Objective:To determine the effectiveness and validity of morphometric analysis made from dental panoramic tomograms(DPTs) for predicting mandibular bone mineral density(BMD) while taking the result of dual energy X-ray absorptiometry(DXA) as gold standard.Methods: Twenty healthy subjects(8 male,12 female) with intact dentition,aged from 1126 years old,were included in the present study.The BMD of each patient was measured at the lumbar spine(L1-L4) by DXA;the results were obtained based on the density of surface(g/cm2).Dental panoramic radiography was carried out using dental panoramic tomography(RTG230/ENR,made in Italy).Mandibular cortical thickness(MCT) and panoramic mandibular index(PMI) values were calculated and their relationship with DXA measurements were subjected to correlation analysis.The validity of MCT and PMI measurements were assessed by sensitivity and specificity.Results: We found mandibular BMD was positively correlated with MCT(r=0.268,P

Objective To observe the changes in contents of ? 1 Microglobulin (? 1 M) in urine after exposure to acceleration of different speeds(+Gz) in order to provide scientific indications for efficient protection for pilots under high +Gz acceleration and efficient flight health service support. Methods Six healthy men were subjected to the following experiments: ①pressurized anti G suit (KH X); ②pressure breathing for +Gz (PBG); ③pressurized anti G suit and PBG and AGSM (up to +9Gz for 10 s). Urine samples were collected before, immediately after, 30 minutes and 24 hour after the exposures for the determination of ? 1 microgolbulin (? 1 M). Results It was found that ①The G tolerances of subjects under 3 conditions were (6 25?0 52) G/10s, (8 17?0 26) G/10s, 6 5G/30s, and 9 00 G/10s, respectively. ②30 minutes after each series of exposure, the contents of ? 1 M in urine samples were increased ( P

Objective: To evaluate the effects of micro-arc oxidation (MAO) and poly-L-lactic acid (PLLA) surface-modification on the biocompatibility of magnesium alloy WE42. Methods: Micro-arc oxidation surface-modificated WE42 (MAO/WE42) materials and MAO+PLLA surface-modificated WE42(MAO+PLLA/WE42) materials were prepared. The surface topography of materials in the physiological environment was observed in vitro by scanning electron microscopy. The human umbilical vein endothelial cells(HUVECs) were treated by leaching liquor of materials. The relative growth rate(RGR) was assessed by MTT assay to evaluate the level of cytotoxicity. The coagulation time(PT, RT) and hemolytic ratio were determined to evaluate the blood compatibility of those materials. Results: The observation of scanning electron microscopy indicated that WE42 corroded seriously after immersion. There were no obvious corrosion holes on the surface of MAO/WE42 and MAO+PLLA/WE42 materials after immersion. It was found that there were good anticoagulant properties but no apparent cytotoxicity in MAO/WE42 and MAO+PLLA/WE42 materials. The results of hemolysis test showed that there were lower hemolysis rates in MAO and MAO+PLLA materials than that of WE42. The material of MAO+PLLA possessed the better anti-hemolytic properties than that of MAO(P < 0.01). Conclusion: Micro-arc oxidation surface modification improved the biocompatibility of WE42. PLLA sealing treatment improved the anti-hemolytic performance of WE42. MAO+PLLA provided a safe drug-loading surface for drug-eluting stents of magnesium alloy.

