Ι2-mediated amination/cyclization of ketones with 2-aminopyridines under high-speed ball milling: solvent- and metal-free synthesis of 2,3-substituted imidazo[1,2-a]pyridines and zolimidine.

Under solvent-free high-speed ball milling, an I[Formula: see text]-promoted condensation/cyclization of easily available methyl ketones or 1,3-dicarbonyl compounds with 2-aminopyridines has been developed, which allows the quick assembly of 2,3-substituted imidazo[1,2-a]pyridines (IPs) with broad molecular diversity, including the antiulcer drug zolimidine. The advantages of high yields, good functional group compatibility, short reaction time (within 90 min), free use of heating, solvent and metal, employment of cheap starting materials, and simple work-up procedure make this protocol a very efficient alternative to traditional synthesis of IPs.

[Treatment of hemolytic uremic syndrome after acute stage].

OBJECTIVE: Hemolytic uremic syndrome (HUS) is a common primary disease that can cause acute renal failure in childhood. Renal disease is the most important long-term complication in patients who survived the acute stage of HUS. Use of angiotensin-converting enzyme inhibitors (ACEI) and a restricted protein intake may be beneficial to the patients. However, it is not established whether such patients should be treated with steroids and immunosuppressors. The present study aimed to probe into the benefit of using steroid and immunosuppressor in patients after acute stage of HUS. METHODS: The subjects included 17 patients (aged 9 months to 15 years, 12 males, 5 females) with HUS. Thirteen patients recovered from the acute stage of HUS, and underwent continuative treatment and follow-up. All the patients were treated with ACEI and early restriction of protein intake. Additionally, 2 children manifested as glomerulonephritis, one was treated with triperygium glycosides. Other 11 children who manifested as nephrotic syndrome were treated with prednisone, among them 5 children had no response or had incomplete response to prednisone, for these children short-term high dose cyclophosphamide or methylprednisolone pulse treatment were added; in 3 of the children short-term high dose methylprednisolone treatment was applied additionally for membranoproliferative glomerulonephritis and/or focal segmental glomerulosclerosis and crescentic glomerulonephritis. RESULTS: After follow-up for 2 months to 8 years, 4 patients with milder disease recovered, their blood pressure, renal function and urinalysis became normal, but 1 patient had recurrence. Among 9 patients with severe disease, 6 maintained normal blood pressure, recovered renal function and urinalysis, the other 3 patients failed to comply with treatment protocol and died during the 3rd, 9th and 13th month. The remainder (4 cases) gave up therapy and died on the 27th to 48th days of the course. CONCLUSION: The treatment applied in this study could improve the prognosis of patients after acute phase of HUS evidently by using the steroid and immuno suppressor according to clinical classification and pathological findings. It is recommended that triperygium glycosides is beneficial to children with glomerulonephritis, proteinuria and hematuria after acute stage of HUS. Adjustment of therapeutic schedule based on pathological findings after renal biopsy is helpful. To the patients with progressive renal failure who have no response to the steroid and immunosuppressors, steroid and immunosuppressor should be discontinued and dialysis treatment should be applied. Protocol compliance is also an important factor.

[Study on cellular and serum concentration of calcium and magnesium in peripheral blood cells of cirrhosis].

OBJECTIVES: To study on the changes of intracellular calcium and magnesium in cirrhosis and its clinical significance. METHODS: The calcium and magnesium were determined in serum (SCa, SMg), platelets (PCa, PMg), mononuclear cells (MNCCa, MNCMg), polymorphonuclear cells (PMNCa, PMNMg) and erythrocytes (RCa, RMg) of 50 patients with uncompensative cirrhosis (group A) and of 35 patients with compensative cirrhosis (group B). 35 health persons were the control group. RESULTS: The SCa and SMg of group A were lower significantly than those of both group B and control group. The MNCCa, PMNCa, RCa, PMg, MNCMg, PMNMg, RMg of group A [(4.76+/-1.91) micromol/10(9), (7.56+/-2.88) micromol/10(9), (0.66+/-0.13) mmol/L, (5.53+/-2.25) micromol/10(11), (6.64+/-3.53) micromol/10(9), (10.12+/-4.32) micromol/10(9), (2.02+/-0.76) mmol/L] and those of group B [(5.34+/-2.41) micromol/10(9), (8.32+/-2.34) micromol/10(9), (0.67+/-0.11) mmol/L, (5.55+/-2.67) micromol/10(11), (6.56+/-3.44) micromol/10(9), (10.95+/-4.45) micromol/10(9), (2.21+/-0.74) mmol/L] were lower significantly than those of control group [(6.86+/-2.02) micromol/10(9), (9.89+/-3.23) micromol/10(9), (0.72+/-0.10) mmol/L, (7.43+/-2.78) micromol/10(11), (8.68+/-4.1) micromol/10(9), (13.96+/-5.76) micromol/10(9), (2.74+/-0.92) mmol/L]; t (group A vs. control group)=4.88, 3.48, 2.31, 3.45, 2.46, 3.52, 4.00, 0.01, 0.01, 0.05, 0.01, 0.02, 0.01, 0.01; t (group B vs. control group)=2.87, 2.34, 2.00, 2.89, 2.33, 2.45, 2.65, 0.01, 0.05, 0.05, 0.01, 0.05, 0.02, 0.02. The PCa of the patients with hepatic encephalopathy was higher, the SMg, PMg, MNCMg, PMNMg and RMg were lower than those of the patients without hepatic encephalopathy significantly. The SCa, SMg, PMg, MNCMg, PMNMg and RMg of the patients in Child stage C were lower significantly than those of the patients in Child stage B. There were no significant differences of PCa, MNCCa, PMNCa and RCa between Child stage C and Child stage B. There were no significant differences of SCa, MNCCa, PMNCa and RCa between the patients with and without hepatic encephalopathy. The ratios of PCa/SCa, MNCCa/SCa and PMNCa/SCa of the patients with decreased SMg were lower than those of control group. The SMg, MNCMg, PMNMg and RMg were correlated directly with the level of serum albumin. CONCLUSION: There are calcium and magnesium deficiencies in the patients with uncompensative cirrhosis and compensative cirrhosis, this deficiency aggravates with the severity of the disease. There is relative increase of intracellular calcium. The magnesium deficiency may be one of the reasons for both hepatic encephalopathy and relative increase of intracellular calcium.