Objective To investigate the relationship between cognitive function and sleep quality in patients with Alzheimer's disease(AD).Methods A case-control trial was conducted on 151 patients admitted to our department from May 2024 to December 2024.The patients with mild-to-moderate AD were assigned into the AD group(59 cases),and the cognitively normal patients in-to the control group(92 cases).All patients received neuropsychological assessment and sleep quality evaluation,including mini-mental state examination(MMSE),Montreal cognitive assess-ment(MoCA)and Pittsburgh sleep quality index(PSQI).The general clinical data and sleep qual-ity were compared between the two groups.Spearman correlation analysis was applied to analyze the relationship between cognitive function and sleep quality in the AD patients.Results The education level,MMSE score,MoCA score,instant story recall(ISR)score,delayed story recall(DSR)score,clock dawning test(CDT)score and Boston naming test score were significantly lower,while the activity of daily living(ADL)score was obviously higher in the AD group than the cognitively normal group(P＜0.05,P＜0.01).The AD patients had notably higher total score of PSQI and scores of sleep efficiency,nocturnal sleep disturbance and daytime dysfunction than the cognitively normal patients(P＜0.05,P＜0.01).In the AD patients,the total sleep time was positively correlated with the DSR score and the CDT score(r=0.300,P=0.021;r=0.308,P=0.018);hypnotic medication was negatively correlated with MMSE score,ISR score,and DSR score,and positively with ADL score(r=-0.320,P=0.013;r=-0.400,P=0.002;r=-0.331,P=0.010;r=0.355,P=0.006).Multiple linear regression analysis showed that benzodiazepines use and education level were independent influencing factors for cognitive function in the AD patients(P＜0.05,P＜0.01).Conclusion In AD patients,sleep quality is closely associated with cognitive function,as manifested by decreased sleep quality,reduced sleep efficiency,and worsened nocturnal sleep disturbances and daytime dysfunction.Administration of benzodiazepines may exacerbate cognitive impairment in AD patients.So,it is recommended that AD patients should be cautious about taking such drugs.

Objective To investigate the associations of immune cells,CD8+and CD4+T cells,and high-sensitivity C-reactive protein(hs-CRP)with cognitive function,and to explore the relation-ships among immunity,chronic inflammation,and Alzheimer's disease-related cognitive impair-ment.Methods A cross-sectional study was conducted on 101 patients with primary complaints of memory decline who visited the Alzheimer's Disease Clinic of Dongzhimen Hospital from June to December 2024.Mini-Mental State Examination(MMSE)and Delayed Story Recall Task(DSR)were performed to assess their cognitive function,and according to the results,they were divided into observation group(cognitively impaired,60 cases)and control group(cognitively normal,41 cases).Peripheral blood levels of CD8+T cells,CD4+T cells,and hs-CRP were compared between the two groups.Results The observation group exhibited significantly lower total scores and scores of different dimensions of MMSE and DSR scores,but notably higher activities of daily liv-ing scores than the control group(P＜0.05,P＜0.01).Serum hs-CRP level was obviously elevated in the observation group than the control group(P＜0.05).Binary logistic regression analysis revealed that CD8+T cells(OR=0.998,95％CI:0.996-1.000,P=0.038)and body mass index(OR=0.843,95％CI:0.719-0.990,P=0.037)were protective factors,while hs-CRP(OR=2.004,95％CI:1.215-3.306,P=0.006)was an independent risk factor for cognitive impairment.Spearman's rank correlation analysis showed a significant positive correlation between hs-CRP and CD4+T cells(P=0.011),but no significant association with CD8+T cells(P＞0.05).Conclusion Chronic inflammation and immune dysregulation synergistically contribute to cogni-tive decline.Hs-CRP may serve as a potential screening biomarker for cognitive impairment in pri-mary care settings.

Objective To retrospectively analyze the clinical risk factors and prognosis of perioperative myocardial injury(MINS)in non-cardiac surgery patients admitted to the intensive care unit(ICU).Methods A total of 478 postoperative patients admitted to the Department of Intensive Medicine,Minhang Hospital,Fudan University from Jan 2020 to Dec 2023 were selected.They were divided into MINS group(n=302)and normal group(n=176)based on whether myocardial injury occurred within 7 days after surgery.The differences in clinical characteristics between the two groups were compared,and risk factors for perioperative myocardial injury were identified.Risk factors for mortality in the MINS group were analyzed with 30-day mortality as the clinical endpoint.Results The prevalence of acute physiology and chronic health evaluation Ⅱ(Apache Ⅱ)score,coronary artery disease,and chronic kidney disease were all higher in the MINS group than those in the normal group,with statistically significant differences(P<0.05).The proportion of emergency surgeries,co-infection,and perioperative hypotension were significantly different between the MINS group and the normal group(P<0.05).Multivariate logistic regression analysis revealed that chronic kidney disease,emergency surgery,co-infection,and intraoperative and postoperative hypotension were risk factors for MINS occurrence.Prognostic analysis indicated that perioperative hypotension was a risk factor for 30-day mortality in MINS patients.Conclusion MINS is closely associated with patients'underlying conditions,timing of surgery,and perioperative hypotension status,and especially perioperative hypotension affects the final outcomes.

