Objective To explore the clinical outcomes of Ligament reconstruction tendon interposition (LRTI) arthro-plasty for first carpometacarpal joint osteoarthritis. Methods From January 2008 to January 2011, 19 patients (21 thumbs) had surgery for thumb carpometacarpal arthritis using ligament reconstruction tendon interposition arthroplasty with flexor carpi radia-lis (FCR). There were 1 male and 18 were females with an average age of 60 years (range, 52-75 years);8 thumbs were on the left side and 13 thumbs on the right side. According to Eaton-Glickel classification, 1 thumb belonged to stageⅡ, 14 thumbs to stageⅢ, and 6 thumbs to stageⅣ. Pain level, grip strength, tip pinch strength, range of motion, and radiographic measurement were re-corded. According to the first metacarpal subsidence, the cases were classified in mild, moderate, and severe groups. Clinical out-comes of different group were evaluated and compared. Results All patients were followed up for 9-28 months with an average of 13.9 months. Comparision with the preoperative X-rays showed the first metacarpal had subsided 54.8% of the arthroplasty space after surgery. Grip strength improved from 18.6±10.1 kg to 20.5±11.9 kg, and tip pinch strength increased from 4.4±2.1 kg to 4.5 ± 1.9 kg after the surgery. Radial abduction increased from 55.7° ± 8.2° to 60.6° ± 7.2° and palmar abduction improved from 56.7° ± 8.5° to 63.5° ± 8.2° after the procedure. Patient pain levels (visual analogue scale, VAS) were significantly reduced, from 6.6 ± 1.4 to 0.5 ± 0.7. There was no difference of grip strength, tip pinch strength, thumbs range of motion, and VAS after LRTI in mild, moderate and severe groups. Conclusion LRTI resulted in excellent relief of pain and increase in range of motion. Howev-er, LRTI cannot sustain the arthroplasty space. Compared with the preoperative X-ray, the first metacarpal subsided more than 50%. Subsidence of the first metacarpal doesn't affect the pain relief, range of motion and strength improvement.

A novel rapid method for detection of the illicit beta2-agonist additives in health foods and traditional Chinese patent medicines was developed with the desorption corona beam ionization mass spectrometry (DCBI-MS) technique. The DCBI conditions including temperature and sample volume were optimized according to the resulting mass spectra intensity. Matrix effect on 9 beta2-agonists additives was not significant in the proposed rapid determination procedure. All of the 9 target molecules were detected within 1 min. Quantification was achieved based on the typical fragment ion in MS2 spectra of each analyte. The method showed good linear coefficients in the range of 1-100 mg x L(-1) for all analytes. The relative deviation values were between 14.29% and 25.13%. Ten claimed antitussive and antiasthmatic health foods and traditional Chinese patent medicines from local pharmacies were analyzed. All of them were negative with the proposed DCBI-MS method. Without tedious sample pretreatments, the developed DCBI-MS is simple, rapid and sensitive for rapid qualification and semi-quantification of the illicit beta2-agonist additives in health foods and traditional Chinese patent medicines.

A liquid chromatography-tandem mass spectrometry ( LC-MSMS ) method has been developed for the simultaneous determination of N3-methyladenine ( N3-MeA ) and N3-ethyladenine ( N3-EtA ) in calf thymus DNA. The DNA samples has been purified and enriched by cation exchange cartridge ( Waters Oasis MCX) . d3-N3-MeA and d5-N3-EtA were used as isotope internal standard. The DNA samples were injected with autosampler. The injected volume was 3 μL and analysis time was 13 min. The sample separation was carried out on hydrophilic interaction chromatograph ( Waters XBridge HILIC ) with 10 mmol/L ammonium formate-acetonitrile (5:92, V/V, pH=4. 0) as mobile phase. The flow rate was set at 250 μL/min. Mass spectrometry was performed by electrospray ionization ( ESI ) with multi-reactions monitoring ( MRM ) . The optimized operation conditions of MS were as follows: nebulizer gas 369 Pa; curtain gas 185 Pa, turbo ionspray temperature 400 ℃, ionspray voltage 5500 V, dwell time 40 ms. The limits of detection were 0. 043 and 0. 007 μg/L for N3-MeA and N3-EtA, respectively. The recoveries were between 87. 8% and 103. 0%for N3-MeA and N3-EtA. This method was successfully applied to the determination of N3-MeA and N3-EtA in calf thymus DNA by cigarette smoke condensate ( CSC) exposure. This method is appropriate for routine analysis and accurate quantification of N3-MeA and N3-EtA by CSC exposure.

