BACKGROUND:Swel ing after knee arthroplasty can produce tension bul ae, worsen pain, and even block venous return. Thus, intraventricular pressure of osseous fascia increases, which can block arterial blood circulation, even induce osteofascial compartment syndrome.
OBJECTIVE:To evaluate efficacy of Cryf/cuff Systems and intermittent cold compress with hypertonic saline fol owing total knee arthroplasty.
METHODS:A total of 60 patients with unilateral total knee arthroplasty were randomly assigned into two groups. Persistent freezing group received treatment with Cryo/cuff Systems after arthroplasty, and intermittent cold group received intermittent cold compress with hypertonic saline after arthroplasty.
RESULTS AND CONCLUSION:Significant differences in circumference differences in superior patel ar pole, patel ar midpoint, and thickest point of gastrocnemius muscle were detected between persistent freezing group and intermittent cold group at 1 and 2 days after total knee arthroplasty (P<0.05), but no significant difference was detectable at day 3. Visual analogue scale scores at rest and during activity were significantly lower in the persistent freezing group than those in the intermittent cold group at 1 and 2 days after total knee arthroplasty (P<0.01), but no significant difference was visible at day 3. Range of motion was better in the persistent freezing group than that in the intermittent cold group at 1, 2 and 3 days (P<0.01), but no significant difference was observed at 1 and 2 weeks. Mean skin temperature was higher in the persistent freezing group than that in the intermittent cold group at 3 days (P<0.05). Results suggested that Cryf/cuff Systems could lessen tissue swel ing and pain, increased range of motion compared with intermittent cold compress with hypertonic saline at 1 and 2 days after total knee arthroplasty, but no significant difference was detected at day 3. That is, intermittent cold compress with hypertonic saline can reach the same effect as Cryf/cuff Systems at day 3.

Objective To elucidate cerebral cortical response to esophageal acid exposure in normal individuals by functional magnetic resonance imaging (fMRI) and the characteristics of activity. Methods Fifteen volunteers were received intraesophageal perfusion with either 0.9% of sodium chloride or acid (0.1 mmol/L HC1) solutions. The modified block-design model of fMRI scanning was performed simultaneously. All of 32 minutes were needed for resting (A, 8 minutes), 0.9% of sodium chloride perfusion (B,8 minutes), acid perfusion (C,8 minutes) and 0.9% of sodium chloride perfusion again (D,8 minutes). Each chunk was consisted of 160 scans and every scan contained 3 seconds. Six hundred and forty scans were collected in all. The clinical response to esophageal acid exposure was observed and the changes in the cerebral regions was statistically analyzed. Results After perfusion of 0.9% of sodium chloride or acid, 10 out of 15 volunteers had chemosensitive complaints, such as pain in pars laryngen pharyngis, heartburn and chest complaint. The initial active domains involved deutocerebrum, anterior part of callosal gyrus, left side of insula, two sides of amygdale and subiculum hippocampi, two outers of forehead cortex. The provoked regions of acid perfusion (C-A) and 0.9% of sodium chloride perfusion again (D-A) were as same as that of the activated domains by initial perfusion of 0.9% sodium chloride (B-A). The intensity and amplitude of most provoked regions increased gradually(D-A> B-A, P< 0.01). Conclusions The two different stimulations of saline and acid provoke similar cerebral regions that may act in the regulation of esophageal sensitivity. There are the evidences of the central mechanism of esophageal visceral hypersensitivity by acid perfusion.

Objective: To develop a method for determination of carnitine in serum using HPLC. Methods: The serum proteins were precipitated by acetonitrile and methanol. The organic extract was added derivatizing reagent and the solution was warmed to 60℃ for 2 hours. Atlantis C18 column (4.6 mm?150 mm,5?m)was used as stationary phase and methanol-ispropand-acetonitrile (35∶45∶20,v/v) as mobile phase; flow rate 1.0ml/min, UV wavelengh at 260nm. Results: The typical chromatogram from serum samples showed clear separation of carnitine. Y= 8490X-48200, r= 0.9999. Intra-day RSD was 1.6%-13.2%, and inter-day 1.8%-12.1%. The recovery rate was 98.5%. Conclusion: A method for determination of carnitine in serum using HPLC by adding derivatizing reagent was developed and it is simple, rapid and precise, and can be used for clinical test.

In recent years, immunotherapy, especially immune checkpoint inhibitors, has shown obvious advantages in prolonging the survival of patients with advanced tumors, and the tumor microenvironment is one of the important factors affecting the efficacy of immunity. Patients with microsatellite-stable colorectal cancer exhibit immune responses in combination with immune checkpoint inhibitor therapy. In-depth exploration of the tumor microenvironment characteristics of microsatellite-stable colorectal cancer and the application of combined immune checkpoint inhibitor therapy can provide new ideas and directions for colorectal cancer immunotherapy.

