Preventive behaviour and attitudes towards early childhood caries amongst mothers of toddlers in Bangladesh.

Background: Our aim was to analyse mothers of toddlers' preventive behaviour towards ECC in Bangladesh.Methods: We conducted a cross-sectional survey of mothers and their 6-24-month-old children visiting vaccination centres in Trishal, Bangladesh in 2021. A cluster-sampling method was applied to select 10 immunization centres and all mothers who attended the centres with a 6-24-month-old child were recruited. Mothers' preventive behaviour and attitude towards oral health was determined using a reliable instrument. Clinical examinations were conducted to assess the presence of dental plaque on the labial surfaces of the upper central incisors and the ICDAS II index criteria were utilized to detect ECC. The associations between preventive behaviours and the plaque score and caries status of the children were determined using multivariable logistic regression analysis after adjusting for confounding variables (mother's age and educational status).Results: The prevalence of ECC among the children was 25.8%. ECC experience was significantly associated with low educational level (p = 0.02) and older age (p = 0.01) of mothers. Of the mothers, 75.2% reported to brush their teeth twice daily and about half of them (48.8%) cleaned their children's teeth daily; and 5.8% with fluoridated toothpaste. The multivariate logistic regression analysis showed that caries preventive behaviour of mothers (AOR = 2.63, 95% CI 1.41-4.91) and the plaque score of the child (AOR = 14.69, 95% CI 7.45-28.9) were significant risk indicators for ECC in the study population.Conclusions: The prevalence of ECC was high among the Bangladeshi toddlers and factors such as the mothers' preventive behaviour and presence of plaque were associated with the occurrence.

Maternal factors associated with early childhood caries among 3-5-year-old children with low socio-economic status in Trishal, Bangladesh.

Introduction: Early Childhood Caries (ECC) is more prevalent in nations where a larger portion of the population resides below the poverty line. This study aimed to evaluate the connections between maternal awareness, attitudes, practices related to oral health, and the occurrence of ECC among children aged 3-5 years in Bangladesh, a low-middle income country with high level of poverty. Methods: This cross-sectional study recruited mother-child pairs with a focus on children aged 3-5 years from low socioeconomic backgrounds in Trishal, Bangladesh. Data collected included maternal oral health knowledge, attitudes, and behaviors. Clinical examinations were conducted to check for dental plaque on the upper central incisors' labial surfaces. ECC was identified using the ICDAS II index criteria. Associations between maternal oral health knowledge, attitudes, behaviors, and children's plaque score and caries status were analyzed using multivariable logistic regression, and adjusting for confounding variables (child's age, gender, mother's age, education, and number of children). Results: Among 532 mother-child pairs, 491 (93.2%) mothers were unaware of the role of fluoride in preventing caries, while 516 (97%) recognized the importance of using fluoridated toothpaste during brushing. Additionally, 520 (97.7%) mothers reported not knowing how to brush their child's teeth, and 87 (16.4%) brushed their children's teeth twice daily. Visible dental plaque was observed in 420 (78.9%) children, and 321 (60.3%) had ECC. Higher plaque score increased the odds of ECC in the study population (AOR: 5.617, 95% CI: 3.511-8.987). Conclusions: Mothers of preschool children with low socioeconomic status were poorly aware of caries preventive behaviors and had suboptimal oral health practices for their children. The plaque score was the only oral health factor that seems to increase the risk for ECC among children with low socio-economic status in Bangladesh. It is imperative to prioritize support and interventions aimed at improving oral hygiene practices to reduce ECC risk in this population.

Validation of the HULL Score clinical prediction rule for unsuspected pulmonary embolism in ambulatory cancer patients.

