Size distribution and antibiotic-resistant characteristics of bacterial bioaerosol in intensive care unit before and during visits to patients.

Airborne bacteria in hospitals have been implicated in nosocomial infections. This investigation studied the characteristics of airborne bacteria and the effect of patient visitation on the bacteria profile in intensive care units (ICUs). Air at a medical ICU and surgical ICU was sampled for one year. Airborne bacteria before and during visits to patients in ICUs were collected using a Six-Stage Viable Andersen Cascade Impactor to analyze the concentration and size distribution of airborne bacteria and the percentage thereof that were antibiotic-resistant. During patient visitation in the ICUs in this study, the number of visitors was 20-80. Airborne bacteria concentration during visiting hours (total averaging 168.5 CFU/m3) was three to four times than before visiting hours (p = 0.043). With increasing the visitors, most of the airborne human-associated bacteria (HAB) concentrations during visitations were higher than before visitations in each season. The two-way ANOVA of HAB concentration before and during visitation (p = 0.028) of combining MICU and SICU in various season (p = 0.007) all revealed statistical agreement. The proportion of particles, from 1.1 to 4.7 µm, during the visits was almost 1-2.4 times that before the visits in most sampling periods (p = 0.028). In addition, the opportunistic pathogens such as Micrococcus spp., Staphylococcus spp. and Acinetobacter spp. were found in the air during visiting times. Small proportions of some environmental strains with a high antibiotic-resistance percentage (42-78%), including Brevundimonas spp., Elizabethkingia spp. and others, were detected during patient visitation. Patient visitation activities affect the bacterial profile in air in ICUs. During the visitation, visitors might bring or generate bacteria into ICUs. Limiting the number of patient visitors to ICUs, wearing respirators and gowns or increasing ventilation rate during and after patient visitation is required to maintain indoor air quality and probably decrease the risk of patient infection.

Involvement of FGFR4 Gene Variants on the Clinicopathological Severity in Urothelial Cell Carcinoma.

Fibroblast growth factor receptor 4 (FGFR4) plays a prominent role in cell proliferation and cancer progression. This study explored the effect of FGFR4 single-nucleotide polymorphisms (SNPs) on the clinicopathological characteristics of urothelial cell carcinoma (UCC). This study was conducted to survey the possible correlation of the polymorphism of FGFR4 to the risk and clinicopathologic characteristics of UCC. Four loci of FGFR4 (rs2011077 T > C, rs351855 G > A, rs7708357 G>A, and rs1966265 A > G) were genotyped via the TaqMan allelic discrimination approach in 428 UCC cases and 856 controls. The results indicated that UCC subjects who carried the SNP rs2011077 TC+CC genotypes were significantly related to a higher tumor stage (odds ratio (OR): 1.751, 95% confidence interval (CI): 1.078-2.846), primary tumor size (OR: 1.637, 95% CI: 1.006-2.662), and histopathologic grading (OR: 1.919, 95% CI: 1.049-3.511). Moreover, the SNP rs1966265 AG+GG genotypes were prominently related to a higher tumor stage (OR: 1.769, 95% CI: 1.082-2.891), primary tumor size (OR: 1.654, 95% CI: 1.011-2.706), and histopathologic grading (OR: 2.006, 95% CI: 1.096-3.674) compared to individuals with AA homozygotes. In conclusion, our data reveal association of FGFR4 polymorphisms with UCC clinicopathologic characteristics. FGFR4 polymorphisms may serve as a marker or therapeutic target in UCC development.

Impact of endothelial nitric oxide synthase polymorphisms on urothelial cell carcinoma development.

