To observe the influence of propofol injection emulsion combined with esketamine injection on hemodynamics and postoperative recovery quality in elderly patients after lower limb arthroplasty.

The elderly patients undergoing lower limb joint replacement were divided into low-dose group (0.25 mg·kg^-1 esketamine), high-dose group (0.50 mg·kg^-1 esketamine) and control group (equal volume of 0.9% NaCl) according to the cohort method. Hemodynamics [heart rate (HR), mean arterial pressure (MAP)], postoperative recovery quality scale-15 (QoR-15) scores, dosages of anesthetic drugs, Ramsay sedation score, recovery quality and adverse reactions were compared among the three groups.

In this study, 39 cases were enrolled in the low-dose group, 40 cases in the high-dose group and 42 cases in the control group. The HR of patients in low-dose group, high-dose group and control group immediately after operation (T1) was (76.39±5.77), (77.16±5.24) and (73.21±4.79) beat·min^-1, respectively; MAP values were (85.11±5.22), (85.21±5.37) and (82.79±4.86) mmHg, respectively; at 15 min after operation, the HR of T2 were (78.36±5.11), (78.24±5.02) and (80.67±4.57) beat·min^-1; the MAP were (85.75±5.11), (85.39±4.97) and (87.93±3.67) mmHg, respectively; the QoR-15 scores 24 h after operation were (108.19±10.29), (109.56±10.12) and (99.66±10.21) points, respectively; the dosage of propofol were (220.66±25.19), (211.66±27.88) and (283.37±26.28) mg, respectively; the dosage of remifentanil were (2.37±0.42), (2.24±0.38) and (2.89±0.35) mg, respectively; Ramsay sedation scores were (1.56±0.27), (1.61±0.22) and (1.58±0.24) points at T0; and (3.18±0.33), (3.29±0.34) and (2.67±0.29) points at T3, respectively. Compared with the control group, there were statistically significant differences in the above indexes between the low-dose group and the high-dose group (all P<0.05), while there were no statistically significant differences in the above indexes between the low-dose group and the high-dose group (all P>0.05). Adverse drug reactions included respiratory depression, nausea/vomiting, dizziness, restlessness, hypotension, etc. The total incidence of adverse drug reactions were 2.56% (1 case /39 cases) in the low-dose group, 15.00% (6 cases/40 cases) in the high-dose group, and 26.19% (11 cases /42 cases) in the control group. The total incidence of adverse drug reactions of low-dose group was significantly lower than the control group, and the difference was statistically significant (P<0.05).

The application of propofol combined with esketamine can reduce the intraoperative dosages of propofol and remifentanil in elderly patients undergoing knee arthroplasty, enhance the sedation effect, improve the hemodynamics, and promote the postoperative recovery.

To investigate the clinical effect of cinacalcet in the treatment of secondary hyperparathyroidism (SHPT) in patients undergoing hemodialysis for chronic kidney disease (CKD).

Patients who underwent hemodialysis for CKD and had SHPT were divided into the control group and the treatment group according to the cohort method. The control group was treated with 0.25 μg of calcitriol capsules once a day via oral administration. On this basis, the treatment group was treated with 25 mg of cinacalcet tablets once a day via oral administration. Patients in both groups were treated for 12 weeks. Clinical efficacy, parathyroid volume, parathyroid function [serum phosphorus, serum calcium, alkaline phosphatase (ALP) and intact parathyroid hormone (iPTH)], and cardiovascular function [creatine kinase-MB (CK-MB), hypersensitive troponin Ⅰ (hs-cTnⅠ) and myoglobin (MYO)]were compared between the two groups. Safety was evaluated.

Sixty-two cases were enrolled in the treatment group and fifty-eight cases in the control group. After treatment, the total effective rates in the treatment group and the control group were 93.55% (58 cases/62 cases) and 77.59% (45 cases/58 cases), with statistically significant difference (P<0.05). After treatment, serum phosphorus levels in the treatment group and the control group were (1.31±0.16) and (1.50±0.34) mmol·L^-1; serum calcium levels were (2.63±0.91) and (2.25±0.72) mmol·L^-1; ALP levels were (83.28±8.40) and (126.46±12.39) U·L^-1; iPTH levels were (215.32±16.69) and (307.65±20.14) pg·mL^-1. The differences were statistically significant (all P<0.05). After treatment, the length of the parathyroid gland in the treatment group and the control group were (0.58±0.10) and (0.77±0.19) cm; width were (0.34±0.08) and (0.45±0.16) cm; thickness were (0.25±0.05) and (0.33±0.15) cm; volume were (0.82±0.15) and (1.13±0.22) cm³. The differences were statistically significant (all P<0.05). After treatment, serum CK-MB levels in the treatment group and the control group were (4.18±0.73) and (6.53±1.26) ng·mL^-1; hs-cTnⅠ levels were (0.04±0.01) and (0.07±0.03) ng·mL^-1; MYO levels were (70.69±9.41) and (112.39±12.60) ng·mL^-1. The differences were statistically significant (all P<0.05). The adverse drug reactions in the treatment group and the control group mainly included nausea and vomiting, increased blood pressure, and myalgia. The total incidence of adverse drug reactions in the treatment group and the control group were 8.06 % (5 cases / 62 cases) and 22.41% (13 cases / 58 cases), respectively, and the difference was statistically significant (P<0.05).