Background: Clinical prediction rules (CPRs) developed to predict adverse outcomes of suspected pulmonary embolism (PE) and facilitate outpatient management have limitations in discriminating outcomes for ambulatory cancer patients with unsuspected PE (UPE). The HULL Score CPR uses a 5­point scoring system incorporating performance status and self-reported new or recently evolving symptoms at UPE diagnosis. It stratifies patients into low, intermediate and high risk for proximate mortality. This study aimed to validate the HULL Score CPR in ambulatory cancer patients with UPE. Patients and methods: 282 consecutive patients managed under the UPE-acute oncology service in Hull University Teaching Hospitals NHS Trust were included from January 2015 to March 2020. The primary end-point was all-cause mortality, and outcome measures were proximate mortality for the three risk categories of the HULL Score CPR. Results: 30-day, 90-day and 180-day mortality rates for the whole cohort were 3.4% (n=7), 21.1% (n=43) and 39.2% (n=80), respectively. The HULL Score CPR stratified patients into low-risk (n=100, 35.5%), intermediate-risk (n=95, 33.7%) and high-risk (n=81, 28.7%) categories. Correlation of the risk categories with 30-day mortality (area under the curve (AUC) 0.717, 95% CI 0.522-0.912), 90-day mortality (AUC 0.772, 95% CI 0.707-0.838), 180-day mortality (AUC 0.751, 95% CI 0.692-0.809) and overall survival (AUC 0.749, 95% CI 0.686-0.811) was consistent with the derivation cohort. Conclusion: This study validates the capacity of the HULL Score CPR to stratify proximate mortality risk in ambulatory cancer patients with UPE. The score uses immediately available clinical parameters and is easy to integrate into an acute outpatient oncology setting.

Recent Advances in Cellular Signaling Interplay between Redox Metabolism and Autophagy Modulation in Cancer: An Overview of Molecular Mechanisms and Therapeutic Interventions.

Autophagy is a fundamental homeostatic process in which certain cellular components are ingested by double-membrane autophagosomes and then degraded to create energy or to maintain cellular homeostasis and survival. It is typically observed in nutrient-deprived cells as a survival mechanism. However, it has also been identified as a crucial process in maintaining cellular homeostasis and disease progression. Normal cellular metabolism produces reactive oxygen (ROS) and nitrogen species at low levels. However, increased production causes oxidative stress, which can lead to diabetes, cardiovascular diseases, neurological disorders, and cancer. It was recently shown that maintaining redox equilibrium via autophagy is critical for cellular responses to oxidative stress. However, little is understood about the molecular cancer processes that connect to the control of autophagy. In cancer cells, oncogenic mutations, carcinogens, and metabolic reprogramming cause increased ROS generation and oxidative stress. Recent studies have suggested that increased ROS generation activates survival pathways that promote cancer development and metastasis. Moreover, the relationship between metabolic programming and ROS in cancer cells is involved in redox homeostasis and the malignant phenotype. Currently, while the signaling events governing autophagy and how redox homeostasis affects signaling cascades are well understood, very little is known about molecular events related to autophagy. In this review, we focus on current knowledge about autophagy modulation and the role of redox metabolism to further the knowledge of oxidative stress and disease progression in cancer regulation. Therefore, this review focuses on understanding how oxidation/reduction events fine-tune autophagy to help understand how oxidative stress and autophagy govern cancer, either as processes leading to cell death or as survival strategies for maintaining redox homeostasis in cancer.

Statistical Bioinformatics to Uncover the Underlying Biological Mechanisms That Linked Smoking with Type 2 Diabetes Patients Using Transcritpomic and GWAS Analysis.

Type 2 diabetes (T2D) is a chronic metabolic disease defined by insulin insensitivity corresponding to impaired insulin sensitivity, decreased insulin production, and eventually failure of beta cells in the pancreas. There is a 30-40 percent higher risk of developing T2D in active smokers. Moreover, T2D patients with active smoking may gradually develop many complications. However, there is still no significant research conducted to solve the issue. Hence, we have proposed a highthroughput network-based quantitative pipeline employing statistical methods. Transcriptomic and GWAS data were analysed and obtained from type 2 diabetes patients and active smokers. Differentially Expressed Genes (DEGs) resulted by comparing T2D patients' and smokers' tissue samples to those of healthy controls of gene expression transcriptomic datasets. We have found 55 dysregulated genes shared in people with type 2 diabetes and those who smoked, 27 of which were upregulated and 28 of which were downregulated. These identified DEGs were functionally annotated to reveal the involvement of cell-associated molecular pathways and GO terms. Moreover, protein-protein interaction analysis was conducted to discover hub proteins in the pathways. We have also identified transcriptional and post-transcriptional regulators associated with T2D and smoking. Moreover, we have analysed GWAS data and found 57 common biomarker genes between T2D and smokers. Then, Transcriptomic and GWAS analyses are compared for more robust outcomes and identified 1 significant common gene, 19 shared significant pathways and 12 shared significant GOs. Finally, we have discovered protein-drug interactions for our identified biomarkers.

