To explore the effects of sleep cognitive behavioral therapy combined with escitalopram tablets on negative emotions and sleep function of patients with depression and anxiety in our hospital.

From April 2021 to May 2023, patients with depression complicated with anxiety in our hospital were divided into control group and experimental group according to treatment methods. The control group was given escitalopram orally, 10 mg each time, qd for 8 weeks; in the experimental group, CBT-I (including sleep health education, stimulation control and other modules) was added on the basis of the control group, once a week for 60-90 min, and the course of treatment was 8 weeks. The clinical efficacy, negative emotional scores [using Hamilton Anxiety Scale (HAMA) and Hamilton Depression Scale (HAMD)], sleep quality [using Pittsburgh Sleep Quality Index (PSQI)], social function [using Social Disability Screening Scale (SDSS)], cognitive function [using Mini-Mental State Examination (MMSE)], serum neuron-specific enolase (NSE) and neuropeptide Y (NPY) levels, medication compliance (using Morisky medication compliance questionnaire), and recurrence rate were compared between the two groups.

A total of 126 patients with depression and anxiety were screened and 100 patients were enrolled, including 48 patients in the control group and 52 patients in the experimental group. After treatment, the total effective rate of the treatment group was 82.69% (43 cases /52 cases), which was significantly higher than that of the control group 62.50% (30 cases/48 cases) (P<0.05). The HAMA scores in the treatment group and control group were (8.33±4.61) and (14.66 ±5.29) scores, respectively; the HAMD scores were (6.87±2.42) and (10.76±2.63), respectively; the PSQI scores were (7.06±1.11) and (10.69±1.03), respectively; the serum NSE levels were (10.35±1.46) and (12.26±1.55) μg·L^-1; the NPY levels were (431.55±97.22) and (314.22±41.38) μg·L^-1, respectively. The above indexes in the treatment group were significantly lower than those in the control group (all P<0.05). The recurrence rate of the treatment group and control group was 3.85% (2 cases /52 cases) and 16.67% (8 cases /48 cases), respectively, without statistically significant difference (P>0.05). No serious adverse events occurred during the intervention period in both groups, and there was no significant difference in the incidence of adverse events (P>0.05).

Cognitive behavioral therapy for insomnia combined with escitalopram tablets can effectively alleviate negative emotions, improve sleep function and reduce recurrence rate in patients with depression complicated with anxiety in our hospital, with good clinical efficacy.

To investigate the effect of β-sitosterol on osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) by regulating the transforming growth factor β1 (TGF-β1)/mothers against decapentaplegic drosophila homolog 3 (Smad3) pathway.

BMSCs were randomly assigned into control group, low-dose β-sitosterol (β-sitosterol-L) group, medium-dose β-sitosterol group (β-sitosterol-M), and high-dose β-sitosterol group (β-sitosterol-H). Control group was cultured normally and β-sitosterol-L, -M and -H group was intervened by 1.5、3.0、6.0 μg·mL^-1 β-sitosterol. BMSCs were randomly divided into control group (normal culture), β-sitosterol group (6 μg·mL^-1 β-sitosterol), SIS3 group (5 μmol·L^-1 SIS3), and β-sitosterol+SIS3 group (6 μg·mL^-1 β-sitosterol+5 μmol·L^-1 SIS3). Enzyme-linked immunosorbent assay (ELISA) was used to detect the alkaline phosphatase (ALP) activity was measured in each group. Alizarin red staining was used to determine the calcium deposition rate of each group, and then the osteogenic differentiation of BMSCs in each group was detected. Western blot was used to detect the osteogenic differentiation of BMSCs and the expression of TGF-β1/Smad3 pathway related proteins in each group.

The ALP activities of the β-sitosterol-L, β-sitosterol-M, β-sitosterol-H and the control groups were (1.24±0.10), (1.53±0.08), (1.84±0.11) and (0.95±0.09) U·mg prot^-1, respectively; the calcium deposition rates were (196.21±13.67)%, (301.73±16.90)%, (423.60±20.25)% and (100.00±0)%, respectively; the relative expression levels of bone morphogenetic protein 2 (BMP-2) protein were 0.49±0.05, 0.89±0.07, 1.30±0.09 and 0.13±0.02, respectively; the relative protein expression of TGF-β 1 were 0.47±0.04, 0.85±0.07, 1.26±0.09 and 0.10±0.01, respectively; the p-Smad3/Smad3 values were 0.32±0.03, 0.59±0.06, 0.94±0.05 and 0.08±0.02, respectively. Compared with the control group, the above indicators of the β-sitosterol-L, β-sitosterol-M and β-sitosterol-H groups showed an increase in a dose-dependent manner, and the differences were statistically significant (all P<0.05). The ALP activities of the β-sitosterol group, SIS3 group, β-sitosterol+SIS3 group and the control group were (1.78±0.14), (0.43±0.08), (0.97±0.13) and (0.91±0.10) U·mg prot^-1, respectively; the calcium deposition rates were (410.35±19.72)%, (45.62±13.91)%, (109.14±16.53)% and (100.00±0)%, respectively; the relative expression levels of BMP-2 protein were 1.79±0.16, 0.27±0.07, 0.87±0.10 and 0.85±0.11, respectively; the relative protein expression levels of TGF-β1 were 1.47±0.10, 0.11±0.03, 0.56±0.09 and 0.55±0.06, respectively; The p-Smad3/Smad3 values were 0.94±0.06, 0.09±0.02, 0.45±0.05 and 0.43±0.04, respectively. Compared with the control group, the above indicators were all increased in the β-sitosterol group, while they were all decreased in the SIS3 group, and the differences were statistically significant (all P<0.05). Compared with the β-sitostero group, the above indicators were all decreased in the β-sitosterol+SIS3 group, and the differences were statistically significant (all P<0.05).

