Objective To discuss the clinicd effect of using nebulised budesonide to treat neonatal laryneal edema caused by mechanical ventilation.Methods 43 newborns with mechanical ventilation were included in this study and divided into two groups:The Observational group(23 newborns)were treated with nebulised budesonide right before excubation once and three times after that,and the control group(20 newborns)were treated with dexamethasone once right before excubation and nebulised adrenine after that for three times.Comparisons were made between two groups about dismissing time of wheeze or hoarseness,tachypnea,PaO2 and PaCO2.Results Observational group:dismissing time of wheeze or hoarseness was(10.26±4.01)hours,dismissing time of tachypnea was(1.63±0.55)days,which was shorter than that of control group[(14.20±5.58)hours/(2.05±0.58)days],P＜0.05).PaO2 and PaCO2 of two groups had no statistical difference(P＞0.05).Conclusion Nebulised budesonide was effective in treatment neonatal laryneal edema caused by mechanical ventilation,using.

Objective To summarize the experiences in the diagnosis and treatment of the hepatic hereditary hemorrhagic telangiectasia (HHHT).Methods The clinical data of 15 HHHT patients who were admitted to the Qilu Hospital,People's Hospital of Mengyin,People's Hospital of Liaocheng,Henan Provincial People's Hospital,the Second Hospital of Hebei Medical University,First Affiliated Hospital of Zhejiang University were retrospectively analyzed.The clinical manifestation,features of imaging and laboratory examination were summarized,and the diagnosis,treatment and prognosis of the disease were investigated.Results HHHT patients had nonspecific symptoms in the early stage,and some patients presented with right upper quadrant discomfort,shortness of breath,anemia and liver bruit.The condition of HHHT patients could be worsened by liver cirrhosis or portal hypertension rapidly.The results of color doppler ultrasound and computed tomography showed intrahepatic telangiectasia,arteriovenous fistula and hepatic artery aneurysm in the 15 patients.Digital subtraction angiography was not clear enough for 2 HHHT patients with more than 1 enlarged hepatic arteries,but computed tomographic angiography was feasible.According to the degree and stages of the HHHT,all the 15 patients were divided into asymptomatic HHHT,simple HHHT and complex HHHT.Among the 6 patients who underwent surgical treatment,5 received ligation or banding of the enlarged hepatic arteries with subsequent disappearance of symptoms.Three patients received interventional treatment,and the treatment for 1 patient with complex HHHT was failed,and the patient died 30 months after medical treatment.Six patients were treated by conservative treatment,2 patients of them had no symptoms at the beginning,then they suffered from hepatic dysfunction and ascites at 21 and 35 months,respectively,and 1 of them died 6 months later.Four patients received medical treatment,and the results of color doppler ultrasound and computed tomography showed the pathological changes were aggravated gradually.Conclusions Telangiectasia,intrahepatic arteriovenous fistula and hepatic artery aneurysm are the main imaging characteristics of HHHT,and imaging diagnosis has significant value in the diagnosis of HHHT.HHHT is a progressive disease,early,active and individualized treatment is beneficial to the patients.The outcome of ligation or banding of the hepatic arteries is satisfactory.

Objective To investigate the effect of proteasome inhibitor MG132 on the proliferation of human lens epithelial cells SRA01/04. Methods The SRA01/04 cells were treated with MG132 by different concentrations (0, 0. 1, 0. 5, 1. 0, 2. 5, 5.0, 10. 0μmol/L) for 36 hours. The cell viability in all groups was determined using methylthiazoltetrazolium (MTT) test. The effect of MG132 on the apoptosis and regulation of cell cycle about SRA01/04 cells were detected by flow cytometry (FCM). The SRA01/04 cells treated with MG132 were observed after Annexin V/FITC-PI staining by fluorescence microscope. Results The inhibitory effect of MG132 on SRA01/04 cells proliferation was enhanced with the increase of MG132 concentration. The 50% inhibiting concentration ( IC50 ) of MG132 was 2. 50μmol/L after SRA01/04 cells were treated with MG132 for 36 hours. The apoptosis index of the cells treated by MG132 at 2. 5μmol/L and 5 μmol/L for 36 hours was 6. 55 ± 0. 35% and 13.75 ± 3.18%, and 0. 75 ± 0. 21% for 5.0μmol/L for 36 hours in control group. After cells were treated with MG132 for 48h, the percentages of cells at G0/G1 phase were (42. 57 ± 0. 64) %, (73.42 ± 3.10) %, ( 80. 95 ± 3.83 ) % 0, 2. 5,5.0 μmol/Lgroups respectively, and those at S phase were (49. 44±1.36)%, ( 17. 40 ± 1.50)%, ( 19. 57 ± 1.29)%.Annexin V/FITC-PI staining was used, and MG132 was found to result to apoptosis. Conclusions MG132 could inhibit the proliferation of SRA01/04 cells by the effect of inducing apoptosis and regulation of cell cycle. The proteasome inhibitor-might play a key role in the prevention of posterior capsular opacification.

