To analyze the clinical characteristics of patients infected with emphysematous pyelonephritis (EPN) and the drug resistance of the strains. To enhance the understanding of EPN, provide a basis for the selection of antibacterial drugs in clinical practice.

Evaluated 15 EPN patients’ clinical characteristics and outcome, analysis of pathogenic bacteria and drug resistance.

Among the 15 EPN patients, 66.67% (10 cases/15 cases) patients were cured, 13.33% (2 cases/15 cases) patients died, and 20.00% (3 cases/15 cases) patients were adverse. Fluid cultures identified 12 strains of pathogenic bacteria, with Escherichia coli being the most prevalent (66.67%, 8 cases/12 cases), followed by Klebsiella pneumoniae (25.00%, 3 cases/12 cases), and Pseudomonas aeruginosa was the least common (8.33%, 1 cases/12 cases), 75.00% (9 cases/12 cases) of the strains were multi-drug resistant. The drug sensitivity test results showed that amikacin, cefotetan, and cefoperazone sulbactam were 100.00% sensitive antibiotics; the sensitivity rates of meropenem, imipenem, and ertapenem were 91.67%.

Patients with EPN have high mortality and poor prognosis. Escherichia coli was the most common pathogenic bacteria, followed by Klebsiella pneumoniae, and the proportion of multi-drug resistant strains was high. We recommend the use of over 90% of the pathogen-sensitive drugs with susceptibility about 90% identified in this study.

To observe the clinical efficacy and safety of different doses of atorvastatin calcium tablets combined with trimetazidine hydrochloride tablets in the treatment of patients with chronic heart failure (CHF).

CHF patients were randomly assigned to low-dose group, high-dose group and control group using a digital randomization method. The control group received conventional heart failure treatment in addition to trimetazidine hydrochloride tablets (20 mg per dose, tid). The low-dose group received conventional atorvastatin calcium tablets (20 mg per dose, qd) on basis of the treatment given to the control group. The high-dose group received higher dose of atorvastatin calcium tablets (40 mg per dose, qd) in addition to the treatment for the control group. All treatment continued for 3 months. The clinical efficacy, heart function indicators, three-dimensional myocardial fibrosis parameters, myocardial cell apoptosis-related factors and safety were compared among the three groups.

A total of 8 cases were dropped during the trial, and 30 cases were included in the low-dose group, 24 cases in the high-dose group, and 26 cases in the control group. After treatment, the efficacy rates were 76.67% (23 cases/30 cases) for the low-dose group, 91.67% (22 cases/24 cases) for the high-dose group, and 61.54% (16 cases/26 cases) for the control group. The difference between the high-dose group and the control group was statistically significant (P<0.05). After treatment, the left ventricular ejection fractions for the low-dose group, high-dose group and control group were (52.25±2.11)%, (55.34±2.76)% and (48.72±2.48)%, respectively; the left ventricular end-diastolic diameters were (51.33±3.94), (48.63±4.79) and (55.79±4.85) mm, respectively; the left ventricular end-systolic diameters were (39.77±3.53), (36.72±3.29) and (42.78±3.69) mm, respectively; troponin Ⅰ levels were (1.62±0.33), (1.36±0.29) and (1.84±0.36) ng·L^-1, respectively; N-terminal pro B-type natriuretic peptide levels were (797.25±79.32), (749.20±84.65) and (854.15±90.57) pg·mL^-1, respectively; global strain values were -29.87±5.19, -32.96±5.82 and -26.33±5.46, respectively; cell membrane receptor protein levels were (2.55±0.46), (2.30±0.36) and (2.84±0.50) μg·L^-1, respectively; soluble Fas ligand levels were (0.23±0.06), (0.19±0.04) and (0.28±0.09) μg·L^-1, respectively; the differences among the three groups and between each pair of groups for the above indicators were statistically significant (P<0.05, P<0.01, P<0.001). The main adverse drug reactions in the low-dose group were gastrointestinal bloating and constipation, while the high-dose group primarily experienced constipation. The control group mainly reported nausea. The incidences of adverse drug reactions in the low-dose, high-dose and control groups were 6.67%, 4.17% and 3.85%, respectively, without statistically significant differences (all P>0.05).

The curative effect of intensive dose atorvastain calcium tablets combined with trimetazidine hydrochloride tablets in the treatment of CHF is better than that of conventional dose atorvastatin combined with trimetazidine hydrochloride tablets, and the safety is good.

To observe the analgesic effects and safety of flurbiprofen axetil injection combined with dezocine injection in postoperative patient-controlled intravenous analgesia (PCIA) for patients with intertrochanteric femoral fractures (IFF).

IFF patients were divided into control group and treatment group based on cohort method. The control group was given 0.5 mg·kg^-1 dezocine injection diluted with 100 mL of 0.9% NaCl and then injected with analgesic pump. The treatment group was given 1.0 mg·kg^-1 flurbiprofen axetil injection + 0.3 mg·kg^-1 dezocine injection diluted with 100 mL of 0.9% NaCl and then injected with analgesic pump Postoperative visual analog scale (VAS), Ramsay sedation score (RSS), mini-mental state examination (MMSE), hemodynamic parameters (heart rate, mean arterial pressure), and safety evaluations were compared between the two groups.

A total of 67 patients were enrolled in the control group; and 53 patients were enrolled in the treatment group. Postoperative VAS scores at 2, 12 and 24 h were (1.95±0.39), (2.52±0.31) and (2.21±0.40) points in the treatment group, and (2.47±0.44), (3.17±0.34) and (2.76±0.37) points in the control group. RSS scores at the same time were (3.15±0.33), (3.39±0.35) and (3.72±0.46) points for the treatment group, and (2.79±0.54), (3.16±0.43) and (3.28±0.68) points for the control group. MMSE scores at 1, 3, and 7 days postoperatively were (25.08±2.40), (26.80±2.01) and (27.64±2.59) points in the treatment group, and (22.36±2.24), (24.53±2.25) and (25.37±1.84) points in the control group. Thirty minutes after surgery, the heart rate was (86.61±4.80) beat·min^-1 in the treatment group and (82.74±4.17) beat·min^-1 in the control group, while the mean arterial pressure was (74.28±4.49) mmHg and (71.76±3.42) mmHg, respectively. These indicators in the treatment group showed statistically significant differences compared to the control group (all P<0.05). The main adverse drug reactions in the treatment group were dizziness, fatigue, drowsiness, and nausea/vomiting, while the control group also had respiratory depression in addition to dizziness, fatigue, drowsiness, and nausea/vomiting. The total incidence of adverse drug reactions was 7.55% (4 cases/53 cases) in the treatment group and 20.90% (14 cases/67 cases) in the control group, with statistically significant difference (P<0.05).

Flurbiprofen axetil injection combined with dezocine injection for postoperative PCIA in IFF patients provides superior analgesic and sedative effects compared to dezocine monotherapy, enhances cognitive function, stabilizes hemodynamics, and has good safety.

To observe the clinical efficacy and safety of general anesthesia induction with different doses of remimazolam in the vascular interventional treatment of intracranial aneurysms, and observe the safety.

