Delirium, commonly observed in critically ill patients following intracerebral hemorrhage (ICH), is an acute neuropsychiatric disorder characterized by disturbances in attention, consciousness, and cognition. The underlying brain network mechanisms remain poorly understood. This study aimed to explore the functional connectivity (FC) of the ascending reticular activating system (ARAS) in delirium patients with basal ganglia ICH and to identify potential biomarkers for predicting delirium onset.

In this cross-sectional study, brain networkomics techniques were used to examine the FC within the ARAS in ICH patients with and without delirium. A two-sample t-test compared differences in ARAS connectivity between delirium and non-delirium groups, identifying abnormal brain regions and their corresponding FC values. Receiver operating characteristic curve analysis was then performed to evaluate the predictive value of FC for delirium onset.

A significant disruption in FC between the brainstem ARAS nuclei and the left parahippocampal gyrus was observed in ICH patients with delirium. The FC strength between these regions was a reliable predictor of delirium occurrence, with an area under the curve of 0.893, indicating high predictive accuracy.

The disruption of FC between the brainstem ARAS nuclei and the left parahippocampal gyrus may represent a key mechanism underlying delirium pathogenesis. The strength of this connectivity could serve as a potential biomarker for predicting delirium onset. Future research should focus on strategies to restore this connectivity as a potential treatment for early reversal of delirium.

Radiation injury poses a serious threat to human health, causing complex and multifaceted damage to cells and tissues. Such injury can be caused by various factors, including nuclear accidents, medical radiation therapy, and space travel. Currently, finding effective treatment methods and drugs to mitigate the harmful effects of radiation injury on the human body is a crucial research direction. This study aimed to explore the protective effects and mechanisms of Licochalcone B (Lico B) on radiation-induced cell damage and radiation-induced mortality in mice.

HaCaT cells, THP-1 cells, and HAEC cells were irradiated with a 10 Gray (Gy) dose of X-rays, while RAW 264.7 cells were irradiated with a 10 Gy dose of γ-rays. The cells were pre-treated with Lico B for 2 h before irradiation, and samples were collected 2 h after irradiation. Cell proliferation viability, oxidative stress levels, DNA damage, expression levels of inflammatory factors, matrix metalloproteinases, guanylate cyclase, and iron death-related factors were measured. C57BL/6 mice were exposed to total-body irradiation with a dose of 8 Gy or a combined dose of 6 Gy + 8 Gy of γ-rays to induce radiation injury. Lico B was injected intraperitoneally one day before irradiation and then administered for two consecutive days, with continuous observation for 20 days.

Mechanistically, Lico B significantly improved antioxidant levels, reduced DNA damage, and lowered the expression of inflammatory factors in HaCaT, THP-1, HAEC, and RAW 264.7 cells. Therapeutically, Lico B increased cell proliferation capacity and significantly extended the survival time of irradiated mice, demonstrating a strong radioprotective effect.

Lico B exhibits significant radioprotective effects and may serve as a potential radioprotective agent.

Helicobacter pylori (H. pylori) infection plays a pivotal role in gastric carcinogenesis and poses a significant burden on global public health. Eradicating H. pylori infection is an important strategy for the primary prevention of gastric cancer but remains a challenge. This consensus, an update of The First Beijing Consensus on Holistic Integrated Medicine (HIM) Combining Traditional Chinese with Western Medicine for the Management of Helicobacter pylori-associated “Disease-Syndrome” released in 2018, aims to further incorporate the HIM perspective and the latest research advances into the management of H. pylori-associated “disease-syndrome”. Forty-three experts from 29 medical institutions were selected to vote and reach a consensus. The consensus consists of five sections addressing 19 key questions with corresponding statements. These cover the current status and challenges of managing H. pylori infection in China, refractory H. pylori infection, the role of HIM in H. pylori management, holistic and individualized assessment/treatment for refractory infections, and the integration of traditional Chinese medicine in treating H. pylori-associated “disease-syndrome”. Finally, three therapeutic schemes for traditional Chinese medicine in treating H. pylori-associated “disease-syndrome” were proposed. Taken together, this consensus incorporates the principles of HIM along with advanced medical knowledge and clinical practice into individualized treatment strategies. It is recommended as a guideline for the management of H. pylori-associated “disease-syndrome” in China.

