The radical compliance of small diameter artificial vascular grafts was measured by a device made of laser micrometer, pressure transducer, A/D card, micro computer and pulsed circulation loop, the volumetric compliance was measured by a device made of micro-syringe and pressure transducer; the longitudinal compliance was calculated from volumetric compliance and radical compliance. The research results showed that the radical compliance, volumetric compliance and longitudinal compliance would rise not only with the increase in polyurethane (PU) elasticity and salt/polymer ratio (or porosity), but also with the decrease in dipping layers (or wall thickness). Circumferential moduli E zeta and longitudinal moduli E theta could be calculated from volumetric compliance and longitudinal compliance respectively; E theta and E zeta would decrease with the increase in PU elasticity and salt/polymer ratio, but was independent on number of dipping layers. Small diameter PU artificial vascular grafts with compliance close to natural vein or artery can be prepared by choosing of more elastic PU materials (Chro or PCU1500), optimization of salt/polymer ratio (6:1), and the number of dipping layers (4-6 layers).
Biocompatible Materials ; chemistry ; Blood Vessel Prosthesis ; Compliance ; Elasticity ; Humans ; Polyurethanes ; chemistry

O-Carboxymethylchitosan (O-CMC) in 1000 g batch was prepared from chitin as starting material and its chemical structure was confirmed by analysis of IR and NMR. O-CMC solution, sodium hyaluronate (HA) solution and physiological saline were used in Sprague-Dawley rat model for prevention of postsurgical adhesions; after 7 days of an abdominal operation, the 3 groups were evaluated according to Belluco standard, the mean scores of O-CMC group, HA group and physiological saline group were 2.5 +/- 3.1, 3.3 +/- 3.6 and 10.3 +/- 1.0, respectively. Histological inspection showed that in O-CMC group, mesothelial cells on peritonaeum or cecum surfaces were almost restored; in HA group the injured surface of peritonaeum was mostly repaired, but in physiological saline group the injured surface of cecum was just a little repaired; there were extensive adhesions between peritonaeum and cecum, and inflammatory response was quite serious. Experimental results indicated that O-CMC and HA had excellent efficiency and O-CMC was slightly better than HA for the prevention of postsurgical adhesions.
Abdomen ; surgery ; Animals ; Chitosan ; analogs & derivatives ; therapeutic use ; Female ; Intestinal Diseases ; prevention & control ; Male ; Postoperative Complications ; prevention & control ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Tissue Adhesions ; prevention & control

Objective: To analyze the incidence rate of occupational noise-induced hearing loss in noise-exposed workers in an iron and steel plant from 2006 to 2015. Methods: Using a cohort study method, workers exposed to occupational noise from Jan 1, 2006 to Dec 12, 2015 were followed up and the pure tone hearing test was conducted. In total, 6 297 subjects completed two or more physical checks and the pure tone hearing test and were included in the analysis. The noise exposure level at the workplace and the equivalent continuous A-weighted sound pressure level for workers was monitored and the cumulative noise exposure dose was evaluated. The subjects were divided into low, middle and high exposure groups according to the noise exposure level, and the equivalent continuous A-weighted sound pressure level for 8 hours for each group was 80.6-85.0, 85.1-90.0 and 90.1-103.4 dB (A), respectively. While the RR and 95% CI were derived from unconditional logistic regression models. In logistic regression analysis, confounding factors such as age, gender, smoking habit, drinking habit, high temperature exposure and chemical hazards exposure level were controlled. Results: During the follow-up period, 392 cases of occupational noise-induced hearing loss were diagnosed among the 6 297 subjects, with an incidence rate of 6.23%; 318 cases of high-frequency hearing loss were diagnosed, with an incidence rate of 5.05%; and 74 cases of occupational noise-induced deafness were diagnosed, with an incidence rate of 1.18% . The incidence rates of hearing loss among the high, medium and low exposure groups were 9.22% (158/1 737), 6.49% (204/3 142) and 2.08% (30/1 442), respectively; the rates of high-frequency hearing loss were 7.41% (127/1 737), 5.25% (165/3 142) and 1.80% (26/1 442), respectively; and the rates of occupational noise-induced deafness were 1.81% (31/1 737), 1.24% (39/3 142) and 0.28% (4/1 442), respectively. For the groups corresponding to cumulative noise exposure doses of ≤84.99, 85.00- 87.99, 88.00- 90.99, 91.00- 93.99, 94.00- 96.99, 97.00- 100.99, 101.00- 102.99 and ≥103.00 dB (A) · year, the incidence rates of hearing loss were 0 (0/185), 1.22% (2/164), 2.52% (17/674), 3.83% (35/913), 5.80% (106/1 827), 6.02% (67/1 113), 9.20% (95/1 003) and 18.04% (70/388), respectively. Compared with the low exposure group, the RR of hearing loss, high-frequency hearing loss and occupational noise-induced deafness for the high exposure group were 4.78 (95% CI: 3.22- 7.11), 4.36 (95% CI: 2.84- 6.69) and 6.63 (95% CI: 2.33- 18.82), respectively; and for the medium exposure group were 3.27 (95% CI: 2.22-4.82), 3.02 (95% CI: 1.99-4.59) and 4.52 (95% CI: 1.61-12.67), respectively. Conclusion The incidence rate of hearing loss for workers exposed to noise in an iron and steel plant was related to the cumulative noise exposure dose, gender, age, educational level, smoking habits, drinking habits and exposure to high temperature.