Aim To investigate the association between cardiovascular health(CVH)score based on life's es-sential 8(LE8)on cognitive function and the mediation role of neutrophil-to-lymphocyte ratio(NLR)between them in ol-der adults,providing basis for the prevention and control of cognitive impairment.Methods The study population was selected from the National Health and Nutrition Examination Survey(NHANES)2011-2014 two cycles of 60 years and a-bove,demographic characteristics,medical history and other variables were collected,the participants'CVH scores were calculated according to LE8 defined by American Heart Association,and cognitive function was assessed using the digit symbol substitution test.The relationship between CVH and cognitive function was explored using a weighted linear re-gression analysis,and the dose-response relationship was analyzed using a restricted cubic spline.Moreover,mediation a-nalysis was used to explore the role of NLR in mediating the relationship between CVH score and cognitive function.Results A total of 2 510 participants were included in this study.After adjusting for relevant factors,cognitive function was positively associated with moderate CVH group score(β=3.36,95％CI:1.43～5.30)and high CVH group score(β=6.01,95％CI:2.89～9.13)compared with the low CVH group score.The LE8 single factor of diet score(β=0.04,95％CI:0.01～0.06),physical activity score(β=0.04,95％CI:0.02～0.05),tobacco exposure score(β=0.05,95％CI:0.02～0.08),blood pressure score(β=0.03,95％CI:0.01～0.05)and blood glucose score(β=0.06,95％CI:0.03～0.09)were positively correlated with cognitive function score.The results of restricted cubic splines showed that the score of CVH was linear positively correlated with the score of cognitive function.The indirect effect of CVH on cognitive function via NLR was 0.002(P＞0.05),and the proportion of mediating effect was 1.29％(P＞0.05),indicating the mediating effect of NLR on the relationship between CVH score and cognitive function was not signif-icant.Conclusions The CVH score based on the LE8 was positively correlated with cognitive function in older adults,underscoring the crucial role of maintaining optimal CVH levels in supporting cognitive health.However,the NLR,as an indicator of inflammation,did not exhibit a significant mediating effect between the CVH score and cognitive function.The relationship between these variables might be influenced by other mechanisms.

The development of traditional Chinese medicine (TCM) diagnosis and treatment has undergone multiple paradigms, evolving from sporadic experiential practices to systematic approaches in syndrome differentiation and treatment and further integration of disease and syndrome frameworks. TCM is a vital component of the medical system, valued alongside Western medicine. Treatment based on syndrome differentiation embodies both personalized treatment and holistic approaches; however, the inconsistency and lack of stability in syndrome differentiation limit clinical efficacy. The existing integration of diseases and syndromes primarily relies on patchwork and embedded systems, where the full advantages of synergy between Chinese and Western medicine are not fully realized. Recently, driven by the development of diagnosis and treatment concepts and advances in analytical technology, Western medicine has been rapidly transforming from a traditional biological model to a precision medicine model. TCM faces a similar need to progress beyond traditional syndrome differentiation and disease-syndrome integration toward a more precise diagnosis and treatment paradigm. Unlike the micro-level precision trend of Western medicine, precision diagnosis and treatment in TCM is primarily reflected in data-driven applications that incorporate information at various levels, including precise syndrome differentiation, medication, disease management, and efficacy evaluation. The current priority is to accelerate the development of TCM precision diagnosis and treatment technology platforms and advance discipline construction in this area.

