HIV-Related Behaviors, Social Support and Health-Related Quality of Life among Men Who Have Sex with Men and Women (MSMW): A Cross-Sectional Study in Chongqing, China

<div><p>Background</p><p>Health-related quality of life (HRQOL) has become commonly used both as a concept and as a field of research. However, little is known about the HRQOL of men who have sex with men and women (MSMW). The aim of this study was to examine HIV-related behaviors, social support, and HRQOL status and explore its predictors among MSMW.</p><p>Methods</p><p>An anonymous cross-sectional study was conducted by snowball sampling method in 2013. A total of 563 Chinese MSM completed a structured questionnaire. The HRQOL and social support were measured with the Chinese version of the World Health Organization Quality of Life Scale (WHOQOL-BRFE) and the Social Support Rating Scale (SSRS), respectively.</p><p>Results</p><p>Of the 563 MSM analyzed, 77 (13.68%) were MSMW who had a higher proportion of in-marriage and preference for an insertive role as compared with the men who have sex with men only (MSMO) (<i>P</i><0.05). As high as 70.13% of MSMW had no regular sex partners and 72.73% of MSMW reported engaging in unprotected anal sex in the last six months. 36.36% had tested for HIV, while only 12.99% had accepted HIV voluntary counseling and testing (VCT) services. The scores of objective support and subjective support in MSMW were significantly higher than that of MSMO (<i>P</i><0.05). No statistically significant difference was found in scores of all the four domains of the HRQOL between MSMW and MSMO. When comparing the HRQOL scores of MSMW with the Chinese general population reference group, the scores of MSMW were significantly lower in physical health domain. In a multivariate regression model, age, monthly income, sexual role, VCT acceptability, subjective support were associated with variability in HRQOL.</p><p>Conclusions</p><p>To improve the HRQOL among MSMW, more attention needs to be paid to those with low social support, low-income, the old and those prefer a receptive role during anal sex populations.</p></div

HRQOL scores of MSMW and the Chinese general population reference group.

<p>Data are shown as the mean±SD; Reference group: Chinese general population reference group.</p><p>HRQOL scores of MSMW and the Chinese general population reference group.</p

Social-demographic characteristics of study population.

<p>Data are shown as the number (%)</p><p>^#Wilcoxon rank tests were used</p><p>*Chi-square tests were used.</p><p>Social-demographic characteristics of study population.</p

HIV-related behaviors of study population.

<p>Data are shown as the number (%).</p><p>^#Wilcoxon rank tests were used</p><p>*Chi-square tests were used.</p><p>HIV-related behaviors of study population.</p

Summary of histopathological diagnoses.

<p>Chc1L+/- and Chc1L-/- mice developed HS and HAL or HS co-occurring with BCL. Chc1L-/- mice developed more cases of HS, while Chc1L+/- mice had more diagnoses of HAL/HS+BCL than HS.</p

Chromosome Condensation 1-Like (<i>Chc1L</i>) Is a Novel Tumor Suppressor Involved in Development of Histiocyte-Rich Neoplasms

<div><p>Human chromosomal region 13q14 is a deletion hotspot in prostate cancer, multiple myeloma, and chronic lymphocytic leukemia. This region is believed to host multiple tumor suppressors. Chromosome Condensation 1-like (<i>CHC1L</i>) is located at 13q14, and found within the smallest common region of loss of heterozygosity in prostate cancer. Decreased expression of <i>CHC1L</i> is linked to pathogenesis and progression of both prostate cancer and multiple myeloma. However, there is no direct evidence for <i>CHC1L</i>’s putative tumor suppressing role in current literature. Presently, we describe the generation and characterization of <i>Chc1L</i> knockout mice. <i>Chc1L</i>^-/- mice do not develop cancer at a young age, but bone marrow and spleen cells from 8–12 week-old mice display an exaggerated proliferative response. By approximately two years of age, knockout and heterozygote mice have a markedly increased incidence of tumorigenesis compared to wild-type controls, with tumors occurring mainly in the spleen, mesenteric lymph nodes, liver and intestinal tract. Histopathological analysis found that most heterozygote and knockout mice succumb to either Histiocytic Sarcoma or Histiocyte-Associated Lymphoma. Our study suggests that <i>Chc1L</i> is involved in suppression of these two histiocyte-rich neoplasms in mice and supports clinical data suggesting that <i>CHC1L</i> loss of function is an important step in the pathogenesis of cancers containing 13q14 deletion.</p></div

Generation of <i>Chc1L</i>^-/- knockout mice by gene targeting.

<p>A) Gene targeting strategy. (a) The start codon is located in exon 4 of murine <i>Chc1L</i>, and a second ATG codon is in exon 5. EcoRI digestion produces a gene fragment of 20 kb. Deleting 6kb of intron 4, a gene targeting vector was constructed, with unidirectional loxP sites flanking exons 4 and 5. (b) The gene-targeted locus produces a 14 kb fragment upon digestion with EcoRI. (c) Exon 4, intron 4 and exon 5 are lost following Cre-mediated recombination. B) Confirmation of gene targeting in ES cells. Successful knockin of neomycin-selected ES cells was detected by Southern Blot using a 5’ probe, visualizing a 20kb WT locus fragment, and a 14kb gene-targeted fragment. C) Confirmation of gene targeting in mice. Gene knockin was confirmed in mice again using Southern Blot. D) Confirmation of loss of Chc1L expression. Loss of Chc1L expression was confirmed by RT-PCR.</p

Western blot.

<p>Lysates of knock-out homozygous <i>aldh7a1</i> zebrafish embryos (at 8 dpf) western blot analysis showing no aldh7a1 protein compared to wild-type.</p

Social support and HRQOL scores of the two groups.

<p>Data are shown as the mean±SD.</p><p>Social support and HRQOL scores of the two groups.</p

<i>Chc1L</i>^+/- and <i>Chc1L</i>^-/- mice have elevated tumor incidence.

<p>A) Splenocyte and bone marrow cell viability. <i>Chc1L</i>^-/- splenocytes and bone marrow cells have increased viability following LPS-stimulation, compared wild-type controls (splenocyte fold-survival <i>Chc1L</i>^-/-/ <i>Chc1L</i>^+/+ = 1.45±0.29, p<0.05, n = 3; bone marrow fold-survival <i>Chc1L</i>^-/-/<i>Chc1L</i>^+/+ = 1.26±0.11, p<0.01, n = 3). B) Tumor incidence. Tumor incidence by genotype. Incidence of observable tumors was highest in <i>Chc1L</i>^+/- and <i>Chc1L</i>^-/- mice (<i>Chc1L</i>^+/+: 26%, <i>Chc1L</i>^+/-: 56%, <i>Chc1L</i>^-/-: 80%). C) Tumor distribution. Tumors were found most often in the spleen, mesenteric lymph nodes and liver. D) Incidence of multiple organs being affected. <i>Chc1L</i>^+/- mice typically had multiple tumor-bearing organs.</p