BACKGROUND:At present, the clinical treatment of lumbar disc degeneration mainly includes conservative treatment, traditional surgery and minimal y invasive surgery. The therapeutic purpose is to relieve symptoms, but the long-term effect is not very satisfactory. Therapeutic methods focusing on biological functional recovery have been concerned gradual y, but the clinical application is far in sight. OBJECTIVE:To review the advances in the treatment of lumbar disc degeneration regarding tissue-engineered repair and biomechanics. METHODS:PubMed database was searched by the first author for relevant articles published before December 2014 using the keywords of“intervertebral disc degeneration, clinical treatment, biological treatment, tissue engineering, biomechanics, repair, progress”in English. A total of 100 articles were searched initial y and final y, 40 articles were included in result analysis. RESULTS AND CONCLUSION:Although the therapeutic schemes are varied, the treatment of intervertebral disc degeneration is a great chal enge for clinicians and basic researchers. Currently there is no perfect clinical treatment, and indications corresponding to various therapies should be paid attention as wel as long-term fol ow-up evaluation. For various reasons, the biological treatment for intervertebral disc degenerative disease is becoming more and more popular, providing a promising prospect for the treatment of intervertebral disc degeneration. So far, large amounts of data have been obtained from animal experiments, but there are stil many problems to be solved. Other chal enges also involve the al aspects of general tissue engineering methods, such as cel s, cytokines and scaffolds. In these studies, the nucleus pulposus tissue engineering based on the combination of heparin-functionalized chitosan hydrogel, cytokines and stem cel s exhibits a promising prospect.

Medication has become the first-line option for the management of lower urinary tract symptoms induced by benign prostatic hyperplasia (LUTS/BPH) for its advantages in controlling the symptoms, inhibiting BPH progression, and reducing serious complications and surgical risks. Recent years have witnessed remarkable achievement in the studies of phosphodiesterase type 5 inhibitors (PDE5-Is) in the treatment of LUTS/BPH. PDE5-Is can effectively alleviate LUTS/BPH, with even better efficacy when combined with al-ARAs.
Humans ; Lower Urinary Tract Symptoms ; drug therapy ; etiology ; Male ; Phosphodiesterase 5 Inhibitors ; therapeutic use ; Prostatic Hyperplasia ; complications

Objective To investigate the value of interphase fluorescence in situ hybridization(FISH)technique and the detection of fusion gene in the diagnosis of acute myeloid leukemia(AML)M2 and M3 Methods FISH was used to detect the AML1/ETO fusion gene and/or PML/RARα fusion gene in incipient cases including 9 AML-M2, 12 AML-M3 and 10 AML undetermined as AML-M2 or AML-M3 primarily diagnosed by routine morphology though bone marrow,cytochemical staining and immunophenotyping,which can help diagnose and guide clinical therapy.Results 4 of 9 AML-M2 cases were AML1/ETO positive.Among 12 AML-M3 cases,10 were PML/RARα positive.1 case was detected AML1/ETO fusion gene.In 10 untonfirmed M3 or M2,3 case8 showed AML1/ETO,5 showed PMIJRARot fusion gene and the rest showed neither of the genes.Conclusion As a new technique of the molecular genetics,FISH is accurate, rapid and efficient.It would be of significance not only at diagnosis of AML,but also for subsequent clinical decision-making.

Based on the Miller Pyramid for assessing clinical competence, this article analyzed the existing problems in the practice of teaching physical examination and provided suggestions for possible reforms.

ObjectiveTo investigate the influence of recombinant thioredoxin (TRX)on apoptosis of myocardium cell in viral myocarditis of mice.MethodsTwenty-four Balb/c mice,weighting 12 - 14 g,were randomly divided into 3 groups:the control group,the virus group and the protective group,8 mice in each group.The virus group and the protective group were injected with 0.1 ml 100TCID50 Coxackie virus B3 (CVB3)intraperitoneally,and the control group was injected equal volume of saline.Therewithal the protective group was injected with TRX(2 mg/kg) by tail vein,and the virus group was injected saline the same way.After 14 days all mice were killed and hearts were taken.Changes of myocardial histopathology was observed with optical microscope,cell apoptosis was checked by TUNEL technique,and the expression of apoptosis-related proteins (Bcl-2,caspase-3)in infiltrated cell of myocardium was determined by immunohistochemistry.Results(①)Lymphocyte infiltration and necrosis were observed in survivals of the virus group,sporadic coagulation necrosis and ballooning degeneration of cells were observed in the protective group,however no myocardial lesion was found in the control group.(②)TUNEL technique showed that the positive ratio of apoptosis in the virus group and the protective group[(90.23 ± 3.63)％,(20.02 ± 2.41)％] was significantly higher than that of the control group(0.00 ± 0.00,all P ＜ 0.05),the positive ratio of apoptosis in the protective group was significantly lower than that of the virus group (P ＜ 0.05 ).(③)Immunohistochemistry showed that the expression of protein Bcl-2(+,++,+++) in the virus group and the protective group was significantly higher than that of the control group (all P ＜ 0.05).The expression of protein Bcl-2 in the protective group was significantly higher than that of the virus group(P ＜ 0.05).The expression of caspase-3 (+,++) was significantly higher in the virus group and the protective group than the control group (all P ＜ 0.05).Compared with the virus group,the expression of caspase-3 in the protective group was significantly lower(P ＜ 0.05).ConclusionTRX could inhibit cardiomyocyte apoptosis in viral myocarditis mice and the inhibition is related to regulation of apoptosis-related protein expression.

