To elucidate the regulatory role and molecular mechanism by which silent information regulator 3 (SIRT3) modulates mitochondrial biogenesis in murine alveolar type II epithelial (MLE-12) cells under oxidative stress.

Oxidative stress was induced in MLE-12 cells by exposure to H₂O₂. MLE-12 cells were transfected with siRNA specifically targeting Sirt3 to achieve knockdown. Thus, the experiment included 6 groups (n=3): normal control group (NC), scrambled negative control siRNA group (NCsiRNA group), Sirt3 siRNA group (siSIRT3 group), H₂O₂ injury group (NC+H₂O₂ group), scrambled negative control siRNA+H₂O₂ injury group (NCsiRNA+H₂O₂ group), and Sirt3 siRNA+H₂O₂ injury group (siSIRT3+H₂O₂ group). Resveratrol was used to stimulate MLE-12 cells to increase SIRT3 protein expression. Another 10 experiment groups (n=3) were also included, that is, normal control group (NC), scrambled negative control siRNA group (NCsiRNA group), DMSO group (DMSO group), Sirt3 siRNA group (siSIRT3 group), resveratrol-treated group (RSV group), H₂O₂ injury group (NC+H₂O₂ group), scrambled negative control siRNA+H₂O₂ injury group (NCsiRNA+H₂O₂ group), DMSO+H₂O₂ injury group (DMSO+H₂O₂ group), Sirt3 siRNA+H₂O₂ injury group (siSIRT3+H₂O₂ group), and resveratrol-treated+H₂O₂ injury group (RSV+H₂O₂ group). Mitochondrial superoxide (O₂•⁻) were detected using MitoSOX Red mitochondrial superoxide indicator, and ATP production was measured by using luciferase-based luminescence assay. The protein levels of SIRT3, AMPKα1, PGC-1α, TFAM, Nrf1, SOD2 and Acetyl-SOD2 were detected with Western blotting.

Exposure to 500 μmol/L H₂O₂ significantly reduced SIRT3 protein level in MLE-12 cells (P<0.000 1). Following H₂O₂ treatment, all H₂O₂-treated groups exhibited a further reduction in ATP level and a more pronounced increase in fluorescence intensity (P<0.000 1). Among these, the siSIRT3+H₂O₂ group demonstrated the most significant decrease in ATP level (P<0.01) and the greatest enhancement in fluorescence intensity (P<0.000 1) relative to the NCsiRNA+H₂O₂ group. Western blot analysis revealed that Sirt3 knockdown resulted in reduced protein levels of AMPKα1, Nrf1, PGC-1α and SIRT3 (P<0.05), while the protein levels of SOD2, acetylated SOD2 (Acetyl-SOD2), and TFAM were increased (P<0.01) when compared to the NCsiRNA group. Resveratrol treatment increased the SIRT3 protein level in MLE-12 cells (P<0.05), subsequently leading to increased protein level of PGC-1α (P<0.05). In H₂O₂ treated groups, the protein expression levels of AMPKα1, Nrf1, PGC-1α and SIRT3 were reduced compared to their corresponding control groups (P<0.05). The NC+H₂O₂ and NCsiRNA+H₂O₂ groups showed increased protein levels of SOD2, Acetyl-SOD2, and TFAM when compared to their corresponding control groups (P<0.05). Compared to the NCsiRNA+H₂O₂ group, the siSIRT3+H₂O₂ group exhibited notably reduced protein levels of AMPKα1, Nrf1, PGC-1α, TFAM, SOD2, Acetyl-SOD2 and SIRT3 (P<0.05). Conversely, the RSV+H₂O₂ group demonstrated significantly higher PGC-1α and SIRT3 protein levels than both the NC+H₂O₂ and siSIRT3+H₂O₂ groups (P<0.05).

SIRT3 enhances mitochondrial biogenesis via the AMPKα1/PGC-1α/Nrf1/TFAM signaling pathway, improves mitochondrial function of lung epithelial cells and alleviates lung injury. Regulation of SIRT3 protein may reduce oxidative damage of type II alveolar cells, suggesting a potential therapeutic target for acute lung injury.

