Sexually transmitted infections (STIs) have risen in the over-40 age group [ [1] Public Health England STI data for the UK; Number and rates of selected STI diagnoses in the UK, 2008–2012. December 2013http://www.hpa.org.uk/web/HPAweb&HPAwebStandard/HPAweb_C/1203348026613#5._STI_data_for_the_UK Google Scholar ] but health promotion is targeted at the younger population. Many infections may be asymptomatic, including HIV, syphilis, chlamydia and gonorrhoea [ [2] Royal College of General Practice and British Association for Sexual Health and HIV Sexually Transmitted Infections in Primary Care. 2013http://www.bashh.org/documents/Sexually%20Transmitted%20Infections%20in%20Primary%20Care%202013.pdf Google Scholar ]. Local data from the North East of England from 2012 showed that 37% of women newly diagnosed with HIV were over the age of 45, with 54% diagnosed late with a poorer prognosis. Women coming out of long-term relationships and entering new sexual relationships may not consider the risks of sexual infection or the need for condoms, due to having a long-acting reversible contraceptive (LARC), or sterilisation. Termination of pregnancy in women over 40 now exceeds the rate in the under 16 age group [ [3] Department of Health Abortion Statistics, England and Wales. July 2013www.gov.uk/government/collections/abortion-statistics-for-england-and-wales Google Scholar ].

Genitourinary medicine clinic attendees who were newly diagnosed as HIV antibody positive in a population with low overall HIV prevalence were compared with HIV-ve control groups in a retrospective study. Demographics and clinical data from the clinic attendance at which the HIV test was performed were analysed. Of 25,627 HIV tests, 113 were positive. Seventy-eight percent had an identified risk factor for HIV and more than half had symptoms of, or were contacts of, a sexually transmitted infection (STI) or HIV. Only eight clients testing HIV+ve had attended for routine STI testing and only two of these had no identified risk factor. Groups shown to be at higher HIV risk included attendees with past history of STI, men-who-have-sex-with-men (MSM) and those requesting HIV test without an STI screen. MSM testing HIV-ve had high rates of HIV risk behaviour.

3beta-Hydroxysteroid dehydrogenase (3beta-HSD) activity is essential for the synthesis of all classes of steroid hormones, converting various Delta(5) -3beta-hydroxysteroids into hormonally active Delta(4) -3-ketosteroids in NAD(+) -dependent reactions. Certain 3beta-HSD isoforms have been reported to exhibit additional dehydrogenase character (e.g., 17-hydroxysteroid dehydrogenase/reductase). We have investigated whether mouse type I (adrenal/gonadal) and type VI 3beta-HSDs (uterine/embryonic) display significant 17beta-HSD-like activity. Nonsteroidogenic HEK 293T cells were transiently transfected with pCMV-based expression vectors containing mouse type I and type VI 3beta-HSDs. Transfected cells expressing either mouse type I or type VI 3beta-HSD converted testosterone to androstenedione, albeit at rates one-tenth of those of pregnenolone to progesterone in similarly transfected 293T cells. Our findings demonstrate that the mouse 3beta-HSD I and VI isoforms can inactivate testosterone within an intact cell milieu. These findings are important not only in establishment of structure-function relationships, but also whenever murine systems are used for developmental/reproductive paradigms associated with human disorders.

3β–Hydroxysteroid dehydrogenase (3β‐HSD) activity is essential for the synthesis of all classes of steroid hormones, converting various Δ5–3β–hydroxysteroids into hormonally active Δ4–3–ketosteroids in NAD+–dependent reactions. Certain 3β–HSD isoforms have been reported to exhibit additional dehydrogenase character (e.g., 17–hydroxysteroid dehydrogenase/reductase). We have investigated whether mouse type I (adrenal/gonadal) and type VI 3β–HSDs (uterine/embryonic) display significant 17β–HSD–like activity. Nonsteroidogenic HEK 293T cells were transiently transfected with pCMV–based expression vectors containing mouse type I and type VI 3β–HSDs. Transfected cells expressing either mouse type I or type VI 3β–HSD converted testosterone to androstenedione, albeit at rates one‐tenth of those of pregnenolone to progesterone in similarly transfected 293T cells. Our findings demonstrate that the mouse 3β–HSD I and VI isoforms can inactivate testosterone within an intact cell milieu. These findings are important not only in establishment of structure‐function relationships, but also whenever murine systems are used for developmental/reproductive paradigms associated with human disorders.