This paper explains the status of science and technology of traditional Chinese medicine in China. Basic conclusions are as follows: policy environment is improved step by step, R&D funds and R&D personnel in traditional Chinese medicine field are increased continuously, and a lot of achievements have been got in traditional Chinese medicine field.
Academies and Institutes ; economics ; statistics & numerical data ; Biomedical Research ; economics ; manpower ; statistics & numerical data ; China ; Medicine, Chinese Traditional

Background Inflammation and adipogenesis are two parallel processes with increasing activity in severe thyroid-associated ophthalmopathy(TAO),and mevastatin was proved to have the inhibiting effect on the differentiation of adipose.Objective The aim of this work was to investigate the effects of mevastatin on the expression of cyclooxygenase-2(COX-2)and peroxisome proliferator activated receptor-γ(PPAR-γ)and differentiation of TAO-derived orbital preadipocytes,and explore its modulation effects on lipopolysaccharide(LPS)induced inflammation and the differentiation of TAO-derived orbital preadipocytes in vitro.Methods The retroorbital adipose tissue was obtained from 4 TAO patients during the surgery.The orbital fibroblasts were cultured from orbital adipose tissues using explant culture method.To study the suppressing effect of mevastatin on inflammatory response,cultured cells were divided into 5 groups.The 1000 μg/L LPS orbital fibroblasts were stimulated for 8 hours in group A,and 1000 μg/L LPS combined with 5 μmol/L,10 μmoL/L or 20 μmoL/L mevastatin were used respectively for the substitute in the group B,group C and group D.The orbital fibroblasts in group E were cultured routinely without any intervention as control.To observe the inhibiting effect of mevastatin on the differentiation of adipose,the group A were then subdivided into group A1-A6.After 1000 μg/L LPS was used to treat the cells for 8 hours,the ceils were induced to differentiate into adipocytes.All orbital preadipocytes from A1 to A6 were stimulated to differentiate into mature adipocytes with cocktail differentiation medium for a 10-day duration.During the procedure,group A2,A3 and A4 were interfered with 5,10 or 20 μmol/L mevastatin,and in the group A5 and A6,10 μmol/L mevastatin were added at the fourth day or eighth day.Intracellular fat accumulation in differentiated adipocytes was determined by oil red O staining.The absorption(A492 nm)was measured in the ceils by enzyme-linked immunosorbent assay(ELISA).Expression of COX-2 and PPAR-γ mRNA was detected by reverse transcription polymerase chain reaction(RT-PCR),and the expression of COX-2 and PPAR-γ protein was detected by Westernblot.The level of PGE2 in the supernatant was detected by ELISA.Results The expression of COX-2 protein and mRNA as well as the PGE2 levels in B,C,D group decreased markedly in comparison with those in A group(P＜0.05).With the increase of mevastatin concentration,the expression of COX-2 protein and mRNA as well as the PGE2 levels in B,C,D groups decreased successively(F =228.380,101.745,1586.881,P＜0.05).The expression of COX-2 protein and mRNA and PGE2 levels in E group were lower significantly than those in A,B and C groups(P＜0.05),but no significant differences were found between E group and D group(P＞0.05).The A492 value and the expressions of PPAR-γ protein and mRNA in differentiated cells showed the successively decrease in A1-A4 group with the elevation of mevastatin concentration(P＜0.05),and the evidently decreased A492 value and the expressions of PPAR-γ protein and mRNA also were seen in A1 and A5 groups compared with A3 group(P ＜ 0.05).Conclusions Mevastatin inhibits LPS-induced COX-2 expression,PPAR-γ expression,PGE2 secretion and differentiation of TAO-derived orbital fibroblasts in vitro in dose-dependent manner.Mevastatin plays these effect more prominently in early stage of adipocytes differentiation.

