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The global TBL cancer burden fell by 15.3%. The joinpoint analysis revealed that the overall trend of age-standardised TBL cancer burden for both females and males significantly changed twice between 1990 and 2017, and it varied across countries with different SDI values and was also different between females and males. Age-standardised TBL cancer burden was more concentrated in higher socioeconomic development countries, but the development of healthy inequality showed a downward trend in males while showing an upward trend in females.
The magnitude and temporal trends of TBL cancer burden varied across countries and sex. This study highlighted the importance of crafting health policy to adapt to local conditions to manage the global burden of TBL cancers.
The magnitude and temporal trends of TBL cancer burden varied across countries and sex. This study highlighted the importance of crafting health policy to adapt to local conditions to manage the global burden of TBL cancers.
Severe acute malnutrition (SAM) and disability are major global health issues. Although they can cause and influence each other, data on their co-existence are sparse. We aimed to describe the prevalence and patterns of disability among a cohort of children with SAM.
A longitudinal cohort study in Malawi followed SAM survivors up to 7 years postdischarge. Clinical and anthropometric profiles were compared with sibling and community controls. Disability at original admission was identified clinically; at 7-year follow-up a standardised screening tool called 'the Washington Group Questionnaire' was used.
60/938 (6.4%) of admissions to SAM treatment had clinically obvious disability at admission. Post-treatment mortality was high, with only 11/60 (18%) surviving till 7-year follow-up. SAM children with a disability at admission had 6.99 (95% CI 3.49 to 14.02; p<0.001) greater risk of dying compared with children without disability. They were also older, less likely to be HIV positive or have oedema and disability-associated SAM have greatly increased risk of dying even if they survive the initial episode of malnutrition. Survivors have poorer growth, physical strength and school achievement. To enable all children to survive and thrive post-SAM, it is vital to focus more on those with disabilities. SAM treatment programmes should consider using not just clinical assessment but structured assessments to better identify at-risk individuals as well as understand the population of children for which they are developing services.
Meeting ambitious global health goals with limited resources requires a precision public health (PxPH) approach. Here we describe how integrating data collection optimisation, traditional analytics and causal artificial intelligence/machine learning (ML) can be used in a use case for increasing hospital deliveries of newborns in Uttar Pradesh, India.
Using a systematic behavioural framework we designed a large-scale survey on perceptual, interpersonal and structural drivers of women's behaviour around childbirth (n=5613). Multivariate logistic regression identified factors associated with institutional delivery (ID). Causal ML determined the cause-and-effect ordering of these factors. Variance decomposition was used to parse sources of variation in delivery location, and a supervised learning algorithm was used to distinguish population subgroups.
Among the factors found associated with ID, the causal model showed that having a delivery plan (OR=6.1, 95% CI 6.0 to 6.3), believing the hospital is safer tML analytics, can help design a PxPH approach that maximise the impact of limited resources.
Microsatellite instability in colon cancer implies favorable therapeutic outcomes after checkpoint blockade immunotherapy. Belnacasan clinical trial However, the molecular nature of microsatellite instability is not well elucidated.
We examined the immune microenvironment of colon cancer using assessments of the bulk transcriptome and the single-cell transcriptome focusing on molecular nature of microsatellite stability (MSS) and microsatellite instability (MSI) in colorectal cancer from a public database. The association of the mutation pattern and microsatellite status was analyzed by a random forest algorithm in The Cancer Genome Atlas (TCGA) and validated by our in-house dataset (39 tumor mutational burden (TMB)-low MSS colon cancer, 10 TMB-high MSS colon cancer, 15 MSI colon cancer). A prognostic model was constructed to predict the survival potential and stratify microsatellite status by a neural network.
Despite the hostile CD8
cytotoxic T lymphocyte (CTL)/Th1 microenvironment in MSI colon cancer, a high percentage of ef neural network, reaching 100%.
Our analysis unraveled the difference in the molecular nature and genomic variance in MSI and MSS colon cancer. The microsatellite status-related gene signature is better at predicting the prognosis of patients with colon cancer and response to the combination of immune checkpoint inhibitor-based immunotherapy and anti-VEGF therapy.
Our analysis unraveled the difference in the molecular nature and genomic variance in MSI and MSS colon cancer. The microsatellite status-related gene signature is better at predicting the prognosis of patients with colon cancer and response to the combination of immune checkpoint inhibitor-based immunotherapy and anti-VEGF therapy.
2,5-dimethylcelecoxib (DMC) is a targeted inhibitor of microsomal prostaglandin E synthase-1 (mPGES-1), a key enzyme in the PGE2 synthesis pathway of inflammatory mediators. Previous studies have confirmed that DMC can inhibit the growth of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). However, it is not known whether DMC is involved in the changes of tumor immune microenvironment.
In this study, we explored the effects of DMC on HBV-related HCC immune microenvironment, and deeply analyzed its unique effect and mechanism on programmed death receptor 1 (PD-1)/and its ligand 1 (PD-L1) pathway.
Clinical hepatoma tissues detection showed that compared with non-virus-related HCC, the level of CD8 of HBV-related HCC was significantly lower, while the levels of PD-L1 and CD163 were higher. In vivo experiments indicated that DMC could increase the level of tumor infiltrating CD8
T cells in hepatitis B virus X (HBx) (+) hepatoma cells implanted mouse models, and inhibit the expression of PD-L1 and CD163 in tumor tissues.