β-sitosterol can promote osteogenic differentiation of BMSCs by activating the TGF-β1/Smad3 pathway.

To explore the molecular mechanism of berberine in improving insulin resistance and liver lipid metabolism in obesity mice.

Sixty clean-grade C57BL/6 mice were randomly divided into control group (normal diet), model group (high fat diet), experimental-L group (model+50.00 mg·kg^-1 berberine), experimental-H group (model+100.00 mg·kg^-1 berberine), inhibitor NC group (model +100.00 mg·kg^-1 berberine + tail vein injection mmu-inhibitor NC), miR-125a inhibitor group (model +100.00 mg·kg^-1 berberine + tail vein injection of mmu-miR-125a inhibitor). Berberine was administered by gavage once a day, and subcutaneous injection was performed every 4 days. After a continuous treatment period of 28 days, the insulin resistance levels were detected, serum lipid levels were analyzed, the expression levels of related genes were detected by real-time quantitative polymerase chain reaction (RT-qPCR), and the expression of related proteins in liver tissue was detected by Western blot (WB).

The levels homeostatis model assessment of insulin resistance (HOMA-IR) in control group, model group, experimental-H group, inhibitor NC group and miR-125a inhibitor group were 2.56±0.11, 7.23±0.67, 5.04±0.20, 4.99±0.34 and 6.46±0.40, respectively; triglyceride (TG) levels were (0.46±0.04), (0.93±0.08), (0.65±0.05), (0.63±0.06) and (0.74±0.06) mmol·L^-1, respectively; the relative expression levels of miR-125a were 1.00±0.12, 0.56±0.07, 0.77±0.10, 0.78±0.11 and 0.21±0.03, respectively; fatty acid synthase (FAS) mRNA were 1.00±0.10, 1.90±0.14, 1.40±0.22, 1.41±0.16 and 1.67±0.14, respectively; the relative protein expression levels of phosphorylated phosphatidylase 3-kinase (p-PI3K) were 0.78±0.09, 0.42±0.05, 0.69±0.06, 0.70±0.03 and 0.51±0.06, respectively; phosphorylated protein kinase B (p-AKT) protein levels were 0.84±0.12, 0.30±0.05, 0.64±0.08, 0.65±0.08 and 0.49±0.07, respectively. Compared between the model group and the control group; between the experimental-H group and the model group; and between the miR-125a inhibitor group and the inhibitor NC group, all differences of the above inclicatovs went statistically significant (P<0.01, P<001).

Berberine may improve insulin resistance and fat metabolism in obesity mice by activating PI3K/AKT signal through miR-125a.

To explore the protective effects and potential mechanism of bifendate against methionine-choline-deficient (MCD) diet-induced metabolic dysfunction-associated steatotic liver disease (MASLD) in mice.

A total of 24 male C57BL/6J mice were randomly divided into control group, model group, and experimental group. The model group was fed with MCD diet to establish the MASLD model, while the experimental group received bifendate (300 mg·kg^-1) in addition to the MCD diet. After 6 weeks, liver pathology was assessed using Hematoxylin-Eosin (H&E) and Oil Red O staining. Hepatic triglyceride (TG) content, serum lipopolysaccharide (LPS) and serum alanine aminotransferase (ALT) levels were measured using assay kits. Gut microbiota composition and diversity were analyzed by high-throughput sequencing. The relative expression levels of the intestinal tight junction protein ZO-1 and Occludin were detected by Western blot.