The study was conducted to investigate the mechanism of Xinyang Tablets( XYP) in modulating the fat mass and obesity-associated protein(FTO)/N6-methyladenosine(m6A) signaling pathway to ameliorate ventricular remodeling in heart failure(HF). A mouse model of HF was established by transverse aortic constriction(TAC). Mice were randomized into sham, model, XYP(low, medium, and high doses), and positive control( perindopril) groups(n= 10). From day 3 post-surgery, mice were administrated with corresponding drugs by gavage for 6 consecutive weeks. Following the treatment, echocardiography was employed to evaluate the cardiac function, and RT-qPCR was employed to determine the relative m RNA levels of key markers, including atrial natriuretic peptide( ANP), B-type natriuretic peptide( BNP), β-myosin heavy chain(β-MHC), collagen type I alpha chain(Col1α), collagen type Ⅲ alpha chain(Col3α), alpha smooth muscle actin(α-SMA), and FTO. The cardiac tissue was stained with Masson's trichrome and wheat germ agglutinin(WGA) to reveal the pathological changes. Immunohistochemistry was employed to detect the expression levels of Col1α, Col3α, α-SMA, and FTO in the myocardial tissue. The m6A modification level in the myocardial tissue was measured by the m6A assay kit. An H9c2 cell model of cardiomyocyte injury was induced by angiotensin Ⅱ(AngⅡ), and small interfering RNA(siRNA) was employed to knock down FTO expression. RT-qPCR was conducted to assess the relative m RNA levels of FTO and other genes associated with cardiac remodeling. The m6A modification level was measured by the m6A assay kit, and Western blot was employed to determine the phosphorylated phosphatidylinositol 3-kinase(p-PI3K)/phosphatidylinositol 3-kinase(PI3K) and phosphorylated serine/threonine kinase(p-Akt)/serine/threonine kinase(Akt) ratios in cardiomyocytes. The results of animal experiments showed that the XYP treatment significantly improved the cardiac function, reduced fibrosis, up-regulated the m RNA and protein levels of FTO, and lowered the m6A modification level compared with the model group. The results of cell experiments showed that the XYP-containing serum markedly up-regulated the m RNA level of FTO while decreasing the m6A modification level and the p-PI3K/PI3K and p-Akt/Akt ratios in cardiomyocytes. Furthermore, FTO knockdown reversed the protective effects of XYP-containing serum on Ang Ⅱ-induced cardiomyocyte hypertrophy. In conclusion, XYP may ameliorate ventricular remodeling by regulating the FTO/m6A axis, thereby inhibiting the activation of the PI3K/Akt signaling pathway.
Animals ; Ventricular Remodeling/drug effects* ; Heart Failure/physiopathology* ; Signal Transduction/drug effects* ; Mice ; Male ; Alpha-Ketoglutarate-Dependent Dioxygenase FTO/genetics* ; Drugs, Chinese Herbal/administration & dosage* ; Mice, Inbred C57BL ; Humans ; Adenosine/analogs & derivatives* ; Myocytes, Cardiac/metabolism* ; Disease Models, Animal

This study investigated the effects of Rehmanniae Radix Praeparata on striatal neuronal apoptosis in rats with attention deficit hyperactivity disorder(ADHD) based on the B-cell lymphoma-2(Bcl-2)/Bcl-2-associated X protein(Bax)/caspase-3 signaling pathway. Twenty-four 3-week-old male spontaneously hypertensive rats(SHR) were randomly divided into a model group, a methylphenidate group(2 mg·kg~(-1)·d~(-1)), and a Rehmanniae Radix Praeparata group(2.4 mg·kg~(-1)·d~(-1)). Age-matched male Wistar Kyoto(WKY) rats were used as the normal control group, with 8 rats in each group. The rats were administered by gavage for 28 days. Body weight and food intake were recorded for each group. The open field test and elevated plus maze test were used to assess hyperactivity and impulsive behaviors. Nissl staining was used to detect changes in striatal neurons and Nissl bodies. Terminal deoxynucleotidyl transferase dUTP nick end labeling(TUNEL) fluorescence staining was used to detect striatal cell apoptosis. Western blot was employed to detect the expression levels of Bcl-2, Bax, and caspase-3 proteins in the striatum. The results showed that compared with the model group, Rehmanniae Radix Praeparata significantly reduced the total movement distance, average movement speed, and central area residence time in the open field test, and significantly reduced the ratio of open arm entries, open arm stay time, and head dipping in the elevated plus maze test. Furthermore, it increased the number of Nissl bodies in striatal neurons, significantly downregulated the apoptosis index, significantly increased Bcl-2 protein expression and the Bcl-2/Bax ratio, and reduced Bax and caspase-3 protein expression. In conclusion, Rehmanniae Radix Praeparata can reduce hyperactivity and impulsive behaviors in ADHD rats. Its mechanism may be related to the regulation of the Bcl-2/Bax/caspase-3 signaling pathway in the striatum, enhancing the anti-apoptotic capacity of striatal neurons.
Animals ; Male ; Apoptosis/drug effects* ; Rats ; Drugs, Chinese Herbal/administration & dosage* ; Caspase 3/genetics* ; Proto-Oncogene Proteins c-bcl-2/genetics* ; bcl-2-Associated X Protein/genetics* ; Rehmannia/chemistry* ; Attention Deficit Disorder with Hyperactivity/physiopathology* ; Signal Transduction/drug effects* ; Neurons/cytology* ; Rats, Inbred SHR ; Rats, Inbred WKY ; Humans ; Corpus Striatum/cytology* ; Plant Extracts

