Non-pharmacological interventions for the prevention of sexually transmitted infections (STIs) in older adults: A systematic review.

BACKGROUND: STIs in older adults (adults aged 50 years and older) are on the rise due to variable levels of sex literacy and misperceived susceptibility to infections, among other factors. We systematically reviewed evidence on the effect of non-pharmacological interventions for the primary prevention of sexually transmitted infections (STIs) and high-risk sexual behaviour in older adults. METHODS: We searched EMBASE, MEDLINE, PSYCINFO, Global Health and the Cochrane Library from inception until March 9th, 2022. We included RCTs, cluster-randomised trials, quasi-RCTs, interrupted time series (ITS) and controlled and uncontrolled before-and-after studies of non-pharmacological primary prevention interventions (e.g. educational and behaviour change interventions) in older adults, reporting either qualitative or quantitative findings. At least two review authors independently assessed the eligibility of articles and extracted data on main characteristics, risk of bias and study findings. Narrative synthesis was performed. RESULTS: Ten studies (two RCTs, seven quasi-experiment studies and one qualitative study) were found to be eligible for this review. These interventions were mainly information, education and communication activities (IECs) aimed at fostering participants' knowledge on STIs and safer sex, mostly focused on HIV. Most studies used self-reported outcomes measuring knowledge and behaviour change related to HIV, STIs and safer sex. Studies generally reported an increase in STI/HIV knowledge. However, risk of bias was high or critical across all studies. CONCLUSIONS: Literature on non-pharmacological interventions for older adults is sparse, particularly outside the US and for STIs other than HIV. There is evidence that IECs may improve short-term knowledge about STIs however, it is not clear this translates into long-term improvement or behaviour change as all studies included in this review had follow-up times of 3 months or less. More robust and higher-quality studies are needed in order to confirm the effectiveness of non-pharmacological primary prevention interventions for reducing STIs in the older adult population.

Granulocyte colony-stimulating factor antibody abrogates radioprotective efficacy of gamma-tocotrienol, a promising radiation countermeasure.

This study aimed to determine the role of granulocyte colony-stimulating factor (G-CSF), induced by a promising radiation countermeasure, gamma tocotrienol (GT3), in protecting mice from lethal doses of ionizing radiation. CD2F1 mice were injected with an optimal dose of GT3 and a G-CSF antibody, and their 30-d survival was monitored. An appropriate antibody isotype was used as a control. Multiplex Luminex was used to analyze GT3-induced cytokines. G-CSF neutralization by exogenous administration of a G-CSF antibody was confirmed by analyzing serum cytokine levels. Our results demonstrate that GT3 significantly protected mice against ionizing radiation, and induced high levels of G-CSF in peripheral blood 24h after administration. Injection of a G-CSF neutralizing antibody to the GT3-treated mice resulted in complete neutralization of G-CSF and abrogation of its protective efficacy. Administration of a G-CSF antibody did not affect levels of other cytokines induced by GT3. Histopathology of bone marrow from GT3-treated and -irradiated mice demonstrated protection of the hematopoietic tissue, and also that such protection was abrogated by administering a G-CSF antibody. Our results suggest that induction of high levels of G-CSF by GT3 administration is responsible for its protective efficacy against radiation injury.

Radioprotective properties of tocopherol succinate against ionizing radiation in mice.

Threats of nuclear and other radiologic exposures have been increasing but no countermeasure for acute radiation syndrome has been approved by regulatory authorities. In prior publications we have demonstrated the efficacy of tocopherol succinate (TS) as a promising radiation countermeasure with the potential to protect against lethal doses of ionizing radiation exposure. The aim of this study was to gain further insight regarding how TS protects mice against a lethal dose of radiation. CD2F1 mice were injected subcutaneously with 400 mg/kg of TS, and 24 h later exposed to (60)Co γ-radiation. Intestinal tissues or spleen/thymus were harvested after irradiation and analyzed for CD68-positive inflammatory cells and apoptotic cells by immunostaining of jejunal cross-sections. Comet assay was used to analyze DNA damage in various tissues. Phospho-histone H3(pH3) and the proliferating cell nuclear antigen (PCNA) were used as mitotic markers for immunostaining jejunal cross-sections. We observed that injecting TS significantly decreased the number of CD68-positive cells, DNA damage and apoptotic cells (BAX, caspase 3 and cleaved poly(ADP-ribose) polymerase-positive cells) as judged by various apoptotic pathway markers. TS treatment also increased proliferating cells in irradiated mice. Results of this study further support our contention that TS protects mice against lethal doses of ionizing radiation by inhibiting radiation-induced apoptosis and DNA damage while enhancing cell proliferation.

Alpha-tocopherol succinate-mobilized progenitors improve intestinal integrity after whole body irradiation.

PURPOSE: The objective of this study was to elucidate the action of α-tocopherol succinate (TS)- and AMD3100-mobilized progenitors in mitigating radiation-induced injuries. MATERIAL AND METHODS: CD2F1 mice were exposed to a high dose of radiation and then transfused intravenously with 5 million peripheral blood mononuclear cells (PBMC) from TS- and AMD3100-injected mice after irradiation. Intestinal and splenic tissues were harvested after irradiation and cells of those tissues were analyzed for markers of apoptosis and mitosis. Bacterial translocation from gut to heart, spleen, and liver in TS-treated and irradiated mice was evaluated by bacterial culture. RESULTS: We observed that the infusion of PBMC from TS- and AMD3100-injected mice significantly inhibited apoptosis, increased cell proliferation in the analyzed tissues of recipient mice, and inhibited bacterial translocation to various organs compared to mice receiving cells from vehicle-mobilized cells. This study further supports our contention that the infusion of TS-mobilized progenitor-containing PBMC acts as a bridging therapy by inhibiting radiation-induced apoptosis, enhancing cell proliferation, and inhibiting bacterial translocation in irradiated mice. CONCLUSIONS: We suggest that this novel bridging therapeutic approach that involves the infusion of TS-mobilized hematopoietic progenitors following acute radiation injury might be applicable to humans as well.