The patients with intracranial aneurysms who will receive vascular interventional treatment for intracranial aneurysms were divided into low-dose group (0.2 mg·kg^-1 remimazolam), middle-dose group (0.3 mg·kg^-1 remimazolam) and high-dose group (0.4 mg·kg^-1 remimazolam) according to cohoert. The three groups completed intravenous injection of 0.2-0.4 mg·kg^-1 remimazolam. When the consciousness of patients disappeared, 10 μg·kg^-1 alfentanil and 0.2 mg·kg^-1 cisatracurium besilate were used for anesthesia induction, and 0.3-1.0 mg·kg^-1·h^-1 remimazolam+ 0.1 μg·kg^-1·min^-1 remifentanil + 0.2 mg·kg^-1·h^-1 cisatracurium besilate were applied for anesthesia maintenance. The anesthetic effect, heart rate (HR) and mean arterial pressure (MAP) during recovery period, oxidative stress indexes at different time points and, remimazolam remedy were compared among the three groups, and the safety was evaluated.

There were 27 cases in low-dose group, 28 cases in middle-dose group and 25 cases in high-dose group. The HR values at extubation in low-dose group, middle-dose group and high-dose group were (79.47±6.85), (75.84±6.71) and (72.03±5.79) beat·min^-1, HR values at 5 min after extubation were (81.92±6.59), (78.09±7.03) and (74.17±7.26) beat·min^-1, serum superoxide dismutase (SOD) levels at 24 h after surgery were (87.61±11.25), (95.49±14.02) and (103.86±15.37) U·mL^-1, serum malondialdehyde (MDA) levels were (19.69±2.74), (17.24±2.45) and (15.08±2.29) mmol·L^-1, serum catalase (CAT) levels were (66.75±8.39), (71.69±8.55) and (76.91±9.13) U·mL^-1, the onset time of sedation was (94.36±4.42), (82.29±4.15) and (75.17±5.38) s, respectively, and there were significant differences between any two groups of the three groups (all P<0.05). There were 4 cases (14.81%), 0 case and 0 case of remimazolam remedy in low-dose group, middle-dose group and high-dose group, respectively, and the index in middle-dose group and high-dose group was significantly different compared with that in low-dose group (P<0.05). In the low-dose group, there was 1 case (3.70%) of hypotension, 1 case (3.70%) of respiratory depression, and 2 cases (7.41%) of intraoperative body movement. In the middle-dose group, there was 1 case (3.70%) of hypotension, 1 case (3.57%) of bradycardia, and 1 case (3.70%) of respiratory depression. In the high-dose group, there was 1 case (4.00%) of hypotension, 2 cases (8.00%) of bradycardia, and 2 cases (8.00%) of respiratory depression. There was no statistically significant difference in the incidence of adverse drug reactions among the three groups (all P>0.05).

The induction of general anesthesia with different doses of remimazolam has a certain application effect in the vascular interventional treatment of intracranial aneurysms, and the induction of general anesthesia with high doses of remimazolam (0.4 mg·kg^-1) is the most ideal. It is not only beneficial to maintaining the stability of hemodynamics during the recovery period, and alleviating the oxidative stress response, but also shortening the onset time of sedation, reduce the number of remedial cases, and it has good safety.

To investigate the effect of arctigenin on bronchial epithelial cell injury caused by Pseudomonas aeruginosa (PA) infection and its mechanism.

BEAS-2B cells were randomly divided into control group (conventional culture), PA group (1.50×10⁸ CFU·mL^-1 PA infection), PA+ low dose group (PA combined with 10.00 mmol·L^-1 burdock aglycone), PA+ high-dose group (PA combined with 20.00 mmol·L^-1 burdock aglycone). The expression of inflammatory factors and glutathione (GSH) was detected by kit assay, glutathione peroxidase 4 (GPX4) protein was detected by Western blot assay, and lipid peroxidation levels were detected by immunofluorescence assay.

The IL-6 contents of control group, PA group, PA+ low dose group and PA+ high dose group were (20.43±2.82), (106.28±8.07), (76.66±5.73) and (50.57±3.98) pg·mL^-1, respectively; the GSH contents were (25.95±1.46), (10.59±0.60), (13.98±0.74) and (21.52±2.36) ng·mL^-1, respectively; GPX4 protein expression levels were 0.76±0.06, 0.33±0.05, 0.46±0.05 and 0.62±0.06, respectively; the lipid peroxidation levels were (100.00±4.29)%, (470.91±36.33)%, (331.16±27.04)% and (160.16±18.65)%, respectively. The above indexes in PA group compared with control group, PA+ low dose group and PA+ high dose group were compared with PA group, and the differences were all statistically significant (all P<0.01).

Arctigenin can reduce the inflammation of PA-infected BEAS-2B cells by inhibiting GPX4-related ferroptosis pathway.

To explore the effect and mechanism of circular RNA RAS p21 protein activator 2 (circRASA2) mediated by nobiletin (NOB) on lipopolysaccharide (LPS)-induced hPDLCs in periodontal ligament cells.

hPDLCs cells were divided into control group, model group (hPDLCs cells were treated with 10 μg·mL^-1 LPS for 24 h), NOB-H group (Based on the model group, 20 μmol·L^-1 NOB was given for 24 h), NOB+oe-NC group (hPDLCs cells transfected with oe-NC were treated with 20 μmol·L^-1 NOB) and NOB+oe-circRASA2 group (hPDLCs cells transfected with oe-circRASA2 were treated with 20 μmol·L^-1 NOB). Quantitative real time polymerase chain reaction was used to detect the mRNA expression levels of circRASA2. The secretion levels of inflammation-related factors were detected by enzyme-linked immunosorbent assay. Western blot analysis of slit homolog 2 (Slit2)/mitogen-activated protein kinase (MAPK) signaling pathway related protein expression levels.

The relative expression levels of circRASA2 in control group, model group and NOB-H group were 1.00±0.15, 2.83±0.50 and 1.36±0.27, respectively. The levels of interleukin-1β in control group, model group, NOB-H group, NOB+oe-NC group and NOB+oe-circRASA2 group were (144.82±24.89), (367.54±65.73), (228.51±40.24), (219.78±36.94) and (324.25±61.57) mg·mL^-1, respectively; interleukin-18 levels were (167.50±27.33), (394.68±74.96), (212.47±39.51), (205.93±41.18) and (358.11±66.27) mg·mL^-1, respectively; the relative expression levels of Slit2 protein were 1.00±0.18, 2.35±0.41, 1.61±0.29, 1.57±0.27 and 2.14±0.38, respectively; the ratios of phospho-p38 mitogen-activated protein kinase/p38 mitogen-activated protein kinase protein were 1.00±0.16, 2.08±0.37, 1.39±0.25, 1.33±0.21 and 1.92±0.34, respectively. The above indexes in the model group were compared with the control group, the NOB-H group was compared with the model group, and the NOB+oe-circRASA2 group was compared with the NOB+oe-NC group, and the differences were statistically significant (all P<0.05).