Oil Red O staining revealed that the number and degree of hepatocellular steatosis were significantly reduced in the experimental group compared to the model group. The MCD diet successfully induced steatohepatitis in mice, characterized by significantly increased hepatic TG, serum ALT, and marked hepatocellular steatosis. Hepatic TG contents were (66.43±14.58), (231.29±20.26), and (190.39±29.33) μmol·g^-1 for the control, model and experimental groups, respectively; serum ALT levels were (52.04±16.80), (219.74±123.37) and (31.68±10.70) IU·L^-1, respectively; serum LPS levels were (0.89±0.57), (4.01±0.65) and (0.52±0.25) EU·mL^-1, respectively. The relative expression levels of ZO-1 were 1.00±0.94, 0.06±0.03 and 0.25±0.27, respectively, and for Occludin were 1.00±0.57, 0.06±0.03 and 0.15±0.15, respectively. Compared with the model group, the experimental group showed statistically significant differences in all the aforementioned indicators (P<0.05, P<0.001). Bifendate intervention significantly reduced serum ALT and hepatic TG levels and markedly alleviated the extent and severity of hepatocellular steatosis. Regarding the gut-liver axis, bifendate significantly improved the diversity and richness of the gut microbiota in model mice, particularly increasing the relative abundance of Bilophila and Desulfovibrio, genera closely related to bile acid metabolism. Furthermore, bifendate intervention significantly up-regulated the expression of intestinal tight junction proteins and decreased serum LPS levels.

Bifendate can effectively ameliorate MCD diet-induced steatohepatitis in mice. Its protective mechanism is closely related to the regulation of the gut-liver axis, including remodeling the intestinal flora structure (increasing the relative abundance of Bilophila and Desulfovibrio), enhancing intestinal barrier function (upregulating tight junction proteins, reducing serum LPS), and potentially affecting bile acid metabolism.

To investigate the bioequivalence of oral torasemide tablets in healthy subjects under fasting and postprandial states.

A single-center, randomized, open-label, single-dose, double-period, double-cross study design was adopted. Each period involved a single oral administration of 10 mg of torasemide under fasting or postprandial conditions. The plasma drug concentration of torasemide was determined by liquid chromatography-tandem mass spectrometry (LC-MS/MS). The pharmacokinetic data were calculated and bioequivalence evaluation was performed.

The pharmacokinetic parameters of the test formulation and reference formulation in the fasting group were as follows: C_max were (1 664.91±353.89) and (1 645.29±363.80) ng·mL^-1, AUC_0-t were (3 459.38±659.07) and (3 468.21±616.06) h·ng·mL^-1, AUC_0-∞ were (3 637.12±700.25) and (3 644.48±651.24) h·ng·mL^-1. The pharmacokinetic parameters of the test formulation and reference formulation in the postprandial group were as follows: C_max were (1 018.18±336.79) and (883.97±172.43) ng·mL^-1, AUC_0-t were (3 974.56±963.76) and (3 924.70±943.83) h·ng·mL^-1, AUC_0-∞ were (4 192.17±1081.81) and (4 143.90±1068.71) h·ng·mL^-1; the 90% confidence intervals of the ratios of the pharmacokinetic parameters of the test formulation and reference formulation (test formulation/reference formulation) under fasting and postprandial conditions were all within the statistically equivalent range.

Torasemide tablets test formulation and the reference formulation have bioequivalence under both fasting and postprandial administration conditions.

To establish a high performance liquid chromatography method for the determination of arecoline in rat plasma, to study the pharmacokinetic behavior of arecoline in rats, and to provide a scientific basis for the pharmacodynamic substance basis of arecoline.

SD rats were given low, medium and high (10, 20 and 30 mg·kg^-1) aqueous solutions of arecine by gavage, and blood was collected from the fundus venous plexus at different time points, and the supernatant was extracted by ethyl acetate and then injected for analysis. Puerarin was used as the internal standard to detect the content of arecine in plasma by HPLC, the mobile phase was acetonitrile-methanol-0.1% triethylamine aqueous solution (6∶16∶78, pH=4.5), isocratic elution, flow rate 1.0 mL·min-1, detection wavelength 215 nm, column temperature 30 ℃, and the pharmacokinetic parameters were calculated by DAS2.0 software.

The linear relationship between arecaine in 0.5-32.0 μg·mL^-1 was good, the standard curve was y=0.0512x-0.0326(r=0.9960), the lower limit of quantification was 0.5 μg·mL^-1, and the precision, repeatability, stability and recovery test results were good. The main pharmacokinetic parameters of arecaine in the low-, medium-, and high-dose groups were (1.36±0.21), (2.15±0.72) and (2.75±0.69) mg·L^-1, and the area under the curve (AUC_0-t) was (3.04±0.24), (3.87±1.02) and (4.49±0.76) mg·L^-1·h, and the elimination half-lives (t_1/2) were (3.67±1.73), (2.88±1.66) and (3.12±1.86) h.

The method is simple and rapid, suitable for the pharmacokinetic study of arecoline in rat plasma.

