Demyelination of the central nervous system often occurs in neurodegenerative diseases， such as multiple sclerosis （MS）. The myelin sheath， a layer of myelin membrane wrapping the axon， plays a role in the rapid conduction and metabolic coupling of impulses for neurons. The exposure of the axon will lead to axonal degeneratio， and further neuronal degeneration， which is the main cause of dysfunction and even disability in patients with demyelinating neurodegenerative diseases. In addition to the demyelination of mature myelin sheath， remyelination disorder is also one of the major reasons leading to the development of the diseases. The myelin sheath is composed of oligodendrocytes （OLs） derived from oligodendrocyte progenitor cells （OPCs） which are differentiated from neural stem cells （NSCs）. The process of myelin regeneration， i.e.， remyelination， is the differentiation of NSCs into OLs. Recent studies have shown that this process is regulated by a variety of genes. MicroRNAs， as important regulators of neurodegenerative diseases， form a complex regulatory network in the process of myelin regeneration. This review summarizes the main molecular pathways of myelin regeneration and microRNAs involved in this process and classifies the mechanisms and targets. This review is expected to provide a theoretical reference for the future research on the treatment of demyelinating diseases by targeting the regulation of microRNAs.

Tumor metastasis is the major cause of death for tumor patients and the key bottleneck of clinical treatment. In recent years， basic and clinical studies have recognized that tumor microenvironment （TME） is highly correlated with tumor metastasis， which provides hope for anti-metastatic drug development and clinical treatment. At present， the mainstream studies on TME represented by immune checkpoint inhibitors （ICIs） mainly focus on the rectification of immune function of T cells and B cells. However， a large number of studies have shown that the significance of other members of TME for tumor metastasis cannot be ignored， which greatly reflects the progress of anti-metastatic research based on TME regulation. This review focused on tumor metastasis， summarized the mechanism of action of non-T and non-B immune cells ［tumor-associated macrophages （TAMs） and tumor-associated neutrophils （TANs）］ and non-immune members ［vascular endothelial cells （ECs）， tumor-associated fibroblasts （CAFs）， and blood platelet］ in the process of tumor metastasis in TME based on the literature over the recent five years， and explored their key value in the treatment of metastasis. At the treatment level， this review focused on the perspective of the integration of frontier and traditional methods and took the functional homeostasis remodeling of TME as the entry point to summarize the activity and mechanism of traditional Chinese medicine （TCM） regulation of non-T and non-B immune cells and non-immune members and highlight its advantages and characteristics in clinical intervention of metastasis. This review helps to break through the limitations of over-reliance on T and B immune cells in anti-metastatic research， make the research rely on a wider range of cell groups， explore the potential value of TME in anti-metastatic drug intervention， and enrich the idea and strategy of understanding the anti-metastatic pharmacological activity. The review is also expected to provide a broader vision for the research and development of new anti-metastatic drugs.

Cytopharmaceutical based on macrophages is a breakthrough in the field of targeted drug delivery. However, it remains a challenge to localize and control drug release while retaining macrophage activity and exerting its immunotherapeutic effect. Herein, a localized light-triggered release macrophage cytopharmaceutical (USIP@M) was proposed, which could utilize the tumor targeting and immunotherapy effects of macrophages to reverse the immune suppression of tumor microenvironment (TME). Amphiphilic block copolymers with ultraviolet (UV)-responsive o-nitrobenzyl groups were synthesized and co-loaded with sorafenib (SF), IMD-0354 (IMD), and upconverting nanoparticles (UCNPs), which were then taken up by macrophages, and the targeted delivery of drugs was realized by using the tumor tropism of macrophages. UCNPs converted near-infrared light with strong penetrability and high safety into UV light, which promoted the photoresponsive depolymerization of block copolymers and production of exosomes from USIP@M, accelerated drug efflux and maintained the activity of macrophages. IMD simultaneously polarized carrier macrophages and tumor-associated macrophages to exert the antitumor effect of macrophages, enhance T cell immunity, and alleviate the immunosuppressive state of TME. Synergistically with the chemotherapeutic effect of SF, it could effectively kill tumors. In conclusion, based on the localized light-triggered release strategy, this study constructed a novel macrophage cytopharmaceutical that could localize and control drug release while retaining the activity of macrophages and exerting its immunotherapeutic effect, which could effectively treat solid tumors.