NOB alleviates LPS-induced inflammation and inhibits pyroptosis in hPDLCs cells by inhibiting circRASA2 expression, possibly by inhibiting Slit2/MAPK signaling pathway.

To investigate the effect of anemoside B4 on the malignant biological behavior of non-small cell lung cancer (NSCLC) cells mediated by microRNA-142-3p (miR-142-3p) on the expression of high mobility group protein A1 (HMGA1).

A549 cells were divided into A549 group (normal culture), anemoside B4 group (100 μg·mL^-1 anemoside B4 treatment), inhibitor NC group (100 μg·mL^-1 anemoside B4+ transfection inhibitor NC treatment), miR-142-3p inhibitor group (100 μg·mL^-1 anemoside B4+ transfected with miR-142-3p inhibitor treatment), si-NC group (100 μg·mL^-1 anemoside B4+ co-transfected with miR-142-3p inhibitor and si-NC treatment), si-HMGA1 group (100 μg·mL^-1 anemoside B4+ co-transfected with miR-142-3p inhibitor and si-HMGA1 treatment). Real-time fluorescence quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting (WB) were used to detect the expression of miR-142-3p and HMGA1. Cell proliferation, migration and apoptosis were detected by 5-acetylidene-2′-deoxyuracil riboside (Edu), Transwell and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL).

The miR-142-3p relative expression levels of A549 group, anemoside B4 group, inhibitor NC group and miR-142-3p inhibitor group were 1.00±0.14, 1.58±0.18, 1.60±0.21 and 1.12±0.16, respectively; the relative expression levels of HMGA1 protein were 1.00±0.23, 0.56±0.07, 0.59±0.08 and 0.95±0.21, respectively; the proliferation rates were (84.62±9.11)%, (62.15±7.20)%, (63.89±7.77)% and (76.35±8.11)%, respectively; the migration number was (156.23±17.54), (80.65±8.67), (82.15±8.96) and (111.55±12.75) cells, respectively; the apoptosis rates were (8.96±0.95)%, (32.56±3.56)%, (33.95±3.79)% and (16.89±1.92)%, respectively. The proliferation rates of si-NC group and si-HMGA1 group were (75.98±8.05)% and (64.52±7.25)%, respectively; the migration number was (118.85±12.98) and (86.95±9.21) cells, and the apoptosis rates were (17.58±2.02)% and (28.15±3.13)%, respectively. The above indexes in A549 group were compared with anemoside B4 group, miR-142-3p inhibitor group were compared with inhibitor NC group, si-HMGA1 group were compared with si-NC group, the differences were all with statistically significant (all P<0.05).

Anemoside B4 may inhibit proliferation and migration of NSCLC cells and promote apoptosis by regulating the miR-142-3p/HMGA1 axis.

To investigate the in vitro inhibitory effects of microRNA-28-5p (miR-28-5p) targeting G antigen 12I antibody (GAGE12I) on the proliferation, migration, and invasion of gastric cancer cells.

SGC-7901 cell were randomly divided into miR-28-5p group (miR-28-5p mimic), miR-NC group (miR-28-5p negative control mimic), shGAGE12I group (GAGE12I knockout) and blank group (GAGE12I not knockout). Cell proliferation, migration, and invasion capabilities were evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) colorimetric assay and invasion chambers. Bioinformatics analysis and luciferase activity assays were conducted to examine the interaction between miR-28-5p and GAGE12I.

The proliferation rates of miR-28-5p and miR-NC groups were (99.90±10.30)% and (48.25±4.15)%; the invasion rates were (145.57±14.52)% and (67.30±6.95)%; the mobility rates were (103.58±10.75)% and (43.18±4.26)%, respectively, the differences were statistically significant (all P<0.05). The proliferation rates of shGAGE12I group and blank group were (99.80±10.20)% and (35.50±3.58)%; the invasion rates were (142.70±13.65)% and (65.30±6.75)%; the mobility rates were (103.55±10.06)% and (48.38±4.52)%, respectively, the differences were statistically significant (all P<0.05). GAGE12I was the target of miR-28-5p.

MiR-28-5p negatively regulates GAGE12I and reduces the proliferation, invasion and migration of gastric cancer cells.

To explore the effects of aloe-emodin on the proliferation, apoptosis, and epithelial-mesenchymal transition (EMT) of pathological scar fibroblasts, as well as its regulatory mechanisms.

Proliferative scar fibroblasts (HSFb) were randomly divided into the following groups: HSFb control group (normal culture), HSFb low-dose group (25.00 μg·mL^-1 aloe-emodin), HSFb medium-dose group (50.00 μg·mL^-1 aloe-emodin), HSFb high-dose group (100.00 μg·mL^-1 aloe-emodin), and HSFb-PFT-α group (100.00 μg·mL^-1 aloe-emodin + 20.00 μmol·L^-1 p53-specific inhibitor PFT-α). Keloid fibroblast (KFb) cells were randomly divided into the following groups: KFb control group (normal culture), KFb low-dose group (25.00 μg·mL^-1 aloe-emodin), KFb medium-dose group (50.00 μg·mL^-1 aloe-emodin), KFb high-dose group (100.00 μg·mL^-1 aloe-emodin), and KFb-PFT-α group (100.00 μg·mL^-1 aloe-emodin + 20.00 μmol·L^-1 p53-specific inhibitor PFT-α). Cell viability was assessed using the cell counting kit-8 (CCK-8) assay, Western blotting was performed to detect the expression of p53 and EMT-related proteins, apoptosis was measured using the TUNEL assay.

The cell survival rates of the KFb control group, KFb low-dose group, KFb medium-dose group, and KFb high-dose group were (100.00±5.17)%, (84.13±8.34)%, (73.81±7.62)% and (54.59±3.47)%, respectively; the cell survival rates of the HSFb control group, HSFb low-dose group, HSFb medium-dose group, and HSFb high-dose group were (100.00±6.77)%, (83.50±6.08)%, (71.43±2.70)% and (61.80±4.79)%, respectively. The relative expression levels of p53 protein in the KFb control group, KFb low-dose group, KFb high-dose group, and KFb-PFT-α group were 0.31±0.04, 0.52±0.04, 0.76±0.06 and 0.38±0.05, respectively; the relative expression levels of E-cadherin protein were 0.35±0.04, 0.58±0.08, 0.76±0.13 and 0.41±0.06, respectively; the apoptosis rates were (4.82±0.59)%, (11.72±1.68)%, (20.36±1.93)% and (12.46±1.28)%, respectively; the relative expression levels of p53 protein in the HSFb control group, HSFb low-dose group, HSFb high-dose group, and HSFb-PFT-α group were 0.37±0.03, 0.48±0.05, 0.65±0.07 and 0.46±0.04, respectively; the relative expression levels of E-cadherin protein were 0.26±0.03, 0.46±0.05, 0.63±0.08 and 0.34±0.05, respectively; the apoptosis rates were (4.89±0.28)%, (13.98±0.83)%, (21.51±1.08)% and (12.95±1.10)%, respectively. The differences between the KFb low- and high-dose groups and the KFb control group, the KFb-PFT-α group and the KFb high-dose group, the HSFb low- and high-dose groups and the HSFb control group, and the HSFb-PFT-α group and the HSFb high-dose group were statistically significant (P<0.05, P<0.01, P<0.001).

