Molecular detection of human papillomavirus prevalence in clinically normal females and identification of high-risk HPV 16 and 18 under low resources setting: a cohort study from Sri Lanka.

High oncogenic risk types of human papillomaviruses are mainly transmitted via sexual contact and are the main cause of cervical cancer in females in developing countries. Molecular detection of HPV infection enables early cancer detection; however, it is not widely used in low-income countries due to resource constraints. The aim of this study was to assess economical yet sensitive HPV detection and genotyping assays for both physician and self-collected cervical samples in a resource limited diagnostic setting. A previously reported polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) based HPV detection and genotyping protocol was verified using direct DNA sequencing to accurately identify the HPV 16 and 18 genotypes in a routine-diagnostic set-up. Then the HPV prevalence in a cohort of 433 clinically normal females was performed using PCR-RFLP diagnostic tool. Finally, the performance of the PCR-RFLP HPV screening tool was further evaluated against self-collected samples. HPV 16 and 18 genotyping with the PCR-RFLP consistently agreed with the sequencing data. The HPV prevalence in the screening cohort was 5.8%. HPV 16 and 18 were the most common high-risk HPV genotypes detected in the study cohort. Self-sampling vs physician collected samples from the same subject resulted in an overall concordance of 93% for HPV detection. The PCR-RFLP protocol can be used effectively under low resource settings for HPV 16/18 diagnosis and genotyping. The self-sampling approach can be recommended to increase HPV screening among women in Sri Lanka. Supplementary Information: The online version contains supplementary material available at 10.1007/s13337-024-00875-w.

Anti-Fibrotic and Anti-Angiogenic Activities of Osbeckia octandra Leaf Extracts in Thioacetamide-Induced Experimental Liver Cirrhosis.

Chronic liver inflammation has become a major global health concern. In the absence of clinical surrogate markers to diagnose inflammatory liver disease, the intervention with effective drugs in modern medicine tends to be late. In Sri Lanka, traditional medical practitioners prescribe herbal preparations from Osbeckia octandra for the prevention and treatment of liver disorders. To test the efficacy of such treatments, we have administered thioacetamide (TAA) to male Wistar rats to induce chronic liver damage (disease control; DC) and examined how various leaf extracts: crude leaf suspension (CLS), boiled leaf extract (BLE), sonicated leaf extract (SLE), methanol leaf extract (MLE) and hexane leaf extract (HLE) of O. octandra ameliorate TAA-induced liver disease. The CLS, BLE and SLE treatments in cirrhotic rats significantly attenuated disease-related changes, such as liver weight and hepato-enzymes. The mRNA levels of Tnf-α were significantly decreased by 3.6, 10 and 3.9 times in CLS, BLE and SLE compared to DC. The same treatments resulted in significantly lower (19.5, 4.2 and 2.4 times) α-Sma levels compared to DC. In addition, Tgf-ß1 and Vegf-R2 mRNA expressions were significantly lower with the treatments. Moreover, BLE expressed a strong anti-angiogenic effect. We conclude that CLS, BLE and SLE from O. octandra have potent hepatic anti-fibrotic effects in TAA-induced liver cirrhosis.

In vitro and in vivo impairment of embryo implantation by commonly used fungicide Mancozeb.

The fungicide Mancozeb is an endocrine-disrupting chemical and the mode of action of Mancozeb on embryo implantation is largely unknown. Mancozeb (1 and 3 µg/ml) significantly reduced Jeg-3 trophoblastic spheroids attachment to endometrial epithelial Ishikawa cells. Mancozeb treatment from gestation day (GD) 1 to GD8 or from GD4 to GD8 significantly lowered the number of implantation sites with higher incidence of morphological abnormalities in the reproductive tissues. However, these were not seen in the treatment from GD1 to GD4. Mancozeb at 30 mg/kg BW/d did not alter the expression of p53, COX-2, or PGFS transcripts in the uterus, but down-regulated the PGES transcript and protein. Mancozeb treatment in human endometrial stromal cells did not alter the decidualization response, but the morphological transformation was impaired. Taken together, exposure to Mancozeb affected embryo implantation probably through the modulation of decidualization and to delineate the exact mode of action needs further investigations.