Objective To construct a system for three dimensional face scanning and measurement. Methods The measurement system was based on the principle of triangulation and the combination of gray-code and phase-shift structured light projection. The system software was developed for Windows XP with the aid of tools such as Visual C++ and Hoops. Results A three dimensional measurement system based on structured light projection was developed. The system hardware was composed of fringe projection unit, image gathering unit, system control unit and mechanical appearance, and the system software was composed of point cloud display and editing module. The lamp house of the system was 12V, the working distance was 900 mm, the scanning time was 5.5 s and the scanning field was 500 mm×400 mm. Conclusion The three dimensional measurement system based on structured light projection is a refined machine with safe light to eyes, and the accuracy and scanning speed are suitable to face scanning.

In recent years, with the development of China's reform of medical and health services, the level of clinical medicine in China has been greatly improved, but there is still a big gap between China and developed countries in Europe and America. China has a large population and rich and diverse clinical resources. However, innovative research and results in key guidelines, diagnosis and treatment programs, and major innovative drugs in the diagnosis and treatment of diseases are insufficient. The key reason is the lack of effective integration of clinical resources. Taking Shanghai Jiao Tong University School of Medicine as an example, under the background of "double first-class" construction, this paper summarized the status quo of clinical resource integration, analyzed the key issues in integration, and tried to put forward the strategies of medical, scientific research, and talent integration in clinical resource integration, to provide path for promoting clinical resource integration and clinical discipline construction.

ObjectiveTo evaluate the curative effect difference between Tong's anterior mesh suspension and modified tension-free vaginal tape-obturator (TVT-O). Methods75 SUI cases were random divided into two groups: Group A (35 cases) were accepted Tong's anterior mesh suspension and group B (40cases) were accepted modified tension-free vaginal tape- obturator. Curative effects, operation safety,and complications and so on, were recorded and compared. ResultsThere had no statistical differences between these two groups on operation time, bleeding lose, operation injury, immediate postoperative urinary retention andcure rates, but the operation expense of group A was cheaper than group B [ (980. 74 ±212.45)yuan vs (2879.06 ±467. 13)yuan , P ＜0.05). ConclusionThe curative effect between two methods were similar. It's a little complicated and fit to be popularized in large hospital to modified tensionfree vaginal tape-obturator. Tong's anterior mesh suspension was performed under completely direct vision,not through pelvic cavity, and it was an economic, convenient and easy way, which not only fit to be popularized in basic hospital, but also a surgical remedial measure to the failures who accepted these operations,such as TVT, SPARC, IVS, MONARC, TOT, TVT-O, etc.

According to the theory of traditional Chinese medicine (TCM), Qi (vital energy) is regarded as a driving force of biological activities in human body, including both nutrient substances and organ functions. Qi-invigorating TCMs are widely used to treat various symptoms and disorders, such as fatigue, obesity, immunosuppression, intestinal flora imbalance, and gastrointestinal diseases, in which Qi is considered to be reduced or depleted. Interestingly, abundant clinical evidences suggest that these disorders are associated with the alternation of intestinal flora, which directly affects disease status. Herein we review the interaction between gut microbiota and Qi-invigorating TCMs under healthy and disease conditions and discuss the mechanisms of action and applications of Qi-invigorating TCMs in enhancing health status through microbial alternation. A better understanding of the role of Qi-invigorating TCMs in modulating microbial composition and the association between intestinal microbiota and diseases would help reveal the clinical consequences of microbiota alteration and explore opportunities to harness this symbiotic relationship to improve public health.
Drugs, Chinese Herbal ; pharmacology ; Gastrointestinal Microbiome ; drug effects ; Humans ; Prebiotics ; Qi