Aloe-emodin may inhibit the proliferation of pathological fibroblasts, EMT, and induce apoptosis by regulating the p53-related signaling pathway.

To investigate the mechanism of quercetin in promoting muscle regeneration in acute skeletal muscle injury.

Satellite cells were randomly divided into blank group (conventional culture), hydrogen peroxide (H₂O₂) group (100 μmol·L^-1 H₂O₂ treated cells for 24 h), quercetin group (10 μmol·L^-1 quercetin treated cells for 24 h), H₂O₂+quercetin group (100 μmol·L^-1 H₂O₂+10 μmol·L^-1 quercetin treated cells for 24 h). Cell proliferation was detected by cell counting kit-8 (CCK-8) method; protein expression was detected by Western blot assay; mitochondrial reactive oxygen species (ROS) levels and related indicators of mitochondrial respiration were detected by kit.

The 24 h proliferation rates of cells in blank group, quercetin group, H₂O₂ group and H₂O₂+quercetin group were (100.00±4.27)%, (148.79±13.17)%, (81.70±3.19)% and (120.83±8.81)%, respectively; the relative expression levels of superoxide dismutase 1 (SOD1) protein were 0.64±0.09, 0.76±0.09, 0.24±0.03 and 0.43±0.06, respectively; the relative expression levels of myosin heavy chain (MyHC) protein were 0.61±0.05, 0.67±0.06, 0.32±0.03 and 0.47±0.06, respectively; the fluorescence intensities of mitochondrial ROS were (52.56±1.97), (48.46±4.05), (119.53±13.06) and (102.91±8.93) a.u., respectively; the catalase (CAT) levels were (28.66±2.18), (35.62±3.89), (18.13±1.78) and (23.97±2.72) μmol·mg protein^-1, respectively; mitochondrial respiratory chain (MRC) complex Ⅰ levels were (19.77±1.01), (23.28±2.48), (9.87±1.01) and (14.19±0.75) μmol·mg protein^-1, respectively. The above indexes in quercetin group and H₂O₂ group were compared with blank group, the above indexes in H₂O₂+quercetin group were compared with H₂O₂ group, the difference was statistically significant (P<0.05, P<0.01, P<0.001).

Quercetin can promote mitochondrial respiration by clearing mitochondrial ROS levels, improve oxidative damage, and then promote satellite cell proliferation, which can promote muscle regeneration in acute skeletal muscle injury.

To investigate the effect of ganoderma lucidum polysaccharides (GLPS) on ferroptosis of hippocampal neuronal (HT22) cell lines induced by hydrogen peroxide (H₂O₂) and its mechanism.

The H₂O₂-induced HT22 cell injury model was first established in vitro. HT22 cells were divided into normal group (conventional culture), H₂O₂ group (200 μmol·L^-1 H₂O₂), GLPS group (200 μmol·L^-1 H₂O₂+100 μg·mL^-1 GLPS), H₂O₂+Fin56 group (200 μmol·L^-1 H₂O₂+5 μmol·L^-1 Fin56), H₂O₂+Fin56+GLPS group (200 μmol·L^-1 H₂O₂+5 μmol·L^-1 Fin56+100 μg·mL^-1 GLPS). The oxidative stress markers were detected by enzyme-linked immunosorbent assay (ELISA); the protein expression levels of iron death markers, nuclear factor erythroid2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were detected by Western blot.

The contents of malondialdehyde (MDA) in normal group, H₂O₂ group, GLPS group, H₂O₂+Fin56 group and H₂O₂+Fin56+GLPS group were (5.56±0.61), (15.53±0.83), (6.51±0.29), (20.92±1.03) and (13.65±0.70) nmol·mL^-1; the contents of superoxide dismutase (SOD) were (37.93±1.37), (22.48±0.59), (37.81±2.56), (16.10±2.28) and (22.21±2.99) μg·mL^-1; Ferritin protein expression levels were 1.52±0.03, 1.22±0.07, 1.42±0.06, 0.64±0.02 and 0.93±0.13; GPX4 protein expression levels were 3.29±0.34, 1.91±0.18, 2.99±0.22, 1.13±0.07 and 2.45±0.05; Nrf2 protein expression levels were 0.90±0.01, 2.24±0.02, 2.97±0.07, 2.45±0.07 and 2.76±0.11; HO-1 protein expression levels were 1.58±0.02, 1.76±0.04, 2.29±0.06, 1.67±0.02 and 2.03±0.06, respectively. H₂O₂ group was compared with normal group and H₂O₂+Fin56 group, GLPS group was compared with H₂O₂ group, H₂O₂+Fin56+GLPS group was compared with H₂O₂+Fin56 group and GLPS group, the differences were statistically significant (P<0.05, P<0.01).

GLPS can improve lipid peroxide accumulation and iron metabolism disorder induced by H₂O₂ in HT22 cells by activating Nrf2/HO-1 pathway, thereby inhibiting the occurrence of ferroptosis.

To investigate the effects of sodium aescinate on the differentiation of human umbilical cord mesenchymal stem cells (HUMSC) into neural-like cells and its possible mechanism.

HUMSC cells were randomly divided into blank group, experiment-L group, experiment-M group and experiment-H group. All the cells were cultured with neurobasal medium (NM) medium, cells in experiment-L group, experiment-M group and experiment-H group were treated with 1.00, 2.00 and 4.00 mg·L^-1 sodium aescinate, respectively. The expression levels of neuron-like cells markers and synaptic markers were detected by reverse transcription-polymerase quantitative chain reaction (RT-qPCR) and Western blot.

The relative mRNA expression levels of microtubule-associated protein 2 (MAP-2) in blank group, experiment-L group, experiment-M group and experiment-H group were 1.00±0.14, 1.26±0.08, 1.74±0.16 and 2.30±0.20, respectively; the relative mRNA expression levels of growth associated protein 43(GAP43) were 1.00±0.10, 1.14±0.15, 1.34±0.15 and 1.53±0.11, respectively; the relative expression levels of synaptophysin(SYN) mRNA were 1.00±0.09, 1.15±0.08, 1.32±0.12 and 1.48±0.13, respectively; the expression levels of neurofilament heavy chain(NF-H) protein were 0.41±0.04, 0.50±0.06, 0.71±0.06 and 1.21±0.09, respectively; postsynaptic density protein 95(PSD95) protein expression levels were 0.27±0.04, 0.41±0.06, 0.52±0.04 and 0.68±0.06, respectively; silent information regulator 1(SIRT1) protein expression levels were 0.31±0.04, 0.52±0.06, 0.67±0.06 and 0.80±0.10, respectively. The above indexes in experiment-L group, experiment-M group and experiment-H group were compared with blank group, the differences were all statistical significant (P<0.05, P<0.01); the above indexes compared among experiment-L group, experiment-M group and experiment-H group, the differences were all statistically significant (P<0.05, P<0.01).