Cinacalcet is effective in the treatment of SHPT in patients undergoing hemodialysis for CKD. It can reduce parathyroid gland volume, maintain calcium and phosphorus metabolism, and protect cardiovascular function, with high safety.

To observe the clinical efficacy and safety of recombinant epidermal growth factor (rhEGF) gel combined with gelatin sponge application under ear endoscopy in the treatment of traumatic tympanic membrane perforations.

Patients with traumatic tympanic membrane perforations were divided into control group and treatment group using cohort method. The control group received intravenous infusion of clindamycin phosphate injection (0.9 g, once daily). The treatment group received rhEGF gel (1 drop per dose, twice daily) combined with gelatin sponge application under ear endoscopy. Both groups received treatment for 1 week. The clinical efficacy, inflammatory markers [white blood cell count (WBC), C-reactive protein (CRP)], hearing status, and safety were compared between the two groups.

A total of 37 patients in the control group and 43 patients in the treatment group were enrolled. The overall treatment efficacy in the treatment and control groups were 95.35% (41 cases /43 cases) and 78.38% (29 cases/37 cases), respectively, with statistically significant difference (P<0.05). After treatment, the WBC levels in the treatment and control groups were (7.74±1.47) and (10.68±1.64) × 10·L^-1, respectively; the CRP levels were (3.37±0.97) and (6.35±1.01) pg·mL^-1, respectively; the air conduction hearing thresholds were (25.64±2.13) and (29.68±2.24) dB HL, respectively; and the air-bone conduction gap were (6.54±1.24) and (12.36±2.47) dB, respectively. The treatment group showed statistically significant differences in all these indicators compared to the control group (all P<0.05). The adverse drug reactions in the treatment group, the main adverse drug reaction was infection, while in the control group mainly included infection and re-perforation. The incidence of adverse drug reactions in the treatment and control groups were 4.65% (2 cases /43 cases) and 10.81% (4 cases /37 cases), respectively, with no significant difference (P>0.05).

The clinical efficacy of treating patients with traumatic tympanic membrane perforation by combining rhEGF gel with absorbable gelatin sponge patch is better than that of conservative treatment. It has a low incidence of adverse drug reactions and high safety.

To evaluate the in vitro antibacterial activity of cefteram against common clinically isolated bacteria in the past three years.

The clinical isolates were collected and the minimal inhibitory concentration (MICs) were determined by the microdilution method.

A total of 484 pathogenic bacteria over the period 2021-2023 were studied. The results show that cefteram has good antibacterial activity against Streptococcus spp other than penicillin-resistant Streptococcus pneumoniae (MICs of penicillin ≥ 2 mg·L^-1), MIC₉₀ value of cefteram was less than or equal 1 mg·L^-1, and the susceptibility rate was 100.0%, which was similar to penicillin, slightly better than cefpodoxime, better than cefuroxime, cefixime, cefaclor and cefalexin. Against gram-negative bacteria, cefteram also showed better antibacterial activity, especially against β-lactamase (ESBLs) negative Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis and Haemophilus influenzae, and Moraxella catarrhalis. The MIC₉₀ value of cefteram was ≤ 2 mg·L^-1, and the susceptibility rate was 100.0%. Especially for Hemophilus influenzae, cefteram was better than all comparator agents, were comparable to cefpodoxime, better than cefuroxime, cefaclor and cefalexin. For Peptostreptococcus spp., cefteram was comparable to cefuroxime, better than all compared agents.

Cefteram had a wide and balanced antibacterial against clinical isolatied of gram-negative bacteria, gram-positive bacteria and anaerobic bacteria in China in recent years. Cefteram also showed better antibacterial activity, especially against penicillin intermediate and ampicillin-resistant Hemophilus influenzae, and is a good variety among oral cephalosporins.