Objective To investigate the correlation between ICRU reference point dose and dosevolume parameters of organs at risk (OARs) under different bladder and rectal filling status in threedimensional conformal brachytherapy for locally advanced cervical cancer.Methods A total of 31 patients who received magnetic resonance imaging-guided three-dimensional conformal brachytherapy for cervical cancer in 96 fractions were enrolled.The ICRU rectal and bladder reference points were determined in the treatment planning system,and the doses at these points were recorded and compared with the dose-volume parameters of the rectum and bladder.The paired t-test was used to analyze the differences between them.Results Bladder DICRU was lower than bladder D0.1cm3 and D1 cm3 (P=0.000 and 0.000),higher than bladder D5 cm3 and D10cm3 (P=0.000 and 0.000),and similar to bladder D2 cm3 (P=0.345).Under the bladder filling status,bladder DICRU was lower than D2cm3.Rectal DICRU was lower than rectal D0.1 cm3 and D1cm3 (P =0.000 and 0.002),higher than rectal D5 cm3 and D 10 cm3 (P =0.000 and 0.000),and similar to rectal D2cm3 (P=0.058).The ICRU bladder and rectal reference point doses were positively correlated with corresponding D2 cm3.In the case of bladder volume ≥ 200 cm3,the ICRU bladder reference point dose underestimated bladder D2 cm3.In the case of rectal volume ≥ 37 cm3,the ICRU rectal reference point dose overestimated rectal D2 cm3.Conclusions In three-dimensional conformal brachytherapy,it is generally safe to use D2 cm3 as an index to evaluate OARs,but when the bladder or rectum is in an empty status,the ICRU bladder or rectal reference point doses should be considered.

Objective To explore the relationship between posttraumatic stress disorder and nurses′ psychological capital. Methods By convenient sampling, totally 550 nurses in 5 first-class upper level general hospitals in Zhejiang province were investigated by the posttraumatic stress disorder (PTSD)Cheeklist-Civilan Version (PCL-C) and Nurses Psychological Capital Questionnaire Revision (NPCQR), and the results were analyzed. Results 18.35%investigated nurses showed a certain degree of PTSD symptoms and 13.71% showed obvious PTSD symptoms. The positive rate was 32.06%.The overall score of nurses′psychological capital was 78.81 ± 16.54, which was in the middle level, and the dimension scores from high to low were self-efficacy (23.80±5.35), hope (23.36±5.24), resilience (19.66 ±4.29), and optimism (11.99 ± 3.21). The nurses′psychological capital had a negative effect on posttraumatic stress disorder (P<0.01). Conclusions Psychological capital of nurses is a negative predictor of PTSD symptoms, which suggested that managers should pay more attention to the development of nurses′psychological capital to reduce and prevent the occurrence of posttraumatic stress disorder,then to improve nursing service quality.

