < 0.05) of total cholesterol (229.0 ± 29.5 to 214.2 ± 25.0 mg/dL), BMI (30.7 ± 5.4 to 29.0 ± 4.0 kg/m²), waist circumference (124.6 ± 11.7 to 117.3 ± 9.3 cm), and daily necessity of insulin. The reduction of total cholesterol occurred independently of the reductions of A1C (9.65 ± 1.03 to 8.18 ± 1.01%) and BMI and the reduction of BMI and WC did not interfere with the improvement of A1C. In conclusion, our study showed the efficacy of the administration of metformin and insulin simultaneously without negative effects. No changes were detected in HDL-cholesterol or blood pressure.

Pancreatic ß cell function and insulin sensitivity, analyzed by the homeostasis model assessment, before and after 24 weeks of insulin therapy were studied and correlated with the presence of autoantibodies against ß cells (islet cell and anti-glutamic acid decarboxylase antibodies), in a group of 18 Brazilian lean adult non-insulin-dependent diabetes mellitus (NIDDM) patients with oral hypoglycemic agent failure (OHAF). Median fasting plasma glucose before and after insulin treatment was 19.1 and 8.5 mmol/l, respectively (P < 0.001); median HbA1c was 11.7% before vs 7.2% after insulin treatment (P < 0.001). Forty-four percent of the patients were positive (Ab+) to at least one autoantibody. Fasting C-peptide levels were lower in Ab+ than Ab- patients, both before (Ab+: 0.16 ± 0.09 vs Ab-: 0.41 ± 0.35 nmol/l, P < 0.003) and after insulin treatment (Ab+: 0.22 ± 0.13 vs Ab-: 0.44 ± 0.24 nmol/l, P < 0.03). Improvement of Hß was seen in Ab- (median before: 7.3 vs after insulin therapy: 33.4%, P = 0.003) but not in Ab+ patients (median before: 6.6 vs after insulin therapy: 20.9%). These results show that the OHAF observed in the 18 NIDDM patients studied was due mainly to two major causes: autoantibodies and ß cell desensitization. Autoantibodies against ß cells could account for 44% of OHAF, but Ab- patients may still present ß cell function recovery, mainly after a period of ß cell rest with insulin therapy. However, the effects of ß cell function recovery on the restoration of the response to oral hypoglycemic agents need to be determined.