BACKGROUND:Coenzyme Q10 participates in the electron transport of respiratory chain and possesses antioxidant, anti-apoptotic and anti-inflammatory properties. It has achieved good outcomes in cardiovascular disease, diabetes and cancer. Coenzyme Q10 may also have a certain application value in the fields of diabetes and periodontitis. OBJECTIVE:To observe the effect of coenzyme Q10 on the expression of interleukin-17 and interleukin-23 in gingival tissue of type 2 diabetic rats with periodontitis.METHODS:Forty-eight healthy male Wistar rats were randomly divided into 3 groups: control, periodontitis+ diabetes+physiological saline and periodontitis+diabetes+coenzyme Q10. Rats in the control group were fed with normal diet and water. Rats in the periodontitis+diabetes+physiological saline and periodontitis+diabetes+ coenzyme Q10 groups were subjected to induction of periodontitis using the method of silk ligation and type 2 diabetes by feeding a high-fat and high-sugar diet and intraperitoneal injection of streptozotocin. After successful modeling, rats in the periodontitis+diabetes+coenzyme Q10 group were intragastricaly administered coenzyme Q10 for 8 successive weeks. Rats in the periodontitis+diabetes+physiological saline group were administered equal amount of physiological saline. At the end of 2nd, 4th and 8th weeks after drug administration, four rats were randomly selected and sacrificed. The expression levels of interleukin-17 and interleukin-23 in gingival tissue were detected by immunohistochemistry. RESULTS AND CONCLUSION: At the end of 8th week, interleukin-17- and interleukin-23-positive expression in the periodontitis+diabetes+physiological saline group was significantly higher than that in the periodontitis+ diabetes+coenzyme Q10 group (P < 0.05). Coenzyme Q10 can reduce the expression levels of interleukin-17 and interleukin-23 in gingival tissue of type 2 diabetic rats with periodontitis, and aleviate periodontal tissue inflammation of type 2 diabetic rats with periodontitis.

Aim To study and compare the pharmaco-kinetic parameters of roxithromycin under normoxic and hypoxic rats. Methods A highly effective and rapid ultra-performance liquid chromatography with tandem mass spectrometry ( UPLC-MS/MS) method with posi-tive electrospray ionization source was successfully de-veloped and validated for quantification of roxithromy-cin in rat plasma. Sprague-Dawley rats were randomly divided into the hypoxia and normoxic groups. Each rat obtained a single dose of roxithromycin with 10 mg · kg-1 via intragastric administration. The pharmacoki-netic parameter comparison between normoxic and hy-poxic groups was calculated by SPSS software using in-dependent sample t test method. Results The main pharmacokinetic parameters of roxithromycin between the normoxic and hypoxic rats were:the AUC(0-t) 7 576 and 3 761 μg·h·L-1 , MRT(0-t) 5. 6 and 7. 7 h, T1/2 3. 4 h and 3. 9 h, CL 1. 5 and 3. 0 L · h-1 · kg-2 , tmax3. 1 and 3. 4 h, Cmax 1 116 and 372 μg·L-1 , re-spectively. The levels of Cmax and AUC of roxithromy-cin in hypoxic rats were statistically lower than those in normoxic rats. Conclusion The exposure level of rox-ithromycin in hypoxic rats markedly decreased. Our re-sults may provide an important experimental basis to adjust the dosage for roxithromycin in hypoxic clinical practice.

Objective To investigate whether naloxone postconditioning could attenuate the focal cerebral ischemia-reperfusion (I/R) injury in rats. Methods Eighty-eight adult male SD nits weighing 270-330 g were randomly divided into 4 groups (n = 22 each) : group I sham operation (S); group Ⅱ I/R; group Ⅲ , Ⅳ I/R + low and high dose naloxone ( N_1, N_2). Focal cerebral I/R was produced by occlusion of right middle cerebral artery for 90 min followed by 24 h reperfusion. In group N_1, and N_2 naloxone 1 and 10 mg/kg were injected intraperitoneally at initiation of reperfusion respectively. In group I/R normal saline was injected instead of naloxone. HR, MAP and EKG were continuously monitored throughout the experiment. He neurological deficits were scored (0 = no deficit, 4 = unable to crawl, mental dysfunction) at 2 h and 24 h of reperfusion. The animals were then decapitated. The brains were immediately removed for determination of infarct size ( n = 10) and the expression of microtubule-associated protein-2 ( MAP-2) in brain tissue ( n = 6) . In the other 6 rats in each group FICT-dextran 1 ml (50 mg/ml) was injected iv at 1 min before decapitation. The cerebral plasma volume and diameter and segment length of cerebral microvessels on the I/R side were measured using laser scanning confocal microscopy (LSCM). Results Focal cerebral I/R significantly increased neurological deficit scores, induced cerebral infarct, and decreased MAP-2 expression in the brain tissue, cerebral plasma volume and the diameter and segment length of cerebral microvessels on the I/R side. Postconditioning with 10 mg/kg naloxone significantly attenuated the above-mentioned focal cerebral I/R-induced changes. Conclusion Postconditioning with naloxone can attenuate focal cerebral I/R injury in a dose-dependent manner.