At present， major depressive disorder （MDD） is highly prevalent with advanced neurological disorders as the main pathological manifestations. As the physiological function bearer of higher neural activity， gray matter has become the focus of MDD treatment. However， recent research has shown that white matter and gray matter are independent of each other in the central nervous system （CNS）， and their functions are integrated and linked. In addition to gray matter damage， white matter damage is also the core driving event of disease progression and determines the outcome of MDD. At the treatment level， the current drug treatment of MDD mainly focuses on gray matter repair， while ignoring the importance of white matter integrity for the treatment of the disease， which has become the weakness of the current treatment of MDD. Traditional Chinese medicine （TCM） has good application potential in white matter repair. This paper elaborated on the following three aspects. ① The roles of white matter damage in the occurrence and development of MDD were summarized. ② The key link of white matter repair in MDD was elaborated with microglia microenvironment regulation as the entry point. ③ The application value of TCM in white matter repair in MDD was analyzed. This review aims to highlight the importance of white matter integrity in the treatment of MDD and is expected to expand the understanding dimension of the activity of related Chinese medicines in MDD from the perspective of white matter repair and analyze its potential application value.

AIM: To verify the role of enhancing or suppressing the expression of glutathione peroxidase 1 (GPx1) in the growth, migration and invasion of glioblastoma multiforme cell lines U87MG and U118MG.METHODS:U87MG and U118MG cell lines were transfected with the vector containing specific siRNA or pcDNA3.1 recombinant plas-mid both targeting GPx1.The mRNA and protein expression levels of GPx1 were detected by real-time PCR and Western blotting.MTS assay was applied for determining the cell activity.The abilities of migration and invasion were examined by Transwell assay.RESULTS:Compared with blank control group and negative group, the inhibitory rate of the cell activity in U87MG cells in siRNA group was significantly reduced by 25.9%, 35.7%and 34.8%at 24 h, 48 h and 72 h, respec-tively (P<0.05).In contrast, the cell activity of U118MG cells in pcDNA3.1-GPx1 group was significantly increased by 22.7%, 45.8%and 39.8%at 24 h, 48 h and 72 h, respectively ( P<0.05) .In siRNA group, the inhibitory rate of mi-gration in U87MG cells was 41.6%±8.2%and the invasion was 41.6%±8.2%compared with blank control group and negative group (P<0.05).The cell migration and invasion rates of the U118MG cells in pcDNA-GPx1 group were in-creased by 55.8%±9.8% and 60.8% ±9.2%, respectively, compared with blank control group and negative group (P<0.05).CONCLUSION:The down-regulation of GPx1 by specific siRNA reduces the capability of cell growth, mi-gration and invasion of U87MG cells, while up-regulation of GPx1 by pcDNA3.1-GPx1 increases the capability of cell growth, migration and invasion of U118MG cells.

Objective To explore the feasibility and effect of laparoscopic Ladd's surgery for the treatment of intestinal malrotation in infants.Methods The clinical data of 50 infants with intestinal malrotation who were admitted to the Wuhan Medical & Health Center for Women and Children from January 2011 to December 2013 were retrospectively analyzed.Of 50 infants, 27 infants receiving the open Ladd's surgery were allocated into the open surgery group and 23 infants receiving the laparoscopic Ladd's surgery were allocated into the laparoscopy group.The operation time, time to anal exsufflation, duration of hospital stay, postoperative incision infection and intestinal obstruction in the 2 groups were observed.All the patients were followed up by outpatient examination or telephone interview till March 2014.The measurement data with normal distribution were presented as x-± s and analyzed by the t test, and count data were analyzed using the chi-square test or Fisher exact probability.Results The operation time, time to anal exsufflation and duration of hospital stay were (69 ± 7)minutes, (41 ±9)hours and (10.4 ± 2.4)days in the open surgery group, which was significantly different from (92 ± 13)minutes, (28 ±5)hours and (6.4 ± 1.5) days in the laparoscopy group (t =6.21, 16.50, 6.34,P ＜ 0.05).Two infants had incision infection and 1 infant had intestinal obstruction in the open surgery group.There was no patient with complications in the laparoscopy group.All the patients were followed up for the median time of 13 months (range, 6-24 months), with a good survival and no other symptoms.Conclusion Laparoscopic Ladd's surgery is safe and feasible compared with open surgery, and it could be used as a prior operation method for treatment of intestinal malrotation in infants.

