Objective To study the effects of selenium deficiency,iodine deficiency and combined selenium and iodine deficiency on bone and cartilage growth in the parental and the first filial generation rats. Methods Forty-eight weanling healthy SD rats were randomly divided into selenium deficieney, iodine deficiency, combined selenium and iodine deficiency and control groups according to their body mass. These rats were fed with selenium deficiency, iodine deficiency, combined selenium and iodine deficiency, and normal fodder, respectively. The parental rats (about 3 months old) were mated in each group 8 weeks after the beginning of the experiment. Right tibias and left knee joints were collected when the parental generation rats were about 6 months and the first filial generation rats were about 3 months old. Tibial length, mid-shaft tibial diameter, and articular cartilage diameters of the right tibias were measured by vernier caliper. Left knee joints were embedded and cut into sections and the thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes in growth plate cartilage were observed under the light microscope. Results The selenium deficiency had significant effect on serum selenium level of the parental and the first filial generation rats(F value were 239.56,232.68, P< 0.01), and also on serum T4 level of the first filial generation rats(F value were 6.95, P < 0.05). The iodine deficiency had significant effect on serum T3 and T4 level in the two generations rats(F value were 14.11,14.05,30.29,34.53, P < 0.01 ). There were interactions between selenium deficiency and iodine deficiency on serum T4 level in the first filial generation rats (F= 5.99, P< 0.05). The serum selenium of selenium deficiency group[ (30.28 ± 6.34), (43.95 ± 9.75)μg/L],combined selenium and iodine deficiency group[ (30.33 ± 5.18), (35.40 ± 3.16)μg/L] were significantly lower than iodine deficiency group[(345.83 ± 29.55), (245.24 ± 9.95)μg/L] and the controls[ (358.64 ± 30.50), (236.50 ±9.75) μg/L] in the two generations. The serum T3 of combined selenium and iodine deficiency group [(0.55 ± 0.05 ),(0.88 ± 0.14)nmol/L] were significantly lower than the controls[(0.75 ± 0.08), (1.26 ± 0.26)nmol/L] in the two generations. The serum T4 of iodine deficiency [ (24.11 ± 2.29), (42.10 ± 8.92) nmol/L ] and combined selenium and iodine deficiency group[ (20.66 ± 1.93), (26.55 ± 5.98)nmol/L] were significantly lower than the controls[ (36.15 ±2.74), (52.79 ± 8.84)nmol/L] and selenium deficiency group[ (28.12 ± 3.33), (52.02 ± ll.99)nmol/L] in the two generations. The selenium deficiency and iodine deficiency had significant effect on tibial length, thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes in first filial generation rats(F values were 24.31,6.98,40.76,56.15,25.24,82.82, 10.07,5.57, P <0.05 or <0.01). There were interactions between selenium deficiency and iodine deficiency on tibial length, thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes (F values were 5.68,24.86,41.82,9.12, P <0.05 or <0.01 ). The tibial length of the selenium deficiency group[ (33.17 ± 0.34)mm] and combined selenium and iodine deficiency group[ (31.30 ± 0.87)mm] were significantly lower than the controls[ (34.12 ± 0.32)mm, P< 0.05]. Thickness of the growth plate cartilage [ (1.60 ± 0.18)mm ], layers of proliferative chondrocyte (8.54 ± 0.81), and hypertrophic chondrocyte (4.95 ± 0.37)of the combined selenium and iodine deficiency group were significantly decreased when compared to the selenium deficiency group[ (3.03 ± 0.10)mm, 14.68 ± 0.84,6.60 ± 0.31], iodine deficiency group[ (2.90 ± 0.09)mm, 13.75 ±0.33,6.61 ± 0.84 ] and the controls [ (3.19 ± 0.09) mm, 14.94 ± 0.36, 6.64 ± 0.26, P <0.05]. Thickness of the growth plate cartilage, layers of proliferative chondrocyte of the iodine deficiency group were lower than the controls(P<0.05). Conclusions Selenium deficiency impair tibial growth in first filial generation rats, iodine deficiency retarded the chondroncyte proliferation and decreases the thickness of growth plate cartilage in first filial generation rats, and combined selenium and iodine deficiency significantly impair the growth of bone and cartilage in first filial generation rats.