Objective To find out the status of prevention and control of iodine deficiency disorders and evaluate the iodine nutritional status of Jinan residents,to explore appropriate iodine level in drinking water,and to provide a scientific basis for adjustment of intervention strategies.MethodsAccording to the Monitoring Program of the National Iodine Deficiency Disorders (Trial),qualified iodized salt consumption rate,drinking water iodine content and urinary iodine levels of women of childbearing age were determined in iodine deficiency areas from 2003 to 2010.Salt iodine was detected by direct titrimetry,urinary iodine by As-Ce catalytic spectrophotometric assay and iodine in drinking water by cerous sulfate catalytic spectrophotometric method.Results Intake rate of qualified iodized salt was up to 90％ and above from 2003 to 2010,median water iodine was 13.65 μg/L in the 10 counties(cities,districts),of which less than 100 μg/L accounted for 79.82％(4560/5713 ) and ＞ 150 μg/L accounted for 12.73％(727/5713).With the increase of water iodine(0 ～ ＜ 10,10 ～ ＜ 50,50 ～ ＜ 100,100 ～ ＜ 150,150 ～ ＜ 300 and ≥300 μg/L),urinary iodine levels of women of childbearing age increased successively(median 156.56,175.81,267.04,349.00,524.22,583.20 μg/L,respectively,x2 =121.20,P ＜ 0.05),while the ratio of urinary iodine ＜ 100 μg/L was significantly lower.The ratio of urinary iodine between 100 and 300 μg/L was decreased gradually,but the ratio of great than 300 μg/L was gradually increased.ConclusionsIodine deficiency areas in Jinan have reached the standard of elimination of iodine deficiency disorders.We should insist to carry out our measures to suit local conditions,classified guidances and scientific principals of iodine supplementation.

Objective:To evaluate the curative efficacy of a buttress plate combined with Kirschner wires for treatment of Regan-Morrey type Ⅱ coronoid fracture after elbow terrible triad injury.Methods:A retrospective study was conducted of the 20 patients who had been surgically treated for Regan-Morrey type Ⅱ coronoid fracture after elbow terrible triad injury from August 2014 to August 2018 at Department of Pelvic Trauma, Henan Luoyang Orthopedic-Traumatological Hospital. They were 12 men and 8 women, aged from 18 to 60 years (average, 39 years), with 6 left and 14 right sides affected. All the coronoid fractures were fixated with Kirschner wires plus a buttress plate through the anterior approach, the radial head and lateral collateral ligaments (LCL) were repaired through the posterolateral approach, and the medial collateral ligament (MCL) was repaired or fixated with a hinged external fixator if necessary. The curative efficacy was evaluated at the last follow-up by range of motion (ROM) of the elbow, Mayo elbow performance score (MEPS), American Shoulder and Elbow Surgeons Scale (ASES) and radiographs of the elbow. Complications were also recorded.Results:The mean follow-up time was 18 months (from 12 to 24 months) and the mean healing time 5 months. At the last follow-up, ROM in flexion and extension of the affected elbow joint averaged 132.5°, ROM in elbow pronation-supination 150°, MEPS 88, and ASES 87. No subluxation or dislocation occurred after elbow surgery. The fracture of coronoid process was slightly displaced in one case but eventually healed without affecting any elbow function; fat liquefaction occurred around the posterolateral incision in 2 cases but healed after debridement; traumatic arthritic changes occurred in 5 patients but no significant dysfunction of the elbow was observed.Conclusion:A buttress plate combined with Kirschner wires can lead to fine curative efficacy for Regan-Morrey type Ⅱ coronoid fracture after elbow terrible triad injury.

OBJECTIVETo investigate the effects of the quinoline derivative PQ1 combined with cisplatin on the proliferation and gap junction communication of prostate cancer PC3 cells.

METHODSWe cultured in vitro prostate cancer PC3 cells and divided them into DMSO blank control, cisplatin control, and cisplatin (10 mg/ml) plus PQ1 (1, 2, 5, 10, and 15 μmol/L) groups. We measured the proliferation of the prostate cancer PC3 cells, determined the expressions of the connexin 43 (Cx43) mRNA and protein by RT-PCR and Western blot, and compared the indexes among different groups.

RESULTSCisplatin combined with PQl at 1 - 10 μmol/L significantly inhibited the proliferation of the PC3 cells and the inhibition rate rose in a concentration- and time-dependent manner, from (48.72 ± 0.98)% vs (50.33 ± 0.62)% at 0 μmol/L to (77.38 ± 1.12)% vs (83.50 ± 1.05)% at 15 μmol/L at 24 and 48 hours (P < 0.05). Compared with the cisplatin control, cisplatin combined with PQ1 at 1, 2, 5, 10, and 15 μmol/L increased the expression of Cx43 mRNA from 0.379 ± 0.113 to 0.669 ± 0.031, 0.831 ± 0. 127, 0.769 ± 0.100, 0.532 ± 0.086, and 0.475 ± 0.134, respectively (P < 0.05), and cisplatin combined with PQ1 at 1, 2, 5, and 10 μmol/L elevated that of Cx43 protein from 0.138 ± 0.146 to 0.263 ± 0.111, 0.306 ± 0.152, 0.415 ± 0.280, and 0.643 ± 0.310, respectively (P < 0.05).