To explore the effect of Sirtuin 1 (Sirt1) on nucleus pulposus cells (NPCs) by regulating histone H3K18 lactylation and its implications for intervertebral disc degeneration (IVDD).

Puncture-induced intervertebral disc degeneration (PIDD) was modeled in the rat caudal vertebrae. The severity of disc degeneration was evaluated, and the expression levels of lactic acid (La), malondialdehyde (MDA), reactive oxygen species (ROS), H3K18la, and Sirt1 were detected in both the normal control (NC) group and the PIDD group using histopathological staining, biochemical assay, flow cytometry, and Western blot analysis. Gradient concentrations of La were used to treat NPCs, and Sirt1 was knocked down or overexpressed via lentiviral transduction. Changes in H3K18la, ROS, and MDA levels were analyzed by immunofluorescence and biochemical assays. The genes regulated by H3K18la and their associated pathways were identified using Cleavage Under Targets and Tagmentation (CUT&Tag) and bioinformatic analyses. Then 24 rats were assigned into normal control (NC), PIDD, PIDD with Sirt1 overexpression (PIDD+oe-Sirt1), and PIDD with viral control (PIDD+Vector) groups, in order to assess the therapeutic effect of Sirt1 overexpression on intervertebral disc degeneration.

The PIDD group had significantly higher histological scores and elevated levels of La, ROS, and MDA, and enhanced expression of H3K18la but decreased Sirt1 expression when compared with the NC group (P<0.01). In cellular experiments, H3K18la, ROS, and MDA levels were in a concentration-dependent increase with the increments of La concentration. Sirt1 overexpression significantly reduced H3K18la expression (P<0.01), whereas its knockdown conversely increased it (P<0.01). CUT&Tag analysis indicated that H3K18la plays a regulatory role in oxidative stress in NPCs. In animal experiments, the PIDD+oe-Sirt1 group exhibited significantly lower histological scores, along with reduced levels of ROS, H3K18la, and MDA in comparison to the PIDD and PIDD+Vector groups (P<0.01).

The expression of Sirt1 is significantly decreased in degenerative intervertebral discs. As a delactylase for histone H3K18la, Sirt1 may play a critical role in intervertebral disc degeneration by modulating oxidative stress in nucleus pulposus cells through H3K18la lactylation.

To investigate the capacity of oxaliplatin (OXA) in inducing cuproptosis in treatment of gastric cancer and explore the underlying mechanisms.

Kaplan-Meier Plotter was used to analyze the data in UALCAN database to explore the key regulatory proteins involved in cuproptosis, dihydrolipoamide S-acetyltransferase (DLAT), ferredoxin 1 (FDX1) and lipoic acid synthase (LIAS) in gastric cancer. The cytotoxic effects of OXA alone and in combination with copper chelator tetrathiomolybdate (TTM) were determined using CCK-8 assays. Immunofluorescence assay and Western blotting were employed to assess the mitochondrial oligomerization of DLAT and the expression levels of FDX1 and LIAS. Intracellular copper levels were measured using a copper-specific fluorescent probe following treatment with OXA and TTM. A subcutaneous tumor model was established through subcutaneous injection of gastric cancer MKN-45 cells in SPF-grade female Balb/c nude mice (5~6 weeks old, weighing 18~25 g). Then the nude mice were randomly assigned into control group, OXA treatment group (intraperitoneal injection), and OXA and tetrasolybdate (TTM) treatment group. Tumor size was monitored regularly to plot a tumor growth curve. Tumor tissues were harvested, embedded in paraffin, sectioned and then subjected to immunohistochemical (IHC) staining to evaluate expression of FDX1 and LIAS. Copper staining was performed to assess copper levels in tumor tissues.