Atherosclerosis is the leading cause of ischemic stroke. As a new inflammation biomarker, lipoprotein-asso-ciated phospholipaseA2 (Lp-PLA2) is largely associated with the development of atherosclerosis and plaque vulnerability. It has been recognized that Lp-PLA2 plays crucial roles on assessing the risk stratification and recurrent risk of is-chemic stroke, and may be a unique prediction factor. This review is going to summarize the relevant data about the biochemical characteristics of Lp-PLA2, the action of Lp-PLA2 on atherosclerosis and the association with carotid atherosclerotic and ischemic stroke.

Objective:To investigate the effects of triptolide (TPL) and BET protein inhibitor JQ1 on proliferation inhibition and apoptosis induction of MLL-rearranged acute myeloid leukemia (AML) cell line MV4-11, and to explore their synergistic mechanisms.Methods:MV4-11 cells in logarithmic growth phase were treated with different concentrations (100, 200, 300, and 400 nmol/L) of JQ1, 4 nmol/L TPL or different concentrations of JQ1 combined with 4 nmol/L TPL for 48 h. Cell proliferation was detected by CCK-8 method, apoptosis was detected by flow cytometry (FCM), mitochondrial membrane potential was detected by JC-1 method, and expressions of mitochondrial apoptosis pathway-related proteins were detected by Western blot.Results:The 50% inhibitory concentration ( IC50) value of MV4-11 cells treated with JQ1 for 48 h was (283.9±10.7) nmol/L. However, 4 nmol/L TPL significantly enhanced the inhibitory effect of JQ1 on proliferation of MV4-11 cells, the IC50 value of MV4-11 cells treated with JQ1 combined with TPL was (148.1±2.6) nmol/L, and the difference was statistically significant ( t = 25.31, P = 0.029). The result of FCM assay showed that compared with the JQ1 alone group [(9.6±2.3)%, (12.6±1.4)%, (19.5±3.3)%, and (22.7±2.1)%], 4 nmol/L TPL combined with different concentrations (100, 200, 300, and 400 nmol/L) of JQ1 acted on MV4-11 cells for 48 h, the proportions of apoptotic cells were (16.4±1.9)%, (27.5±2.1)%, (32.9±3.6)%, and (35.5±3.0)%, respectively, the difference was statistically significant ( F = 9.25, P < 0.01). After treated with 4 nmol/L TPL and JQ1 for 12 h, the level of cell membrane potential in MV4-11 cells was significantly lower than that of JQ1 single agent group, and the difference was statistically significant ( P < 0.05). After treated by 4 nmol/L TPL combined with JQ1 for 24 h, the levels of anti-apoptotic proteins bcl-2 and Mcl-1 decreased, and the level of pro-apoptotic protein bax increased. Conclusion:TPL can significantly enhance the proliferation inhibition and apoptosis induction effects of BET protein inhibitor JQ1 on MLL-rearranged AML cells, and the mechanism may be related to enhancing the mitochondrial apoptosis pathway.