BACKGROUND:Hyperbaric oxygen (HBO) can increase oxygen diffusing capacity, thereby, improve hypoxic state of brain edema and brain tissue and promote the recovery of physiological function of brain cells in focal zone, the establishment of bypass circuit, and regeneration and repair of brain cells.OBJECTIVE: To observe the effect of hyperbaric oxygen on c-fos oncogene expression of rats at different time points following acute focal cerebral ischemia/reperfusion(I/R) injury.DESIGN : Randomized grouping animal experiment.SETTING: Department of Emergency, Tangdu Hospital, Fourth Military Medical University of Chinese PLA; Department of Laboratory Medicine, Xi'an Gaoxin Hospital;The General Hospital of the Air Force of Chinese PLA; Hyperbaric Oxygen Treatment Center, Department of Aerospace Medicine, Fourth Military Medical University of Chinese PLA.MATERIALS: This experiment was carried out in the Hyperbaric Oxygen Treatment Center, Department of Aerospace Medicine, Fourth Military Medical University of Chinese PLA in April 2002. Sixty-five 2-month-old healthy male SD rats.METHODS: The involved rats were randomized into: model group (n =20), normal control group (n =5), pure oxygen treatment group (n =20) and HBO treatment group (n =20). In the model group, following the method of Koizumi et al, rat models of middle cerebral artery (MCA) ischemia were developed. In the normal control group, only occlusion of arterial blood flow was omitted; In the pure oxygen treatment group, the operation procedure was the same as that of model group, and embolus being drawn out at ischemia for 1 hour, rats were placed in the hyperbaric cabin at 2,9,21, 45 and 69 hours after embolus being inserted, and they inhaled pure oxygen under the normal pressure; In the HBO treatment group, the operation procedure was the same as that of model group, and rats inhaled pure oxygen for 1 hour under 0.25 MPa pressure. MAIN OUTCOME MEASURES: By means of immunohistochemical and pathohistological methods, neutrophilic infiltration,c-fos oncogene protein and positive cell expression in cerebral cortex, preoptic area and corpora striatum of rats in each group were observed at cerebral I/R 5, 12, 24 and 72 hours; Neuronal necrosis degree in cerebral cortex, medial area of corpora striatum and preoptic area, and cerebrovascular leakage area of left cerebral hemisphere of rats were calculated.RESULTS: Sixty-five rats were involved in the final analysis. ① c-fos positive products mainly focused in the center of the preoptic area, but they were occasionally seen in the contralateral cortex, slightly expressed in the preoptic area and moderately expressed in the corpora striatum, c-fos positive products began to reduce in the above-mentioned area at ischemia 12 hours, and were obviously reduced at ischemia 24 hours; c-fos positive products in the cerebral cortex and preoptic area were obviously weakened in the HBO treatment group than in the simple ischemia group; At I/R 12 hours,neutrophils in the preoptic area and corpora striatum were significantly lower in the HBO treatment group than in the model group, respectively(P ＜ 0.05); At I/R 24 hours, neutrophils in the cerebral cortex, preoptic area and corpora striatum were significantly lower in the HBO treatment group than in the model group (P ＜ 0.05). ② Cerebrovascular leakage area was more significantly contracted in the HBO treatment group than in the model group (P＜ 0.05); At I/R 72 hours, the number of injured nerve cells in the optic chiasm cortex, medial area of corpora striatum and preoptic area was significantly smaller in the HBO treatment group than in the model group (P＜0.05). Neuronal damage was not found in the sham-operation group.CONCLUSION: HBO can markedly contract cerebrovascular leakage area of rats with acute focal cerebral ischemia/reperfusion injury, alleviate the symptoms of nervous system, inhibit neutrophilic infiltration and c-fos oncogene protein expression in the infarct area, and reduce neuronal necrosis in the "penumbral region".