Objective To investigate the infections caused by Staphylococcus aureus carrying Panton-Valentine leukocidin(PVL)genes.Methods 26 isolates of Staphylococcus aureus carrying Panton- Valentine leukocidin(PVL)genes were determined by multiplex PCR.Multilocus sequence typing(MLST) was used to determine the STs of the isolates.The genotypes of SCCmec were also determined by another multiplex PCR in the isolates of methicillin-resistant Staphylococcus aureus(MRSA).Results Among 26 isolates,there were 6 isolates of ST88 MRSA,7 isolates of ST88 methicillin-susceptible Staphylococcus aureus (MSSA),5 isolates of ST239 MRSA,5 isolates of ST398 MRSA,1 isolate of ST25 MRSA,1 isolate of ST30 MRSA and 1 isolate of ST59 MRSA.20 isolates were hospital-acquired(HA)which mainly caused pulmonary infection and post-operative pyogenic infection.6 isolates were community-acquired(CA)which mainly caused soft tissue necrosis.Among 19 isolates of MRSA,ST88-SCCmec Ⅲ A,ST239-SCCmec Ⅲ,ST398- SCCmec Ⅳ and ST398-SCCmec Ⅲ were main types.26 isolates were isolated from 14 wards.ST88-SCCmec Ⅲ A-MRSA caused clone spread in maternity department in our hospital.Conclusion ST88,ST239 and ST 398 are main STs in Staphylococcus aureus carrying PVL in our hospital.The isolates not only cause nosocomial infections but also cause community infection.

OBJECTIVETo investigate the role of Caspase-8 and Bcl-2 in the formation of loose bodies in Kashin-Beck disease (KBD).

METHODSSpecimens of cartilage loose bodies were collected from 50 adult patients with KBD, and the samples of articular cartilage were collected from 10 healthy adults to serve as control. Avidin-biotin alkaline phosphatase immunohistochemistry was employed to examine Bcl-2 and Caspase-8 positivities in the chondrocytes in the loose bodies.

RESULTSIn KBD loose bodies, the percentage of chondrocytes positive for Bcl-2 and Caspase-8 [(18.40∓8.78)% and (67.54∓12.29)%, respectively] were significantly higher than those of the control group [(12.25∓1.58)% and (24.70∓4.35)%, respectively]. Caspase-8 was found to promote chondrocyte apoptosis in the loose bodies, and this effect overrode the apoptosis-suppressing effect of Bcl-2. Bcl-2 and Caspase-8 positivities were found mainly in the deep hypertrophic chondrocytes in the cartilage or in cells adjacent to the bone tissues.

CONCLUSIONKBD loose bodies contain an increased percentage of apoptotic chondrocytes positive for Bcl-2 and Caspase-8. The apoptosis-inducing effect of Caspase-8 was a dominant feature in the cartilage pathology of KBD compared to the apoptosis-suppressing effect of Bcl-2.

Adult ; Apoptosis ; Cartilage ; pathology ; Case-Control Studies ; Caspase 8 ; metabolism ; Female ; Humans ; Joint Loose Bodies ; metabolism ; Kashin-Beck Disease ; metabolism ; pathology ; Male ; Middle Aged ; Proto-Oncogene Proteins c-bcl-2 ; metabolism

OBJECTIVETo study the effect of butenolide (BUT) on cultured chondrocytes differentiation and the possible protective effects of selenium (Se).

METHODSEx-vivo cultured chondrocytes were divided into six groups: (1) Control group (without BUT and Se); (2) Se 0.1 microg/ml control group; (3) BUT 0.1 microg/ml group; (4) BUT 1.0 microg/ml group; (5) BUT 5.0 microg/ml group; and (6) BUT 1.0 microg/ml + Se 0.1 microg/ml group. The expression of collagen II (Col II), collagen X (ColX), basic fibroblast growth factor (bFGF), and parathyroid hormone-related peptide (PTHrP) in (or around) chondrocytes in all groups were analyzed by immunohistochemistry.