To investigate the effect and mechanism of ursodeoxycholic acid on bronchial epithelial cell injury induced by toluene diisocyanate (TDI).

BEAS-2B cells were randomly divided into control group (conventional culture), TDI-human serum albumin (HSA) group (120.00 mg·L^-1 TDI-HSA), low-dose group (100 μmol·L^-1 ursodeoxycholic acid+120.00 mg·L^-1 TDI-HSA), high-dose group (200 μmol·L^-1 ursodeoxycholic acid+120.00 mg·L^-1 TDI-HSA) and rapamycin group (25 nmol·L^-1 rapamycin+120.00 mg·L^-1 TDI-HSA). The expression of inflammatory factors was detected by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA); the level of reactive oxygen species (ROS) was detected by DCFH-DA; and the protein expression of each cell was detected by Western blot.

The mRNA levels of interleukin (IL)-6 in control group, TDI-HSA group, low-dose group and high-dose group were 1.00±0.13, 2.20±0.24, 1.87±0.12, 1.48±0.14, respectively; IL-8 levels were (22.65±1.96), (81.42±6.35), (56.36±5.88), (38.28±3.25) pg·mL^-1, respectively; ROS levels were (100.00±3.47)%, (351.25±22.52)%, (312.80±26.59)%, (242.15±13.60)%, respectively; the protein levels of dynamic associated protein 1 (DRP1) were 0.23±0.03, 0.82±0.08, 0.69±0.10, 0.55±0.05, respectively; benzyl chloride 1 (Beclin1) protein expression levels were 0.23±0.04, 0.60±0.07, 0.44±0.04, 0.37±0.03, respectively; phosphorylated adenylate activates protein kinase (p-AMPK) protein expression levels were 0.20±0.05, 0.49±0.05, 0.40±0.03, 0.34±0.04, respectively. Beclin1 protein expression levels in high-dose group and rapamycin group were 0.35±0.04 and 0.69±0.07, respectively; IL-6 levels were (17.63±1.36) and (29.52±3.49) pg·mL^-1, respectively; IL-18 levels were (65.22±5.30) and (95.58±6.80) pg·mL^-1, respectively. The above indexes: TDI-HSA group was compared with control group, low- dose group and high- dose group were compared with TDI-HSA group, rapamycin group compared with high dose group, the differences were significant (all P<0.05).

Ursodeoxycholic acid may mediate ROS/AMPK/ autophagy pathway to improve the inflammatory response and mitochondrial dysfunction induced by TDI-HSA.

To investigate the effects of almonertinib on the proliferation, invasion, epithelial-mesenchymal transition (EMT), and stemness of non-small-cell lung cancer (NSCLC) cells by regulating microRNA-22 (miR-22) targeting ubiquitin-conjugating enzyme E2O (UBE2O).

Human lung adenocarcinoma cell line NCI-H1975 was randomly divided into control group (normal culture with no treatment), medium-dose group (4 μmol·L^-1 almonertinib), inhibitor negative control (NC inhibitor) group (4 μmol·L^-1 almonertinib + miR-22 inhibition negative control), miR-22 inhibitor group (4 μmol·L^-1 almonertinib + miR-22 inhibition), miR-22 inhibitor+short hairpin negative control (sh-NC) group (4 μmol·L^-1 almonertinib + miR-22 inhibition + short hairpin negative control), and miR-22 inhibitor+short hairpin UBE2O (sh-UBE2O) group (4 μmol·L^-1 almonertinib + miR-22 inhibition + short hairpin UBE2O). The expression of miR-22 was detected by quantitative real-time polymerase chain reaction (qRT-PCR) ; Western blot analysis was performed to detect the expression of octamer-binding transcription factor 4 (OCT4), SRY-Box transcription factor 2 (SOX2), and Nanog; the cell proliferation rate was assessed using the 5-ethynyl-2-deoxyuridine (EdU) assay; and Transwell assays were conducted to evaluate cell invasion ability.