The expression levels of FDX1 and DLAT were significantly elevated in gastric cancer tissues than normal tissues (P<0.001), and the expression levels of FDX1, DLAT and LIAS were associated with the prognosis of gastric cancer. OXA treatment inhibited cell proliferation in both MKN-45 and BGC-823 cells, with the IC₅₀ values of 44.89 and 19.02 μmol/L, respectively. Its cytotoxicity was significantly attenuated by TTM (P<0.001). OXA induced pronounced mitochondrial oligomerization of DLAT, intracellular copper accumulation, and reduced FDX1/LIAS expression. In nude mice of transplanted tumor, OXA monotherapy significantly suppressed tumor growth (P<0.01), which was weakened by TTM treatment (P<0.001), and decreased the protein levels of FDX1 and LIASr than those in the control and OXA+TTM groups. Copper staining revealed elevated intracellular copper levels in the OXA-treated group, consistent with in vitro findings.

OXA inhibits the progression of gastric cancer by inducing cuproptosis in tumor cells.

To explore the effects of long non coding RNA FGD5-AS1 (LncRNA FGD5-AS1) on the migration and invasion of gastric cancer cells by regulating the microRNA-302b-3p (miR-302b-3p)/E2F transcription factor 1 (E2F1) axis.

Real-time fluorescence quantitative PCR (qRT-PCR) was used to detect the mRNA expression of LncRNA FGD5-AS1, miR-302b-3p, and E2F1 in gastric cancer cell lines (SGC-7901, MKN-45, HGC-27, AGS, BGC-823) and human gastric epithelial cell line GES-1, in order to screen for the best intervention cells. Gastric cancer cells were separated into control group (NC group), sh-NC group, sh-FGD5-AS1 group, sh-FGD5-AS1+anti-miR-NC group, and sh-FGD5-AS1+anti-miR-302b-3p group. qRT-PCR was performed to detect the expression of LncRNA FGD5-AS1, miR-302b-3p, and E2F1 in the cells. MTT assay and flow cytometry were applied to measure cell proliferation and apoptosis, respectively. Scratch and Transwell assays were carried out to measure cell migration and invasion, respectively. Western blotting was carried out to measure the protein levels of E2F1, Ki-67, Bax and Bcl-2. Nude mouse model of transplantable subcutaneous tumor was established to verify the effect of LncRNA FGD5-AS1 on the growth of gastric cancer transplant tumors. Dual luciferase reporter gene and RNA pull-down assays were used to detect the targeting relationship of LncRNA FGD5-AS1 and E2F1 with miR-302b-3p.

Compared with the GES-1 cells, the gastric cancer cell lines SGC-7901, MKN-45, HGC-27, AGS and BGC-823 exhibited significantly increased mRNA levels of LncRNA FGD5-AS1 and E2F1, while decreased level of miR-302b-3p (P<0.05). AGS cells were finally selected for the following experiments. Silencing LncRNA FGD5-AS1 prominently up-regulated miR-302b-3p, down-regulated E2F1, and inhibited cell proliferation, migration, and invasion, and promoted cell apoptosis in gastric cancer AGS cells (P<0.05). Inhibition of miR-302b-3p partially weakened the effects of silencing LncRNA FGD5-AS1 on the proliferation, migration, invasion, and apoptosis of gastric cancer cells (P<0.05). In vivo experiments showed that silencing LncRNA FGD5-AS1 could prominently inhibit the growth of transplanted tumors in mice (P<0.05). RNA pull-down and dual luciferase reporter gene assays confirmed the targeted regulatory relationship of LncRNA FGD5-AS1 and E2F1 with miR-302b-3p.

LncRNA FGD5-AS1 is up-regulated in gastric cancer cells, and its silencing can inhibit the malignant progression of gastric cancer by regulating the miR-302b-3p/E2F1 axis.

To explore whether dexmedetomidine (Dex) improves sevoflurane (Sev)-induced cognitive impairment in neonatal rats by regulating mammalian rapamycin target protein (mTOR)/nuclear factor-κB (NF-κB) signaling pathway.