RESULTSThe expressions of Col II in 1.0 microg/ml BUT group and 5.0 microg/ml BUT group were significantly lower than those in the control group (P < 0.05). The expression of Col II in 1.0 microg/ml BUT + Se group were significantly higher than those in the 1.0 microg/ml BUT group and 5.0 microg/ml BUT group (P < 0.05). The expressions of bFGF and PTHrP of BUT groups were significantly higher than those in the Se and control groups (P < 0.05). No expression of ColX was observed in all groups.

CONCLUSIONBUT can affect the collagen II synthesis of the chondrocytes. Selenium supplementation may play a protective role.

4-Butyrolactone ; analogs & derivatives ; pharmacology ; Cell Differentiation ; Cells, Cultured ; Chondrocytes ; cytology ; Humans ; Protective Agents ; pharmacology ; Selenium ; pharmacology ; T-2 Toxin ; toxicity

OBJECTIVETo evaluate the early operative treatment and clinical results of pelvic fractures associated with urethra disruption.

METHODSFrom January 1995 to January 2005, 25 patients suffered from pelvic fractures combined urethra disruption treated by operation were retrospectively analyzed. According to Tile's classification, 1 case was stable pelvic fracture, 17 rotational unstable fractures, and 7 rotational combined vertical unstable fractures. The complete urethra rupture were in 23 cases and incomplete in 2 cases. The operative methods included: (1) emergency open reduction and internal fixation of the pelvis combined primary urethra suturing in 2 cases, partial suturing after realignment in 4 cases, realignment in 2 cases, and urethrovaginal penetrating wound repairing in 1 case; (2) primary urethra realignment only and delayed (range, 7 to 21 days) pelvic internal fixation in 10 cases; (3) early cystostomy and delayed (range, 3 to 21 days) urethra realignment and pelvic internal fixation in 6 cases.

RESULTSThe mean follow-up time of all patients was 34 months (range from 6 to 120 months). According to Majeed's evaluation, 17 cases of pelvic injury showed excellent results, 5 good, and 3 fare. After urinary catheter removed, the mean maximal urine flow rate of 19 (76%) patients was 18.6 ml/s and the mean scar length between both disrupted ends on the film of excretion urethrography was 0.51 cm. Five (20%) cases suffered in dysuria needed urethral dilatation or further surgery. One (4%) female could not control urination who need a second-look operation. The primary suprapubic soft tissue avulsion wound infection secondary to retropubic abscess was found in 1 case, posterior urethra-stenosis in 5 cases, sexual impotence in 3 cases, and incontinence in 1 case.

CONCLUSIONSThe satisfactory reduction and effective fixation of the pelvic fractures is an anatomical basis for receiving "tension-free urethral anastomosis".

Adult ; Female ; Follow-Up Studies ; Fracture Fixation, Internal ; Fractures, Bone ; surgery ; Humans ; Male ; Middle Aged ; Pelvic Bones ; injuries ; Postoperative Complications ; prevention & control ; Retrospective Studies ; Time Factors ; Treatment Outcome ; Urethra ; injuries

Objective To investigate the genetic polymorphism of mec Ⅰ in the clinical isolates of methicillin-resistant Staphylococcus anreus(MRSA).Methods 40 isolates(MRSA)carrying mecA gene were selected randomly from the clinical isolates of Staphylococcus anreus from Jan,2005 to Aug,2006 in our hospital.The mec Ⅰ gene was detected by PCR followed with sequencing.Staphylococcal cassette chromosome mec(SCCmec)in MRSA were detected by multiplex-PCR.Agar dilution method was used for determining the MICs of oxacillin against MRSA.Results 35 of 40(87.5%)MRSA carried mec Ⅰ gene.All isolates carrying mec Ⅰ gene have mecI 202C→T substitution,which resulted in Gln at 68 aminophenol position replaced by stop condon.32 isolates carried single point mutation.3 isolates carried double-point mutation,including additonal A at 3 positon,A→C at 41 position and C→T at 142 position beside C→T at 202 position,respectively.Among 35 isolates carrying mec Ⅰ gene,there were 27 isolates of SCCmec Ⅲ, 7 isolates of SCCmec Ⅲ A and 1 isolate of SCCmec Ⅱ.Among 5 isolates with deletion of mec Ⅰ gene,there were 3 isolates of SCCmecⅣ,1 isolate of SCCmec Ⅰ and 1 isolate of non-known SCCmec tpye.The MICs of oxacillin were 256-512 ?g/ml,≥512 ?g/ml and 8-256 ?g/ml in 31 isolates with single point mutation at 202 position in mec Ⅰ gene,3 isolates with double-point mutation in mecI gene and 5 isolates with deletion of mec Ⅰ gene,respectively.1 isolate with single point mutation in mec Ⅰ gene had contrary result(MIC

