BACKGROUND:Transforming growth factor-βsignaling widely existing in cel s mediates cel growth, proliferation, migration, differentiation, and apoptosis. The activation of transforming growth factor-βsignaling can result in muscular dystrophy. However, there have been some contradictions regarding the effects of the transforming growth factor-βsignaling on muscular dystrophy. OBJECTIVE:To summarize the latest progress in the effects of the transforming growth factor-βsignaling on muscle mass and function regulation to provide the solutions for the treatment of muscular dystrophy. METHODS:A computer-based online search was conducted in PubMed and Wanfang databases from 2005 to 2015 to screen the relevant literatures using Chinese and English key words“transforming growth factor-β, muscle, regulation mechanism, treatment”. A total of 102 literatures were retrieved, and 22 eligible literatures were included, summarized, and analyzed. RESULTS AND CONCLUSION:The activation of transforming growth factor-βsignaling as a common cause of most muscle disorders promotes the activation of muscle satel ite cel s, differentiation of myocytes, myoblast infusion, the expression of muscle-specific proteins, and the inhibition of col agen synthesis, which facilitates muscular fibrosis and scar formation. Transforming growth factor-βsignaling is involved in Duchenne muscular dystrophy, spinal scoliosis, type I diabetes induced skeletal muscle regenerative disorders, myocardial and cardiac remodeling. The inhibition of transforming growth factor-βsignaling may result in incomplete muscle recovery.

BACKGROUND:There is an urgent need to explore the loss of skeletal muscle mass during aging (sarcopenia), and its molecular mechanisms of action, and prevention and treatment strategies. OBJECTIVE:To summarize the latest progress in molecular mechanisms of sarcopenia, and to provide a fundamental for promoting functional recovery and regeneration of skeletal muscle. METHODS:A computer-based online search was conducted in PubMed and Wanfang databases from 2005 to 2015 to screen the relevant literatures using Chinese and English key words“sarcopenia, skeletal muscle, mechanism, therapy”, respectively. Consequently, 31 eligible literatures were col ected, summarized, and analyzed. RESULTS AND CONCLUSION:Sarcopenia is closely correlated with oxidative stress caused by mitochondrial respiratory failure, inhibition of activating factors for regulating satel ite cel s, reduction in insulin secretion, decreased sensitivity, protein synthesis, and low protein diet. There are common features and molecular mechanisms in sarcopenia and disuse muscle atrophy. Further exploration of exercise and diet strategies for the treatment of sarcopenia is required.

Most previous researches on nuclear factor κB (NFκB) are limited to immune cells. Recently, however, researches on NFKB in muscle cells attract more attention. Target genes of NFκB encodes proteins with different functions, accordingly NFκB can not only induce inflammation deterioration, protein degradation and tissue injury but also promote cell growth and maintenance. But the inhibitation effect of NFκB inhibitors is not related with its antioxidant capacity. Exercise can activate NFκB during which process NFκB may act as an inducer of cell growth and development which is different from its role under pathological situation. This article sums up and analyzes the effect of NFκB on cell growth, the changing trend and effect of NFκB in skeletal muscle under exercise, providing data for the researches on muscle rehabilitation and motion fitness change.

Lactate shuttle is the process of lactic migration thmugh membrane with monocarboxylate transporters(MCTs)and anti-exchange ion,including intracellular and extracellular modes.The effect of MCTs specific distribution on lactate shuffle and the structure and mechanism of anti-exchange ion transporter is unclear.Any factor which infiuences lactate production.oxidation,MCTs expression and blood circulation can regulate lactate shuttle.That lactate induces ASIC channel to open may affect the Sensory nerve bnnging about pain.Various lactate shuttles may induce vanous kinds of pain,Ageing,but not inactivity,decrease lactate accumulation and shuttle leading to the decreased fatigability of skeletal muscle.The regulation mechanism and energy supply extend of lactate shuttle need to be investigated.Lactate shuttle may be one important factor to regulate the biological effect of lactate such as vanous muscle pain,fatigability and etc.Lactate shuffle effect on body function regulation is a noticeable problem in muscle rehabilitation and excise-inducad adaption fields.

Otoneurological operations were performed in 96 patients through the retrosigmoidal approach. The anatomical structures in the cerebello-pontine angle can be clearly exposed with this procedure. The approach has the advantage that it is of convenience in manipulation with only gentle trauma, and that some drawbacks of suboccipital or retrolabyrimhine approach may be overcome. On the other hand, operation indications can be extended and operation complications reduced. It is an ideal approach which enters the cerebello-pontine angle. The surgical technique and clinical experience have been reported in detail in this paper.

Objective To explore the possibility of rapamycin to up-regulate radiosensitivity of nasopharyngeal carcinoma (NPC) and its molecular mechanism.Methods In vitro,with untreated cells as the control,NPC cells were treated with rapamycin,irradiation (IR),or both rapamycin and IR.Phosphorylation of S6 and GSK3β,expression of Cyclin D1,clonogenic survival,number of residual γH2AX foci,and cell cycle status between study groups were compared.In vivo,athymic mice bearing CNE1 tumor were similarly treated.Tumor weight,Cyclin D1 and phosphorylated S6 in the xenograft model were compared between study groups.Results The results showed that rapamycin alone decreased the phosphorylation of S6 and glycogen synthase kinase 3 β (GSK3β),and the expression of Cyclin D1 in NPC cells.Thus,rapamycin-treated NPC cells had lower cell viability,higher DNA damage and more G1 arrest than the control,which was reflected by the in vivo study that rapamycin significantly attenuated tumor growth and decreased the levels of Cyclin D1 and phosphorylated S6.Moreover,the combination of rapamycin and IR caused the highest cell death,DNA damage,G1 arrest and tumor regression compared to those treated either alone.Conclusions Rapamycin up-regulate NPC radiosensitivity by inhibiting signal transduction of Akt/mammalian target of rapamycin (mTOR)/S6 pathway and Akt/GSK3β pathway,and by downregulating Cyclin D1 expression.