Fifty neonatal SD rats (aged 6 d, weighing 9.5~11.5 g) were randomly divided into 5 groups: sham operation (Sham) group, model (Model) group, low-dose Dex (Dex-L) group, high-dose Dex (Dex-H) group, and phorbol 12-myristate 13-acetate (PMA) group (an activator of mTOR/NF-κB signaling pathway), with 10 animals in each group. The rats in the Sham group were placed in a sealed chamber containing fresh air, while those rats from the other 4 groups were exposed to 2% Sev+21% O₂ for modeling. In 2 h before chamber placement, the Dex-L and Dex-H groups received an intraperitoneal injection of 10 and 30 μg/kg Dex, respectively, and the PMA group received an intraperitoneal injection of 30 μg/kg Dex and 5 mg/kg PMA. The rats in the Sham and Model groups were given an intraperitoneal injection of equivalent volume of normal saline. Cognitive function and learning and memory abilities were evaluated with novel object recognition test and step-down inhibitory avoidance test. Laser speckle contrast imaging (LSCI) was used to observe cerebral blood flow; Nissl staining and transmission electron microscopy were employed to observe the ultrastructure of hippocampal neurons and synapses. TUNEL staining was perform to detect the cell apoptosis. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to measure the expression levels of mTOR, NF-κB, postsynaptic density protein 95 (PSD95), synaptophysin (SYP), synapsin (SYP), microtubule-associated protein-2 (Map-2), B-cell lymphoma-2 (Bcl-2), and Bcl-2-associated X protein (Bax) in the hippocampal tissue. Western blotting was conducted to detect the protein levels of mTOR, p-mTOR, NF-κB, p-NF-κB, Bcl-2, and Bax in the hippocampal tissue.

Compared with the Sham group, the Model group exhibited significantly lower discrimination index and shorter platform jumping latency, increased number of errors (P<0.05), reduced cerebral blood perfusion, decreased number of hippocampal neurons, damaged synaptic structure, raised apoptotic rate, enhanced expression of p-mTOR, p-NF-κB and Bax at mRNA and protein levels (P<0.05), while down-regulated mRNA levels of SYN, Map-2, SYP and PSD95 (P<0.05), and reduced mRNA and protein expression of Bcl-2 (P<0.05). After the intervention of Dex, all the above indexes were significantly improved (P<0.05), and the effects of high dose were better. PMA partially reversed the protective effects of Dex-H, reactivated the signal of mTOR/NF-κB, and aggravated the neuronal damage (P<0.05).

Dex may alleviate cognitive dysfunction in neonatal rats by inhibiting the mTOR/NF-κB signaling pathway and suppressing Sev-induced hippocampal neuronal apoptosis.

To evaluate the effects of a compound nutritional preparation on postoperative wound healing, immune function, inflammatory response, nutritional status, and intestinal barrier function in patients after cardiovascular surgery, so as to provide a new nutritional intervention strategy for rapid recovery of trauma patients.

From September 2024 to January 2025, 65 eligible patients scheduled for open cardiovascular surgery at the Second Affiliated Hospital of Army Medical University were recruited, and randomly assigned via sealed envelopes to either an experimental group (n=32) or a control group (n=33). From the first day after operation, both groups received isocaloric and isonitrogenous enteral nutritional support for 7 d, and the control group was given a standard formula, while the experimental group took the compound nutritional preparation. Wound healing was assessed with REEDA scale on postoperative days 7 and 14. Inflammatory markers, including the neutrophil-to-lymphocyte ratio (NLR), white blood cell (WBC) count, C-reactive protein (CRP), TNF-α and IL-6 were measured preoperatively and on postoperative days 3 and 7. Immune function was evaluated by T-lymphocyte subsets (CD3⁺, CD4⁺, CD8⁺) and serum immunoglobulins (IgA, IgG, IgM). Nutritional status was assessed via serum albumin (ALB), prealbumin (PA), and total protein (TP). Intestinal barrier function was indicated by serum levels of diamine oxidase (DAO), lipopolysaccharide (LPS) and D-lactate. Body composition analysis was performed preoperatively and on postoperative day 7. Incidence of postoperative infectious complications and length of hospital stay were compared between the 2 groups.