Cannabinoid receptors are one of the most expressed G protein-coupled receptors in the central nervous system, which are potential drug targets for inflammation, pain and drug abuse. Cannabinoid receptors are composed of type 1 receptor (CB1R), type 2 receptor (CB2R) and other receptors, of which CB1R plays a vital role in regulating central memory, cognition, and motor function. Therefore, screening CB1R agonists has potential value in treating nervous system diseases. In this study, the intracellular loop 3 (ICL3) domain of CB1R was replaced with a circular-permutated enhanced green fluorescent protein (cpEGFP). After infecting HEK 293T cells with lentivirus particles, we obtained a stable cell line that was overexpressed human CB1R-cpEGFP after puromycin selection. The interaction between receptor agonists and CB1R led to the change of receptor conformation, resulting in de-protonation of the EGFP, and enhancing the fluorescence intensity. Therefore, active CB1R compounds could be verified by measuring the fluorescence intensity. Using CB1R agonist arachidonyl-2′-chloroethylamide (ACEA) as a positive control to evaluate the reliability of this model, studies have shown that ACEA could induce receptor activation and increase fluorescence intensity, while antagonist rimonabant inhibited receptor activation with unchanged fluorescence intensity. In conclusion, this study successfully constructed a fluorescent probe screening model for CB1R agonists.

Objective To investigate the therapeutic effect of enteral drip infusion with modified Baitouweng Decoction for the treatment of ulcerative colitis(UC) with damp heat in large intestine at active phase , and to observe its influence on serum levels of inflammatory factors. Methods Sixty patients suffering from mild to moderate UC with damp heat in the large intestine were randomly divided into treatment group and control group, 30 cases in each group. The treatment group was given enteral drip infusion with modified Baitouweng Decoction and the control group was given Mesalazine Enemas enema. The medication lasted for 8 continuous weeks. Before and after treatment, the scores of traditional Chinese medicine (TCM) syndromes and intestinal mucosal signs under enteroscopy, and serum levels of inflammatory factors were observed. Therapeutic effect on single TCM syndrome and clinical safety were also evaluated after treatment. Results After treatment, the scores of each TCM syndrome and intestinal mucosal signs under enteroscopy in the treatment group were much improved (P<0.05 compared with those in the control group); serum interleukin-8 (IL-8) and tumor necrosis factor beta (TNF-β) levels in both groups were decreased, serum IL-10 and IL-13 levels were increased (P <0.05 compared with those before treatment), and the effect in the treatment group was superior to that in the control group (P < 0.05). Except for the abdominal pain, the treatment group had better effect on relieving diarrhea, anal expansion, tenesmus, mucous stool and bloody purulent stool than the control group, the difference being statistically significant (P < 0.05). During the medication, no obvious adverse reaction was found in the treatment group, but 4 cases from the control group had anal burning sensation which had no effect on the mediciation. Conclusion Enteral drip infusion with modified Baitouweng Decoction can inhibit the release of proinflammatory cytokines, reduce the inflammatory response, and promote the healing of intestinal mucosa, which is effective for the treatment of UC with damp heat in large intestine at active phase.

The E2F-1 transcription factor is post-translationally modified and stabilized in response to various forms of DNA damage to regulate the expression of cell-cycle and pro-apoptotic genes. The sustained overexpression of E2F-1 is a characteristic feature of gastric cancer. In this study, we investigated the role of short hairpin RNA (shRNA) targeting E2F-1 gene on human gastric cancer MGC-803 cell growth in vivo, and preliminarily revealed the mechanism. Thus, we constructed recombinant pGCSIL-GFP-shRNA-E2F-1 lentiviral vector to knock down E2F-1 expression in human gastric cancer MGC-803 cells in vivo, and studied the effect of E2F-1 shRNA on growth of MGC-803 tumor and evaluated its treatment efficacy. Our data demonstrated that in a mouse model of established gastric cancer, intratumor injection of lentiviral shRNA targeting E2F-1 definitely decreased the endogenous E2F-1 mRNA and protein expression in MGC-803 tumor, and inhibited tumor growth and promoted tumor cells apoptosis. Moreover, we found that E2F-1 shRNA increased the expression of phosphatase and tensin homolog (PTEN), activated caspase-3 and caspase-9, and suppressed nuclear factor (NF)-kappaB expression in tumor tissue as determined by reverse transcription (RT)-PCR and western blotting. In summary, shRNA targeting of E2F-1 can effectively inhibits human gastric cancer MGC-803 cell growth in vivo and may be a potential therapeutic strategy for gastric cancer.
Animals ; Apoptosis ; Blotting, Western ; Caspase 3/metabolism ; Caspase 9/metabolism ; Cells, Cultured ; E2F1 Transcription Factor/antagonists & inhibitors/genetics/*metabolism ; Genetic Vectors/administration & dosage ; Humans ; Lentivirus/*genetics ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; RNA Interference ; RNA, Small Interfering/*genetics ; Stomach Neoplasms/*genetics/pathology/*prevention & control