Sodium aescinate may induce the differentiation of HUMSC into neural-like cells by regulating SIRT1 in vitro.

To explore the omalizumab via microRNA (miR)-26a-5p reduced the inflammasome, or the NOD-like receptor themal domain associated protein 3 (NLRP3) mediated pyroptosis on airway remodeling in asthmatic rats, based on the inhibition of the Toll-like receptor 4 (TLR4)/myeloid differentiation primary response protein 88 (MyD88)/nuclear factor kappa-B (NF-κB) signaling pathway.

Fifty SD rats were divided into control group, model group, omalizumab group, omalizumab+agomir NC group and omalizumab+miR-26a-5p agomir group, with 10 rats in each group. The control group was intraperitoneally injected with 0.9% NaCl; the model group established the asthma model; the omalizumab group was intraperitoneally injected with 100 mg·kg^-1·d^-1 omalizumab daily on the basis of model group; the omalizumab + agomir NC group received tail vein injection of agomir NC on the basis of the omalizumab group; the omalizumab+ miR-26a-5p agomir group received tail vein injection of miR-26a-5p agomir on the basis of omalizumab group. Hematoxylin-eosin (HE) staining was used to observe the pathological changes of lung tissue; enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of inflammatory factors; real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR) and fluorescence in situ hybridization (FISH) were used to detect the expression of miR-26a-5p; Western blotting (WB) was used to detect the pyroptosis and TLR4/MyD88/NF -κB pathway-related proteins expression levels.

The tube wall thickness in control group, model group and omalizumab group were (35.16±2.95), (52.94±4.63) and (44.07±3.78) μm; interleukin-13 (IL-13) levels were (18.23±3.94), (61.84±10.94) and (34.23±6.11) pg·mL^-1; interferon gamma (IFN-γ) levels were (68.43±11.59), (22.94±4.70) and (43.10±8.04) pg·mL^-1; miR-26a-5p mRNA were 1.00±0.15, 2.26±0.31 and 1.37±0.19. The relative expression levels of NLRP3 in control group, the model group, the omalizumab group, the omalizumab +agomir NC group and omalizumab+miR-26a-5p agomir group were 1.00±0.11, 3.21±0.47, 1.77±0.24, 1.69±0.27 and 2.53±0.38; the relative expression levels of TLR4 were 1.00±0.13, 2.54±0.39, 1.86±0.39, 1.90±0.30 and 2.24±0.34; the relative expression levels of MyD88 were 1.00±0.15, 1.97±0.26, 1.44±0.21, 1.41±0.18 and 1.69±0.23; the relative expression levels of NF-κB were 1.00±0.12, 2.88± 0.37, 1.83±0.29, 1.77±0.25 and 2.54±0.41, respectively. The differences of the above indexes were statistically significant when compared the model group with the control group, the omalizumab group with the model group, and the omalizumab+miR-26a-5p agomir group with the omalizumab+agomir NC group (P<0.05, P<0.01).

Omalizumab may reduce NLRP3 inflammasome-mediated pyroptosis by inhibiting the activation of TLR4/MyD88/NF-κB pathway, thus achieving omalizumab inhibited airway remodeling and improved lung function in bronchial asthmatic rats.

To explore the effect of fingolimod (FTY720) on depressive behavior in depressive disorder rats and its related mechanism.

The SD rats were divided into the following groups: Control group (normal feeding), model group (depression model construction), and low, medium, high groups (administering 0.1, 0.3 and 1.0 mg·kg^-1 FTY720 prior to constructing the depression model, respectively), with 10 rats in each group. The hippocampal tissue morphology was assessed using hematoxylin-eosin (HE) staining; depression symptoms were evaluated through the sucrose preference test; cognitive function was assessed using the Morris water maze test; neuronal apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL); levels of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome pathway-related proteins were measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and immunofluorescence; dopamine (DA) content in different brain regions was analyzed by high-performance liquid chromatography.

After different treatments, the sugar-water preference rates in control, model and low, medium, high groups were (81.95±9.06)%, (59.72±8.32)%, (62.34±7.58)%, (68.08±7.94)% and (79.61±9.25)%, respectively; the escape latencies were (18.73±2.06), (34.25±3.87), (31.64±2.92), (25.97±2.43) and (19.86±1.95) s, respectively; apoptosis rates were (3.93±0.65)%, (28.75±5.94)%, (24.63±3.21)%, (15.27±2.58)% and (6.08±1.74)%, respectively; NLRP3 mRNA relative expression levels were 1.00±0.17, 4.89±0.64, 4.31±0.72, 2.52±0.58 and 1.87±0.25; ASC mRNA relative expression levels were 1.00±0.14, 2.67±0.53, 2.28±0.39, 1.54±0.26 and 1.39±0.21; DA contents in PFC region were (795.42±64.38), (547.93±52.65), (571.08±51.97), (662.45±73.89) and (748.96±81.53) μg·g^-1; DA contents in NAc region were (2 186.53±124.97), (1 672.84±109.25), (1 769.65±112.14), (1 904.27±106.63) and (2 065.92±127.58) μg·g^-1; DA contents in the VTA region were (1 765.83±108.29), (1 316.73±115.84), (1 378.52±94.36), (1 494.76±103.21) and (1 653.94±108.45) μg·g^-1. Compared with the control group, the above indexes in the model group were statistically significant (all P<0.001). Compared with the model group, the above indexes in the middle dose group were statistically significant (all P<0.05). Compared with the model group, the above indexes in the high dose group were statistically significant (all P<0.001).

FTY720 can regulate neuronal damage and cognitive function in depressed model rats, and its antidepressant mechanism may be related to inhibiting the activation of NLRP3 inflammasome pathway and increasing the content of DA in the neural circuit of PFC-ARC-VTA.

To investigate the mechanism of action of bezafibrate (BEZ) targeting nuclear factor of activated T cells 5 (NFAT5) through microribonucleic acid (miR)-486-5p on the kidney tissues of mice with diabetic nephropathy.

Db/m mice were used as control group. Db/db mice were used to construct a diabetic nephropathy model, which was divided into 4 groups according to the random number table method: Model group, experimental group (75 mg·kg^-1·d^-1 BEZ), miR-486-5p antagomir group (75 mg·kg^-1·d^-1 BEZ+10 mg·kg^-1 miR-486-5p antagomir), sh-NFAT5 group (75 mg·kg^-1·d^-1 BEZ+10 mg·kg^-1 miR-486-5p antagomir+recombinant adenovirus containing NFAT5 knockdown plasmid). The kit was used to detect the levels of renal function and oxidative stress in mice; and the expression levels of glucose metabolism and renal fibrosis-related proteins in renal tissues of mice in each group were detected by Western blot.