Finally, 60 patients completed the whole study, with 30 participants in each group. No significant differences were found in baseline indicators between the 2 groups. When compared with the control group, the experimental group exhibited significantly lower postoperative REEDA scores, reduced incidence of infectious complications, and shorter length of hospital stay (P<0.05), along with obviously higher skeletal muscle mass index (SMI) and 50 kHz whole-body phase angle (P<0.05). On postoperative day 3, there were no significant differences in above indicator between the 2 groups (P>0.05). On postoperative day 7, notably higher CD3⁺ and CD4⁺ T-cell counts and serum PA levels were observed in the experimental group than the control group (P<0.05). Significant group × time interactions were observed in CD3⁺, CD4⁺, and CD8⁺ T-cell counts and IgA level (P<0.05). Additionally, the experimental group had remarkably lower levels of NLR, CRP, TNF-α, IL-6, DAO, LPS, and D-lactate (P<0.05), with significant group×time interactions for NLR, CRP, IL-6, DAO, and D-lactate (P<0.05). There existed significant group×time interactions in NLR, CRP, IL-6, DAO, and D-lactate.

The compound nutritional preparation can promote wound healing, improve immune function and nutritional status, attenuate the inflammatory response, protect intestinal barrier function, and thereby facilitate postoperative recovery in patients undergoing open cardiovascular surgery.

To investigate the value of tumor vascular habitat characteristic parameters constructed based on dynamic susceptibility contrast-enhanced perfusion-weighted imaging (DSC-PWI) in differentiating between newly diagnosed glioblastoma (GBM) and solitary brain metastasis (SBM).

A case-control study design was adopted to analyze the imaging data of 109 patients with malignant brain tumors (including 57 cases of GBM and 52 cases of SBM) confirmed by postoperative pathology or comprehensive clinical diagnosis retrospectively collected from Department of Radiology of Daping Hospital between January 2019 and March 2025. Based on DSC-PWI images, hemodynamic tissue signature (HTS) was used to segment the lesions and construct 4 tumor vascular habitats, that is, high angiogenic tumor (HAT), low angiogenic tumor (LAT), potentially infiltrated peripheral edema (IPE), and vasogenic peripheral edema (VPE). Volume parameters and blood flow parameters for each habitat region were calculated, including volume of each habitat region, tumor core volume, peritumoral edema volume, and relative cerebral blood volume (rCBV). Baseline data and habitat characteristic parameters were compared between the 2 groups. Receiver operating characteristic (ROC) curves were drawn to evaluate the differential diagnostic efficacy. Pearson correlation analysis was performed to assess the correlations among habitat characteristic parameters to quantify the spatial interactions between habitats.

In the GBM group, the median rCBV (rCBV_median) at HAT, LAT, IPE, and VPE habitats were 6.143±1.687 (95%CI: 5.695~6.591), 3.249±0.988 (95%CI: 2.987~3.511), 1.913 (1.578, 2.588) (95%CI: 1.794~2.110) and 0.836 (0.676, 1.110) (95%CI: 0.710~0.949), respectively. These values were all significantly higher than the rCBV_median at above habitats in the SBM group [4.634±1.647 (95%CI: 4.175~5.092), 2.255±0.807 (95%CI: 2.031~2.480), 1.291 (1.022, 1.767) (95%CI: 1.125~1.677), 0.600 (0.459, 0.742) (95%CI: 0.519~0.682); P<0.001]. ROC curve analysis showed that the rCBV_median at LAT habitat had good diagnostic efficacy for differentiation, with an AUC value of 0.792 (95%CI: 0.704~0.864) (P<0.001). The optimal cutoff value of rCBV_median at LAT habitat was 2.660 (sensitivity: 75.44%, specificity: 78.85%). The ratio of IPE volume to peritumoral volume (V_(IPE)/V_(P)) in the GBM group was 0.216 (0.101, 0.351) (95%CI: 0.165~0.267), notably higher than that in the SBM group [0.079 (0.055, 0.153) (95%CI: 0.066~0.102), P<0.001]. ROC curve analysis indicated that V_(IPE)/V_(P) ratio had good diagnostic efficacy, with an AUC value of 0.765 (95%CI: 0.674~0.840). The optimal cutoff value of the ratio was 0.122 (sensitivity: 71.93%, specificity: 73.08%). Pearson correlation analysis suggested that in the GBM group, the correlation coefficients between IPE-rCBV_median and HAT-rCBV_median, and between VPE-rCBV_median and HAT-rCBV_median were 0.620 (P<0.01) and 0.283 (P=0.033), respectively, indicating significant positive correlations.