OBJECTIVES: Urothelial cell carcinoma (UCC), a major malignancy of the genitourinary tract, is induced through carcinogenic etiological factors. Endothelial nitric oxide synthase (eNOS) is one of the major isoforms of nitric oxide synthase and is involved in various pathophysiologic and physiologic processes. In this study, eNOS single-nucleotide polymorphisms were investigated to evaluate UCC susceptibility and clinicopathological characteristics. MATERIALS AND METHODS: Two single-nucleotide polymorphisms of eNOS in 431 patients with UCC and 862 controls without cancer were analyzed using real-time polymerase chain reaction. RESULTS: The results showed that 272 men with UCC having eNOS 894 G > T rs1799983 "GT + TT" variants had a high risk of developing a large tumor (T1-T4, P = 0.038). Furthermore, a correlation was observed between the expressions of eNOS and invasive tumor, metastasis and poor survival in urothelial carcinoma in The Cancer Genome Atlas data set. CONCLUSION: Our results indicated that male patients with UCC carrying eNOS 894 G > T rs1799983 "GT + TT" genetic variants have a high risk of developing a large tumor, and eNOS polymorphisms may serve as a marker or therapeutic target in UCC treatment.

Effects of genetic polymorphisms of programmed cell death 1 and its ligands on the development of ankylosing spondylitis.

OBJECTIVES: There is a known association of imbalanced peripheral tolerance and autoimmune diseases. The binding of programmed cell death 1 (PD-1) with its ligands 1 and 2 (PD-L1 and PD-L2) inhibits T-cell proliferation through a negative signal via recruitment of src homology 2-domain-containing tyrosine phosphatase 2. Therefore we evaluated the effect of the PD-1, PD-L1 and PD-L2 genotypes on the occurrence of AS in a population of Taiwanese patients. METHODS: Genetic polymorphisms of PD-1 G-536A, PD-L1 A8923C and PD-L2 C47103T were identified by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) for 330 AS patients and 330 healthy controls who were matched by age and gender. RESULTS: Subjects with the PD-1 GG genotype [matched relative risk (RR(m)) 1.78; 95% CI 1.13, 2.81] and the GA genotype (RR(m) 1.59; 95% CI 1.09, 2.31) had significantly greater risk for AS than those with the AA genotype. Subjects with the PD-L2 CT genotype had lower risk for AS than those with the CC genotype (RR(m) 0.01; 95% CI 0.001, 0.06). Interestingly, the combined genotypes of PD-1 G-536A, PD-L1 A8923C and PD-L2 C47103T also appear to be associated with AS development. CONCLUSIONS: Our results suggest that PD-1 G-536A, PD-L1 A8923C and PD-L2 C47103T polymorphisms are associated with the presence of AS.

Osteoprotegerin genetic polymorphisms and age of symptom onset in ankylosing spondylitis.

OBJECTIVES: Osteoporosis is one of the recognized features of AS. It is known that RANK ligand (RANKL), which binds to RANK, can cause the activation of bone resorption. Osteoprotegerin (OPG) also competes with RANK by binding to RANKL and inhibiting bone absorption. Therefore, we designed a case-control study to evaluate the association between occurrence and clinical features of AS and RANK, RANKL and OPG genetic polymorphisms. METHODS: A total of 330 AS patients and 330 age- and gender-matched controls were recruited. PCR-restriction fragment length polymorphism was applied to identify RANK C575T, RANKL C-290T and OPG G1181C genotypes. RESULTS: OPG GG genotype carriers had an elevated risk of AS compared with those with the GC and CC genotypes (matched odds ratio 1.74; 95% CI 1.26, 2.40). Age of symptom onset and frequency of peripheral arthritis significantly differed among AS patients by OPG G1181C genotypes. HLA-B27(+) patients with the OPG C allele had the earliest age of symptom onset [mean (s.d.) 26.6 (9.6) years], followed by HLA-B27(+) patients with the OPG G allele [32.6 (12.2) years], HLA-B27(-) patients with the OPG G allele [38.1 (13.6) years] and HLA-B27(-) patients with the OPG C allele [38.6 (9.8) years]. CONCLUSION. OPG G1181C polymorphism may be associated with AS development and clinical manifestations.