Prevalence, associated factors, and relationship to quality of life of lower urinary tract symptoms: a cross-sectional, questionnaire survey of cancer patients.

BACKGROUND: Few studies conducted outside of Asia have shown that lower urinary tract symptoms (LUTS) could be a concern for cancer patients. This gap necessitates more research on LUTS among cancer patients in Asia, particularly regarding associated factors and the relationship between quality of life and LUTS. OBJECTIVES: This study investigates the prevalence, associated factors, and relationship to quality of life of LUTS based on a sample of cancer patients. DESIGN: A cross-sectional, questionnaire survey. SETTINGS/PARTICIPANTS: This study was conducted at two oncology outpatient departments in two hospitals in Taiwan, and included 134 Asian cancer patients. METHODS: We collected information about each participant's individual characteristics, personal habits, LUTS, and quality of life by using a questionnaire. We calculated descriptive statistics to demonstrate the distribution of collected information, and used multivariate logistic regression to identify the factors associated with LUTS. We used Student's t-test to compare the mean quality of life scores for participants with and without LUTS. RESULTS: Ninety-nine (73.9%) participants experienced at least one type of LUTS, and the prevalence rates for various types of LUTS ranged from 3.7% to 52.2%. Radiotherapy and the time since the diagnosis of cancer were associated with LUTS. Participants with LUTS reported lower quality of life scores than participants without LUTS. CONCLUSIONS: The high prevalence of LUTS suggests that cancer treatment might be linked to LUTS, which in turn has a negative effect on a patient's quality of life. These results suggest that future research should involve studies in larger, more homogeneous samples. Health care providers should monitor the presence of LUTS and deliver the management and treatments of LUTS to optimise cancer patients' quality of life.

Novel mutations at carboxyl terminus of CIC-1 channel in myotonia congenita.

OBJECTIVES: Myotonia congenita (MC), caused by mutations in the muscle chloride channel (CLCN1) gene, can be inherited dominantly or recessively. The mutations at the carboxyl terminus of the CLCN1 gene have been identified in MC patients, but the functional implication of these mutations is unknown. MATERIAL AND METHODS: Direct sequencing of polymerase chain reaction products covering the whole coding region of the CLCN1 gene was performed in a MC family. This study was designed to investigate the clinical manifestations and genetic analysis of the CLCN1 gene. RESULTS: We identified two novel mutations, 2330delG and 1892C>T, from a genetic screening of the CLCN1 gene in the MC family. The 2330delG mutant allele producing a fs793X truncated protein was identified in a heterozygous state in all the patients. The 1892C>T nucleotide change induced a missense mutation (T631I) found in several asymptomatic individuals, indicating that it may not be associated with MC. Intriguingly, the 2330delG mutation was also found in an asymptomatic subject who also carried the 1892C>T mutation. CONCLUSION: The data indicate that the fs793X mutant protein causes dominantly inherited MC. Because the mutation has been found in a recessive pedigree, the fs793X mutation may have a dual inheritance pattern.

Study on construction of cDNA libraries from rat normal liver and regeneration liver with smart technique.

The aim of the study is to construct cDNA libraries from the normal liver and regeneration liver of rat by SMART (switching mechanism at 5' end of RNA transcript) technique and analyze their quality. The total RNA was separated from the normal liver and regeneration liver of rat and the frist-strand cDNA was synthesized through reverse transcription by a modified oligo (dT) primer (contained sfi IB site) while the SMART oligonucleotide (contained sfi IA site) was utilized as a template so that the first-strand cDNA could be extended over the 5' end of mRNA. The double-strand cDNA was amplified by LD-PCR (long-distance PCR) with the above two primers and then digested by sfi I (IA & IB) restriction, enzyme. After cDNA size fractionation through Chroma Spin 400 column, the double-strand cDNA was ligated into the sfi I-digested lambda TripIEx2 vector and then the recombinant DNA was packagedin vitro. The unamplified rat normal liver cDNA library consists of 1.3×10(7) pfu/ml, and regeneration liver cDNA library consists of 1.6×10(7) pfu/ml in which the percentage of recombinant clones both are about 100%. Through testing, the high quality cDNA libraries containing full-length cDNA of rat normal liver and regeneration liver have been constructed. The titer of the amplified cDNA library is 4.5×10(10) pfu/ml and 3.6×10(10) pfu/ml. the average exogenous inserts of the recombinants both are about 1.5 kb. These results show that the normal liver and regeneration liver of rat cDNA libraries both have an excellent quality and lay solid foundation to study liver functions and the mechanism of liver regeneration.

Cancer, heart disease, and diabetes in workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

BACKGROUND: In 1997, the International Agency for Research on Cancer classified 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as a group 1 human carcinogen, based largely on four highly exposed industrial cohorts that showed an excess of all cancers combined. In this study, we extended the follow-up period for the largest of these cohorts by 6 years and developed a job-exposure matrix. METHODS: We did cohort mortality analyses involving 5132 chemical workers at 12 U.S. plants by use of life table techniques (U.S. population referent) and Cox regression (internal referent). We conducted exposure-response analyses for 69% of the cohort with adequate work history data and adequate plant data on TCDD contamination. All P values are two-sided. RESULTS: The standardized mortality ratio (SMR) for all cancers combined was 1.13 (95% confidence interval = 1.02-1.25). We found statistically significant positive linear trends in SMRs with increasing exposure for all cancers combined and for lung cancer. The SMR for all cancers combined for the highest exposure group was 1.60 (95% confidence interval = 1.15-1.82). SMRs for heart disease showed a weak increasing trend with higher exposure (P = .14). Diabetes (any mention on the death certificate) showed a negative exposure-response trend. Internal analyses with Cox regression found statistically significant trends for cancer (15-year lag time) and heart disease (no lag). CONCLUSIONS: Our analyses suggest that high TCDD exposure results in an excess of all cancers combined, without any marked specificity. However, excess cancer was limited to the highest exposed workers, with exposures that were likely to have been 100-1000 times higher than those experienced by the general population and similar to the TCDD levels used in animal studies.