Objective: To investigate the relationship between workplace bullying and posttraumatic stress disorder (PTSD) in nursing staff, and to analyze the role of psychological capital between workplace bullying and PTSD. Methods: From December 2014 to June 2015, convenience sampling was used to collect 496 nurses from 5 grade A tertiary hospitals in a province of China. Their workplace bullying, psychological capital, and PTSD status were assessed using the Negative Acts Questionnaire, Psychological Capital Questionnaire, and Posttraumatic Stress Disorder Self-Rating Scale, respectively. The correlation between variables was analyzed using a structural equation model. Results: Among these nurses, the scores of negative acts, psychological capital, and PTSD were 37.15±12.83, 78.81±16.54, and 34.56±12.52, respectively. The score on each dimension of negative acts was positively correlated with that on each dimension of PTSD (P<0.01) ; the score on each dimension of psychological capital was negatively correlated with that on each dimension of PTSD and negative acts (P<0.01). Negative acts had a positive predictive effect on PTSD (β=0.539, P<0.01) , which was reduced after inclusion of psychological capital (β=0.513, P<0.01). The path coefficient was 0.62 for the effect of negative acts on PTSD, -0.18 for the effect of negative acts on psychological capital, and -0.11 for the effect of psychological capital on PTSD (P<0.05) . Conclusion Workplace bullying is a predictive factor for PTSD, and psychological capital plays a mediating role between workplace bullying and PTSD. The manager should reduce workplace bullying to improve the psychological capital in nursing staff and to prevent and reduce PTSD.

Objective To investigate the relation between intrauterine growth and the development of carotid atherosclerosis in later life. Methods The intima-media thickness of carotid was measured with ultrasonography in 2036 people aged above fifty who had complete birth records, and divided into normal and abnormal group. They were asked to fill in the cardio-cerebrovascular questionnaire, and venous blood samples were taken and analysed for various biochemical parameters. The relation between carotid atherosclerosis and various parameters at birth and in adult life was assessed. Results The birthweight and head circumference in abnormal group were less than those in normal. The prevalence of carotid atherosclerosis was greatest in those weighed 2500g or less, whose risk of carotid atherosclerosis was greater than those weighed between 3000g and 3500g, after adjustment for cardiovascular risk factors. Conclusions Increased atherogenesis may be one independent mechanism mediating the epidemiological link between impaired fetal growth and vascular disease.

BACKGROUND:The content of serum thrombin in patients with osteoarthritis is significantly higher than that in normal individuals,and thrombin can induce inflammatory degeneration of rat chondrocytes,suggesting that inhibiting the function of thrombin may become a method for treating osteoarthritis.Celecoxib is a common therapeutic drug for the clinical treatment of osteoarthritis.It is not yet known whether it improves chondrocyte degeneration by inhibiting the activity of thrombin. OBJECTIVE:To investigate the effect of celecoxib on thrombin-induced degeneration of rat chondrocytes. METHODS:Thrombin levels in the serum of osteoarthritis patients and normal individuals were detected by an ELISA kit.Primary chondrocytes of neonatal Sprague-Dawley rats were isolated,and all experiments were performed with cells from passage one.Chondrocytes were randomly divided into three groups:control group,thrombin group,and celecoxib group.The cell morphology of the three groups was observed under an inverted microscope,and an Edu kit was used to detect the cell proliferation.qRT-PCR was used to detect the expression of extracellular matrix components(aggrecan,elastin,cartilage oligomeric matrix proteins),inflammatory factors(interleukin-1,interleukin-6,and tumor necrosis factor-α),and chemokines(monocyte chemotactic protein 2,monocyte chemotactic protein 7,granulocyte chemotactic protein 6).The expression of type 2 collagen α1 was detected by immunofluorescence.Western blot method was used to detect the expression of catabolic metabolism genes,such as matrix metalloproteinase 9,matrix metalloproteinase 13,and cyclooxygenase 2. RESULTS AND CONCLUSION:Patients with osteoarthritis had higher levels of thrombin in the serum compared with normal individuals.Under the microscope,celecoxib was found to significantly inhibit fibroid changes in chondrocytes.Compared with the thrombin group,celecoxib inhibited the proliferation of chondrocytes.The downregulation of extracellular matrix gene expression,such as type II collagen α1,in the thrombin group was inhibited by celecoxib(P<0.05).Thrombin promoted the expression of inflammatory factors(interleukin-1,interleukin-6,and tumor necrosis factor-α),chemokines(monocyte chemotactic protein 2,monocyte chemotactic protein 7,granulocyte chemotactic protein 6),as well as catabolic genes(matrix metalloproteinase 9,matrix metalloproteinase 13,and cyclooxygenase 2),and under the intervention of celecoxib,the expression of these genes could be downregulated(P<0.05).Overall,these findings indicate that celecoxib inhibits the pro-inflammatory effects of thrombin and thereby ameliorates chondrocyte degeneration in rats.