Objective To evaluate the effect of micronutrient selenium on atopic dermatitis-like skin lesions in mice.Methods After 4-week feed with forages lacking selenium,40 BALB/c mice were randomly and equally divided into 4 groups:selenium deficiency group fed with forages containing 0.01 mg/kg selenium for 4 weeks,normal selenium supplementation group fed with forages containing 0.25 mg/kg selenium for 4 weeks,excessive selenium supplementation group fed with forages containing 3.00 mg/kg selenium for 4 weeks,and control group fed with forages containing 0.25 mg/kg selenium for 4 weeks.Then,atopic dermatitis-like skin lesions were induced by dinitrochlorobenzene (DNCB) in the mice in sensitized groups,including the selenium deficiency group,normal selenium supplementation group and excessive selenium supplementation group.During sensitization,the severity of dermatitis in mice was monitored.Three weeks after the sensitization,the total plasma IgE level and inflammatory cell count in whole blood were measured.Skin tissues from the back of mice were subjected to histopathological examination and the selenium level was detected.Statistical analysis was carried out by one-way analysis of variance for comparisons of IgE levels and cell counts among different groups,as well as by Pearson correlation analysis and linear regression analysis for analyzing the correlation of various indices with the selenium level.Results Six days after the sensitization,the dermatitis severity scores were significantly higher in the sensitized groups than in the control group (On day 6,8,11,13,15 and 18 after the sensitization,F =44.897,76.622,114.866,33.352,28.605 and 11.271 respectively,all P ＜ 0.01).On day 11 after the sensitization,the dermatitis severity score was significantly higher in the excessive selenium supplementation group than in the selenium deficiency group and normal selenium supplementation group (both P ＜ 0.05).Compared with the control group,obvious pathological changes of dermatitis were observed in the sensitized mice,but there was no significant difference in the number of inflammatory cells in skin lesions among the 3 sensitized groups (all P ＞ 0.05).The inflammatory cell count in whole blood and total plasma IgE level in the sensitized mice increased along with the increase of dietary selenium levels,and the excessive selenium supplementation group showed higher total plasma IgE level ([167.17 ±8.49] μg/L) compared with the selenium deficiency group ([124.78 ± 5.32] μg/L,t =3.919,P ＜ 0.05),normal selenium supplementation group ([132.61 ± 4.71] μg/L,t =3.222,P ＜ 0.05) and control group ([109.13 ± 0.79] μg/L,t =6.485,P ＜ 0.05).The selenium level in the skin tissues of sensitized mice was positively linearly correlated with the total plasma IgE level (r =0.579,P ＜ 0.001),whole-blood white blood cell count (r =0.414,P ＜ 0.05),neutrophil count (r =0.439,P ＜ 0.05),lymphocyte count (r =0.417,P ＜ 0.05)and eosinophil count (r =0.505,P ＜ 0.01).Conclusion Different dietary selenium levels showed different effects on the severity of dermatitis in mice,and more severe dermatitis occurred in the excessive selenium supplementation group.

Objective:To explore the effects of apatinib on the proliferation and apoptosis of FLT3-ITD mutant acute myeloid leukemia (AML) cells, and to explore the related mechanisms.Methods:The logarithmic growth phase FLT3-ITD mutant AML cell lines MV4-11 and MOLM-13 were treated with different concentration of apatinib for 48 hours. The cell proliferation was detected by CCK-8 method. Flow cytometry was performed to examine the effect of apatinib on apoptosis. The cell mitochondrial membrane potential changes were detected by JC-1. Then the expression changes of vascular endothelial growth factor receptor 2 (VEGFR2) pathway-related proteins were examined by Western blot.Results:Apatinib had proliferation inhibitory effects on both MV4-11 and MOLM-13 cells, and the half-maximal inhibitory concentration (IC 50) at 48 hours was (2.23±0.42) μmol/L and (4.08±2.62) μmol/L, respectively. After exposure to apatinib with increasing concentrations (10, 20, 30, and 40 μmol/L) for 48 h hours, the percentage of apoptotic cells was significantly increased in MV4-11 cells [(81.95±1.15)%, (88.80±0.23)%, (97.46±0.49)%, and (99.29±0.05)%] and MOLM13 cells [(47.30±0.87)%, (67.00±3.71)%, (82.60±2.89)%, and (98.06±5.34)%] in a dose-dependent manner, and the differences were statistically significant ( F = 6 915.0, P < 0.01; F = 5 385.0, P < 0.01). Detection of mitochondrial membrane potential by JC-1 method showed that after MV4-11 and MOLM-13 cells were treated by 10, 20, 30, and 40 μmol/L apatinib for 24 hours, the JC-1 aggregate/monomer mean fluorescence intensity (MFI) ratios were 0.45±0.06, 0.19±0.07, 0.12±0.03, 0.09±0.01, and 0.84±0.05, 0.66±0.13, 0.35±0.11, 0.27±0.02, which were different from the control group (0.67±0.15 and 0.97±0.42), and the differences were statistically significant ( F = 372.3, P < 0.05; F = 276.4, P < 0.05). Western blot was performed to detect different concentration of apatinib (2.5, 5.0 and 10.0 μmol/L) on the MV4-11 cells for 24 hours, the results showed that apatinib could down-regulate the phosphorylation of VEGFR2, Src and Stat3 in a dose-dependent manner. Conclusions:Apatinib can inhibit cell proliferation and induce apoptosis in AML with FLT3-ITD mutation. The possible mechanism is related to the down-regulation of phosphorylation of VEGFR2 and its downstream targets Src and Stat3.

