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Pengaruh Menopause Terhadap Kardiovaskular Guadelupe Maria Melisa Wiriadinata; Dewa Ayu Agus Sri Laksemi
Journal of Pharmaceutical and Sciences JPS Volume 9 Nomor 2 (2026)
Publisher : Fakultas Farmasi Universitas Tjut Nyak Dhien

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.36490/journal-jps.com.v9i2.1556

Abstract

Menopause is the permanent cessation of menstruation for 12 consecutive months without any underlying pathological cause. This occurs due to ovarian follicular atresia, which leads to the cessation of estrogen production. The menopausal transition begins 5 to 10 years before menstruation ceases. During menopause, estrogen levels decline, leading to biological changes in the body, such as an increase in total cholesterol, low-density lipoproteins (LDL), triglycerides, and apolipoprotein B, as well as a decrease in high-density lipoprotein (HDL), an increase in visceral fat, and the development of metabolic syndrome. Various characteristics of menopause have been evaluated in relation to cardiovascular disease (CVD) risk, including age at menopause onset, type and stage of menopause, endogenous estradiol levels, and menopause-related symptoms. These factors have been found to be associated with CVD risk, with the highest risk occurring in women with ovarian failure and relatively early menopause. Women with early menopause (aged 40–44 years) have a hazard ratio of 1.55 (95% CI: 1.38–1.73) for coronary artery disease events compared to women with menopause at age 50–54 years. Women with premature ovarian failure tend to have a shorter life expectancy compared to those who experience late menopause, primarily due to an increased risk of cardiovascular disease.
Cytochrome P450 Monooxygenase and Pyrethroid Resistance in Anopheles: A Narrative Review I Gusti Ayu Avinya Chintya Devi; Dewa Ayu Agus Sri Laksemi; Putu Ayu Asri Damayanti
Indonesian Journal of Global Health Research Vol. 8 No. 4 (2026): Indonesian Journal of Global Health Research
Publisher : GLOBAL HEALTH SCIENCE GROUP

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37287/ijghr.v8i4.2054

Abstract

Malaria remains a major global public health problem, with approximately 282 million cases reported in 2024. Although vector control interventions such as long-lasting insecticide-treated nets (LLINs) and indoor residual spraying (IRS) have significantly reduced malaria transmission, their effectiveness is increasingly compromised by pyrethroid resistance in Anopheles mosquitoes. This review examines the role of cytochrome P450 monooxygenase enzymes in mediating pyrethroid resistance. A literature search was conducted in PubMed, Springer, and Google Scholar for articles published between 2016 and 2026 using the keywords “Cytochrome P450,” “P450 monooxygenase,” “Insecticide Resistance,” “metabolic resistance,” “Pyrethroid,” “Anopheles,” and “malaria vector.” Of 10,854 articles identified, 142 were screened, and six relevant studies were included, focusing on resistance mechanisms, P450 characteristics, gene regulation, and vector control implications. The findings indicate that overexpression of specific P450 genes significantly enhances the detoxification of pyrethroids, thereby reducing insecticide susceptibility. Furthermore, interactions between metabolic resistance and target-site mutations contribute to elevated resistance levels. Recent evidence suggests that non-coding RNAs (ncRNAs) regulate detoxification pathways and contribute to adaptive resistance. In conclusion, insecticide resistance in Anopheles is a multifactorial process involving genetic, biochemical, and regulatory mechanisms. Understanding these mechanisms is crucial for developing more effective and sustainable vector control strategies.