Objective To observe the interfering effect of different doses of penehyclidine hydrochloride (PHC) on the mRNA expressions of nuclear factor kappa B (NF-κB) and inducible nitric oxide synthase (iNOS) in the lung tissue of rats with traumatic shock so as to investigate the protective role of PHC in secondary long injury following traumatic shock and the underlying mechanism.Methods The traumatic shock model was established.A total of 104 Wistar rats were randomly divided into four groups:control group,shock group,low dose PHC group ( P1 group) and high dose PHC group ( P2 group).At the beginning of resuscitation,the rats in P1 and P2 groups were given transjugular intravenous injection of 2 ml/kg isotonic saline containing 0.15 mg/kg and 0- 45 mg/kg PHC respectively,while the rats in shock and control groups were injected only isometric isotonic saline.The rats in the four groups were killed at 2 h,6 h,12 h and 24 h after resuscitation respectively to detect the mRNA expressions of NF-κB and iNOS by using RT-PCR and determine the lung wet/dry weight (W/D) ratio,lung permeability index (LPI) and lung injury score (LIS).Results The mRNA expressions of NF-κB and iNOS,lung W/D ratio,LPI and LIS at all the time intervals in the shock,P1 and P2 groups were all significantly increased as compared with those in the control group (P＜0.05).Howerver,the P2 group showed significant reduction in aspects of the mRNA expressions of NF- κB and iNOS,lung W/D ratio,LPI and LIS at all time points and P1 group also had significant decrease regarding the mRNA expressions of NF-κB and iNOS,lung W/D ratio at2 h,6 h,and LPI and LIS at 2 h,6 h,12 h,as compared with the shock group.Meanwhile,P2 group showed evident decrease at 6 h concerning the mRNA expressions of NF-κB and iNOS,lung W/D ratio,LPI and LIS as compared with P1 group (P ＜ 0.05 ).Conclusions PHC,especially at a large dosage,can significantly mitigate the long injury secondary to traumatic shock,and the mechanism may be associated with the inhibition of mRNA expressions of NF-κB and iNOS.

Objective:To investigate whether the susceptibility of human colon adenocarcinoma cell SW1116 to lymphokine-activated killer cell (LAK)-mediated lysis could be enhanced by low concentration of sodium butyrate, and the possible involvement of intercellular surface adhesion molecule-1 (ICAM-1) and carcinoembryonic antigen (CEA). Methods:Standard MTT assay was used to evaluate the cytotoxic activity of LAK cells to SW1116 cells, flow cytometric and immunofluorescent techniques were used to determine the expression of ICAM-1 and CEA on tumor cells. Results:Treatment of SW1116 with sodium butyrate leads to an increased resistance to LAK-mediated lysis, accompanied by downregulation of ICAM-1 expression and upregulation of CEA expression. Conclusion: Sodium butyrate inhibits rather than enhance LAK activity against SW1116, probably by changing the expression of ICAM-1 and CEA on target cells, which impair the adherence of effector on target cells.

Objective To investigate possible reasons of different incidence of femoral head necrosis between two populations exposed to corticosteroid: severe acute respiratory syndrome (SARS) and renal allograft transplantation. Methods 67 cases of SARS and 59 cases of renal allograft transplantation were enrolled in the study. The following relevant data were reviewed: cumulative dosage (intravenous methylprednisolone and oral prednisone respectively), maximum single dosage, corticosteroids-exposing days, body weight, weight-load index, and minimum arterial oxygen pressure. MRI of bilateral hips was taken in all the patients. Results The incidence of femoral head necrosis of SARS (23.9%) was significantly higher than the renal allograft transplantation patients (6.8%) (P0.05). There was a very significant difference in minimum arterial oxygen pressure between two groups (P