Objective: To investigate the pathogen spectrum distribution and drug resistance of febrile neutropenic patients with hematological diseases in Shanghai. Methods: A retrospective study was conducted on the clinical isolates from the febrile neutropenic patients hospitalized in the departments of hematology in 12 general hospitals in Shanghai from January 2012 to December 2014. The drug susceptibility test was carried out by Kirby-Bauer method. WHONET 5.6 software was used to analyze pathogenic bacteria and drug susceptibility data. Results: A total of 1 260 clinical isolates were collected from the febrile neutropenic patients. Gram-positive bacteria accounted for 33.3% and Gram-negative bacteria accounted for 66.7%. Klebsiella pneumoniae (12.5%) , Stenotrophomonas maltophilia (9.5%) , Escherichia coli (9.1%) , Pseudomonas aeruginosa (8.7%) , Acinetobacter baumannii (6.6%) , Staphylococcus aureus (5.6%) and Enterococcus faecium (5.0%) were ranked in the first 7 of all pathogens. In the respiratory tract secretions specimens, non-fermented strains accounted for 56.2%. Stenotrophomonas maltophilia accounted for 15.2%. Enterobacteriaceae and coagulase-negative Staphylococci accounted for 42.3% (104/246) and 32.6% (85/246) respectively in blood samples. Enterobacteriaceae and Enterococcus bacteria accounted for 39.4% (76/193) and 28.5% (55/193) respectively in pus specimens. The detection rates of methicillin resistant Staphylococcus aureus (MRSA) and methicillin resistant coagulase negative Staphylococci (MRCNS) were 54.3% and 82.5%, respectively. Staphylococcus bacterial strain was not found to be resistant to linezolid, vancomycin and teicoplanin. The detection rate of Enterococcus vancomycin-resistant strains was 8.9%. Enterococcus was not detected resistance to oxazolidinone strains. Enterobacteriaceae bacteria were highly sensitive to carbapenems. The resistance rate of Pseudomonas aeruginosa to imipenem and meropenem was 34.1% and 15.8%, respectively. Stenotrophomonas maltophilia was more sensitive to minocycline hydrochloride, levofloxacin and sulfamethoxazole. The resistance rate of Acinetobacter baumannii only to cefoperazone-sulbactam was less than 10.0%. The antibiotic resistance rate of Klebsiella pneumoniae, Stenotrophomonas maltophilia, Pseudomonas aeruginosa and Acinetobacter baumanii to most of common antibiotics was lower than that of the CHINET surveillance. Conclusions The pathogenic strain distribution in common infection sites of febrile neutropenic patients was characterized. Bacterial resistance surveillance was better than the CHINET nationwide large sample surveillance in China.

OBJECTIVE: To explore the effects of nano-silicon dioxide( SiO_2) on the survival and poly( ADP-ribose)polymerase-1( PARP-1) expression in human bronchial epithelial cells( 16 HBE cells). METHODS: i) The 16 HBE cells were treated with nano-SiO_2 at concentrations ranging from 0 to 100 mg/L for 24. 0 hours,and CCK-8 assay was used to examine cell viability. ii) The 16 HBE cells were divided into 6 groups: solvent control group( equal volume solvent treatment),micro-SiO_2 control group( treated with 20 mg/L micro-SiO_2),5,10,and 20 mg/L nano-SiO_2 groups( treated with the corresponding final dose of nano-SiO_2),and curcumin group. The curcumin group was given pretreatment with curcumin at a final concentration of 10 μmol/L for 2. 0 hours followed by treatment with a final concentration of 20 mg/L of nano-SiO_2. Cells in each group were harvested at time points of 4. 0,12. 0 and 24. 0 hours after treatment. The relative expression of PARP-1 mRNA and protein in 16 HBE cells was detected by quantitative real-time polymerase chain reaction and Western blotting respectively. RESULTS: i) The survival of 16 HBE cells decreased with increasing nano-SiO_2 treatment dose,showing a dose-effect relationship( P < 0. 01). ii) The expression of PARP-1 mRNA and protein in 16 HBE cells were dose-dependently decreased after nano-SiO_2 stimulation at the 12. 0 and 24. 0 hours time points( P < 0. 01). The expression of PARP-1 mRNA and protein in 5,10,and 20 mg/L nano-SiO_2 groups decreased at the above mentioned time points( P < 0. 05),compared with the solvent control group at the same time points. The expression of PARP-1 mRNA and protein in 20 mg/L nano-SiO_2 group was lower than that in the micro-SiO_2 control group at the same 12. 0 and 24. 0 hours time point( P < 0. 05). The above two indexes of cells were higher in curcumin group than that of 20 mg/L nano-SiO_2 group at the 12. 0 hours time point( P < 0. 05). CONCLUSION: Nano-SiO_2 stimulation can lead to decrease survival of 16 HBE cells in a dose-dependent manner and down-regulation of PARP-1 expression may be one of the mechanisms of proliferation and inhibition of 16 HBE cells induced by nano-SiO_2. Curcumin has certain protective effect on nano-SiO_2-induced 16 HBE cell injury.