Objective To investigate feasibility and early stage postoperative complications of lapa-roscopic radical cystectomy ( LRC) . Methods We retrospectively analyzed the data of 63 consecutive pa-tents (58 males and 5 females) who underwent LRC from Oct .2011 to Oct.2013 in our institute.Of these patients, 46 patients underwent ileal conduit , 9 patients underwent ureterocutaneostomy , and 8 patients un-derwent orthotopic ileal neobladder urinary diversion .The average age and body mass index of patients were 67.7±11.1 (33-84) years and 23.3±2.1 (18.8-28.7) kg/m2, respectively.The mean hemoglobin and al-bumin of patients were (130.7±20.3) g/L and (38.9±4.1) g/L, respectively.Comorbidities of hyperten-sion, diabetes, coronary heart disease and decompensated liver cirrhosis were found in 10, 6, 2 and 1 pa-tient, respectively.10 of 61 patients had a history of abdominal surgery .The indications for cystectomy were classified as muscle invasive bladder cancer for 30 patients, unresectable superficial bladder cancer for 19 patients and recurrent bladder cancer for 14 patients.Postoperative data and early stage postoperative compli-cations within 3 months after surgery were collected . Results The median operative time for LRC and uri-nary diversion was 390 (260-480) min, with a median estimated blood loss of 400 (100-1 500) ml.This was one patient converted to open surgery .The mean postoperative hemoglobin and albumin of patients was 108.5±14.7 g/L and 29.5±3.7 g/L, respectively, both of which significantly reduced compared with pre-operative data (P<0.01).The median duration of hospital stay was 15 days.The median time for liquid in-take, abdominal drainage removal and ureteral stent removal was 4 days, 9 days and 2 months after surgery , respectively.Catheter was removed 2 weeks after laparoscopic orthotopic cystectomy .21 (33.3%) of 63 pa-tients suffered from perioperative complications .15 of 46 patients (32.6%) in ileal conduit group had com-plications including ileus ( 5, 1 of 5 need re-operation ) , lymphatic fistulas ( 5) , pulmonary infection ( 1) , pyelonephritis (1), delirium (1), anastomotic leak (1, re-operation was needed) and pneumothorax (1). 2 of 9 patients (22.2%) in ureterocutaneostomy group had complications such as ileus (1) and lymphatic fistulas (1).4 of 8 patients (50.0%) in orthotopic ileal neobladder group suffered from complications like ileus (2, 1 of 2 required re-operation), lymphatic fistulas (1) and arrhythmia (1). Conclusions LRC is technically feasible and safe .It reduces the estimated blood loss and postoperative complications .It is noteworthy to surgeons that serum albumin significantly reduced after LRC , nutrition should be kept balanced after surgery.

OBJECTIVETo investigate chondrocyte apoptosis and expression of Fas and inducible nitric oxide synthase (iNOS) in articular cartilage in the pathogenesis of Kashin-beck disease (KBD) and primary osteoarthritis (OA).

METHODSThe collected samples of articular cartilage were divided into three groups: normal control (15 cases), KBD adults (15 cases) and OA (15 cases). Chondrocyte apoptosis was detected by terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling method, and Fas and iNOS in articular cartilage were stained by immunohistochemistry.

