This paper makes persuasive demonstrations on some problems about the human ear sound transmission principle in existing physiological textbooks and reference books, and puts forward the authors' view to make up for its literature. Exerting the knowledge of lever in physics and the acoustics theory, we come up with an equivalent simplified model of manubrium mallei which is to meet the requirements as the long arm of the lever. We also set up an equivalent simplified model of ossicular chain--a combination of levers of ossicular chain. We disassemble the model into two simple levers, and make full analysis and demonstration on them. Through the calculation and comparison of displacement amplitudes in both external auditory canal air and internal ear lymph, we may draw a conclusion that the key reason, which the sound displacement amplitude is to be decreased to adapt to the endurance limit of the basement membrane, is that the density and sound speed in lymph is much higher than those in the air.
Acoustics ; Ear Canal ; Ear Ossicles ; physiology ; Ear, Inner ; physiology ; Humans ; Lymph ; Models, Anatomic ; Sound

Objective To investigate the preoperative biliary drainage on the effect of surgical treatment for hilar cholangiocarcinoma patients.Methods A total of 52 hilar cholangiocarcinoma patients who underwent resection operation in Renmin Hospital of Wuhan University from January 2005 to December 2015 were divided into preoperative biliary drainage group (24 cases) and non-preoperative biliary drainage group (28 cases).To compare the operation time,intraoperative blood loss,hospital stay,perioperative changes in liver function,and incidence of postoperative complications,tumor recurrence rate,1-,3-,and 5-year survival rate and some other indicators.The data was analyzed using SPSS 19.0 software.The patients of two groups were followed up by telephone,out-patient review and hospital examination.Patients were followed up for 8-60 monthes.Results The hospital stay for biliary drainage group was longer than that in non-preoperative biliary drainage group and the difference was statistically significant (P ＜ 0.05).The differences of operation time,intraoperative blood loss,postoperative tumor recurrence rate,postoperative complications (including bile leakage,blooding,fever,pleural effusion,abdominal infection,wound infection,pulmonary infection,liver failure and some others) and 1-,3-,and 5-year survival rate were not statistically significant (P ＞ 0.05).Alanine aminotransferase,aspartate aminotransferase,total bilirubin and direct bilirubin in preoperative biliary drainage group before biliary drainage were(98.0 ± 51.7) U/L,(94.2 ± 44.2) U/L,(177.5 ± 64.1) μmol/L and (160.2 ± 61.9) μmol/L,respectively,and after biliary drainage were (71.2 ± 13.8) μmol/L,(60.0 ± 12.1) μmol/L,(93.5 ± 20.7) μmol/L and (76.3 ± 18.1) μmol/L,respectively.The differences of the above parameters before and after biliary drainage were statistically significant (P ＜ 0.05).However,the changes of albumin before and after biliary drainage were not significant (P ＞ 0.05).The follow-up patients of biliary drainage group were 21 cases and the follow-up patients of non-preoperative biliary drainage group were 25 cases.The differences of 1-,3-,and 5-year survival rate between the two groups were not statistically significant (P ＞ 0.05).Conclusions Preoperative biliary drainage for hilar cholangiocarcinoma patients may improve the liver function to a certain extent.However,preoperative biliary drainage cannot improve the prognosis of the hilar cholangiocarcinoma patients.Therefore preoperative biliary drainage is not suggested for patients with good general conditions.

