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Objective@#To investigate the hearing loss and speech disorders in the elderly, to analyze the risk factors of the elderly deafness, as well as to provide reference for the clinical research of the elderly deafness.@*Methods@#From March 2016 to March 2018, 913 elderly people, who were tested for hearing and speech disorders, were examined by a unified questionnaire to investigate the demographic data of the subjects and the related factors of deafness, and the hearing and speech recognition tests were carried out. According to the hearing loss, the hearing impaired group was divided into the hearing impaired group (500, 1 000, 2 000 and 4 000 Hz, the average hearing threshold>25 dBHL) and the non hearing impaired group (the average hearing threshold of the four frequencies ≤25 dBHL), and then the single factor analysis and the unconditional Logistic regression analysis were used. Finally, the risk factors of senile deafness were analyzed.@*Results@#Of the 913 elderly subjects in the survey, 389 (42.61%, 389/913) had no hearing impaired, 345 (37.79%, 345/913) were mild hearing impaired, and 149 (16.32%, 149/913) had moderate hearing loss. Twenty-six patients were severe hearing loss (2.85%, 26/913); 4 patients had severe hearing loss (0.44%, 4/913). Among the 524 hearing-impaired elderly, there were 244 speech-recognition disorders (46.56%, 244/524), of whom 106 were mild hearing-impaired, accounting for 30.72% (106/345), 108 were moderate hearing loss, accounting for 72.48% (108/149), 26 were severe hearing loss, accounting for 100% (26/26), and 4 were the profound hearing loss, accounting for 100% (4/4). Statistical analysis showed that the age, job status, history of hypertension, history of hyperglycemia, and smoking history were independent risk factors for senile hearing loss (P<0.05).@*Conclusions@#High incidences of hearing and speech recognition obstacle are found in health examination for the elderly patients. Noise exposure, age, history of hypertension, high blood sugar, and smoking history are high-risk factors for senile deafness, therefore, prevention and rehabilitation programs are urgent to be developed.
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Objective To approach the effect of ulinastatin (UTI) on protection of vascular endothelial cells in rats with sepsis and its mechanism.Methods Fifty-two Sprague-Dawley (SD) male rats were randomly divided into a normal saline pretreatment group (control group) and a UTI pretreatment group (UTI group), each groupn = 26. The rats in two groups were given lipopolysaccharide (LPS, 10 mg/kg) intra-peritoneal injection for the establishment of rat septic models. In UTI group, 18 hours before LPS injection, intraperitoneal injection of UTI 100 kU/kg dissolved in 5 mL normal saline was given, while in the control group, 3 hours before LPS injection, intraperitoneal injection of 5 mL normal saline was given to the rats for pretreatment. Respectively, at 0.5, 2, 4, 12, 24, 72 hours after model establishment, tail venous blood and myocardial tissue were taken. The levels of tumor necrosis factor-α (TNF-α), interleukins (IL-6, IL-10), vascular cell adhesion molecule (VCAM) and intercellular adhesion molecule-1 (ICAM-1) were detected by enzyme-linked immunosorbent assay (ELISA); the correlation between TNF-α and ICAM-1 was analyzed; the expression of ICAM-1 in myocardial cell was determined by immunohistochemistry.Results After model establishment, the levels of TNF-α, IL-6, IL-10, ICAM and VCAM in two groups were gradually increased, reaching the peaks at 24, 12, 12, 72, 72 hours, respectively. Compared with control group, the levels of TNF-α, IL-6, ICAM-1, VCAM of UTI group were significantly lower at various time points [24 hours TNF-α (ng/L): 119.8±28.9 vs. 190.2±30.4, 12 hours IL-6 (ng/L): 327.8±26.9 vs. 948.7±63.8, 72 hours VCAM (ng/L): 36.3±3.2 vs. 68.8±2.4, 72 hours ICAM-1 (ng/L): 115.6±11.6 vs. 129.4±8.2,P < 0.05 orP < 0.01], IL-10 was significantly increased [12 hours (ng/L): 80.7±1.9 vs. 42.3±4.9,P < 0.01]. TNF-αwas positively correlated to ICAM significantly (UTI group:r = 0.907,P = 0.050; control group:r = 0.961, P = 0.010). Immunohistochemistry showed that after modeling for 0.5 hour, basically no positive expression of ICAM-1 in myocardial cells was found in the two groups; in the control group, at 12 hours the positive expression of ICAM-1 was increased, and in UTI group, a little expression of ICAM-1 was seen; at 72 hours, the expression of ICAM-1 was significantly increased in both groups.Conclusion UTI can protect the function of endothelial cells in rats with sepsis by regulating the expressions of proinflammatory cytokine, anti-inflammatory cytokine, adhesion molecules, and improving the microvascular permeability.
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Objective To investigate whether early goal-directed therapy ( EGDT ) could lower the mortality rate in patients with severe sepsis and septic shock. Methods Articles with items sepsis, severe sepsis, septic shock, EGDT were retrieved from MEDLINE, EMBASE, Cochrane, Wanfang Data and CNKI. Inclusion criteria included randomized controlled trial, subjects concerning patients with severe sepsis or septic shock, endpoints with short-term mortality [ in-hospital, intensive care unit ( ICU ) or 28-day ] and long-term mortality ( 60-day or 90-day ). Related risk ( RR ) and 95% confidence interval ( 95%CI ) were used as indices to judge the difference in mortality rate between EGDT group and standard treatment group. RevMan 5.2 software was used for Meta analysis. Results There were 8 studies meeting inclusive criteria with a total of 4 853 patients. For patients with severe sepsis and septic shock, compared with the group with routine treatment, EGDT showed a decrease in the short-term mortality ( RR = 0.74, 95%CI=0.66-0.82, P<0.000 01 ), but did not decrease the long-term mortality ( RR=0.99, 95%CI=0.92-1.06, P=0.81 ). Conclusion EGDT strategy may decrease the short-term mortality in patients with severe sepsis and septic shock, but it showed no influence on the long-term mortality.