The report quality of randomized controlled trials (RCTs) of moxibustion for knee osteoarthritis (KOA) in China was evaluated by Consolidated Standards for Reporting of Trials (CONSORT) and Standards for Reporting Interventions in Controlled Trials of Moxibustion (STRICTOM). Computer and manual retrieval was used. Four databases of China National Knowledge Infrastructure (CNKD, China Biomedicine (CBM), VIP and WNFANG were searched in combination with manual retrieval for relevant journals to screen the literature that: met the inclusive criteria, and CONSORT and STRICTOM were used to assess the report quality. A total of 52 RCTs were included. It was found that unclear description of random methods, low use of blind methods, no allocation concealment, no sample size calculation, no intention-to-treat analysis,inadequate report of moxibustion details and no mention of practitioners background existed in the majority of the RCTs. Although the quality of RCTs of moxibustion for KOA was generally low, reducing the reliability and homogeneous comparability of the reports ,the quality of heat-sensitive moxibustion RCTs was high. It was believed that in order to improve the reliability and quality of RCTs of moxibustion, CONSORT and STRICTOM should be introduced into the RCT design of moxibustion and be strictly performed.
China ; Databases, Factual ; Humans ; Moxibustion ; methods ; standards ; Osteoarthritis, Knee ; therapy ; Randomized Controlled Trials as Topic ; standards ; Research Design

Objective To investigate the relationship between neurogenic bowel dysfunction (NBD) and substance P in rats suffering from spinal cord injury (SCI). Methods 60 male Sprague-Dawley rats, weighted (220±40) g, were randomly divided into three groups: sham group (n=20), normal group (n=20) and model group (n=20) and then were subdivided into subgroups of 24 h, 1 week, 3 weeks, and 5 weeks respectively after SCI. SCI model was established at thoracic 10 segment of rat with NYU impactor device. The colon tissue of the rats was resected and stored. Substance P in serum and tissue was measured by ELISA. The tissue was examined by real-time RT-PCR and Western blotting to analyze the expression of substance P. Results The colon intestinal transmission function decreased and delineated at minimum value at 3 weeks in the model group. There was statistical significance with respect to the content of substance P in serum and tissue between the sham group and model group at 3 weeks. The expression of substance P in the sham group was (3.12±0.51) times of the model group (P<0.05). Conclusion Substance P may take part in NBD after SCI in rats.

Objective To analyze the effects of adenohypophysis function after treating with thyrotropin releasing hormone and its clinical significance in patients with brain trauma. Methods There were 22 cases with traumatic brain injuries from July 2010 to September 2012 in Chinese people's Liberation Army nine eight hospital,after injuried within 4 to 12 hours,then 1 1 cases who were given thyrotropin-releasing hormone(TRH)were selected as experimental group,while 1 1 cases who were given the same amount of isotonic saline were selected as control group,then the score of GCS, ICS,RLS85 and the improvement of adenohypophysis function were observed. Results After treatment,the score of glasgow coma scale (GCS ), innsbruck coma scale (ICS),and the reaction level scale (RLS85)between two groups were significantly increased in three days compared with before treatment,and within three days after injury situation,the improvements of ICS and RLS85 in experimental group were better than control group(P<0.05 ). Compared with control group,the levels of each gland pituitary hormone in experimental group were significantly increased(P<0.05 ),and on the third day,the growth hormone (GH)was reduced significantly,finally 50%of that in control group. Conclusion Patients with brain injury treated with thyrotropin releasing hormone,has no significant adverse reactions,with the characteristics of safe and effective.

Several studies have demonstrated the role of 4-1BBL in T cell activation. Furthermore, enhanced 4-1BB/4-1BBL interaction has been shown to amplify T-cell-mediated antitumor immunity in several mouse models. However, when applied in humans, it was difficult to generate sufficient T cells ex vivo and whole cell vaccines to transfer back into patients. To overcome this difficulty, we have focused on producing the human 4-1BBL extracellular domain/anti-CD20 Fab' fusion protein. In this report, PCR and overlap PCR were used to construct the human 4-1BBL extracellular domain/anti-CD20 Fab' expression vector. DNA sequence was analyzed by the Terminus of Dideoxy Nucleotide. The product was purified by affinity chromatography and analyzed by SDS-PAGE and HPLC; its antigen binding activity was examined by rosetting assay. The data of DNA sequence showed that the human 4-1BBL extracellular domain/anti-CD20 Fab' fusion protein was corrected. The fusion protein was recovered in high yield (up to 200 microg/mL) after E-taq purification. The fusion protein was capable of simultaneous binding to stimulated Jurkat cells and Raji cells as shown by cellular rosetting. In conclusion, the human 4-1BBL extracellular domain/anti-CD20 Fab' fusion protein was induced to express in E. coli 16C9. The results of some biological activity experiments indicated that the fusion protein could bind to stimulated Jurkat cells and Raji cells. Furthermore, 4-1BBL-negative tumors can be converted into 4-1BBL-positive tumors by the fusion protein without the need for 4-1BBL gene transfer to the malignant cells.
4-1BB Ligand ; biosynthesis ; genetics ; Antibodies, Bispecific ; immunology ; Antigens, CD20 ; immunology ; Humans ; Immunoglobulin Fab Fragments ; biosynthesis ; genetics ; Immunotherapy ; methods ; Lymphoma, Non-Hodgkin ; therapy ; Recombinant Fusion Proteins ; biosynthesis ; genetics ; immunology

Central nervous system (CNS) injuries, including stroke, traumatic brain injury, and spinal cord injury, are essential causes of death and long-term disability and are difficult to cure, mainly due to the limited neuron regeneration and the glial scar formation. Herein, we apply extracellular vesicles (EVs) secreted by M2 microglia to improve the differentiation of neural stem cells (NSCs) at the injured site, and simultaneously modify them with the injured vascular targeting peptide (DA7R) and the stem cell recruiting factor (SDF-1) on their surface via copper-free click chemistry to recruit NSCs, inducing their neuronal differentiation, and serving as the nanocarriers at the injured site (Dual-EV). Results prove that the Dual-EV could target human umbilical vascular endothelial cells (HUVECs), recruit NSCs, and promote the neuronal differentiation of NSCs in vitro. Furthermore, 10 miRNAs are found to be upregulated in Dual-M2-EVs compared to Dual-M0-EVs via bioinformatic analysis, and further NSC differentiation experiment by flow cytometry reveals that among these miRNAs, miR30b-3p, miR-222-3p, miR-129-5p, and miR-155-5p may exert effect of inducing NSC to differentiate into neurons. In vivo experiments show that Dual-EV nanocarriers achieve improved accumulation in the ischemic area of stroke model mice, potentiate NSCs recruitment, and increase neurogenesis. This work provides new insights for the treatment of neuronal regeneration after CNS injuries as well as endogenous stem cells, and the click chemistry EV/peptide/chemokine and related nanocarriers for improving human health.