ABSTRACT:Objective To study the effects of arotinolol,propranolol and carvedilol on rat portal hypertension and make a comprehensive evaluation of the three drugs.Methods Portal hypertension was induced with CCl4 in rats.Arotinolol,propranolol,and carvedilol were administered for 2 weeks after the model was stable.Mean arterial pressure (MAP),heart rate (HR)and portal venous pressure (PVP)were measured at intubation;α-SMA expression was measured by immunohistochemistry;Masson staining was used to test collagen fibers area.Results Compared with model group,both arotinolol and carvedilol could significantly reduce PVP level (P <0.001),which was lower than that in propranolol group (P <0.001,P =0.032).Compared with those in model group,both MAP and HR in arotinolol group and carvedilol group were significantly reduced (P <0.05),MAP in carvedilol group was lower than in arotinolol group (P = 0.01 1 ).MAP was obviously decreased in propranolol group compared with model group (P =0.003),but HR had no sighificant difference between the two groups (P =0.143).Only TBIL in arotinolol and propranolol groups reduced significantly compared with model group (P <0.001 ).However,ALT, ALB and TBIL were obviously ameliorated in carvedilol group compared with model group (P <0.001,P <0.001, P =0.045).The expression ofα-SMA and the area of collagen fibers in arotinolol,carvedilol and propranolol groups
significantly declined compared with those in model group (P <0.05 ).Conclusion Arotinolol can significantly reduce cirrhotic rats’ portal pressure,with effects similar to those of carvedilol.The effect of arotinolol in improving liver function is weaker than that of carvedilol,but the side effects on MAP are milder than those of carvedilol.

AIM: To study the role of peroxisome proliferator-activated receptor-α (PPAR-α) signal transduction pathway in cardiac hypertrophy induced by high glucose and insulin (HGI). METHODS: The cultured neonatal rat cardiomyocytes were used to observe the effect of fenofibrate (FF), a selective PPAR-α agonist, on cardiomyocyte hypertrophy induced by HGI (glucose at concentration of 25.5 mmol/L and insulin at 0.1 μmol/L). The cardiomyocyte hypertrophic responses were assayed by measuring the cell surface area, protein content, and mRNA expression of atrial natriuretic factor (ANF). The expressions of mRNA and protein were assayed by real -time PCR and Western blotting. RESULTS: In cultured cardiomyocytes, HGI induced profound change of hypertrophic morphology, the significant increase in cell surface area, protein content and ANF mRNA expression compared to those in vehicle control (P<0.01), but the expressions of PPAR-α mRNA and protein decreased significantly (P<0.05). At the same time, the expression of cyclooxygenase 2 (COX-2), one of the PPAR-α downstream effectors was obviously elevated (P<0.05). However, FF (0.1, 0.3 and 1 μmol/L) inhibited the cardiomyocyte hypertrophy induced by HGI in a concentration-dependent manner (P<0.01). FF at concentration of 0.3 μmol/L increased the expressions of PPAR-α in both mRNA and protein levels (P<0.05) and inhibited the expressions of COX-2 (P<0.05), which were abolished by MK 886 (0.3 μmol/L), a selective PPAR-α antagonist (P<0.05). CONCLUSION: PPAR-α signal transduction pathway and its downstream effector COX-2 might involve in the cardiomyocyte hypertrophy induced by HGI.

Objectives To investigate the clinical significance of CYP2C19 genotype detection for antiplatelet therapy of elder cardiovascular and cerebrovascular diseases(CCVD).Methods We enrolled all elderly patients with either cardiovascular or cerebrovascular disorders who received clopidogrel as mono drug or in combination with another antiplatelet drug aspirin as secondary prevention for more than 12 months in our hospital from January to August 2015.Somatotypes of CYP2C19 genotypes of all participants were assessed to analyze the relapse of cardiac-cerebral vascular diseases in these patients.Results A total of 250 patients were enrolled,including 179 male and 71 female,with average age of (85.2 ± 7.9) years.Among these patients,there were 97 (38.8％) cases with EM CYP2C19 genotypes,110 cases(44.0 ％) with IM CYP2C19 genotypes,43 cases(17.2 ％) with PM CYP2C19 genotypes.When treated with clopidogrel for antiplatelet in secondary prevention process,the rate of the relapse in cardiovascular event was 34.9％ and higher in PM CYP2C19 genotype than in EM and IM CYP2C19 genotype (19.6 ％ and 15.5 ％,respectively) (x2 =7.251,P =0.027).This phenomenon was similar to patients who received stent implantation(x2=6.393,P =0.041).However,no statistically significant difference was observed in the recurrence rate of cerebral vascular disease between three different genotypes(EM 29.9 ％,IM 20.0 ％,PM 27.9％,x2 =2.880,P =0.237).Conclusions Our results highlight that CYP2C19 genotype might be a potential guidance for secondary prevention of cardiovascular and cercbrovascular disorders among elderly patients.Clopidogrel may be less effective in patients with SM CYP2C19 genotype than those with EM or PM CYP2C19 genotype for secondary prevention of cardiovascular disease.