To systematically screen potential antioxidant targets for the treatment of Alzheimer’s disease (AD) based on network pharmacology strategy.

Firstly, the structure-data file (SDF) of the antioxidant compound library was converted into the standard simplified molecular input line entry system (SMILES) molecular structure format usingrational discovery kit (RDKit), and then the potential targets of antioxidant compounds were predicted using the SwissTargetPrediction platform. After the obtained targets were analyzed with the differentially expressed genes of AD, a protein interaction network (PPI network) was constructed, and the functional interaction relationship was mined based on the STRING database. Further, the "compound-disease target-signaling pathway" network diagram was established with the help of Cytoscape software to screen key therapeutic targets. Finally, the core targets were annotated with Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis using the DAVID database.

Finally, 10 core targets with potential anti-Alzheimer’s disease effects were screened. Among them, the top three key nodes in degree value were heat shock protein 90α family class B member 1 (HSP90AB1), catenin β1 (CTNNB1) and proto-oncogene tyrosine protein kinase (SRC). Enrichment analysis suggested that these core targets may be mainly involved in the pathogenesis and intervention of Alzheimer’s disease through calcium signaling pathway and phosphatidyqinositol-3 kinase/protein kinase B (PI3K-Akt) signaling pathway, and had important therapeutic potential.

This study systematically identified the core antioxidant targets and key pathways for the treatment of Alzheimer’s disease from the perspective of network pharmacology, providing theoretical support for further research on antioxidant drugs.

To collect the case reports of hypersensitivity reactions induced by etoposide and systematically summarize the characteristics, clinical manifestations, and treatment outcomes of hypersensitivity reactions, in order to provide corresponding reference for the safe use of etoposide.

The related case reports of hypersensitivity reactions induced by etoposide were retrieved and collected from databases such as China National Knowledge Infrastructure China Hospital Knowledge Base, Wanfang, VIP, Pubmed and Web of Science, and basic information such as patient gender, age, medication use, time of hypersensitivity reaction occurrence, and treatment outcomes was statistically analyzed as well.

A total of 27 case reports were finally included, involving 34 patients which included 21 males and 12 females and 1 patient whose gender was not mentioned. The average age of the patients was (45.83±15.50) years, with approximately 60% being over 40 years old. The majority of included cases were lung cancer patients, and the occurrence time of hypersensitivity reactions induced by etoposide was relatively short, with 18 patients experiencing hypersensitivity reactions within 1-10 minutes of medication, while only 3 patients had hypersensitivity reactions that occurred for more than 1 hour. Hypersensitivity reactions could affect many systems of the body, such as respiratory, circulatory, skin and its appendages. Common clinical manifestations of hypersensitivity reactions included difficulty breathing, chest tightness, papules, palpitations, hypotension, cyanosis; in addition, there were many serious cases such as anaphylactic shock. All cases showed improvement after treatment, and the patient did not experience any hypersensitivity reactions after receiving another infusion of etoposide, which had been pre treated with hormones or anti allergic drugs.

Hypersensitivity reactions induced by etoposide belong to immediate hypersensitivity reactions, characterized by short onset time, rapid progression, and good prognosis. In clinical practice, it is necessary to closely observe the status of patients during infusion of etoposide, strengthen medication monitoring, which can ensure the safety use of etoposide.

This study systematically evaluated its clinical efficacy and safety of ceftolozane/tazobactam for gram-negative bacterial (GNB) infections.

Clinical studies on ceftolozane/tazobactam for GNB infections were retrieved from PubMed, Embase, Cochrane Library, CNKI, VIP, and WanFang databases from inception to April 2025. Study quality was assessed using the Cochrane Risk of Bias tool and Newcastle-Ottawa Scale (NOS). Meta-analysis was performed using RevMan 5.4.1.

Twenty-two studies involving 5 728 patients were included. Ceftolozane/tazobactam demonstrated superior clinical efficacy against Pseudomonas aeruginosa infections compared to control drugs (OR=1.61; 95% CI: 1.07-2.42; I²=60%; P=0.02) and significantly higher bacterial eradication rates (OR=1.27; 95% CI: 1.05-1.55; I²=11%; P=0.01). No significant differences were observed in adverse event rates (OR=0.90; 95% CI: 0.70-1.15; I²=55%; P=0.40), serious adverse event rates (OR=0.83; 95% CI: 0.53-1.29; I²=73%; P=0.40), or all-cause mortality (OR=0.92; 95% CI: 0.78-1.10; I²=0%; P=0.37).

For GNB infections, ceftolozane/tazobactam exhibits non-inferior clinical efficacy and safety to comparator drugs with higher bacterial eradication rates. It may represent a preferred alternative for Pseudomonas aeruginosa nfections.