CONCLUSIONThe quinoline derivative PQ1 can promote the gap junction communication of prostate cancer PC3 cells and enhance the killing effect of cisplatin on PC3 cells by upregulating the expressions of Cx43 mRNA and protein.

Aminoquinolines ; pharmacology ; Antineoplastic Combined Chemotherapy Protocols ; pharmacology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Cisplatin ; pharmacology ; Connexin 43 ; genetics ; metabolism ; Dose-Response Relationship, Drug ; Gap Junctions ; drug effects ; physiology ; Humans ; Male ; Prostatic Neoplasms ; metabolism ; pathology ; physiopathology ; RNA, Messenger ; metabolism ; Time Factors

OBJECTIVETo evaluate the efficacy and safety of testosterone undecanoate (TU) in the treatment of late-onset hypogonadism (LOH) by meta-analysis.

METHODSWe searched Pubmed (until April 1, 2014), Embase (until March 28, 2014), Cochrane Library (until April 17, 2014), CBM (from January 1, 2001 to February 2, 2014), CNKI (from January 1, 2001 to February 2, 2014), Wanfang Database (from January 1, 2000 to February 2, 2014), and VIP Database (from January 1, 2000 to Febru ary 2, 2014) for randomized controlled trials of TU for the treatment of LOH. We evaluated the quality of the identified literature and performed meta-analysis on the included studies using the Rveman5. 2 software.

RESULTSTotally, 14 studies were included after screening, which involved 1 686 cases. Compared with the placebo and blank control groups, TU treatment significantly increased the levels of serum total testosterone (SMD = 6.22, 95% CI 3.99 to 8.45, P < 0.05) and serum free testosterone (SMD = 4.35, 95% CI 1.86 to 6. 85, P < 0.05) but decreased the contents of luteinizing hormone (WMD = -2.23, 95% CI -4.03 to -0.42, P < 0.05), sex hormone binding globulin (WMD = 2.00, 95% CI 1.38 to 2.63, P < 0.05). TU also remarkably reduced the scores of Partial Androgen Deficiency of the Aging Males (WMD = -9.49, 95% CI -12.96 to -6.03, P < 0.05) and Aging Males Symptoms rating scale (WMD = -2.76, 95% CI -4.85 to -0.66, P <0.05) but increased the hemoglobin level (SMD = 2.35, 95% CI 0.29 to 4.41, P < 0.05) and packed-cell volume (SMD = 4.35, 95% CI 1.36 to 7.33, P < 0.05). However, no significant changes were shown in aspertate aminotransferase, alanine transaminase, prostate-specific antigen, or prostate volume after TU treatment (P > 0.05).

CONCLUSIONTU could significantly increase the serum testosterone level and improve the clinical symptoms of LOH patients without inducing serious adverse reactions. However, due to the limited number and relatively low quality of the included studies, the above conclusion could be cautiously applied to clinical practice.

Androgens ; therapeutic use ; Hemoglobin A ; metabolism ; Humans ; Hypogonadism ; blood ; drug therapy ; Luteinizing Hormone ; blood ; Male ; Prostate-Specific Antigen ; Randomized Controlled Trials as Topic ; Sex Hormone-Binding Globulin ; metabolism ; Testosterone ; adverse effects ; analogs & derivatives ; blood ; pharmacology

Objective To investigate drug resistance mechanism of aminoglycoside-resistant Acinetobacter baumannii by detecting 16S rRNA methylase gene and three common genes of aminoglycoside-modifying enzymes in Acinetobacter baumannii infected patients at EICU. Methods The 48 Acinetobacter baumannii strains were collected,and antimicrobial susceptibility tests were performed by VITEK automicroscan. The MIC was detected by 2-fold agar dilution method,and genes were analyzed by polymerase chain reaction( PCR) . Results Among 48 strains,28 were highly resistant to aminoglycosides and 20 showed lower resistances. The 16S rRNA armA,APH(3')-I,ANT(3'')-Ia,AAC(6')-Ib genes were detected in 71. 43%,60. 71%,82. 14%, and 53. 57%of the 28 highly resistant strains,but only present in 0. 00%,0. 05%,0. 05%,and 0. 05%of the low-resistant isolates(P<0. 01). Conclusion The aminoglycoside-modifying enzymes and 16S rRNA methylase were frequently found in Acinetobacter baumannii clinical isolates,which is closely related to the high-level resistance to aminoglycoside antibiotics.