Objective: The aim of this study was to investigate whether genetic variability in the protocadherin 15 (PCDH15) gene may correspond with increased susceptibility to noise-induced hearing loss (NIHL) in a Chinese population. Methods: A nested case-control study was performed that followed a cohort of 7 445 noise-exposed workers in a steel factory of Henan province in China from January 1, 2006 to December 31, 2015. In this study, 394 cases who had an average hearing threshold of more than 40 dB (A) in high frequency were defined as the case group, and 721 controls who had an average hearing threshold of less than 35 dB (A) in high frequency and less than 25 dB (A) in speech frequency were defined as the control group. A questionnaire was completed by participants and a physical test was also conducted. SNP genotyping was performed using the SNPscan^TM Kit. Multivariate unconditional logistic regression additive models were used to analyze the genotypes in different groups, and the association with NIHL. Unconditional logistic regression models were used to assess the associations between the genotypes and NIHL. Results: The average age of study participants was (40.5±8.3) years and the median number of noise-exposed working years M (P₂₅, P₇₅) was 21.1 (9.1, 27.3). The range of noise exposed levels and the levels of cumulative noise exposure (CNE) were 80.1- 98.8 dB(A) and 86.6- 111.2 dB(A), respectively. Only the distribution of the genotypes (TT/CC/CT) of rs11004085 in the PCDH15 gene showed a significant difference between the case and control groups (P=0.049). In the case group, the distribution was 370 (93.9%), 24 (6.1%) and 0; in the control group, the distribution was 694 (96.3%), 23 (3.2%) and 1 (0.1% ). After smoking, drinking, hypertension, height and CNE adjustment, compared with the TT genotype individuals with the CC/CT genotype had a 1.90-fold increased risk of NIHL (95% CI: 1.06- 3.40). After stratified these data by the noise exposure level or CNE when the noise exposure level was>85 dB (A), compared with cases with the AA genotype of rs10825113, individuals with the GA/GG genotype had a 2.63-fold increased risk of NIHL (95% CI: 1.12- 6.14). When the CNE was ≤ 98 dB(A), compared with cases with the TT genotype of rs11004085, individuals with the CC/CT genotype had a 2.96-fold increased risk of NIHL (95% CI: 1.33- 6.56). However, these differences were not significant after Bonferroni correction had been applied. Conclusions The results confirmed that genetic variation within the PCDH15 gene may affect the susceptibility to NIHL.

Objective: To identify the association between genetic polymorphisms in the eye absent homolog 4 (EYA4) gene and noise-induced hearing loss (NIHL). Method: A nested case control study was conducted based on a cohort of noise-exposed subjects. In total, 292 cases were selected from a steel factory from 6 297 subjects during Jan 1, 2006 to Dec 12, 2015,who had an average hearing threshold of more than 40 dB(A); 584 matched control subjects for each case were designated on the basis of matched criteria including same gender, age (±5 years) and duration of exposure to noise (±2 years). What's more, the control group had an average hearing threshold of less than 35 dB(A) in high frequency and less than 25 dB(A) in speech frequency. Four single nucleotide polymorphisms (SNPs) of the EYA4 gene were genotyped using a SNPscan^TM multiplex SNP genotyping kit. Hardy-Weinberg equilibrium tests were performed using a χ² test for goodness-of-fit for each SNP among the control group, and the effects of genotypes of the EYA4 gene on NIHL were analyzed by logistic regression. The haplotypes were established and their frequencies in the two groups were assessed using Haploview 4.2 and Phase 2.1 software, and interactive effects between haplotypes and cumulative noise exposure were analyzed. Results: The average age of the subjects was (40.1±8.4) years and the average number of noise-exposed working years was 20.3 (8.4, 27.3) years. The range of noise exposure levels and the cumulative noise exposure were 80.2- 98.8 dB (A) and 86.6- 111.2 dB(A) · year, respectively. After adjustment for covariates including height, blood pressure, drinking status and smoking status, in the noise intensity>85 dB (A) group, subjects carrying the rs3813346 TT genotype had a higher NIHL risk than those carrying the GG genotype, and the adjusted OR (95% CI) value was 2.12 (1.21- 3.69). In the cumulative noise exposure>98 dB (A) · year group, compared with haplotype TGC, haplotype CGT showed a protective effect in the development of NIHL, with an adjusted OR (95% CI) value of 0.60 (0.37-0.97), however, the significance of intercation between EY4 gene of noise was lost after Bonferroni correction. Conclusion Genetic polymorphism in the EYA4 gene may be a genetic susceptibility factor for NIHL.