ObjectiveTo observe the recovery of proprioception of the affected ankle over time after lateral ankle sprain accepting routine rehabilitation. MethodsFrom June, 2020 to June, 2022, 18 patients with lateral ankle sprain in Kunshan Rehabilitation Hospital underwent routine rehabilitation for twelve weeks. They were measured active and passive position sense of bilateral ankles using an isokinetic dynamometer before treatment, and four, eight and twelve weeks after treatment, respectively. ResultsThe active presentation difference of affected ankle reduced after treatment (F = 22.533, P < 0.001), but it was more than that of the healthy ankle at the same time (t > 4.419, P < 0.001). No significant improvement was found in passive presentation difference of affected ankle after treatment (F = 1.175, P > 0.05), and it was not significantly different from those of the healthy ankle at the same time (|t| < 0.646, P > 0.05). ConclusionProprioception of affected ankle has been impaired after lateral ankle sprain, and it can be recovered after rehabilitation, but cannot achieve the healthy level even after three months of training. Passive position sense as an index of proprioception needs more researches.

Clinical application of doxorubicin (DOX) is heavily hindered by DOX cardiotoxicity. Several theories were postulated for DOX cardiotoxicity including DNA damage and DNA damage response (DDR), although the mechanism(s) involved remains to be elucidated. This study evaluated the potential role of TBC domain family member 15 (TBC1D15) in DOX cardiotoxicity. Tamoxifen-induced cardiac-specific Tbc1d15 knockout (Tbc1d15^CKO) or Tbc1d15 knockin (Tbc1d15^CKI) male mice were challenged with a single dose of DOX prior to cardiac assessment 1 week or 4 weeks following DOX challenge. Adenoviruses encoding TBC1D15 or containing shRNA targeting Tbc1d15 were used for Tbc1d15 overexpression or knockdown in isolated primary mouse cardiomyocytes. Our results revealed that DOX evoked upregulation of TBC1D15 with compromised myocardial function and overt mortality, the effects of which were ameliorated and accentuated by Tbc1d15 deletion and Tbc1d15 overexpression, respectively. DOX overtly evoked apoptotic cell death, the effect of which was alleviated and exacerbated by Tbc1d15 knockout and overexpression, respectively. Meanwhile, DOX provoked mitochondrial membrane potential collapse, oxidative stress and DNA damage, the effects of which were mitigated and exacerbated by Tbc1d15 knockdown and overexpression, respectively. Further scrutiny revealed that TBC1D15 fostered cytosolic accumulation of the cardinal DDR element DNA-dependent protein kinase catalytic subunit (DNA-PKcs). Liquid chromatography-tandem mass spectrometry and co-immunoprecipitation denoted an interaction between TBC1D15 and DNA-PKcs at the segment 594-624 of TBC1D15. Moreover, overexpression of TBC1D15 mutant (∆594-624, deletion of segment 594-624) failed to elicit accentuation of DOX-induced cytosolic retention of DNA-PKcs, DNA damage and cardiomyocyte apoptosis by TBC1D15 wild type. However, Tbc1d15 deletion ameliorated DOX-induced cardiomyocyte contractile anomalies, apoptosis, mitochondrial anomalies, DNA damage and cytosolic DNA-PKcs accumulation, which were canceled off by DNA-PKcs inhibition or ATM activation. Taken together, our findings denoted a pivotal role for TBC1D15 in DOX-induced DNA damage, mitochondrial injury, and apoptosis possibly through binding with DNA-PKcs and thus gate-keeping its cytosolic retention, a route to accentuation of cardiac contractile dysfunction in DOX-induced cardiotoxicity.