Objective To detect the expression of β-catenin in the tissues of primary central nervous system lymphoma (PCNSL), and to discuss its function in PCNSL.Methods The paraffin embedded tissues from 10 patients diagnosed as PCNSL from October 2010 to April 2012 were collected as the experimental group.The paraffin embedded tissues from 10 patients with lymphadenitis were collected as the control group.Quantitative real-time PCR and immunohistochemical method were used to detect the expression of β-catenin in these tissues, and the relationships between β-catenin and clinical data were analyzed.Results Immunohistochemistry results showed that β-catenin protein was localized in the cytoplasm and (or) nucleus.Among 10 PCNSL patients, β-catenin protein was positive in 4 patients, while it was no positive in all of 10 lymphadenitis patients, with the significant differences between both groups (P ＜ 0.05).The β-catenin gene relative expression level was 4.70±0.57 and 1.00±0.27 in the experimental group and the control group, respectively.β-catenin expression was no correlation to age, PS score, cerebrospinal fluid protein level and serum lactate dehydrogenase level of patients with PCNSL.Conclusions Whether in mRNA level or in protein level, β-catenin expression is always high in PCNSL tissues, and its protein is expressed in the cytoplasm, however, this phenomenon was not observed in the tissue of lymphadenitis.

This article reports one hepatic echinococcosis patient complicated with systemic sclerosis. His clinical manifesta?tions were the progressive fibrosis of the skin,sour regurgitation,and belching. The blood examination showed that eosinophils was reduced,and antinuclear antibody(ANA)was positive at 1∶100 in cytoplasm particle type. He was given prednisone ace?tate 25 mg,q. d.,aspirin 100 mg,q. d.,centella triterpenes cream 12 mg t. i. d.,esomeprazole 40 mg q. d.,and domperidone 10 mg t. i. d. After one week,the Rodnan skin score reduced from 27 to 17. The liver hydatid cyst resection was performed,and the follow?up showed that his clinical manifestations improved and the Rodnan skin score reduced further.

Objective To screen the anti-nasopharyngeal carcinoma scFv from a human anti-nasopharyngeal carcinoma single-chain phage antibody library, and identify its characteristics. Methods The single-chain phage antibody library was subjected to three rounds of positive and negative cell panning and enrichment, and then it was selected by ELISA. The binding specificity of phage antibodies with naso-pharyngeal carcinoma cells was confirmed by immunohistochemistry. Results After panning, enrichment and testing by ELISA, 3 phage an-tibody clones reacting with CNE2 more strongly than HUVEC and NP69 were picked out from 4212 clones. One clone, HNSAO33, was fur-ther analyzed after DNA sequencing. The results of immunohistochemistry with cultured cells were similar to those of ELISA. HNSAO33 spe-cifically reacted to nasopharyngeal carcinoma cells in most human nasopharyngeal carcinoma tissue sections except a few human normal naso-pharyngeal tissue sections. The distinction of positive rates was of a great statistical significance. Conclusion ELISA and immunohisto-chemistry results confirmed HNSAO33 specifically bind with nasopharyngeal carcinoma cells. The seFv fragment against nasopharyngeal carci-noma may be further developed and applied in clinical diagnosis and therapy of nasopharyngeal carcinoma.

Objective To study the imaging characteristics of the ligaments in craniocervical junction (CCJ), and to optimize the examination methods and scanning sequences of the ligaments in this region. Methods Two groups of 51 healthy volunteers in each were selected to undergo CT and MRI examination respectively. The CT and MRI features of the ligaments in CCJ were assessed. Two senior imaging doctors compared the results of showing the ligaments in CCJ by several MRI sequences, including T1 WI ,T2 WI, proton density weighted imaging (PDWI), T2 * WI and short time inversion recovery (STIR) ,and proton density fat saturate (PDFSAT). Standard normal rank transformation was done according to the primary data,and then analysis of variance of repeated measurement was applied. Results CT and MRI could both demonstrate the ligaments (except the anterior atlantooccipital membrane only seen on MRI) and their adjoins in CCJ, while MRI had more advantages than CT. The display ratio of the anterior atlantooccipital membrane was 100% (51/51) by MRI. The display ratio of the apical ligament was 29.4%(15/51) by CT and 43.1% (22/51) by MRI. The posterior atlantooccipital membrane-dura complex,tectorial ligament-dura complex, transverse ligament, and alar ligament could be demonstrated clearly by CT and MRI, the display ratio was 100% respectively (51/51). The results of PDWi scored by two doctors were both 5.0, there were no significant differences between them (F = 0.000, P > 0.05), which were significantly higher than T, WI (M = 3.0), T2Wi (M = 3.0), T2 * WI (M = 1.0), STIR (M = 1.0), and PDFSAT(M = 3.0)(P < 0.01). Conclusion MRI was superior to CT in demonstrating the ligaments in CCJ. PDWI was the optimal MRI sequence. Imaging research of normal ligamentous structures in CCJ could provide valuable diagnostic and therapeutic information for evaluating the ligamentous diseases.