The levels of malondialdehyde (MDA) in the control group, model group, experimental group, miR-486-5p antagomir group, and sh-NFAT5 group were (2.78±0.56), (4.96±0.97), (3.02±0.54), (4.51±0.79) and (3.24±0.58) nmol·mg^-1, respectively; the levels of aldose reductase (AR) were 1.00±0.12, 3.61±0.43, 1.82±0.29, 3.09±0.58 and 2.25±0.47, respectively; the levels of pyruvate dehydrogenase (PDH) were 1.00±0.11, 0.53±0.10, 0.91±0.15, 0.64±0.12 and 0.82±0.14, respectively; the levels of pyruvate dehydrogenase E1 subunit α1 (PDHA1) were 1.00±0.14, 0.36±0.07, 0.83±0.16, 0.51±0.11 and 0.74±0.13, respectively; the levels of pyruvate dehydrogenase kinase (PDK) were 1.00±0.10, 2.59±0.52, 1.34±0.31, 2.11±0.43 and 1.56±0.39, respectively; the levels of transforming growth factor-β1 (TGF-β1) were 1.00±0.11, 3.15±0.52, 1.43±0.38, 2.72±0.43 and 1.89±0.57, respectively; the levels of fibronectin (FN) were 1.00±0.09, 2.84±0.57, 1.46±0.41, 2.59±0.52 and 1.73±0.49, respectively; the levels of collagen type I (Collagen I) were 1.00±0.13, 4.28±0.71, 2.03±0.46, 3.64±0.68 and 2.51±0.53, respectively. The above indicators of the control group were compared with the model group, the above indicators of the model group were compared with the experimental group, the above indicators of the experimental group were compared with the miR-486-5p antagomir group, and the above indicators of the miR-486-5p antagomir group were compared with the sh-NFAT5 group. The differences were statistically significant (P<0.05, P<0.01, P<0.001).

BEZ can effectively protect the kidney tissue of mice with diabetic nephropathy, and the mechanism may be realized through the miR-486-5p/NFAT5 signaling pathway.

To explore the mechanism of tacrolimus mediating the protective effect on chronic glomerulonephritis (CGN) rats through regulating the expression of microRNA-145-5p (miR-145-5p) and modulating the C-X-C motif chemokine ligand 16/Ras homolog family member A/Rho-associated coiled-coil-containing protein kinase (CXCL16/RhoA/ROCK) pathway.

SD rats were randomly divided into the control group (administered an equal volume of 0.9% NaCl), model group (CGN model + equal volume of 0.9% NaCl), experimental group (CGN model + 3 mg·kg^-1·d^-1 tacrolimus) and combined group (experimental group + tail vein injection of 140 nmol·L^-1 miR-145-5p antagomir). Enzyme-linked immunosorbent assay was used to measure 24-hour urinary protein (PRO), blood urea nitrogen (BUN), and serum creatinine (SCr) levels. Real-time quantitative polymerase chain reaction was used to detect the relative expression level of miR-145-5p in rat kidney tissue; Western blotting was used to determine protein expression levels.

The 24-hour PRO levels in the control, model and experimental groups were (7.44±2.16), (85.29±17.35) and (49.81±9.52) mg, respectively; the BUN levels were (5.82±1.03), (9.65±1.78) and (6.97±1.14) mmol·L^-1, respectively; the SCr levels were (46.31±7.69), (93.57±16.94) and (58.72±8.36) μmol·L^-1, respectively. The relative expression levels of miR-145-5p in the control, model, experimental and combined groups were 1.00±0.14, 0.56±0.07, 0.83±0.12 and 0.68±0.09, respectively; the TNF-α levels were (116.42±14.53), (237.56±26.18), (164.79±18.35) and (205.12±21.64) pg·mL^-1, respectively; the IL-1β levels were (15.76±1.84), (52.41±6.27), (21.35±2.92) and (43.63±4.58) pg·mL^-1, respectively; the IL-6 levels were (26.28±3.47), (71.53±8.64), (38.92±5.06) and (59.78±6.21) pg·mL^-1, respectively; the CXCL16 expression levels were 1.00±0.12, 1.62±0.17, 1.23±0.14 and 1.45±0.15, respectively. Statistical analysis revealed significant differences between the model group and the control group, between the experimental group and the model group, and between the combined group and the experimental group for these indicators (P<0.05, P<0.01, P<0.001).

Tacrolimus can upregulate miR-145-5p, activate the CXCL16/RhoA/ROCK pathway, reduce inflammatory factors, and improve kidney damage in CGN rats.

To investigate the mechanism of soyisoflavones (SIF) alleviate the rats with polycystic ovary syndrome (PCOS) by regulating the miR-29a-3p/insulin-like growth factor 1 (IGF1) molecular axis.

The female SD rats were divided into normal, model and experimental groups, with 12 rats in each group. The model and experimental groups were induced with gavage letrozole to construct the PCOS rat model. After successful modeling, the normal and model groups were given 100 mg·kg^-1 cellulose sodium carboxymethyl by gavage, and the experimental group was given 100 mg·kg^-1 SIF by gavage. Three groups were treated for 21 d with once a day. The apoptosis rate of ovarian tissues was detected by TdT-mediated dUTP nick-end labeling, the serum sex hormone levels were detected by enzyme-linked immunosorbnent assay, the expression levels of miR-29a-3p and IGF1 were detected by real-time fluorescence quantitative plymerase chain reaction, and the positive expression level of IGF1 was detected by immunohistochemistry in ovarian tissues. Ovarian granulosa cells from PCOS model rats were divided into blank group (normal culture), experimental group (100 μg·L^-1 SIF), miR-29a-3p group (after transfection with miR-29a-3p inhibitor, 100 μg·L^-1 SIF culture was given) and IGF1 group (after transfection with miR-29a-3p inhibitor and si-IGF1, 100 μg·L^-1 SIF culture was given). Apoptosis of ovarian granulosa cells was measured by mitochondrial membrane potential analysis, and the expression level of apoptosis-related proteins was detected by Western blotting.

In the animal experiments, the apoptosis rates of experimental, model and normal groups were (16.14±4.09)%, (23.75±5.68)% and (10.83±3.54)%; the luteinizing hormone levels were (26.81±5.99), (41.55±9.84) and (17.63±3.19) mU·mL^-1; the follicle stimulating hormone levels were (51.09±8.72), (41.66±9.87) and (67.91±18.58) pg·mL^-1; the relative expression levels of miR-29a-3p were 0.89±0.08, 0.47±0.06 and 1.00±0.11; the relative expression levels of IGF1 mRNA were 1.42±0.39, 2.36±0.54 and 1.00±0.07; the positive expression levels of IGF1 were 1.37±0.31, 1.98±0.41 and 1.00±0.12, respectively. The differences of above indexes in the experimental and normal groups were statistically different from those in the model group (all P<0.05). In the cell experiments, the mitochondrial membrane potentials of the experimental, miR-29a-3p, IGF1 and blank groups were 1.28±0.13, 0.66±0.05, 1.47±0.19 and 0.54±0.06; the relative expressions levels of the B-cell lymphoma-2-associated X protein were 0.73±0.06, 0.97±0.11, 0.62±0.07 and 1.00±0.08; the relative expression levels of B-cell lymphoma-2 were 1.74±0.23, 1.14±0.18, 2.11±0.37 and 1.00±0.05, respectively. The differences of above indexes in the experimental and IGF1 groups were statistically different from those in the miR-29a-3p group (all P<0.05).

