Objective To prepare nifedipine( NF)sustained-release pellet tablets,and study of its release behavior in vitro. Methods Soluplus was selected as a carrier to prepare solid dispersion of NF by hot melt extrusion technique( HME), and the ratio of the drug to carrier was 1:1. The samples were validated as the solid dispersion by differential scanning calorimetry(DSC). Extrusion-spheronization technique was introduced to prepare NF pellets and EudragitRS 30D was used as the coating material. The NF sustained-release tablets were prepared by direct compression of the coated pellets and suitable excipients. Results The release data in vitro proved that the drug release from the tablets was steady and complete over 24 hours. Conclusion The release of NF from sustained-release tablets is slow and steady. The method is easy to operate. The in vitro drug release pattern follows first-order kinetics.

Objective To investigate the risk factors for early neurological deterioration (END) in patients with ischemic stroke. Methods The consecutive patients with new acute ischemic stroke within 24 h were enrol ed. They were divided into either an END or a non-END group. Their relevant medical history, baseline clinical data, imaging examinations and laboratory test results in both groups were compared. Results A total of 95 patients with acute ischemic stroke were enrol ed, including 32 in the END group and 63 in the non-END group. There were significant differences in the proportion of patients in diabetes mel itus (χ2 =6. 081, P=0. 014), baseline National Institutes of Health Stroke Scale (NIHSS) score >15 (χ2 =9. 851, P=0. 002), baseline infarct volume >30 cm3 (χ2 =10. 815, P=0. 001), and fever (χ2 =6. 642, P=0. 010), as wel as the fasting glucose (t=2. 632, P=0. 010), homocysteine (t =2. 997, P=0. 003), C-reactive protein (t=2. 349, P=0. 021), baseline NIHSS (Z=497. 5, P=0. 001), and baseline infarct volume (Z=544. 5, P<0. 001) between the 2 groups. Furthermore, there were significant differences in the proportions of patients in large artery atherosclerotic stroke (χ2 =24. 539, P<0. 001 ) and smal arterial occlusive stroke (χ2 = 27. 913, P< 0. 001 ) in the TOAST classification, as wel as the total anterior circulation stroke (χ2 =7. 578, P<0. 006) and partial anterior circulation stroke (χ2 =4. 818, P<0. 028) in the OSCP classification. Multivariate logistic regression analysis showed that fasting glucose >6. 0 mmol/L (odds ratio [OR] 6. 951, 95%confidence interval [CI] 2. 159-22. 348; P=0. 001), homocysteine >15 μmol/L (OR 3. 301, 95% CI 1. 028-10. 595; P=0. 045), NIHSS score >15 (OR 4. 174, 95% CI 1. 772-14. 870;P=0. 028), infarct volume >30 cm3 (OR 4. 996, 95% CI 1. 334-18. 717; P=0. 017), and fever (OR 4. 528, 95% CI 1. 334-15. 372;P=0. 015) were the independent risk factors for occurring END in patients with acute ischemic stroke. Conclusions The baseline glucose, NIHSS score, infarct volume, homocysteine, and increased body temperature are the independent risk factors for occurring EDN in patients with acute ischemic stroke.

As a potent anticoagulant, leech a traditional Chinese medicine, has become increasing topics. Hirudin, which is the primary effective component in leech, is a specific and efficient inhibitor of thrombin, mainly used in prevention and treatment of thrombus on the clinic practice. However, there is still no accurate and convenient method reported about the determination of it's biological activity. This paper reported a method for the determination of the biological activity the of extract from hirudo. The extra thrombin, which was not inhibited by hirudin in the extract from hirudo, reacted with N-benzoyl-L-arginine ethyl ester and was determined. The biological activity of the hirudo extract was determined, indirectly. The linear of calibration curve and accuracy were both perfect, the method was accurate and reliable.
Animals ; Arginine ; analogs & derivatives ; analysis ; Biological Factors ; analysis ; isolation & purification ; pharmacology ; Enzyme Assays ; methods ; Enzyme Inhibitors ; analysis ; isolation & purification ; pharmacology ; Hirudins ; analysis ; isolation & purification ; pharmacology ; Hirudo medicinalis ; chemistry ; Thrombin ; analysis ; antagonists & inhibitors

Cryptogenic stroke refers to ischemic stroke that is not clear to the cause of the disease through routine examinations. With the development of medical technology, studies have found that most cryptogenic stroke is caused by embolism.Therefore,the concept of embolic stroke of undetermined source (ESUS) is proposed. The main causes of ESUS include subclinical atrial fibrillation, patent foramen ovale, aortic arch atherosclerotic plaque, non-stenotic complex carotid atherosclerotic plaques, and tumor-related embolism, etc. This article reviews the etiology and secondary prevention of ESUS.

