Objective To study the middle ear damage caused by high pressure. Methods The finite element model of human middle ear was established based on CT scanning, and the change of stress, strain and displacement of the tympanic membrane and the stapes footplate was analyzed when the model was applied with time-varying pressure. Results The satisfactory agreement between the computational results and the corresponding experimental data in the literature indicated the validity of the model. High pressure would cause damage to the middle ear, and the damage would increase with the pressure increasing. Rapid pressurization could severely damage the middle ear, but with a small effect on the inner ear. Slow pressurization could also lead to the middle ear damage, but the inner ear might be damaged before the damage to the middle ear. Conclusions High pressure can easily lead to the ear damage; therefore, the pressurized rate should be controlled strictly during pressurization in order to protect the hearing.

Objective To study the middle ear damage caused by high pressure.Methods The finite element model of human middle ear was established based on CT scanning,and the change of stress,strain and displacement of the tympanic membrane and stapes footplate was analyzed when the model was applied with timevarying pressure.Results The satisfactory agreement between the computational results and the corresponding experimental data in the literature could indicate the validity of the model.High pressure would cause damage to middle ear,and the damage would be aggravated with the pressure increasing.Rapid pressurization could make severely damage to middle ear,but have minor effect on inner ear.Slow pressurization could also lead to middle ear damage,but inner ear might be damaged before the injury to middle ear.Conclusions High pressure can easily lead to the ear damage;therefore,the pressurized rate should be controlled strictly to protect the hearing during pressurization.

AIM: To study the inhibitory effects of nm23-H1 gene on proliferation and invasion of human lung adenocarcinoma A549 cell line. METHODS: Recombinant eukaryotic expression vector pcDNA3.1-nm23-H1 containing full length of human nm23-H1 cDNA was constructed and transfected into a human lung adenocarcinoma A549 cell line by lipofectamine. Cell strain that expressed nm23-H1 stably was screened out by G418 and named pcDNA-nm23-A549. Expression of nm23-H1 was identified by RT-PCR and immunohistochemistry. Growth curves were drawn to detect the inhibitory effects on cell proliferation. Cell cycle of pcDNA-nm23-A549 was examined by flow cytometry. Atomic force microscopy was used to observe the filopodia on the surface of the cells. RESULTS: Introduction of nm23-H1 obviously inhibited the proliferation of A549. Expression of nm23-H1 did not induce apotosis in A549 cells but increased the percentage of phase G_1 cells and decreased phase S cells. Meanwhile, phase G_1 to phase S transition was restrained. Filopodia in the cell surface was much fewer and its structure changed in cells transformed. CONCLUSION: nm23-H1 is capable of inhibiting A549 proliferation and decreasing its metastatic ability, probably by interfering with cell cycle and cell surface structure.

0.05), but the level of albumin dropped significantly(P

Objective To observe myocardial tolerance to ischemia/reperfusion (I/R) injury in rats after exposure to X-ray irradiation.Methods Twelve male rats were randomly divided into control group and radiation group.The rat model of radiation-induced heart disease was established in the radiation group by precordial irradiation with 20.0 Gy of 6 MV X-ray in a single fraction.At 14 days after model establishment,the Langendorff perfusion technique was performed in the two groups and the cardiac parameters including left ventricular developing pressure (LVDP),left ventricular end diastolic pressure (LVEDP),maximal rate of left ventricular pressure rise/fall (+/-LVdp/dtmax),and coronary flow (CF)were recorded.Myocardial infarct size after I/R was compared between the two groups by 2,3,5-triphenyltetrazolium chloride staining.Results After 30 minutes of ischemia and 60 minutes of reperfusion,the irradiation group had a significantly slower CF than the control group (5.64±0.35 vs.8.38±0.52 ml/min,P=0.002).Moreover,the irradiation group had substantially poorer recovery of cardiac function in isolated hearts compared with the control group,as shown by a significantly reduced LVDP (25.4±2.31 vs.52.76±2.76 mm Hg(1 mm Hg=0.133 kPa),P=0.000),significantly reduced+/-LVdp/dtmax(547.04±78.74 vs.1 100.05±83.35 mm Hg(1 mm Hg=0.133 kPa)/s,P=0.001;-408.81±56.74 vs-813.62±73.82mm Hg(1 mm Hg =0.133 kPa)/s,P=0.002),and a significantly increased LVEDP (85.29±4.61 vs.65.65±3.65 mm Hg (1 mm Hg =0.133 kPa),P=0.012).X-ray irradiation induced a significantly increased percentage of myocardial infarct size in rats (44.67％±0.95％ vs.30.46％±0.96％,P=0.000).Conclusions X-ray irradiation can induce coronary injury,reduce myocardial tolerance to I/R injury,and increase myocardial infarct size after I/R in rats.