SIF may delay the progression of PCOS rats by regulating miR-29a-3p/IGF1 pathway to mediate the apoptotic process in ovarian cells.

To investigate the possible mechanism of action of sinomenine (Sin) in the treatment of collagen-induced arthritis (CIA) rats by regulating macrophage polarization.

Wistar rats were randomly divided into control group (normal diet and care), model group (CIA model was established with bovine type Ⅱ collagen at the tail), experimental-L, -M, -H groups (all on the basis of the model group, 40, 80 and 160 mg·kg^-1 Sin by gavage respectively), inh-NC group and inh-miR-885-5p group[on the basis of the experimental-H group, the two groups were injected with a negative control of microRNA-885-5p (miR-885-5p) and miR-885-5p inhibitor in the tail vein, respectively)], for four weeks, with 10 rats in each group. The arthritis index (AI) and plantar swelling of rats in each group were statistically analyzed. The pathological conditions of the synovial tissue of the ankle joint were observed by hematoxylin-eosin staining. Real-time fluorescent quantitative polymerase chain reaction was performed to examine the relative expression level of miR-885-5p in rat synovial tissue. Western blot was carried out to detect the expression of related proteins in the synovial tissue of rats. Enzyme-linked immunosorbent assay was used to detect the level of serum inflammatory factors. Terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) was used to detect the apoptosis of rat synovial cells.

The AI scores of the control group, model group and experimental-H group were 0, (7.20±1.38) and (5.50±1.10) scores, respectively; the paw swelling were 35.32±7.05, 72.46±14.47 and 51.65±10.31, respectively; the relative expression levels of miR-885-5p were 1.00±0.18, 0.52±0.10 and 0.71±0.14, respectively. The relative expression levels of suppressor of cytokine signaling 1 (SOCS1) protein in the control, model group, experimental-H group, inh-NC group and inh-miR-885-5p group were 1.00±0.18, 0.51±0.10, 0.75±0.15, 0.71±0.14 and 0.55±0.11, respectively; the levels of interleukin (IL)-6 were (35.29±7.05), (215.82±43.15), (121.33±24.25), (115.62±23.08) and (207.39±41.36) pg·mL^-1, respectively; the apoptosis rates were (31.47±6.29)%, (12.19±2.43)%, (22.03±4.41)%, (20.16±4.03)% and (13.37±2.66)%, respectively. The above indexes in the experimental-L, -M, -H groups were dose-dependent, and the differences in the above indexes between the experimental-H group and the control group were statistically significant compared with the model group (P<0.05, P<0.01, P<0.001), and the differences in the above indexes between the inh-miR-885-5p group and the inh-NC group were also all statistically significant (all P<0.05).

Sin can regulate macrophage polarization, and improve synovial inflammation in CIA rats, which may be related to the up-regulation of miR-885-5p expression and activation of SOCS1/signal transducer and activator of transcription 3 (STAT3) signaling pathway.

To evaluate the bioequivalence of rotigotine patches after a single dose in healthy Chinese subjects.

Using randomized, open, fasting, single-dose, two-preparation, four-cycle, two-sequence exact repeat crossover design, 24 healthy subjects applied one of the test preparation or reference preparation (4.5 mg·10 cm^-2) to the abdominal skin. To determine the drug concentration in human plasma by liquid chromatography-tandem mass spectrometry. Pharmacokinetic software was used to calculate the relevant pharmacokinetic parameters, and the bioequivalence evaluation was carried out.

The C_max of the test preparation and the reference preparation of rotigotine patches were (275.04±98.93) and (277.11±96.78) pg·mL^-1, the AUC_0-t were (5 011.91±2 015.32) and (4 934.28±2 095.76) h·pg·mL^-1, the AUC_0-∞ were (5 092.68±2 033.23) and (5 160.61±2 052.04) h·pg·mL^-1, respectively. C_max, AUC_0-t and AUC_0-∞ geometric mean (90% confidence interval) were all in the equivalent interval of 80.00%-125.00%.

The test preparation and reference preparation of rotigotine patches are bioequivalent in healthy Chinese subjects.

To establish a method for the determination of carfilzomib in rat plasma by high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS), and to investigate the pharmacokinetic characteristics of carfilzomib in rat plasma.

The rat plasma samples were processed by a protein precipitation approach using methanol∶acetonitrile (1∶1, v/v). Chromatographic column: Thermo Scientific^TM Hypersil GOLD^TM C₁₈ Column (2.1 mm×50.0 mm, 3 μm); mobile phase: 2 mmol·L^-1 ammonium acetate-0.02% formic acid water (A)-methanol (B) in gradient elution mode; flow rate: 0.45 mL·min^-1; injection volume: 5 μL. Electrospray ionization source in positive ion mode and multiple reaction monitoring were adopted. The specificity, standard curve and lower limit of quantification, residue effect, precision and extraction recovery rate, dilution reliability, matrix effect and stability of this method were examined. After a single intravenous injection of 4 mg·kg^-1 carfilzomib into 6 healthy male SD rats, blood was collected from the inner corner of the eye, and the concentration of carfilzomib in the plasma was detected. The pharmacokinetic parameters were calculated using DAS 3.0.

Carfilzomib exhibited good specificity and linearity within the range of 0.5 to 1 250.0 ng·mL^-1, with a standard curve of y=2.40×10^-2x+6.81×10^-2 (r=0.996 4), the quantitative limit of detection was 0.5 ng·mL^-1, the sample residues were 7.64% and 1.00% of the quantitative limit of detection and the internal standard, respectively, the intra-day and inter-day precision were ≤7.51% and ≤8.16%, respectively, the intra-day and inter-day accuracy were -4.54% to 5.14% and -4.41% to 8.26%, respectively, the extraction recovery were 92.49% to 108.33%, and the methodological evaluation results of sample dilution effect, matrix effect and stability were all in accordance with the requirements for the validation of biological sample analysis methods. The main pharmacokinetic parameters of carfilzomib were: C_max was (1.10×10⁶±5.45×10⁵) ng·L^-1, t_1/2 was (23.10±7.38) min, AUC_0-t was (1.85×10⁷±9.85×10⁶) ng·L^-1·min.

The approach formulated in this study is operationally facile, highly discriminatory, sensitive, precise, dependable, and is appropriate for the determination and analysis of carfilzomib in rat plasma specimens.

To devolope a liquid chromatography-tandem mass spectrometry (LC-MS/MS) method for the determination of furmonertinib in human plsama and apply this method to analyze the blood concentration of non-small cell lung cancer (NSCLC) patients after taking medicine.

Furmonertinib -d3 was employed as the internal standard. The analyte and internal standard were extracted from plasma by protein precipitation with acetonitrile and chromatographed on Agilent Poroshell 120 SB-C₁₈(2.1 mm×100.0 mm, 3.5 μm); mobile phase consisted of acetonitrile-10 mmoL^-1 ammonium acetate(both of containing 0.1% formic acid); the whole analytical time was 3 min. The quantitative analysis were ionized with an electrospray ionization (ESI) source and operated in positive ion, multiple reaction monitoring (MRM) mode, the specificity, linear range, precision and accuracy, extraction recovery rate, matrix effect, dilution validation, and stability were all investigated.

