BACKGROUND:For evaluation of risks of periprosthetic fractures in elderly patients aged>75 years old after hemiarthroplasty, we should perform dynamic observation of postoperative physical health status, quality of life, hip function and bone mineral density. Presently, there is lack of general investigation.
OBJECTIVE:To provide references for clinical diagnosis and prediction of periprosthetic fractures after hemiarthroplasty in elderly patients.
METHODS:On the basis of arranging the exploration results of recent studies on risk factors for periprosthetic fractures of hip joint, we analyzed the monitoring method of scholars concerning fracture-associated risk factors. Simultaneously, in combination of the development of modern inspection sciences, the method was applied in the clinic. Thus, we summarized general evaluation methods with clinical significance for risk factors of prosthesis fracture in elderly patients after hemiarthroplasty.
RESULTS AND CONCLUSION:For elderly patients with femoral neck or intertrochanteric fracture combined with various medical il ness, hemiarthroplasty is an effective manner presently. Fractures surrounding the prosthesis in elderly patients postoperatively gradual y increased. Once fracture appeared, it would bring a great attack on patients’ spirit, economy and even life. Therefore, early evaluation on the risk factors for fractures surrounding the prosthesis is a necessary measure for preventing and saving this disastrous consequence by selecting general correct prevention and treatment strategies. This wil greatly improve patients’ prognosis and elevated patient’s quality of life and survival rate. Present short-term smal-sample prospective fol ow-up studies suggested that comprehensive dynamic evaluation possibly has a certain clinical significance for the evaluation of risks of fractures after hemiarthroplasty in elderly patients, and deserves further investigations.

Objective To evaluate the effect of propofol on invasiveness of human gastric cancer MKN-45 cells.Methods Human gastric cancer cell line MKN-45 were seeded in culture plates.After being cultured for 24 h,the cells were randomly divided into 5 groups(n =12 each):control group (group C),intralipid group (group Ⅰ),4 μg/ml propofol group (group P1),8 μg/ml propofol group (group P2) and 16μg/ml propofol group (group P3).The cells were treated with 10％ intralipid and 4,8 and 16 μg/ml propofol for 24 h in I and P1-3 groups,respectively.The cells were then cultured for another 24 h.The migration of cells was determined by cell scratch test.The invasion of cells was determined by Transwell invasion assay.The expression of RhoA and ROCK1 was detected by Western blot.Results Compared with group C,the cell migration and invasion were significantly decreased,and the expression of RhoA and ROCK1 was down-regulated in P1-3 groups,and no significant changes were found in the parameters mentioned above in group Ⅰ.With the increasing concentrations of propofol,the cell migration and invasion were gradually decreased,and the expression of RhoA and ROCK1 was gradually down-regulated in P1-3 groups.Conclusion Propofol can inhibit the invasiveness of human gastric cancer MKN-45 cells cultured in vitro dose-dependently and inhibition of RhoA/ROCK1 signaling pathway may be involved in the mechanism.

Objective To evaluate the role of interleukin-4 receptor (IL-4R) in renal fibrosis following renal ischemia-reperfusion (I/R) injury in mice.Methods Twelve male wild type BALB/C mice and 12 IL-4Rα gene-knockout mice,aged 8-10 weeks,weighing 20-30 g,were used in the study.The mice of either type were divided into 2 groups (n =6 each) using a random number table:sham operation group (group S) and group I/R.In group I/R,renal I/R was induced by occlusion of the right renal artery for 1 h with atraumatic microclips followed by 2 weeks of reperfusion.The right renal artery was only isolated in group S.At 2 weeks of reperfusion,blood samples were taken from the orbital vein for determination of the concentrations of serum blood urea nitrogen (BUN) and creatinine (Cr).The renal tissues were obtained,and the renal fibrosis area was measured by Sirius Red staining.The expression of fibronectin (FN),collagen Ⅰ (COL-Ⅰ) and α-smooth muscle actin (α-SMA) in renal tissues was detected by immunofluorescence.The expression of signal transducer and activator of transcription 6 (STAT6) and phospho-STAT6 in renal tissues was determined by Western blot.The ratio of phoshop-STAT6 to STAT6 was calculated to reflect the phosphorylation of STAT6.Results Compared with group S of wild type mice,the serum BUN and Cr concentrations and renal fibrosis area were significantly increased,the expression of FN,COL-Ⅰ and α-SMA in renal tissues was significantly up-regulated,and the phosphorylation of STAT6 in renal tissues was significantly increased in group I/R of wild type and IL-4Rα KO mice (P＜0.05).Compared with group I/R of wild type mice,the serum BUN and Cr concentrations and renal fibrosis area were significantly decreased,the expression of FN,COL-Ⅰ and α-SMA in renal tissues was significantly down-regulated,and the phosphorylation of STAT6 in renal tissues was significantly decreased in group I/R of IL-4RαKO mice (P＜0.05).Conclusion The mechanism of renal fibrosis following renal I/R injury is partially related to IL-4R,and IL-4R results in renal fibrosis through promoting activation of STAT6 signaling pathway in mice.

