Annals of medicine
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Accurately identifying persons with addiction is critically important for effectively targeting treatment and harm reduction interventions. Misdiagnosis of addictive disorders can lead to a cascade of negative outcomes, including stigma, discontinuation of needed medications, undue scrutiny of both patients and physicians, and even criminal consequences. A recent study raises significant concerns about the accuracy of diagnosis code data, likely rooted in confusingly-worded International Classification of Diseases (ICD)-9 and ICD-10 codes and a general misunderstanding of the difference between addiction and physiologic dependence. ⋯ Key messagesIt is not surprising that physicians frequently conflate patients with "addiction" and "dependence" when the ICD terms used to code for addiction are themselves misleading. ICD codes have not been updated to reflect what we know about the nature of addiction, unlike those in the DSM-5. This commentary calls for the ICD to update their codes to reflect current understanding of addiction.
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This study aims to identify potential prognostic biomarkers of bladder cancer (BCa) based on large-scale multi-omics data and investigate the role of SRC in improving predictive outcomes for BCa patients and those receiving immune checkpoint therapies (ICTs). ⋯ This study first performed the large-scale multi-omics analysis, distinguished the IPRPs (BECLIN, EGFR, PKCALPHA, SRC, ANNEXIN1 and AXL) and revealed novel prediction model, outperforming the currently traditional prognostic indicators for anticipating BCa progression and better clinical strategies. Additionally, this study provided insight into the importance of biomarker SRC for better prognosis, which may inversely improve predictive outcomes for patients receiving ICT and enable patient selection for future clinical treatment.
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To investigate the association between overweight/obesity and fatty liver index (FLI) on the odds of incident prediabetes/type 2 diabetes and non-alcoholic fatty liver disease (NAFLD) in 2020 participants after 10 years follow up. ⋯ An increased FLI significantly increases the odds of incident prediabetes, type 2 diabetes and NAFLD in individuals with overweight/obese highlighting the contributory role of liver fat accumulation in the pathophysiology of prediabetes/type 2 diabetes.Key messagesObesity is a risk factor for non-alcoholic fatty liver disease (NAFLD), prediabetes and type 2 diabetes.Additionally, NAFLD is more prevalent in people with prediabetes and type 2 diabetes when compared to age- and BMI-matched individuals.The presence of a raised fatty liver index (FLI) confers a significantly increased risk of developing prediabetes, type 2 diabetes and NAFLD above that conferred by being overweight/obese.The degree of elevation of FLI can risk stratify for incident prediabetes and type 2 diabetes in people with obesity.
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Background and aim: Since the relation between Helicobacter pylori (H. pylori) and atherosclerosis has been evidenced, we aimed to analyze whether there is a relationship between the patient's H. pylori infection and age, gender, BMI, blood lipids, and carotid plaque formation. Methods: 810 patients from January 2016 to December 2019 were enrolled in this study, and divided the subjects into H. pylori (+) group and H. pylori (-) group based on the results of UBT. To analyze whether H. pylori infection is related to gender, age, BMI, blood lipids, and neck vascular plaque formation. ⋯ The multi-variant analysis showed that patients with H. pylori infection are prone to have higher BMI, triglycerides, and neck vascular plaque formation over 1.4-times higher in non-infected individuals. KEY MESSAGESH. pylori infection is an independent risk factor for higher BMI, triglyceride, and neck vascular plaque formation. H. pylori can accelerate vascular plaque formation through increasing BMI and triglyceride.
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Long noncoding RNAs (LncRNAs) are regulatory molecules that play important roles in various biological and pathological processes. Herein, we aimed to explore whether maternally expressed gene 8 (MEG8) promotes M1 macrophage polarization among Henoch-Schonlein purpura (HSP) rats, and to investigate the underlying mechanism. ⋯ The lncRNA MEG8 sponged miR-181a-5p, which contributes to M1 macrophage polarization by regulating SHP2 expression in HSP rats.Key MessagesLncRNA MEG8 downregulation and M2 polarization in Henoch Schonlein purpura rats.MEG8 upregulation enhances M1 polarization and suppresses JAK2/STAT3 pathway.MEG8 sponges miRNA-181a-5p to regulate SHP2 expression.MiRNA-181a-5p upregulation reverses lncRNA MEG8-mediated enhancement of M1 polarization and inhibition of JAK2/STAT3 pathway.SHP2 downregulation reverses lncRNA MEG8-mediated enhancement of M1 polarization and inhibition of JAK2/STAT3 pathway.