The standard curves were demonstrated to be liner in the range of 0.50-100.00 μg·L^-1 with y=3.95×10^-2x-4.16×10^-4 (r=0.995 4). The accuracy was 95.8%-107.3%. The coefficient of variation (CV) of inter-day (n=6) and intra-day (n=3) for four different concentration levels were less than 15%. The average recoveries and matrix effects were between 83.1%-88.2% and 94.6%-105.8%.

The established LC-MS/MS method for determining the concentration of vormetinib meets the requirements of biological sample analysis and can be used for the concentration determination of vormetinib in clinical practice.

To establish a quantitative analysis method for serum vitamin D (VD) based on liquid chromatography-tandem mass spectrometry (LC-MS/MS) and evaluate its clinical application value in pediatric nutritional support.

Serum samples were processed with acetonitrile, using 25-hydroxyvitamin D₂-d₆ (25-OH-VD₂-d₆) and 25-hydroxyvitamin D₃-d₆ (25-OH-VD₃-d₆) as internal standards. The chromatographic column was Kinetex C18 (50.0 mm × 3.0 mm, 2.6 μm). The mobile phase consisted of 0.1% formic acid aqueous solution and 0.1% formic acid methanol solution, with gradient elution at a flow rate of 0.5 mL·min^-1 and an injection volume of 10 μL. The column temperature was set to 30 ℃. Electrospray ionization was used in positive ion mode, with multiple reaction monitoring. The LC-MS/MS method was evaluated for specificity, calibration curves, lower limits of quantification, precision, recovery rate, stability, and matrix effects. The method was applied to detect VD levels in the serum of infants from the external group (oral 10 μg·kg^-1 VD drops, qd) and the parenteral group [parenteral nutrition solution with injectable fat-soluble vitamin (Ⅰ) administered intravenously, it was equivalent to 10 μg·mL^-1 VD, qd].

Both 25-OH-VD₂ and 25-OH-VD₃ showed good linearity in the range of 5-100 ng·mL^-1, with the 25-OH-VD₂ standard curve of y=1.00x+2.34×10^-2 (R=0.999 8), and a lower limit of quantification (LLOQ) of 0.5 ng·mL^-1; 25-OH-VD₃ standard curve of y=1.00x+5.6×10^-3 (R=0.999 8), and LLOQ of 1 ng·mL^-1. The recovery rate of 25-OH-VD₂ quality control samples was 95.59%-105.38%, with intra- and inter-day precision ≤ 4.75% and ≤ 4.68%, respectively. The recovery rate of 25-OH-VD₃ was 98.38%-113.63%, with intra- and inter-batch precision ≤5.64% and ≤7.83%, respectively. Stability of 25-OH-VD₂ and 25-OH-VD₃ samples at different concentrations was good under various conditions, with matrix effects ranging from 85%-110% and 88%-112%, respectively. After enteral or parenteral VD supplementation, the serum levels of 25-OH-VD₂ and 25-OH-VD₃ in both groups of preterm infants significantly increased, with the parenteral group showing significantly higher concentrations of 25-OH-VD₂ and 25-OH-VD₃ compared to the enteral group (P<0.05). The daily weight gain rate of preterm infants in the parenteral group was also significantly higher than those in the enteral group (all P<0.05).

The quantitative analysis method of serum VD based on LC-MS/MS has strong specificity and high sensitivity, which is suitable for the monitoring of VD level in premature infants.

To evaluate the efficacy, safety, and economy of trastuzumab emtansine (T-DM1) in the treatment of human epidermal growth factor receptor 2(HER2)-positive metastatic breast cancer based on the rapid health technology assessment methodology, and to provide a reference for the rational use of the drug in the clinic.

A systematic search of Chinese and English databases such as PubMed, Embase, the Cochrane Library, CNKI, Wanfang, SinoMed, etc. was performed to screen the literature according to the inclusion and exclusion criteria, extract the data, evaluate the quality of the literature, and qualitatively analyze the results.

T-DM1 had comparable or even superior efficacy in terms of progression-free survival (PFS) and overall survival (OS) compared with conventional anti-HER2 treatment regimens as well as other chemotherapeutic regimens. Some regimens, such as docetaxel+trastuzumab+patuximab, and pyrrolitinib+capecitabine, might be superior to T-DM1 in terms of PFS and OS. Adverse effects of T-DM1 were mainly liver function abnormalities and thrombocytopenia, and overall the safety profile was better, with a lower probability of serious adverse effects. In terms of economy, T-DM1 was more favorable than T-Dxd, and further evaluation was still needed compared with other regimens.

T-DM1 has favorable efficacy and safety, with economics to be further evaluated.

To explore the design and application of digital intelligence quality control technology in drug clinical trials, aiming to improve the quality and efficiency of these trials.

Based on the characteristics and requirements of quality control in drug clinical trials, a digital intelligence quality control model was designed and applied throughout the entire process of drug clinical trials. The system’s performance and security were evaluated.

The digital intelligence quality management system can significantly enhance the accuracy and completeness of clinical trial data, improve the efficiency of drug clinical trials, and strengthen real-time monitoring capabilities to ensure compliance and safety of the trials.

The digital intelligence quality management system can optimize resource allocation, shorten trial duration, and reduce overall costs. It provides new perspectives and methodologies for quality control in drug clinical trials, laying a reliable foundation for the digital transformation of the biopharmaceutical industry.

To investigate prescription of semaglutide and analyzed status of semaglutide administration in China’s real-world.

The prescription including semaglutide were extracted from 9 cities across China in first quarter of 2023. We analyzed the current administration of semaglutide and risk factors of off-label use of semaglutide by multivariant logistic regression.

A total of 10 884 patients were included after data screening, about 70% patients were 34-64 years old. Endocrinology was the most common prescription department. Diabetes was diagnosed in 76.78% patients and 765 patients combined chronic complications of diabetes, of which diabetic neuropathy (470 cases, 4.32%) and diabetic nephropathy (248 cases, 2.28%) were the most common complications. Cardiovascular diseases and risk factors were diagnosed in 2 429 patients. Hypertension (1 379 cases, 12.67%) and hyperlipemia (1 342 cases, 11.31%) were the most common cardiovascular disease and risk factors. While 56.74% (6 176 cases) patients were treated by semaglutide singe-agent in general, 36.79% (3 075 cases/ 8 357 cases) patients with diabetes combined oral hypoglycemic drugs or insulin, and biguanides and sodium-dependent glucose transporters 2 inhibitors were used mostly. About 1/4 patients without diabetes off-label administrated semaglutide. According to the logistic regression, risk factors of off-label use were elder age, came from first-tier cities, prescription from endocrinology and a greater number of combined cardiovascular diseases and risk factors.

Semaglutide -based therapy regimens in patients with diabetes are fairly standardized according to clinical guidelines, while off-label use in patients without diabetes are supported by clinical evidence and guidelines to some extent.