ObjectiveTo establish a rat model of nerve damage induced by intrathecal(IT) lidocaine.MethodsFifty-five adult male SD rats weighing 200-220 g were randomly divided into 5 groups (n =11 each):group normal control (group C); group dimethyl sulfoxide (DMSO)-the solvent(group D) and groups IT 5％,10％,15％ lidocaine (groups L5.10.15 ).IT catheter was successfully implanted without complication in groups D,L5,L1o,L15.DMSO,5％,10％ and 15％ lidocaine 20 μl were injected IT in groups D,L5,L10,L15 respectively.Motor dysfunction of hindlimb was assessed and scored (0 =normal,2 =complete block) and paw withdrawal threshold to mechanical stimulation (von Frey filaments) (MWT) and paw withdrawal latency to thermal nociceptive stimulus (TWL) were measured before (baseline) and at 1,2,3,4,5,7 d after IT administration in 8 animals in each group.Three animals in each group were sacrificed at 1 d after IT administration.The lumbar segment (L4-5) was removed for microscopic examination.ResultsThere was no significant difference in motor dysfunction score,MWT and TWL among groups C,D and L5.MWT was significantly increased and TWL prolonged at 1 and 2 d after IT administration in group L10,while in group L15 motor dysfunction score was significantly increased at 1,2 d after IT administration and MWT was significantly increased and TWL prolonged at 1,2,3 d after IT administration.There was significant histologic damage to spinal cord in groups L10 and L15.Conclusion Nerve damage can be induced by IT 10％ lidocaine.

Objective To investigate the effects of different concentrations of parecoxib on proliferation and apoptosis of colon cancer LoVo cells.Methods The colon cancer LoVo cells were inoculated in cuhure plate and cultured for 24 h.The cells were randomly divided into 4 groups (n =6 each):control group (C group) and different concentrations of parecoxib groups (P1-3 groups).The cells were incubated with parecoxib 10,40 and 160μmol/L for 24 h in P1-3 groups respectively.The rates of proliferation inhibition were measured by MTT assay.The colony formation rates were measured by colony formation assay.The apoptotic rate was determined by flow cytometry.The Survivin and caspase-3 mRNA expression in the cells was detected by RT-PCR.Results Compared with C group,the rates of proliferation inhibition and apoptotic rate were significantly increased,the colony formation rates were significantly decreased,the expression of Survivin mRNA was down-regulated,and the expression of caspase-3 mRNA was up-regulated in a concentration-dependent manner in P1-3 groups (P ＜ 0.05).Conclusion Parecoxib can inhibit the proliferation of LoVo cells and induce the apoptosis in LoVo cells in a concentration-dependent manner through down-regulating the expression of Survivin mRNA and up-regulating the expression of caspase-3 mRNA.