Objective:To explore the correlation between the expression of signaling lymphocyte activation molecule family 6 (SLAMF6) on peripheral blood CD8 +T cells and perforin and granzyme B and the clinical significance in patients with newly diagnosed severe aplastic anemia(SAA). Methods:The indicators of blood routine and bone marrow and peripheral blood samples of 32 newly diagnosed SAA patients admitted to Henan Provincial People′s Hospital from January 2016 to June 2019 were collected for retrospective analysis. Flow cytometry was used to detect the expression of SLAMF6, perforin and granzyme B on samples CD8 +T cell before therapy and 6 months after therapy (11 cases received transplantation, 21 cases received immunosuppressive therapy [IST]). Spearman correlation analysis was performed to determine the association between clinical indicators and laboratory test results. The expression of SLAMF6, perforin and granzyme B was also detected in 10 healthy people (normal group) and 13 myelodysplastic syndromes/paroxysmal nocturnal hemoglobinuria (MDS/PNH) patients (MDS/PNH group). Results:(1) At diagnosis: the expression of SLAMF6 was significantly lower in the SAA group than that in the normal group and the MDS/PNH group ([56.40±6.37]% vs [84.34±5.81]% and [82.24±4.98]% (both P<0.001]). The expression of perforin was significantly higher in the SAA group (32.73±8.46) than that in the normal control group (23.75%±5.10%), and the MDS/PNH group (26.12%±5.53%) (both P<0.05). The expression of granzyme B was also significantly higher in the SAA group (36.23%±7.94%) than that in the normal control group (21.67%±5.05%) and the MDS/PNH group (21.79%±5.10%) (both P<0.001). The expression of SLAMF6 was positively correlated with the hemoglobin ( r=0.804), and reticulocyte absolute values ( r=0.656) in peripheral blood, percentage of granulocytes ( r=0.643) and erythrocytes ( r=0.622) in bone marrow of SAA patients (all P<0.05). Expression of SLAMF6 was negatively correlated with perforin ( r=-0.792) and granzyme B ( r=-0.908) on CD8 +T cells in patients with SAA (both P<0.001). (2) After treatment: the expression of SLAMF6 in peripheral blood CD8 +T cells of 30 surviving patients was higher than pre-treatment ([79.19±12.69]% vs [56.40±6.37]%, P<0.001). The expressions of perforin and granzyme B were lower than pre-treatment level (both P<0.05). The expression of SLAMF6 on CD8 +T cells in 11 transplanted patients was higher than before transplantation ([86.54±3.75]% vs [56.40±7.35]%, P<0.001). The expressions of perforin and granzyme B were lower than before transplantation (both P<0.05). The expression of SLAMF6 on CD8 +T cells in 12 IST-respond patients was higher than that before treatment, while the perforin and granzyme B levels were lower than pre-treatment (all P<0.05). The post-treatment expressions of SLAMF6, perforin and granzyme B were similar as before treatment levels in 7 IST-unrespond patients (all P>0.05). Conclusion:SLAMF6 is significantly down-regulated on CD8 +T cells in newly diagnosed SAA, negatively correlated with the effective factors of CD8 +T cells, which might participate in the immune regulatory of CD8 +T cells as a negative regulatory factor in patients with SAA. The SLAMF6 is significantly up-regulated after hematopoietic recovery, while there is no significant change in treatment-unrespond patients, which could thus serve as an useful diagnostic and therapeutic index of patients with SAA.

Traditional Chinese medicine (TCM) formulas have attracted increasing attention worldwide in the past few years for treating complex disease including rheumatoid arthritis. However, their mechanisms are complex and remain unclear. Guan-Jie-Kang (GJK), a prescription modified from "Wu Tou Decoction," was found to significantly relieve arthritis symptoms in rats with adjuvant-induced arthritis after 30-day treatment, especially in the 24 g/kg/day group. By analyzing 1749 targets related to 358 compounds in the five herbs of GJK, we identified the possible anti-arthritis pathways of GJK, including the calcium signaling and metabolic pathways. Bone damage levels were assessed by micro-computed tomography, and greater bone protective effect was observed with GJK treatment than with methotrexate. Receptor activator of nuclear factor κB ligand (RANKL)-RANK signaling, which is related to calcium signaling, was significantly regulated by GJK. Moreover, a target metabolomics assay of serum was conducted; 17 metabolic biomarkers showed significant correlations with treatment. An integrated pathway analysis revealed that pyruvate metabolism, purine metabolism, and glycolysis metabolism were significantly associated with the effects of GJK in arthritis treatment. Thus, this study establishes a new omics analytical method integrated with bioinformatics analysis for elucidating the multi-pathway mechanisms of TCM.