Cardiac fibrosis(CF) is a cardiac pathological process characterized by excessive deposition of extracellular matrix(ECM). When the heart is damaged by adverse stimuli, cardiac fibroblasts are activated and secrete a large amount of ECM, leading to changes in cardiac fibrosis, myocardial stiffness, and cardiac function declines and accelerating the development of heart failure. There is a close relationship between heart yin deficiency and cardiac fibrosis, which have similar pathogenic mechanisms. Heart Yin deficiency, characterized by insufficient Yin fluids, causes the heart to lose its nourishing function, which acts as the initiating factor for myocardial dystrophy. The deficiency of body fluids leads to stagnation of blood flow, resulting in blood stasis and water retention. Blood stasis and water retention accumulate in the heart, which aligns with the pathological manifestation of excessive deposition of ECM, as a tangible pathogenic factor. This is an inevitable stage of the disease process. The lingering of blood stasis combined with water retention eventually leads to the generation of heat and toxins, triggering inflammatory responses similar to heat toxins, which continuously stimulate the heart and cause the ultimate outcome of CF. Considering the syndrome of heart Yin deficiency, traditional Chinese medicine capable of nourishing Yin, activating blood, and promoting urination can reduce myocardial cell apoptosis, inhibit fibroblast activation, and lower the inflammation level, showing significant advantages in combating CF.
Humans ; Fibrosis/drug therapy* ; Animals ; Yin Deficiency/metabolism* ; Myocardium/metabolism* ; Medicine, Chinese Traditional ; Drugs, Chinese Herbal/therapeutic use*

This study investigates the effect and underlying mechanism of Guizhi Tongluo Tablets(GZTL) in treating atherosclerosis(AS) in a mouse model. Apolipoprotein E-knockout(ApoE~(-/-)) mice were randomly assigned to the following groups: model, high-, medium-, and low-dose GZTL, and atorvastatin(ATV), and age-matched C57BL/6J mice were selected as the control group. ApoE~(-/-) mice in other groups except the control group were fed with a high-fat diet for the modeling of AS and administrated with corresponding drugs via gavage for 8 weeks. General conditions, signs of blood stasis, and body mass of mice were monitored. Aortic plaques and their stability were assessed by hematoxylin-eosin, Masson, and oil red O staining. Serum levels of total cholesterol(TC), triglycerides(TG), and low-density lipoprotein cholesterol(LDL-C) were measured by biochemical assays, and those of interleukin-1β(IL-1β), tumor necrosis factor-α(TNF-α), and interleukin-6(IL-6) were determined via enzyme-linked immunosorbent assay. Apoptosis was assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling(TUNEL). Single-cell RNA sequencing(scRNA-seq) was employed to analyze the differential expression of CD72hi macrophages(CD72hi-Mφ) in the aortas of AS patients and mice. The immunofluorescence assay was employed to visualize CD72hi-Mφ expression in mouse aortic plaques, and real-time fluorescence quantitative PCR was utilized to determine the mRNA levels of IL-1β, TNF-α, and IL-6 in the aorta. The results demonstrated that compared with the control group, the model group exhibited significant increases in body mass, aortic plaque area proportion, necrotic core area proportion, and lipid deposition, a notable decrease in collagen fiber content, and an increase in apoptosis. Additionally, the model group showcased elevated serum levels of TC, TG, LDL-C, IL-1β, TNF-α, and IL-6, alongside marked upregulations in the mRNA levels of IL-1β, TNF-α, and IL-6 in the aorta. In comparison with the model group, the GZTL groups and the ATV group showed a reduction in body mass, and the medium-and high-dose GZTL groups and the ATV group demonstrated reductions in aortic plaque area proportion, necrotic core area proportion, and lipid deposition, an increase in collagen fiber content, and a decrease in apoptosis. Furthermore, the treatment goups showcased lowered serum levels of TC, TG, LDL-C, IL-1β, TNF-α, and IL-6. The data of scRNA-seq revealed significantly elevated CD72hi-Mφ signaling in carotid plaques of AS patients compared with that in the normal arterial tissue. Animal experiments confirmed that CD72hi-Mφ expression, along with several pro-inflammatory cytokines, was significantly upregulated in the aortas of AS mice, which were downregulated by GZTL treatment. In conclusion, GZTL may alleviate AS by inhibiting CD72hi-Mφ activity.
Animals ; Drugs, Chinese Herbal/administration & dosage* ; Atherosclerosis/immunology* ; Mice ; Mice, Inbred C57BL ; Macrophages/immunology* ; Male ; Humans ; Apolipoproteins E/genetics* ; Tablets ; Tumor Necrosis Factor-alpha/genetics* ; Apoptosis/drug effects* ; Interleukin-1beta/genetics* ; Interleukin-6/genetics* ; Disease Models, Animal ; Mice, Knockout