RESULTSThe positive percentages of chondrocyte apoptosis stained in articular cartilage of KBD and OA were significantly higher than that of the control (P < 0.01), and the positive percentage of chondrocytes apoptosis in the eroded areas of articular cartilage were significantly higher than in the non-eroded areas in articular cartilage of the same patient with KBD and OA (P < 0.05). There was no significant difference in positive percentage of chondrocytes apoptosis between KBD and OA. The positive percentages of Fas and iNOS in chondrocytes were significantly higher in KBD and OA than in control (P < 0.01). Significant differences in Fas and iNOS expression between the eroded areas and non-eroded areas were seen in articular cartilage of patients with KBD and OA (P < 0.05), but such difference did not exist between KBD and OA.

CONCLUSIONCell apoptosis seems to be associated with the pathogenesis of both KBD and OA. Fas and iNOS might mediate chondrocyte apoptosis.

Adult ; Apoptosis ; Cartilage, Articular ; pathology ; Chondrocytes ; cytology ; Endemic Diseases ; Female ; Humans ; In Situ Nick-End Labeling ; Male ; Nitric Oxide Synthase ; metabolism ; Osteoarthritis ; pathology ; physiopathology ; Osteoarthritis, Knee ; pathology ; physiopathology ; fas Receptor ; metabolism

OBJECTIVETo observe cell apoptosis and Bcl-2 and Bax expression changes of chondrocytes induced by butenolide (BUT) and the inhibitory effect of selenium against BUT-induced chondrcyte apoptosis, to gain insights into the mechanism by which BUT induces chondrcyte apoptosis.

METHODSCartilage tissue reestablished from human fetal articular chondrocytes in vitro were treated with BUT at the concentrations of 0.1, 1.0 and 5.0 microg/ml and with the protective factor selenium. TUNEL method was used to detect chondrocyte apoptosis, which was quantified by flow cytometry. Immunohitochemistry was performed to analyze the expression of Bcl-2 and Bax in the reestablished cartilage tissue.

RESULTSBUT exposure induced chondrocyte apoptosis, and the apoptosis rate increased with the concentration increment of BUT from 0 to 1.0 mg/ml, resulting also increased positive expression rate of Bcl-2 and Bax(P<0.05). The apoptosis rate of chondrocytes in BUT+ selenium group was significantly lower than that of BUT groups (P<0.05), as was the positivity rate of Bcl-2 and Bax expression (P<0.05).

CONCLUSIONBUT induces chondrocyte apoptosis in positive relation with BUT concentration (from 0 to 1.0 mg/ml) and causes increased expressions of Bcl-2 and Bax. Selenium can inhibit the chondrocyte apoptosis induced by BUT.

4-Butyrolactone ; analogs & derivatives ; pharmacology ; Apoptosis ; drug effects ; Cells, Cultured ; Chondrocytes ; drug effects ; Humans ; In Situ Nick-End Labeling ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Selenium ; pharmacology ; bcl-2-Associated X Protein ; metabolism

OBJECTIVETo explore the effects of selenium and/or iodine deficiency on chondrocyte apoptosis in articular cartilage in rats.

METHODSForty-eight Sprague-Dawley rats were randomly divided into selenium deficiency group, iodine deficiency group, combined selenium and iodine deficiency group, and control group. Chondrocyte apoptosis was detected by terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) method, and Bcl-2 and Bax in articular cartilage were stained by immunohistochemistry in F3 generation of rats.

RESULTSIn articular cartilage, the positive rate of apoptotic chondrocytes stained by TUNEL in the upper and middle zones in selenium deficiency group, iodine deficiency group, and combined selenium and iodine deficiency group (all P < 0.05) were significantly higher than that in control group. The apoptotic chondrocytes were prominent in the middle zone. The positive percentage of chondrocytes apoptosis was not significantly different among these three groups (P > 0.05). Compared with the control group, the expressions of both Bcl-2 and Bax were significantly higher in the upper and middle zone in the selenium deficiency group, iodine deficiency group, and combined selenium and iodine deficiency group (all P < 0.05); however, the expressions of Bcl-2 and Bax were not significantly different among these three groups (P > 0.05).

CONCLUSIONSelenium and/or iodine deficiency may induce chondrocyte apoptosis.

Animals ; Apoptosis ; Cartilage, Articular ; metabolism ; pathology ; Chondrocytes ; metabolism ; pathology ; Female ; Iodine ; deficiency ; Male ; Rats ; Rats, Sprague-Dawley ; Selenium ; deficiency