DSC-PWI-based vascular habitat characteristic parameters show significant differences between newly diagnosed GBM and SBM. Both the volumetric parameter V_(IPE)/V_(P) ratio and the hemodynamic parameter LAT-rCBV_median have good differential diagnostic efficacy, and can serve as imaging markers for distinguishing between GBM and SBM.

To investigate the effect of continuous intravenous nicorandil administration during the perioperative period on ventricular arrhythmia (VA) in patients with acute ST-segment elevation myocardial infarction (STEMI).

A randomized controlled trial was conducted on 140 patients with acute STEMI undergoing emergency percutaneous coronary intervention (PCI) in our department from January 2024 to May 2025. They were randomly allocated into a control group (n=70) and a nicorandil group (n=70). The nicorandil group received an intravenous bolus of 6 mg nicorandil as a loading dose before emergency PCI, followed by a continuous intravenous infusion at 6 mg/h for 48 h. The control group received normal saline following the same dosage and administration schedule. The incidences of in-hospital VA (including frequent ventricular premature beats, non-sustained ventricular tachycardia, sustained ventricular tachycardia, ventricular flutter, and ventricular fibrillation) and major adverse cardiovascular events (MACE) were compared between the 2 groups.

The total incidence of VA (31.4% vs 58. 6%, P=0.001) was significantly lower in the nicorandil group than in the control group. The incidence of MACE was slightly lower in the nicorandil group compared to the control group, but the difference did not reach statistical significance (15.7% vs 27.1%, P=0.099). Multivariate logistic regression analysis indicated that nicorandil was an independent protective factor against VA (OR=0.205, 95% CI: 0.083~0.506, P=0.001). Subgroup analysis suggested that the protective effect of nicorandil was particularly significant in patients aged <65 years, without diabetes, and with Killip class I.

Based on conventional STEMI treatment regimen, continuous intravenous administration of nicorandil during the peri-PCI period effectively reduces the incidence of in-hospital VA.

To investigate the current status of compliance with endoscopic follow-up in patients with chronic atrophic gastritis (CAG) and analyze its influencing factors.

Clinical data of 1 196 patients with gastroscopy-diagnosed CAG in our department from May 1 to July 31, 2022 were retrospectively collected in this study. According to the status of gastroscopy reexamination in this hospital and other hospitals within the subsequent nearly 3 years, they were divided into a compliant group (n=473) and a non-compliant group (n=723). General demographic data of, and past medical history, including positive history of Helicobacter pylori (H.pylori) infection, intestinal metaplasia, and atrophy classification, as well as disease cognition of CAG, hospital distance, and medical background were collected during follow-up. The current status of compliance with endoscopic follow-up surveillance was analyzed. Univariate and logistic regression analyses were used to evaluate the independent influencing factors for patient compliance with gastroscopy reexamination, while receiver operating characteristic (ROC) curve and area under the curve (AUC) were adopted to determine the predictive efficiency of the logistic regression model on patient compliance with endoscopic follow-up monitoring.