Objective To estimate the characteristics of gastroesophageal reflux (GER) and its clinical association with pulmonary arterial hypertension (PAH) in systemic sclerosis (SSc) patients.Methods Two hundred and five patients with SSc,who fulfilled the American College of Rheumatology criteria were consecutively recruited.GER was recognized in patients with symptom of heartburn or regurgitation.Demographic,clinical,and laboratory data were analyzed.A six minute walk test,pulmonary function test and modified Rodnan's skin score (mRSS) were also calculated for GER and non-GER groups.x2 test,Fisher's exact test and t-test were used for statistical analysis.Logistic regression test was used for the analysis of risk factors.Results There were 90 patients with GER among 205 patients,the prevalence of GER was 43.9％.The presence of PAH (23.3％ vs 9.6％),Raynaud's phenomenon (98.9％ vs 92.2％ ) and fingertip ulcers (56.7％vs 51.3％) were significantly higher in patients with GER than those without GER.There was no difference in autoantibody profile between GER patients and non-GER patients (P＞0.05).The New York Heart Association (NYHA) functional class of SSc-related GER was worse than patients without GER (P=0.015).Pulmonary function test showed that diffuse capacity (DLCO)％,forced vital capacity (FVC)％,and forced expiratory volume (FEV1)％ were lower and the FVC％/DLCO％ ratio was higher in patients with GER than non-GER (P＜0.05).GER was an independent risk factor of PAH in SSc patients (P=0.047,OR=3.41 ).Conclusion GER frequently occurs in SSc patients,SSc patients presenting with GER should be screened for PAH.Targeting the underlying vascular dysfunction might prevent not only PAH,but also GER in SSc patients.

Aim To investigate whether necroptosis mediates chemical hypoxia-induced HT22 mouse hippocampal cell injury and inflammation.Methods HT22 hippocampal cells were exposed to cobalt chloride (CoCl2) to establish a model of the chemical hypoxia-induced injury and inflammation.The expression level of RIP3 (an index of necroptosis) was determined by Western blot.Cell counter kit-8 (CCK-8) assay was used to test the cell viability.Lactate dehydrogenase (LDH) activity in the culture medium was measured with commercial kits.Mitochondrial membrane potential (MMP) was examined by rhodamine123 staining followed by photofluorography.The intracellular level of reactive oxygen species (ROS) was detected by 2', 7'-dichlorfluorescein-diacetate (DCFH-DA) staining followed by photofluorography.The secretion levels of interleukin-1β (IL-1β) and tumor necrosis factor-a (TNF-α) were measured by ELISA.Results Treatment of HT22 hippocampal cells with 600 μmol·L-1 CoCl2 for 36 h markedly induced cytotoxicity, leading to a decrease in cell viability to (52.0±2.65) % , indicating that chemical hypoxia-induced cellular injury model was successfully set up.Besides, CoCl2 induced considerable injuries and inflammation, evidenced by increases in LDH activity, ROS production, MMP loss, as well as the secretion levels of IL-1β and TNF-α.Co-treatment of the cells with 40~100 μmol·L-1 Nec-1 (a specific inhibitor of necroptosis) and CoCl2 markedly attenuated the decrease in viability induced by CoCl2, reaching the best anti-cytotoxicity inhibitory effect at 80 μmol·L-1.Meanwhile, the co-treatment with 80 μmol·L-1 Nec-1 blocked the above injuries and inflammatory response induced by CoCl2.In addition, treatment of HT22 hippocampal cells for 6~48 h up-regulated the expression of RIP3, and Nec-1 alleviated the up-regulation of RIP3 expression level induced by CoCl2.Conclusion Necroptosis mediates chemical hypoxia-induced HT22 hippocampal cell injury and inflammation.

A high-throughput three-dimensional (3D) hepatocyte culture model is constructed in this study. It is capable of replicating the 3D in vivo environment and offers the advantages of high throughput, enhanced reproducibility, low cost, and simplified operation, rendering a valuable tool for hepatotoxicity screening of traditional Chinese medicine (TCM). First, we constructed the 3D high throughput liver chip model using collagen hydrogel. The precision and its difference with traditional cell culture plates were assessed using acetaminophen, Tripterygium hypoglaucum, and Qili San as the references. The feasibility of this model was also investigated by comparing the hepatotoxicity among four batches of T. hypoglaucum and Qili San. The methodology verification shows that the 3D hepatocyte model is better than traditional two-dimensional (2D) cell culture model in precision and feasibility. Subsequently, we compared the hepatotoxicity of different samples over a period of three or seven days and found that the hepatotoxicity of TCM extracts increased over time. Finally, we compared the hepatotoxicity of T. hypoglaucum and its compound formula Kunxian capsule under equivalent concentration. The results showed that the compound Kunxian capsule could significantly reduce hepatotoxicity of T. hypoglaucum. Generally, we constructed a high-throughput, robust 3D liver-on-a-chip model with the potential of rapid assessing TCM-induced liver toxicity.

