Objective:To evaluate the clinical efficacy of Sini-Jia-Huanglian Decoction on chronic heart failure (CHF) with qi deficiency and blood stasis syndrome. Methods:A total of 100 patients with CHF and qi deficiency and blood stasis syndrome in Handan Mingren hospital from January 2018 to June 2019 who met the inclusion criteria were divided into two groups according to the random number table method, 50 cases in each group. The control group was treated with conventional western medicine therapy, and the treatment group was treated with Sini-Jia-Huanglian Decoction on the basis of the control group. Both groups were treated for 30 days. TCM syndrome score was performed before and after treatment. The level of N-terminal-pro-B-type natriuretic peptide (NT-proBNP) was detected by radioimmunoassay. The levels of peptide and galectin 3 (Gal-3) were detected by ELISA. The exercise tolerance was measured by 6-minute walking test, the clinical efficacy was tevaluated. Results:The total effective rate of the treatment group was 92.0% (46/50), and the control group was 76.0% (38/50), there was significant difference between the two groups ( χ2=4.762, P=0.029). After treatment, the scores of shortness of breath, palpitation, dyspnea, dizziness, chest pain and total scores in the treatment group were significantly lower than those in the control group ( t values were 4.257, 8.493, 8.211, 4.481, 5.500, 6.977, respectively, all Ps<0.01). After treatment, the levels of NT-proBNP (2 349.61 ± 683.50 ng/L vs. 3 026.27 ± 714.35 ng/L, t=4.840), and peptide (12.16 ± 3.43 ng/L vs. 17.52 ± 3.98 ng/L, t=7.214) and Gal-3 (3.01 ± 0.82 μg/L vs. 3.94 ± 0.93 μg/L, t=5.304) in the treatment group were significantly lower than those in the control group ( P<0.01), and the walking distance of 6 minutes (450.66 ± 79.25 m vs. 384.49 ± 70.16 m, t=4.421) was significantly longer than that of the control group ( P<0.01). Conclusions:The Sini-Jia-Huanglian Decoction can improve the heart function and clinical symptoms of CHF patients with qi deficiency and blood stasis syndrome, and improve the clinical efficacy.

Glioma is the most common lethal tumor of the human brain. The median survival of patients with primary World Health Organization grade IV glioma is only 14.6 months. The World Health Organization classification of tumors of the central nervous system categorized gliomas into lower-grade gliomas and glioblastomas. Unlike primary glioblastoma that usually develop de novo in the elderly, secondary glioblastoma enriched with an isocitrate dehydrogenase mutant typically progresses from lower-grade glioma within 5-10 years from the time of diagnosis. Based on various evolutional trajectories brought on by clonal and subclonal alterations, the evolution patterns of glioma vary according to different theories. Some important features distinguish the normal brain from other tissues, e.g., the composition of the microenvironment around the tumor cells, the presence of the blood-brain barrier, and others. The underlying mechanism of glioma recurrence and evolution patterns of glioma are different from those of other types of cancer. Several studies correlated tumor recurrence with tumor heterogeneity and the immune microenvironment. However, the detailed reasons for the progression and recurrence of glioma remain controversial. In this review, we introduce the different mechanisms involved in glioma progression, including tumor heterogeneity, the tumor microenvironment and drug resistance, and their pre-clinical implements in clinical trials. This review aimed to provide new insights into further clinical strategies for the treatment of patients with recurrent and secondary glioma.
Aged ; Brain Neoplasms/genetics* ; Drug Resistance ; Glioblastoma ; Glioma/genetics* ; Humans ; Mutation ; Neoplasm Recurrence, Local/drug therapy* ; Tumor Microenvironment