BACKGROUND:Acute carbon monoxide (CO) poisoning may lead to delayed amnesia in rats,and which is similar to delayed neurologic syndrome caused by acute CO in human.So,this experiment is to investigate the pathogenesis of delayed neurologic syndrome by studying acute CO poisoning in the rats.OBJECTIVE:To observe the changes in delayed neuronal damage and memory after acute CO poisoning in the rats,and analyze their correlation.DESIGN:Randomized controlled animal experiment.SETTING:Department of Emergency,Tangdu Hospital,Fourth Military Medical University of Chinese PLA;Department of Laboratory Medicine,Xi'an Gaoxin Hospital;The General Hospital of the Air Force of Chinese PLA,Center for Hyperbaric Oxygen Treatment,Department of Aerospace Medicine,Fourth Military Medical University of Chinese PLA.MATERIALS:This experiment was carried out in the Laboratory of Aviation Pathology and Molecular Biology,Department of Aerospace Medicine.Fourth Military Medical University of Chinese PLA from July to November 2005.Fiftyhealthy male Sprague-Dawley(SD)rats were randomized into control group and CO poisoning group,with 25 rats each.METHODS:The awake rats in the CO poisoning group were placed in self-made jar for poisoning,then which was pumped with 0.999 volume fraction of CO.Rats in the jar inhaled the mixture of CO and air for 60 minutes.The average volume fraction of CO in the jar was 3.451×10-3.Rats in the control group were untouched.MAIN OUTCOME MEASURES:①The step down test was carried out in the rats before and 1,3,5 and 7 days after Coexposure.Escape latency was used as an index for evaluating the ability of memory retention.Shorter escape latencyindicated poor memory ability.②Pathological changes of brain tissue:After step down test was carried out following 1,3,5 and 7 days of CO exposure,6 rats were separately sacrificed in each group,and their brains were harvested.The brain tissue sections were performed haematoxylin & eosin (HE) staining for observing pathological injury degree and the amount of pyramidal neurons in hippocampal CA1 region.③SPSS 10.0 software was used to analyze the relationship of the amount of pyramidal neurons in hippocampal CA1 region and escape latency.RESULTS:Forty-eight rats were involved in the final analysis.①There were no significant differences in escape latencyon the 1"and 3"days after CO exposure between two groups. but escape latency in the CO poisoning group was significantly shorter than that in the control group on the 5th and 7th days after CO exposure(P＜0.05,0.01).②There were no significant changes in the amount of pyramidal neurons in hippocampal CA1 region on the 1st day after CO exposure between CO poisoning group and control group,but pyramidal neurons in hippocampal CA1 region in the CO poisoning group were significantly reduced on the 3rd,5th and 7th days after CO exposure,and 1 5%dead pyramidal neurons were found on the 7th day after CO exposure.③Decrease of pyramidal neurons in hippocampal CA1 region was significantly correlated with shortening of escape latency of rats in the CO poisoning group(r=0.270,P＜0.01).CONCLUSION:Acute CO poisoning leads to delayed neuronal damage,which causes delayed amnesia.