Objective To evaluate the cytogenetic, molecular responses and safety of generic imatinib in newly diagnosed patients with chronic myelogenous leukemia in chronic phase (CML-CP) in 1-year at different stages. Methods From January 2014 to November 2014, 50 CML-CP patients received oral generic imatinib 400 mg/d. The cytogenetic examinations, bcr-abl transcript levels and safety were monitored after 3, 6, 9 and 12 months respectively. Results 46 of 50 patients insisted on oral generic imatinib and followed up 1 year. At 3-month, 52.0 % (26/50) patients reached the complete hematologic responses (CHR) rate, and patients at least achieved minor cytogenetic response (mCyR) and bcr-ablIS≤10 % were 84.0 % (42/50) and 42.0 % (21/50). At 6-month, patients at least achieved part cytogenetic response (PCyR) and bcr-ablIS≤10 %were 73.5 % (36/49) and 59.2 % (29/49). At 12-month, patients achieved complete cytogenetic response (CCyR), bcr-ablIS≤1 % and bcr-ablIS≤0.1 % were 60.9 % (28/46), 63.1 % (29/46) and 45.7 % (21/46). The grade 3 leukopenia, thrombocytopenia and anemia rates were 34 % (17/50), 40 % (20/50) and 30 % (15/50), respectively. No grade 4 hematologic toxicity occurred. The common non-hematologic toxicities included edema [84 % (42/50)], nausea [46 % (40/50)], muscle pain [20 % (10/50)], rash [16 % (8/50)], and impaired liver function [8 % (4/50)]. Conclusion Generic imatinib has a favorable effect in treatment of patients with CML-CP, and without serious adverse reactions.

Objective To explore the effect of heat shock protein 70(HSP70)expression in the role of Curcumin inhibited staurosporine(STS)-mediated neurons toxic injury.Methods The primary cultured hippocampal neurons was cultured in vitro and the stress damage model of STS-induced nerve cell toxicity was established.The experiment were divided into six groups according to the added drugs:normal control group,the STS model group (final concentration was 20μmol/L),Quercetin+STS model group(final concentration were 10 μmol/L and 20 μmol/L,respectively),Curcumin+STS pretreatment group(for 20μmol/L final concentration),Curcumin+Quercetin+STS treatment group(final concentration were 20μmol/L,10μmol/L and 20μmol/L,respectively)and Curcumin treatment group(final concentration was 20μmol/L).The cell viability were determined by thiazole blue (MTT)method,cell toxicity were measured by lactate dehydrogenase(LDH)release rate and HPS70 expression were detected by Western Blot. Results MTT results showed that the cell viability of Curcumin+STS pretreatment group was significantly higher than STS model group(P<0.001).Compared with Quercetin+STS model group,the cell viability of Curcumin+Quercetin+STS treatment group had little change.LDH results show that the nerve cell toxicity of Curcumin+STS pretreatment group was obviously less than that of STS model group(P<0.001).Western Blot results show that compared with STS model group,HSP70 protein expression in Curcumin+STS pretreatment group was significantly increased(P<0.001).Conclusion Curcumin can inhibit STS-mediated neurons toxicity stress damage though increasing HSP70 expression,when added Quercetin to block HSP70 expression in nerve cells,the inhibiting effect of Curcumin on STS-mediated neuron toxic stress injury is counteract.