Chronic liver cirrhosis (LC) and acute-on-chronic liver failure (ACLF) are interconnected hepatic disorders associated with substantial morbidity and mortality. Despite their distinct clinical characteristics, both conditions share common pathogenic pathways that remain inadequately understood. This study aimed to identify shared gene signatures and elucidate underlying molecular mechanisms.

In this study, we employed Weighted Gene Co-Expression Network Analysis to explore transcriptomic data from the Gene Expression Omnibus for LC and ACLF.

Key co-expression modules enriched with genes involved in glycolysis and gluconeogenesis pathways were identified, implicating metabolic dysfunction as a central feature in both conditions. Furthermore, microRNA analysis revealed that hsa-miR-122 and hsa-miR-194 play pivotal roles in regulating these metabolic pathways, potentially contributing to immune dysregulation.

Our findings indicate that these shared molecular mechanisms are critical in the progression from LC to ACLF, providing novel insights into potential therapeutic targets for mitigating disease severity and improving clinical outcomes.

Prognostic scores are valuable tools for predicting survival in patients with chronic liver disease. Recently, the albumin-bilirubin (ALBI) score has emerged as a potential prognostic indicator in liver-related conditions. This study aimed to compare the prognostic efficacy of the ALBI score with the Model for End-stage Liver Disease (MELD), MELD-Na+, and Child-Turcotte-Pugh (CTP) scores in predicting survival among patients with alcohol-associated liver disease (ALD).

This study included consecutive ALD patients admitted to the Medicine and Gastroenterology wards of MKCG Medical College and Hospital, Berhampur, Odisha, India, between November 2019 and November 2022. Upon hospitalization, baseline characteristics, clinical and laboratory parameters, ALBI, MELD, MELD-Na+, and CTP scores were recorded. The accuracy of these scores in predicting survival up to three years was compared.

A total of 490 ALD patients were included. Higher ALBI scores were observed in patients who died during hospitalization (p < 0.001), at 28 days (p < 0.001), 90 days (p < 0.001), six months (p < 0.001), one year (p < 0.001), two years (p < 0.001), and three years (p < 0.001), compared to those who survived. However, the area under the receiver operating characteristic (AUROC) curves showed that the ALBI score was inferior to MELD, MELD-Na+, and CTP scores in predicting survival at admission [AUROC: ALBI (0.719), MELD-Na+ (0.823), MELD (0.817), CTP (0.770)] and at three years [AUROC: ALBI (0.755), MELD-Na+ (0.787), MELD (0.758), CTP (0.784)]. Furthermore, Cox regression analysis revealed that components used in the MELD, MELD-Na+, and CTP scores—such as serum creatinine, serum sodium, and hepatic encephalopathy—were independent predictors of mortality, whereas the components of the ALBI score (serum albumin and serum bilirubin) were not.

All hospitalized ALD patients had a grade 3 ALBI score, with significantly higher scores observed among non-survivors compared to survivors. However, MELD, MELD-Na+, and CTP scores were superior to the ALBI score in predicting survival both during hospitalization and over a three-year follow-up period.

Metabolic syndrome (MetS) is associated with a plethora of different comorbidities. Exploring its key molecular mechanisms, such as advanced glycation end product and its receptor (AGE/RAGE) pathway, holds great potential. Numerous sources agree that targeting the AGE/RAGE pathway is a potential therapeutic strategy for MetS. However, the regulation of AGE/RAGE by microRNAs (miRNAs) in the context of MetS is still poorly understood. This review aimed to provide a systematic picture of the influence of miRNAs on AGE/RAGE in the context of MetS, with a particular focus on its ligands and receptors. This review achieves this in two ways: through an inductive “bottom-up” approach realized by a classical descriptive literature search, and through a deductive/synthetic “top-down” approach based on carefully selected miRNA profiling studies in MetS and its comorbidities. Although the initial inductive approach allowed the identification of some miRNAs of interest, almost all articles on this topic focus on the regulation of processes exclusively involved in atherogenesis. The new deductive approach has broadened the research horizon: It has enabled the discovery of new promising miRNAs and allowed for ranking different comorbid pathologies in MetS according to the degree of miRNA dysregulation of AGE/RAGE. Thus, in addition to atherosclerosis, significant miRNA dysregulation of AGE/RAGE was also described in MetS, particularly in immune cells, as well as in subcutaneous adipose tissue in obesity. This review, along with the novel approaches to systematizing the data contained therein may contribute to the understanding of MetS pathogenesis and the search for targets for the treatment of MetS.