ObjectiveTo compare the effects of different general anesthesia protocols on perioperative cellular immune function in patients undergoing laparoscopic surgery for colorectal cancer.MethodsNinety ASA Ⅰ or Ⅱ colorectal cancer patients aged 40-64 yr weighing 50-85 kg undergoing laparoscopic surgery were randomly divided into 3 groups (n ＝ 30 each):group total intravenous anesthesia (group Ⅰ ); group inhalational anesthesia (group Ⅱ ) and group combined intravenous-inhalational anesthesia(group Ⅲ ).Anesthesia was induced with iv midazolam,sufentanil,TCI of propofol and remifentanil and vecuronium in groups [ and Ⅲ.In group Ⅰ anesthesia was maintained with TCI of propofol and remifentanil and intermittent iv boluses of vecuronium,while in group Ⅲ with inhalation of sevoflurane and intermittent iv boluses of vecuronium.In group Ⅱ anesthesia was induced and maintained with inhalation of sevoflurane and intermittent iv boluses of vecuronium.Narcotrend index was used to monitor depth of anesthesia and maintained at 37-64 during operation.Venous blood samples were taken for determination of the levels of T lymphocyte subsets (CD3+,CD4+,CD8+,CD4+/CD8+ ) and natural killer cells at 30 min before induction of anesthesia (T0 ),2 h after skin incision (T1),at the end of operation (T2 ) and 24 hafter operation (T3 ).ResultsThe levels of CD3+,CD4+,CD4+/CD8+ and natural killer cells were significantly decreased at T2 in group Ⅱ,while the levels of natural killer cells were decreased at T2 in group Ⅲ as compared with the baseline at T0,and were significantly lower than those in group Ⅰ.The levels of CD3 + and CD4+were significantly lower at T2 in group Ⅱ than in group Ⅲ.ConclusionIntravenous anesthesia with midazolam,propofol,sufentanil,remifentanil and vecuronium has less inhibitory effect on perioperative cellular immune function than inhalational anesthesia and combined intravenous-inhalational anesthesia in patients undergoing laparoscopic surgery for colorectal cancer.

Objective To evaluate the effects of dexmedetomidine on the cellular immune function of the rats with scald.Methods Seventy-two healthy male Sprague-Dawley rats,weighing 200-220 g,aged 120-150 days,were randomly divided into 3 groups (n =24 each):normal control group (group C),scald group (group S) and dexmedetomidine group (group D).Thirty percent of the total body surface was shaved and then exposed to 94 ℃ water for 12 s in S and D groups.The rats were resuscitated according to Parkland formula after scald in S and D groups,and in addition,dexmedetomidine 30 μg/kg was also intraperitoneally injected immediately after scald in D group.Before the model was established (T1) and at 12 and 24 h after scald (T2,3),blood samples from the inferior vena cava were collected for determination of T lymphocyte subsets CD3 +,CD4 + and CD8 +,NK cell,C-reactive protein (CRP),interleukin-6 (IL-6),IL-10 and tumor necrosis factor-alpha (TNF-α) level.CD4+/CD8+ was calculated.Arterial blood samples were collected for blood gas analysis.Results Compared with C,the CD3+,CD4+ and NK cell levels,CD4+/CD8+,pH value,PaCO2 and PaO2 were significantly decreased,and CD8+ levels,IL-6,IL-10,TNF-α,CRP and BE negative value were increased at T2,3 in S and D groups.Compared with group S,the CD3+,CD4+,NK cell and IL-10 levels,CD4+/CD8+,pH value,PaCO2 and PaO2 were significantly increased,and CD8+ levels,IL-6,TNF-α,CRP and BE negative value were decreased at T2,3 in group D.Conclusion Dexmedetomidine can improve the cellular immune function of the rats with scald.

Objective To evaluate the role of calcium/calmodulin-dependent protein kinase Ⅱ (CaMK Ⅱ) in the up-regulation of expression of Cav3.2 T-type calcium channels in spinal cord in a rat model of neuropathic pain (NP).Methods Forty-eight male Sprague-Dawley rats,aged 3 months,weighing 220-250 g,were randomly divided into 6 groups (n =8 each)∶ sham operation group (group S),group NP,dimethyl sulfoxide group (group D) and different concentrations of a specific CaMK Ⅱ inhibitor KN93 groups (groups K1-3).NP was produced by chronic compression of dorsal root ganglion.The rats in groups D and K1-3 received a single intrathecal injection of dimethyl sulfoxide and KN93 15,30,60 nmol/L (10 μl),respectively,on 5th day after NP.Paw withdrawal threshold to von Frey filament stimulation (MWT) and paw withdrawal latency to thermal nociceptive stimulus (TWL) were measured before NP,before intrathecal injection on 5th day after NP,and at 30 and 60 min and 3,6 and 8 h after intrathecal injection on 5th day after NP (T1-7).The rats were sacrificed after the measurement of pain threshold at T7 and their lumbar enlargements were removed to detect the expression of Cav3.2 mRNA and protein using Western blot and RT-PCR.Results Compared with group S,MWT was significantly decreased,TWL was shortened and the expression of Cav3.2 mRNA and protein was up-regulated in NP,D and K1-3 groups (P ＜ 0.05).Compared with NP group,MWT was significantly increased,TWL was prolonged and the expression of Cav3.2 mRNA and protein was down-regulated in a concentration-dependent manner in K1-3 groups (P ＜ 0.05),and no significant change was found in the parameters mentioned above in group D (P ＞ 0.05).Conclusion CaMK Ⅱ is involved in the development and maintenance of chronic NP by up-regulating the expression of Cav3.2 T-type calcium channels in rat spinal cord.