Despite being advised by attending physicians to undergo reexamination within 2~3 years after CAG diagnosis, only 473 (39.55%) patients complied with the follow-up recommendation, while 723 (60.45%) patients did not. Univariate analysis showed statistical differences were observed between the 2 groups in terms of residence, education level, monthly income, history of coronary heart disease, symptoms, H. pylori infection history, intestinal metaplasia history, atrophy grade, disease cognition, health awareness score, initial department of visit, hospital distance, and medical background (all P<0.05). Logistic regression analysis revealed that the factors associated with higher compliance included having disease cognition (OR=6.280, 95%CI: 4.442~8.878, P<0.01), higher health awareness score (OR=2.219, 95%CI: 1.943~2.535, P<0.01), presence of symptoms (OR=2.537, 95%CI: 1.822~3.531, P<0.01), history of H. pylori infection (OR=2.159, 95%CI: 1.496~3.116, P<0.01), history of intestinal metaplasia (OR=3.452, 95%CI: 2.100~5.675, P<0.01), history of coronary heart disease (OR=2.306, 95%CI: 1.325~4.015, P<0.01), monthly income of 5 000~10 000 Yuan (OR=2.525, 95%CI: 1.693~3.766, P<0.01) or ≥10 000 Yuan (OR=4.268, 95%CI: 2.472~7.370, P<0.01) (both higher than those with monthly income<5 000 Yuan), type O atrophy (OR=2.523, 95%CI: 1.319~4.827, P<0.01) (higher than type C atrophy), and initial visit to gastroenterological department (OR=1.988, 95%CI: 1.345~2.939, P<0.01) (higher than visits to other departments). Conversely, longer hospital distance was associated with lower compliance (OR=0.981, 95%CI: 0.963~0.998, P<0.05). The patients with college or higher education level (OR=0.250, 95%CI: 0.138~0.453, P<0.01) had lower compliance than those with primary school education level or below, and those with medical background had lower compliance than those without (OR=0.289, 95%CI: 0.150~0.557, P<0.01).

Compliance with endoscopic follow-up surveillance in CAG patients is associated with disease cognition of CAG, health awareness score, monthly income, symptoms, H. pylori infection history, intestinal metaplasia history, atrophy grade, initial department of visit, history of coronary heart disease, hospital distance, and education level. Clinicians should formulate targeted individualized interventions to improve patient compliance and early warning for gastric cancer.

To investigate the short-term efficacy and safety of deep cervical lymphatic-venous anastomosis (LVA) in treating Alzheimer disease.

This case series included 30 patients who underwent LVA at the Department of Neurosurgery, First Affiliated Hospital of Chongqing Medical University between December 2024 and February 2025. All patients had confirmed Alzheimer disease and were assessed preoperatively and at 1 week, 1 month, and 3 months postoperatively using three standardized neuropsychological scales: Neuropsychiatric Inventory (NPI), Clinical Dementia Rating Scale Sum of Boxes (CDR-SB), and Activities of Daily Living (ADL) scale. Changes in these scores served as efficacy endpoints.

All patients successfully underwent LVA with no mortality or severe adverse events. Median NPI scores decreased from 25.5 (13.8, 47.5) preoperatively to 16.0 (7.2, 21.5) at 1 week postoperatively (P<0.001, r=0.74), remaining stable at 17.0 (8.5, 23.8) and 17.5 (12.0, 21.0) at 1 and 3 months respectively (P<0.001 vs. baseline). Mean ADL scores decreased from 56.7±16.6 preoperatively to 54.9±16.2 at 1 week (P<0.001), further declined to 53.7±16.0 at 1 month (P<0.001), and returned to 56.2±13.9 at 3 months (P=0.701 vs baseline). Median CDR-SB significantly improved from 16.0 (13.2, 17.0) preoperatively to 15.0 (13.0, 16.0) at 1 week (P<0.001, r=0.63), with sustained improvements at 1 and 3 months (P<0.001).

LVA demonstrates favorable safety and modest short-term efficacy in ameliorating neuropsychiatric symptoms and cognitive function in Alzheimer disease.