Deficient DNA mismatch repair and persistence of SARS-CoV-2 RNA shedding: a case report of hereditary nonpolyposis colorectal cancer with COVID-19 infection.

BACKGROUND: Several independent risk factors have been reported to influence viral shedding following COVID-19 infection, but the influence of host-related molecular factors has not yet been described. We report a case of a cancer patient with Lynch syndrome (hereditary nonpolyposis colorectal cancer, HNPCC) who manifested SARS-CoV-2 PCR (polymerase chain reaction) positivity for at least 54 days after contracting mild COVID-19 illness. We propose that deficient mismatch repair (MMR) may play a role in the prolonged SARS-CoV-2 RNA shedding. CASE PRESENTATION: A patient with Lynch syndrome was under surveillance for metastatic adenocarcinoma after completing palliative chemotherapy in October 2019. Between the period of April 2020 to June 2020, he was admitted multiple times to address several clinical needs mainly related to his underlying malignancy. These included progressive disease observed in the aortocaval lymph nodes leading to recurrent episodes of upper gastrointestinal bleeding, dehydration resulting in acute kidney injury and a short-lived episode of pyrexia. A SARS-CoV-2 PCR of the nasopharyngeal swab (NPS) was positive at his initial admission with mild COVID-19 symptoms. He remained positive on subsequent admissions when tested routinely for SARS-CoV-2 without demonstrating any apparent clinical features of COVID-19 infection. The MMR pathway, a component of DNA damage response (DDR), is impaired in Lynch syndrome due to an inherited genetic mutation. This pathway is also required for viral clearance from the host cells following certain RNA viral infections like influenza virus and other coronaviridae. Here we provide a current understanding of the importance of DDR deficiencies in the clearance of RNA virus and suggest how this may play a similar role in the clearance of COVID-19, as evident in our case that demonstrated persistent positivity. CONCLUSION: The importance of understanding the scientific basis of extended viral shedding during the COVID-19 pandemic is now centre-stage in the establishment of robust track and trace services to allow the recovery and function of societies and economies. This patient with Lynch syndrome recovered from infection but had prolonged viral positivity, which might merit further investigation to better understand the effect of this condition on infection duration and outcome.

Increased dose primary thromboprophylaxis in ambulatory patients with advanced pancreatic ductal adenocarcinoma, a single centre cohort study.

BACKGROUND: Advanced pancreatic ductal adenocarcinoma (aPDAC) patients have a lifetime all type thromboembolic event (ATTE) rate of 25-35%. Efficacy and safety of increased dose primary thromboprophylaxis (IDPTP) with low molecular heparin (LMWH) given for 3 months has been shown in two prospective randomized trials. OBJECTIVES: To report on efficacy -reduction of all type thromboembolic events (ATTE)-, safety -incidence of Major Bleeding (MB)- and compliance in a single-centre cohort of aPDAC patients receiving first line chemotherapy and LMWH-IDPTP. METHODS: From May 2009 to October 2016, 82 patients received IDPTP -LMWH with dalteparin. Schedule: 55 kg and below: 7500 IU, between 55 and 80 kg: 10,000 IU, above 80 kg: 12,500 IU. MB is reported using the International Society of Thrombosis and Haemostasis (ISTH) criteria. ATTE was defined as any arterial or venous event, incidental or clinically symptomatic, including visceral VTE. RESULTS: Mean and median time on dalteparin was 10.2 (95%CI 8.1, 12.4) and 8.0 (95%CI 6.2, 9.7) months respectively. ATTE was observed in 7 (8.5%) of patients, with a median time on IDPTP of 6.2 months (95% CI 10.0, 13.2). MB was seen in 10 (12.2%) patients with a median time on IDPTP of 4.5 months (95% CI 1.6, 7.4). Six major bleeds (60%) were the direct or indirect result of aPDAC. Eighty-one patients had died at the time of data collection with a median overall survival time of 8.7 months (95%CI 6.4, 11.0). Thromboembolism and bleeding were late events. No impact of thromboembolism or bleeding on overall survival was observed. CONCLUSIONS: IDPTP-dalteparin was associated with lower ATTE occurrence rates than expected and comparable major bleeding rates. ATTE and MB were late events, the majority of MB was from direct or indirect result of locally progressing aPDAC. Since these conditions can frequently arise in aPDAC, IDPTP should be regularly reviewed beyond 3 months.