Objective: To explore the relationship between mitochondrial 12 S rRNA gene variation, tRNA gene variation and cytochrome oxidase Ⅱ gene point mutations and the risk of noise-induced hearing loss (NIHL). Methods: A nested case-control study was performed that followed a cohort of 7 445 noise-exposed workers in a steel factory in Henan province, China, from January 1, 2006 to December 31, 2015. Subjects whose average hearing threshold was more than 40 dB(A) in high frequency were defined as the case group, and subjects whose average hearing threshold was less than 35 dB(A) in high frequency and less than 25 dB (A) in speech frequency were defined as the control group. Subjects was recruited into the case group (n=286) and the control group (n=286) according to gender, age, job category and time of exposure to noise, and a 1∶1 case-control study was carried out. We genotyped eight single nucleotide polymorphisms in the mitochondrial 12 S rRNA gene, the mitochondrial tRNA gene and the mitochondrial cytochrome oxidase Ⅱ gene using SNPscan high-throughput genotyping technology from the recruited subjects. The relationship between polymorphic sites and NIHL, adjusted for covariates, was analyzed using conditional logistic regression analysis, as were the subgroup data. Results: The average age of the recruited subjects was (40.3±8.1) years and the length of service exposure to noise was (18.6±8.9) years. The range of noise exposed levels and cumulative noise exposure (CNE) was 80.1- 93.4 dB (A) and 86.8- 107.9 dB (A) · year, respectively. For workers exposed to noise at a CNE level<98 dB (A) · year, smokers showed an increased risk of NIHL of 1.88 (1.16-3.05) compared with non-smokers; for workers exposed to noise at a CNE level ≥98 dB(A) · year, smokers showed an increased risk of NIHL of 2.53 (1.49- 4.30) compared with non-smokers. For workers exposed to noise at a CNE level<98 dB (A) · year, the results of univariate analysis and multifactor analysis, adjusted by smoking and CNE, suggested that the risk of NIHL in workers exposed to noise carrying the GG genotype (G827A) was lower than that of NIHL workers exposed to noise carrying the AA genotype (G827A) [OR (95% CI) were 0.18 (0.04- 0.82) and 0.19 (0.04- 0.88), respectively]. Conclusion Smoking increased the risk of NIHL in the present study. For workers subjected to a CNE<98 dB(A)·year, the mitochondrial genetic variant G827A was found to be significantly associated with the risk of NIHL.

Objective To prepare ultrasound(US)responsive nanodroplets(NDs)simultaneously loaded with anticancer drug Sorafenib(SF)and Doxorubicin(DOX),and to characterize its ultrasound responsibility in vitro and in vivo.Methods The SF/DOX NDs were prepared using the thin-film hydration method.The particle diameter,Zeta potential and drug-encapsulation efficiency were characterized.The acoustic droplets vaporization activity was monitored by in vitro ultrasound imaging and light microscope. The cavitation effect was monitored by in vitro ultrasound imaging and transmission electron microscopy. Results SF/DOX NDs were round in shape,the mean diameter and Zeta potential of SF/DOX NDs was (498 ± 67.34)nm,-(38.87 ± 3.78)mV,respectively.The entrapment efficiency of SF and DOX was (58.14±2.93)%,(51.23±4.11)%,respectively.SF/DOX NDs underwent a phase transition into bubbles and could be continuously imaged for more than 25 min in vitro,and afterward therapeutic ultrasound pulse induced inertial cavitation and substantially enhanced treatment.Conclusions US-responsible SF/DOX NDs are prepared using thin-film hydration mehtod,it can enhance ultrasonic echo in vitro and release anticancer drug by the aid of US exposure,which possesses greater researching and applicating value.