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Coronavirus Disease 2019 (COVID-19) pandemic created a global health crisis. Prolonged exposure to PM, NO2, CO, O3 has a negative effect on COVID-19 patients. Several studies have shown a significant relationship between genetic susceptibility to the effects of air pollutants on disease, such as COVID-19 patients with ACE rs4646994 or ACE2 rs2285666 polymorphisms can have a more severe degree. The aim of this study was to analyze the effect of exposure to PM2.5, NO2, O3, weather conditions, ACE rs4646994 and ACE2 rs2285666 polymorphisms, age, BMI, and comorbidities (hypertension, heart disease, asthma, and DM) on the degree of COVID-19. Environmental data were obtained from the BMKG and the subjects were domiciled within a radius of <3 km from the Kemayoran Meteorological Station by dividing the patients into asymptomatic-mild and moderate-severe groups. Polymorphism examination was taken from a buccal swab sample. Logistic regression was used to analyze the data. The results of this study found that COVID-19 patients with the polymorphism ACE2 rs2285666 genotype AA would be 9.128 times more at risk of experiencing a more severe degree. Polymorphism ACE rs4646994, exposure to PM2.5, NO2 and comorbidities were not significantly related to the degree of COVID-19. O3 exposure, low temperature, high average humidity, fewer durations of sunlight, and high BMI significantly aggravate COVID-19 in bivariate analysis. This study concluded that the polymorphism ACE2 rs2285666 genotype AA is a risk factor for the severity of COVID-19. Exposure to O3, BMI, minimum temperature, average temperature, average humidity, and duration of sunlight can play a role in the degree of COVID-19.
Hipertensi merupakan salah satu kondisi medis yang cukup serius karena dapat meningkatkan risiko penyakit jantung, otak, ginjal dan penyakit lainnya. Wilayah di DKI Jakarta dengan prevalensi hipertensi tertinggi berdasarkan diagnosis dokter yaitu Kota Jakarta Pusat sebesar 12,16%. Partikulat meter organik dan komponen partikulat meter dapat memicu proinflammatory effects pada paru-paru karena kemampuannya mengakibatkan stress oksidatif. Penelitian ini bertujuan untuk menyusun model pengaruh pajanan PM2,5 di udara ambien terhadap kejadian hipertensi melalui stress oksidatif dan sitokin inflamasi pada penduduk di Jakarta Pusat. Penelitian dilakukan pada penduduk dewasa (18-65 tahun) di Kota Jakarta Pusat dengan disain studi hybrid cross sectional ecology. Pengumpulan data secara cluster random sampling dengan analisis data dilakukan melalui pemodelan regresi logistik multilevel dan cox regresi proporsional hazard.
Hasil analisis menunjukkan terdapat asosiasi antara PM2,5 di udara ambien dengan biomarker stress oksidatif (IOR PM2,5: 2,185173-2,185176) dan dengan biomarker sitokin inflamasi (IOR PM2,5: 1,21-1,91). Pemodelan multivariat dengan cox regresi proporsional hazard menunjukkan bahwa variabel umur dan indeks massa tubuh merupakan confounder hubungan antara stress oksidatif dengan hipertensi dan antara sitokin inflamasi dengan hipertensi dengan nilai Rasio Prevalens adjusted (95% CI) masing-masing sebesar 1,19 (0,69-2,03) dan 0,99 (0,58-1,72). Dapat disimpulkan bahwa variabel konsentrasi PM2,5 di udara ambien memiliki peran terhadap terjadinya hipertensi, stress oksidatif dan sitokin inflamasi pada penduduk di Jakarta Pusat.
Hypertension is a serious medical condition that can increase the risk of heart, brain, kidney and other diseases. The area in DKI Jakarta with the highest prevalence of hypertension based on doctor diagnosis is Central Jakarta city about 12.16%. Organic particulate matters and particulate matter components can trigger proinflammatory efects in the lung due to their ability to cause oxidative stress. This study aims to develop a model of the Influence of PM2,5 Exposure in Ambient Air on Hypertension Occurrence through Oxidative Stress and Inflammatory Cytokines among residents in Central Jakarta. The study was conducted among adult residents (age 18-65 years) in Central Jakarta with hybrid cross sectional study design. Data collected using cluster random sampling with data analysis carried out through multilevel logistic regression modeling and cox proportional hazard regression. Results show there is an association between PM2.5 in ambient air with oxidative stress biomarkers (IOR PM2.5: 2.185173-2.185176) and with inflammatory cytokine biomarkers (IOR PM2.5: 1.21-1.91). Multivariate modeling with Cox regression proportional hazard shows that age and body mass index are confounders of the relationship between oxidative stress with hypertension and between inflammatory cytokines with hypertension with an adjusted prevalence ratio (95% CI) value of 1.19 (0.69-2.03) and 0.99 (0.58-1.72). It can conclude that concentration of PM2.5 in ambient air has a role on hypertension, oxidative stress and inflammatory cytokine among residents in Central Jakarta.
This cohort study examined the effect of secondhand smoke exposure in pregnant women on fetal growth restriction. The study recruited 128 pregnant women in the third trimester pregnancy, single pregnancy, no chronic illness, non-active smokers, non-exsmokers, and who were willing to participate in the study. Pregnant women with the secondhand smoke exposure referred to those with the umbilical cord blood nicotine level of 1ng/ml or higher. Fetal growth disorder was assessed according to the newborn weight, length, head circumference, and palcental weight measured immediately after birth. The independent t-test analysis was used to determine the difference in average size of fetal growth between two groups of pregnant women: exposed and the notexposed to the secondhand smoke. A multiple linear regression analysis was employed to find out the effect of secondhand smoke exposure on birth weight, length, head circumference, and palcental weight controlling for the birth size confounders including weight gain during pregnancy, body mass index, parity, maternal age, and maternal hemoglobin. The study found that mean of nicotine in umbilical cord blood was 1.3±2.5 ng/ml, the birth weight and the placental weight of infants were lower among mothers who exposed than among mothers who did not expose to the secondhand smoke. Exposed to the secondhand smoke reduced the birth weight by 205.6 grams (p value = 0.005) and placental weight by 51 grams (p value=0.010).