OBJECTIVETo study the effects of E2F-1-silencing lentivirus vector on the growth and chemoresistance of subcutaneous human gastric cancer in nude mice.

METHODSThirty-six nude mice were inoculated subcutaneously with chemoresistant SGC-7901/DDP cells to establish subcutaneous tumor models of gastric carcinoma. The mice were randomly divided into E2F-1/RNAi-LV group, LV-scrRNAi group and PBS group (n = 12). E2F-1/RNAi-LV, LV-scrRNAi or PBS (0.1 ml per time) was injected into the mice, respectively, every two days. The nude mice received an intraperitoneal injection of cisplatin (25 mg/kg) every two days. The tumor volume was measured and histopathological changes of the tumors were observed by HE staining. The expressions of E2F-1, c-Myc, survivin, MDR1 and MRP were detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) and Western blot. Apoptosis in tumor xenografts was determined by in situ TUNEL labeling technique.

RESULTSThe mean tumor growth rate of the E2F-1/RNAi-LV group was significantly slower than that of the LV-scrRNAi and control groups (P < 0.05). The tumor volume of the E2F-1/RNAi-LV group was (745.13 ± 154.42)mm(3), significantly lower than that of the LV-scrRNAi and PBS groups (P < 0.05). Compared with that in the LV-scrRNAi and PBS groups, the expressions of mRNA and protein of E2F-1, c-Myc, survivin, MDR1 and MRP were significantly decreased in the E2F-1/RNAi-LV group (P < 0.05). The apoptotic rate in the E2F-1/RNAi-LV treatment group was (27.5 ± 9.7)%, significantly higher than (7.0 ± 1.1)% in the LV-scrRNAi group and (7.3 ± 1.2)% in the PBS group (P < 0.05).

CONCLUSIONIntra-tumoral injection of E2F-1/RNAi-LV shows significantly inhibitory effect on the tumor growth and chemoresistance of subcutaneous human gastric cancer in nude mice.

ATP-Binding Cassette, Sub-Family B, Member 1 ; genetics ; metabolism ; Animals ; Antineoplastic Agents ; pharmacology ; Apoptosis ; Cell Line, Tumor ; Cisplatin ; pharmacology ; Drug Resistance, Neoplasm ; E2F1 Transcription Factor ; genetics ; metabolism ; Female ; Gene Silencing ; Genetic Vectors ; Humans ; Inhibitor of Apoptosis Proteins ; genetics ; metabolism ; Lentivirus ; genetics ; Mice ; Mice, Nude ; Multidrug Resistance-Associated Proteins ; genetics ; metabolism ; Neoplasm Transplantation ; Proto-Oncogene Proteins c-myc ; genetics ; metabolism ; RNA, Messenger ; metabolism ; Random Allocation ; Repressor Proteins ; genetics ; metabolism ; Stomach Neoplasms ; genetics ; metabolism ; pathology ; Transfection ; Tumor Burden

OBJECTIVEThe objective of this study was to review the research on clinical genetics of Wilson's disease (WD).

DATA SOURCESWe searched documents from PubMed and Wanfang databases both in English and Chinese up to 2014 using the keywords WD in combination with genetic, ATP7B gene, gene mutation, genotype, phenotype.