Objective:To investigate the change of biological characteristics after stable knockdown of CKLF-like MARVEL transmembrane domain containing 3 (CMTM3)expression in PC3 by lentivirus shRNA and to reveal new therapeutic targets.Methods:The research includes two groups:sh393 is the experimental group in which CMTM3 is knocked down in PC3 cell line;shN is the control group in which CMTM3 is negatively knocked down.The expression of CMTM3 was detected by Western blot.The mi-gration ability of PC3 after stable knockdown was detected by Transwell and Wound healing assay.The invasion ability of PC3 was detected by Matrigel assay.Results were obtained from at least three indivi-dual experiments.Results:The expression of CMTM3 in sh393 group is significant lower than shN group (0.004 0 ±0.000 4 vs.0.490 0 ±0.055 7,P <0.001)detected by Western blot.It also had statistical significance in Matrigel assays (248.6 ±4.5 vs.113.0 ±3.3),Transwell (203.6 ±1.9 vs.103.0 ± 1.2)and Wound healing assays (95.0 ±2.9 vs.33.0 ±1.5)that knockdown of CMTM3 promoted mi-gration,and invasion of PC3 cells in vitro (P <0.001).Conclusion:Negative correlation exists between the stable knockdown of CMTM3 and change of biological characteristics in PC3 cells,and knocking down CMTM3 affects migration,and invasion ability in PC3 cells.

BACKGROUND:Classical drug for Parkinson’s disease is levodopa, but long-term application of levodopa can induce complications such as dyskinesias.
OBJECTIVE:To observe the effects of levodopa on learning and memory capacities of Parkinson’s disease rats and to study its mechanisms.
METHODS:The rat models of Parkinson’s disease were established using 6-hydroxydopamine. The 228 model rats were randomly divided into control group and experimental group. Rats in the experimental group were intraperitoneal y injected with 10, 20 and 30 mg/(kg?d) levodopa for 28 consecutive days. At 1, 3, 5, 7, 14 and 28 days after intraperitoneal injection, we observed the rats’ learning and memory capacities and tested plasma concentration of homocysteine and folic acid. Acetylcholinesterase activities in the rat hippocampus were measured. Hippocampal neurofibril ary tangles were observed using Bielschowsky staining.
RESULTS AND CONCLUSION:Increased dose of levodopa and prolonged application time obviously decreased learning and memory capacities in rats (P<0.001), increased plasma homocysteine levels, reduced folic acid levels (P<0.001), diminished acetylcholine esterase activities in the rat hippocampus (P<0.001), and increased neurofibril ary tangles in the rat hippocampus (P=0.000). Results suggested that a large dose of levodopa could significantly decrease the learning and memory capacities, and disease acetylcholine esterase activities, and increase neurofibril ary tangles in hippocampus. Its mechanism possibly associated with the increased plasma concentration of homocysteine.

Animals ; Astrocytes ; immunology ; metabolism ; Male ; Microglia ; immunology ; metabolism ; Neurons ; metabolism ; Oxidopamine ; metabolism ; Parkinson Disease ; immunology ; Rats ; Rats, Sprague-Dawley

Adolescent ; Brain Diseases ; diagnostic imaging ; Brain Neoplasms ; diagnostic imaging ; surgery ; Diagnosis, Differential ; Hematoma, Epidural, Cranial ; diagnostic imaging ; Hernia ; diagnostic imaging ; Humans ; Male ; Plasmacytoma ; diagnostic imaging ; surgery ; Tomography, X-Ray Computed

Objective To investigate the water quality and running status of the dringking water improving project in Xuchang,Pingdingshan and Nanyang,thus to provide basis for scientifically evaluating social effects.Methods Stratified sampling was used in the levels of counties and townships and villages,with the number of checked counties greater than or eaquel to half of the projected counties(13/24),the checked townships more than 40 percent of the projected townships(42/102),the checked villages greater than or eaquel to 30% of the projected villages(56/186).We listened their statement,reviewed the documents,examined carefully the water projects before we made the appraisal.Results More than 95%(129/136)of the projects had water quality reports,among which 90%(122/136)were provided by county level centers for disease prevention and control,75% (102/136) of water samples were collected by centers for disease prevention and control,80%(109/136)ofcounties organized an acceptance check-up group,92%(125/136)projects well preserved water source.Conclusions The dringking water improvement projeets in countryside are basically normal in terms of construction and management,the water supplied is qualified,so the expected goal is achieved.However,duties of each department are not explicit and the communication is inadequate,so collaboration should be reinforced.