Schistosomiasis is a neglected tropical disease affecting 40 million women of childbearing age worldwide. Its global disease prevalence among pregnant women is still unknown. This meta-analysis determined the pooled prevalence of schistosomiasis among pregnant women globally. Additionally, this study also determined the pooled prevalence based on infection intensity based on eggs per gram. Observational studies on the prevalence of schistosomiasis among pregnant patients were obtained from Medline, Scopus, and CINAHL from January 2001 until August 2020. A review of titles and abstracts was done independently by six reviewers. The quality of the included studies was assessed using the Newcastle–Ottawa Scale for case–control, cohort, and cross-sectional studies. A total of 27 studies were included in the meta-analysis and meta-regression. The pooled prevalence of S. haematobium was 13.44 (CI: 8.90–19.80) per 100 observations, while the pooled prevalence of S. mansoni was 12.18 (CI: 4.47–29.12) per 100 observations. The prevalence of S. japonicum infection in one study was 53.54 (CI: 43.23–63.62) per 100 observations. Our results showed a prevailing health problem of schistosomiasis during pregnancy in various countries worldwide. This strengthens the need to conduct more schistosomiasis research, prevention, and control programs in pregnant women.

HPV infection is one of the most studied risk factors in cervical cancer—the second most common cancer site and cause of death due to cancer in the Philippines. However, there is a lack of population-based epidemiological data on cervical HPV infection in the Philippines. Local reports on co-infections with other lower genital tract pathogens, commonly reported globally, are also lacking, which emphasizes the need to increase efforts in targeting HPV prevalence, genotype, and distribution. Hence, we aim to determine the molecular epidemiology and natural history of HPV infection among reproductive-age Filipino women using a community-based prospective cohort design. Women from rural and urban centers will be screened until the target sample size of 110 HPV-positive women (55 from rural sites and 55 from urban sites) is reached. Cervical and vaginal swabs will be collected from all screened participants. For HPV-positive patients, HPV genotypes will be determined. One hundred ten healthy controls will be selected from previously screened volunteers. The cases and controls will comprise the multi-omics subset of participants and will be followed up after 6 and 12 months for repeat HPV screening. Metagenomic and metabolomic analyses of the vaginal swabs will also be performed at baseline, after 6 months, and after 12 months. The results of this study will update the prevalence and genotypic distribution of cervical HPV infection among Filipino women, determine whether the current vaccines used for HPV vaccination programs capture the most prevalent high-risk HPV genotypes in the country, and identify vaginal community state types and bacterial taxa associated with the natural history of cervical HPV infection. The results of this study will be used as the basis for developing a biomarker that can help predict the risk of developing persistent cervical HPV infection in Filipino women.

The cholesterol biosynthesis pathway is upregulated during breast cancer development and progression. Inhibition of the aberrantly upregulated cholesterol pathway by statins reduces breast tumor incidence and burden by 50% in SV40 C3(1) TAg mice, a mouse model of triple negative breast cancer. We hypothesized that fluvastatin’s preventive efficacy could be further enhanced by co-targeting the statin-induced restorative feedback pathways that tightly control the cholesterol pathway and are involved in resistance to statins. Acyl-coenzyme A: cholesterol acyltransferase (ACAT)2 is a cholesterol esterification gene that is upregulated in statin-resistant MCF10.DCIS cells, and in mammary tumors of statin-non-responsive SV40 C3(1) TAg mice. In support of this hypothesis, a combination of fluvastatin and avasimibe effectively inhibited the cell growth of statin-resistant MCF10.DCIS cells. However, this combination failed to prevent breast tumor formation in SV40 C3(1) TAg mice. Although avasimibe inhibited fluvastatin-induced ACAT2 mRNA expression in the breast tissue of the combination-treated mice, confirming that avasimibe effectively hit its target, the fluvastatin and avasimibe combination was completely ineffective in preventing breast cancer in vivo, with approximately 90% of mice developing tumors by 22 weeks, similar to the vehicle control group animals. These findings, along with avasimibe’ s known interactions with CYP450 gene family members, suggest that AVA abrogates the efficacy of fluvastatin through enhanced metabolism of fluvastatin in vivo. The findings reported in this brief communication provide a cautionary note for studies proposing the use of avasimibe in combination therapy for cancer prevention and treatment.