STUDY SELECTIONPublications about the ATP7B gene and protein function associated with clinical features were selected.

RESULTSWilson's disease, also named hepatolenticular degeneration, is an autosomal recessive genetic disorder characterized by abnormal copper metabolism caused by mutations to the copper-transporting gene ATP7B. Decreased biliary copper excretion and reduced incorporation of copper into apoceruloplasmin caused by defunctionalization of ATP7B protein lead to accumulation of copper in many tissues and organs, including liver, brain, and cornea, finally resulting in liver disease and extrapyramidal symptoms. It is the most common genetic neurological disorder in the onset of adolescents, second to muscular dystrophy in China. Early diagnosis and medical therapy are of great significance for improving the prognosis of WD patients. However, diagnosis of this disease is usually difficult because of its complicated phenotypes. In the last 10 years, an increasing number of clinical studies have used molecular genetics techniques. Improved diagnosis and prediction of the progression of this disease at the molecular level will aid in the development of more individualized and effective interventions, which is a key to transition from molecular genetic research to the clinical study.

CONCLUSIONSClinical genetics studies are necessary to understand the mechanism underlying WD at the molecular level from the genotype to the phenotype. Clinical genetics research benefits newly emerging medical treatments including stem cell transplantation and gene therapy for WD patients.

Adenosine Triphosphatases ; genetics ; Cation Transport Proteins ; genetics ; Copper-transporting ATPases ; Hepatolenticular Degeneration ; genetics ; Humans ; Phenotype

To investigate the role and mechanism of ceramide (Cer) regulation in alcohol-induced neuronal proliferation and the newborn neurons formation, we used sphingomyelin synthase 2 (predominant enzyme of Cer metabolism) knockout (SMS2(-/-)) and wild type (WT) female mice to establish the model of prenatal alcohol exposure. In 24 h after being given birth (postnatal day 0, P0), the offspring of model mice received blood sphingomyelin (SM) measurement with enzymatic method. On P0, P7, P14 and P30, the proliferation of granule cells in the dentate gyrus and newborn neurons were investigated with immunofluorescent labeling. The expression of protein kinase Cα (PKCα) in the hippocampus was tested with Western blot analysis. The results showed that the SM level of blood in SMS2(-/-) pups was significantly lower than that in WT pups. No matter in SMS2(-/-) or WT mice, the prenatal alcohol exposure down-regulated the SM levels in pups with dose-dependency. In both SMS2(-/-) and WT pups, the number of proliferative neurons and newborn neurons in the dentate gyrus gradually decreased with the growing age. Compared with the WT pups, SMS2(-/-) pups showed significantly more proliferative neurons and newborn neurons in the dentate gyrus. Notably, prenatal alcohol exposure dose-dependently increased proliferative neurons and newborn neurons in the dentate gyrus in both WT and SMS2(-/-) pups. The hippocampal expression of PKCα protein in SMS2(-/-) mice was lower than that in WT mice, and prenatal alcohol exposure could up-regulate the PKCα protein expression in both WT and SMS2(-/-) mice with dose dependency. These results suggest that alcohol exposure during pregnancy can induce the compensatory neural cell proliferation and the production of newborn neurons in offspring, and the Cer-ceramide-1-phosphate (C1P) pathway is involved in alcohol-induced neural cell proliferation. The activation of PKCα may be a key step to start the Cer-C1P pathway and up-regulate the alcohol-induced neural cell proliferation and the newborn neurons formation.
Animals ; Animals, Newborn ; Cell Proliferation ; drug effects ; Cells, Cultured ; Ceramides ; metabolism ; Dentate Gyrus ; cytology ; Ethanol ; toxicity ; Female ; Mice ; Mice, Knockout ; Neurons ; cytology ; Pregnancy ; Prenatal Exposure Delayed Effects ; physiopathology ; Protein Kinase C-alpha ; metabolism ; Signal Transduction ; Transferases (Other Substituted Phosphate Groups) ; genetics