Objective To evaluate the role of calcium/calmodulin-dependent protein kinase Ⅱ (CaMK Ⅱ) in the neuronal damage induced by lidocaine.Methods SH-SY5Y cells were seeded in 96-well plates (100 μl/hole) with a density of 5 × 105/ml and randomly divided into 4 groups (n =63 each):normal culture group (C group),CaMK Ⅱ inhibitor KN93 (K group),lidocaine group (L group) and KN93 + lidocaine group (KL group).KN93 (final concentration 1 μmol/L) was added to the culture medium and the cells were then cultured for 24 h in group K.Lidocaine (final concentration 10 mmol/L) was added to the culture medium and the cells were then cultured for 24 h in group L.KN93 (final concentration 1 μmol/L) and lidocaine (final concentration 10 mmol/L) were added to the culture medium and the cells were then cultured for 24 h in group KL.The cell morphology was examined with microscope after 24 h of incubation.The viability of cells was measured by MTT assay before incubation and at 1,6,12 and 24 h of incubation.The apoptosis in the cells was assessed by flow cytometry.The apoptotic rate was calculated.Results Compared with C and K groups,the cell viability was significantly decreased and the apoptotic rate was increased in L and KL groups (P ＜ 0.05).The cell viability was significantly higher and the apoptotic rate was lower in group KL than in group L (P ＜ 0.05).There was no significant difference in the cell viability and apoptotic rate between C group and K group (P ＞ 0.05).The pathological changes were obviousin group L and significantly reduced in group KL.Conclusion CaMK Ⅱ is involved in the neuronal damage induced by lidocaine.

Objective To investigate the effects of dexmedetomidine on perioperative cellular immune function and micro-metastasis in blood circulation in patients undergoing radical operation for colon cancer.Methods Sixty ASA Ⅰ or Ⅱ patients,aged 38-69 yr,weighing 45-67 kg,undergoing radical operation for colon cancer,were randomly divided into 2 groups (n =30 each) ∶ dexmedetomidine group (D group) and control group (C group).Anesthesia was induced with midazolam,cisatracurium and sufentanil,and maintained with propofol,remifentanil and sevoflurane.After tracheal intubation,a loading dose of dexmedetomidine 1 μg/kg was injected intravenously,followed by infusion at 0.5μg· kg-1 · h-1 until the end of operation in D group.The equal volume of normal saline was administered in C group.Venous blood samples were obtained at 5 min before induction of anesthesia (T0),1 h after beginning of operation (T1),the end of operation (T2) and 24 h after the end of operation (T3) for determination of the levels of T lymphocyte subsets (CD3+,CD4+,CD8+) and NK cells by flow cytometry.CD4+/CD8+ ratio was calculated.Cytokeratin 20 (CK20) expression in circulation was detected by RT-PCR at T0 and T3 and the positive rate was calculated.Results Compared with the baseline value at T0,the levels of CD3+ and CD4+,CD4+/CD8+ ratio and level of NK cells were significantly decreased at T2 and T3 in group C,and the levels of CD3+ and CD4+ were significantly decreased at T2 and T3 in group D (P ＜ 0.05).The levels of CD3+,CD4+ and NK cells at T2 and T3 were significantly higher and positive rate at T3 was significantly lower in group D than in group C (P ＜ 0.05).Conclusion Dexmedetomidine can improve the cellular immune function and decrease the probability of micro-metastasis in blood circulation in patients undergoing radical operation for colon cancer.