Objective To investigate the expressions of carbohydrate antigen 19-9(CA19-9), carbohydrate antigen 15-3(CA15-3) and carbohydrate antigen 125(CA125) and their clinical significance in papillary thyroid carcinoma (PTC). Methods The expressions of CA19-9, CA15-3 and CA125 were detected by immunohistochemical MaxVision method in 80 cases of PTC and 80 cases of benign thyroid lesions (BTL), including 34 cases of nodular goiter, 26 cases of Hashimoto's thyroiditis and 20 cases of follicular adenoma. The relationship between expressions of CA19-9, CA15-3 and CA125 and the clinical pathological characteristics were analyzed. Results The expression rates of CA19-9, CA15-3 and CA125 in 80 cases of PTC were 85%, 100%and 43.8%respectively, compared with BTL, the difference was statistically significant (P < 0.01). There was no significant correlation between expressions of CA19-9, CA15-3 and CA125 and age, gender, number and diameter of tumor nodules, lymph node metastasis, and TNM staging (P > 0.05). The sensitivity of CA19-9, CA15-3 and CA125 in the differential diagnosis of PTC and BTL were 85%, 100% and 43.8% respectively, and the specificity were 91.3%, 36.3%and 91.3%, respectively. Conclusion The expressions of CA19-9, CA153 and CA125 are helpful for the differential diagnosis of PTC and BTL.

AIMTo explore the effects of different doses of tyrosine modulation on behavioral performances in open field test of psychological stress rats.

METHODSThe animal model of psychological stress was developed by restraint stress for 21 days. Wistar rats were randomly assigned to five groups (n = 10) as follows: control group (CT), stress control group (SCT), low, medium and high-doses of tyrosine modulation stress groups (SLT, SMT and SIT). The changes of behavioral performances were examined by open-field test. Serum levels of cortisol, norepinephrine and dopamine were also detected.

RESULTSThe levels of serum cortisol were all increased obviously in the four stress groups, and their bodyweight gainings were diminished. The behavioral performances of SCT rats in open-field test were changed significantly in contrast to that of CT rats. However, The behavioral performances of SMT and SHT rats were not different from that of CT rats. In addition, the serum levels of norepinephrine and dopamine were downregulated obviously in SCT and SLT groups, and no differences were observed in other groups.

CONCLUSIONPsychological stress can impair body behavioral performances, and moderate tyrosine modulation may improve these abnormal changes. The related mechanisms may be involved with the changes of norepinephrine and dopamine.

Animals ; Behavior, Animal ; drug effects ; Dopamine ; blood ; Male ; Norepinephrine ; blood ; Random Allocation ; Rats ; Rats, Wistar ; Restraint, Physical ; psychology ; Stress, Psychological ; drug therapy ; physiopathology ; Tyrosine ; therapeutic use

AIMTo evaluate the effects of different doses of zinc on the expression of metallothionein isoforms in stressed hippocampal neurons in vitro.

METHODSThe cell stress model was developed by corticosterone. The cultured hippocampal neurons were assigned to seven groups as follows: control group, zinc deficiency group, and their corresponding stressed groups, as well as three different levels of zinc complementarity groups.

RESULTSIn zinc deficiency group, the expressions of metallothionein and MT-1 mRNA, MT-3 mRNA were downregulated. On the other hand, inductions of metallothionein and it's mRNAs in stressed zinc complementarity group were increased. In addition, the levels of supernatant IL-6 and NO were increased clearly in zinc deficiency group and corticosterone stressed groups.

CONCLUSIONOur results suggest that zinc deficiency may decrease while zinc complementarity increase the expressions of metallothioneins and MT-1 mRNA, MT-3 mRNA in stressed hippocampal neurons in vitro.

Animals ; Animals, Newborn ; Hippocampus ; cytology ; metabolism ; In Vitro Techniques ; Metallothionein ; metabolism ; Neurons ; metabolism ; RNA, Messenger ; Rats ; Zinc ; pharmacology

AIMTo observe the impairment of homocysteine (Hcy) on neurons in vitro and the related mechanisms.

METHODSWe examined the consequences of treatment of cultured rat cortical and hippocampal neurons with Hcy and detected the neurons' apoptosis, calcium influx, DNA damage and oxidative injury.

RESULTSPrimary cortical and hippocampal neurons were treated with Hcy (250 micromol/L) for 4 h resulted in apoptosis time-dependently. S-adenosyl methionine (SAM) could significantly, but MK-801, an NMDA receptor inhibitor, couldn't repress the Hcy induced neuron apoptosis. Hcy could induce neuron calcium overload through activating the NMDA receptors. The DNA of neurons was damaged by Hcy because the methylation reactions were inhibited. Hcy treatment also induced MDA level significantly increased, but did not affect the neurons' T-AOC.

CONCLUSIONThese findings indicate that Hcy compromises neuronal homeostasis by multiple, divergent routes, including DNA damage, neuron exitotoxicity, and oxidative injury. Hcy mediated neuron apoptosis was mainly due to DNA damage.

Animals ; Apoptosis ; Calcium ; metabolism ; DNA Damage ; Hippocampus ; drug effects ; pathology ; Homocysteine ; metabolism ; pharmacology ; Neurons ; drug effects ; metabolism ; Oxidative Stress ; Rats ; Rats, Wistar