Objective To establish a scientific and normative process for using physical restraint,and to increase the safety and efficiency of physical restraint.Methods On the basis of the previous studies,combined with the literature and clinical,we drafted a process framework of using physical restraint and then conducted consultation from 11 experts by using the Delphi technique.Results After 2 rounds of consulting,an evaluation form,consisted of 4 first-dimensions and 11 second-dimensions,and a process,consisted of 4 first-dimensions and 26 second-dimensions,were established.Kendall's W were 0.37 and 0.38 respectively,and expert authority coefficient was 0.84.Conclusions The results from the study is valid,feasible and reliable,however it still need to be further perfected.

Objective To explore extracellular signal-regulated kinase ( ERK1/2 ) expression in the role of curcumin inhibited staurosporine (STS)-mediated neurons toxic injury through added PD098059, and to clarify ERK1/2 mediated inhibitory role of curcumin on STS-induced neurons toxic injury.Methods The neurons toxic injury model of primary cultured hippocampal neurons was established by STS.The experiment was divided into six groups:normal control group, STS model group, PD098059 +STS model group, curcumin +STS pretreatment group, curcumin+PD098059+STS treatment group and curcumin treatment group.The cell viability were determined by MTT method, lactate dehydrogenase (LDH) release rate, cell toxicity were detected, nuclear shape were observed by DAPI staining, and ERK1/2 expression were detected by Western blot method.Results The cell viability of curcumin +STS pretreatment group was significantly higher than STS model group ( P <0.001 ); the cell viability had no significant difference between PD098059 +STS model group and curcumin +PD098059 +STS treatment group;compared with curcumin +STS model group , the cell viability of curcumin +PD098059 +STS treatment group was significantly decreased ( P<0.001 ).LDH results showed that the nerve cell toxicity of curcumin +STS pretreatment group was obviously less than STS model group (P<0.001).The cell nuclear shape showed typical apoptosis morphological characteristics in STS model group, and curcumin inhibited the effect of STS mediated-neuronal apoptosis.ERK1/2 protein expression in curcumin +STS pretreatment group significantly increased compared with STS model group ( P <0.001 ) .Conclusion Curcumin inhibited STS-mediated neurons toxicity injury by up-regulating ERK1/2 expression.After PD098059 blocking the nerve cells ERK1/2 synthesis, the inhibitory action of curcumin failed to implemented, which illustrated that ERK1/2 mediated curcumin to inhibit STS-induced neuronal toxic injury.

Objective To investigate the prognostic significance of serum cystatin C in multiple myeloma (MM).Methods 160 cases of newly diagnosed MM patients with average age of 61.38 years old.Determine the levels of serum cystatin C,serum creatinine,β 2-microglobulin,lactate dehydrogenase and hemoglobin before the treatment; median follow-up of 38 months,observe the relationship between serum cystatin C with overall survival (OS) and event-free survival (EFS).Results Median serum cystatin C level in 160 MM patients was higher than that in the 80 healthy controls [(0.96 ± 0.32) mg/L vs (0.71 ± 0.16) mg/L,P ＜ 0.000].All the patients in ISS stage were divided into 3 stages.Median serum cystatin C levels significantly increased in higher ISS stages [stage Ⅰ (0.70±0.13) mg/L,stage Ⅱ (0.87±0.16) mg/L,stage Ⅲ(1.23±0.33) mg/L (P ＜ 0.05)],serum cystatin C level was positively correlated with levels of serum creatinine (r =0.669,P ＜ 0.000),β2-microglobulin (r =0.672,P ＜ 0.000).lactate dehydrogenase (r =0.521,P ＜ 0.000),and negatively correlated with hemoglobin levels (r =-0.436,P ＜ 0.000).Using ROC analysis,patients with serum cystatin C levels ＞ 0.95 mg/L had significantly shorter EFS and OS patients with serum cystatin C levels ≤0.95 mg/L (median EFS:30 vs 57 months,P ＜ 0.05; median OS:43 vs 68 months,P ＜ 0.05).Conclusion Serum cystain C is not only a sensitive marker of kidney damage,but also reflects tumor burden and delivers prognostic information in MM.