The expression levels of miR-22 in the control group, medium-dose group were 1.00±0.16, 2.07±0.34. The expression levels of OCT4 in the control group, medium-dose group, NC inhibitor group, and miR-22 inhibitor group were 1.00±0.16, 0.63±0.09, 0.67±0.08 and 0.94±0.12, respectively; SOX2 expression levels were 1.00±0.14, 0.48±0.06, 0.54±0.07 and 0.81±0.11; and Nanog expression levels were 1.00±0.18, 0.45±0.08, 0.52±0.11 and 0.89±0.15. The cell proliferation rates in the control group, medium-dose group, NC inhibitor group, miR-22 inhibitor group, miR-22 inhibitor+sh-NC group, and miR-22 inhibitor+sh-UBE2O group were (87.29±10.73)%, (41.65±7.82)%, (48.47±6.54)%, (79.31±10.26)%, (84.50±11.98)% and (36.82±6.79)%, respectively. The numbers of invading cells were (156.92±24.81), (72.53±9.06), (64.41±10.75), (143.27±26.19), (137.58±21.46) and (75.23±11.94), respectively. Compared between the control group and medium-dose group, NC inhibitor and miR-22 inhibitor groups, as well as miR-22 inhibitor+sh-NC and miR-22 inhibitor+sh-UBE2O groups showed statistically significant differences (all P<0.05).

Almonertinib can inhibit the proliferation and invasion of NSCLC NCI-H1975 cells, likely by regulating miR-22 to target UBE2O.

To investigate the effects of circCSPP1 mediated autophagy on the proliferation and metastasis ability of gastric cancer cells.

The human gastric cancer cells NCI-N87 were divided into Vector group (transfected with Vector), circCSPP1 group (transfected with circCSPP1) and inhibitor group (transfected with circCSPP1 and incubated with 10 μmol·L^-1 chloroquine). The MKN-45 cells were divided into sh-NC group (transfected with circCSPP1 shRNA-NC), sh-circCSPP1 group (transfected with circCSPP1 shRNA) and agonist group (transfected with circCSPP1 shRNA + 1 μmol·L^-1 sirolimus). Flow cytometry was used to detect cell apoptosis. Transwell was used to detect cell migration and invasion. Western blot were used to detect the expression levels of microtubule associated protein light chain 3-Ⅱ (LC3-Ⅱ) and p62 protein.

In NCI-N87 cells: the apoptosis rates of Vector, circCSPP1 and inhibitor groups were (7.95±0.66)%, (3.93±0.62)% and (7.37±0.85)%; the number of cell migrations were 122.50±12.25, 169.40±16.09 and 109.00±8.22; the number of cell invasions were 73.38±12.33, 117.30±12.78 and 55.25±8.73; the relative expression levels of LC3-Ⅱ protein were 0.40±0.06, 1.13±0.11 and 0.44±0.08; the relative expression levels of p62 protein were 1.62±0.15, 0.21±0.08 and 1.43±0.16. The differences of above indexes were statistically significant between the circCSPP1 group and the inhibitor and Vector groups (all P<0.05). In MKN-45 cells: the cell apoptosis rates of sh-NC, sh-circCSPP1 and agonist groups were (6.81±0.68)%, (12.02±0.78)% and (5.76±1.21)%; the number of cell migrations were 191.60±21.43, 87.50±10.76 and 155.60±10.36; the number of cell invasions were 150.00±11.55, 61.63±11.39 and 154.50±17.99; the relative expression levels of LC3-Ⅱ protein were 1.08±0.05, 0.13±0.03 and 1.18±0.06; the relative expression levels of p62 protein were 0.15±0.03, 1.29±0.08 and 0.19±0.04. Compared with the sh-circCSPP1 group, the differences of above indicators in the agonist and sh-NC groups were statistically significant (all P<0.05).

circCSPP1 can improve the proliferation and metastasis ability of gastric cancer cells by inducing autophagy.

To investigate the effect of microRNA-183-5p (miR-183-5p) targeting RNA-binding motif single-stranded-interacting protein 1 (RBMS1) on autophagy and migration of breast cancer cells and its mechanism.

Human breast cancer cells MCF-7 were divided into control group, NC inhibitor group (transfected with NC inhibitor) and miR-183-5p inhibitor group (transfected with miR-183-5p inhibitor), miR-183-5p inhibitor+si-NC group (transfected with miR-183-5p inhibitor and empty vector si-NC), miR-183-5p inhibitor+si-RBMS1 group (transfected with miR-183-5p inhibitor and RBMS1 knockdown plasmid si-RBMS1). The expression levels of autophagy and phosphatidylinositol-3-kinase (PI3K)/ protein kinase B (Akt)/ mammalian target of rapamycin (mTOR) pathway-related proteins in each group were detected by Western blot, and the mobility of cells in each group was detected by scratch test.

Control group, NC inhibitor group, miR-183-5p inhibitor group, miR-183-5p inhibitor+si-NC group and miR-183-5p inhibitor+si-RBMS1 group the relative expression levels of light chain 3 Ⅱ (LC3-Ⅱ)/light chain 3 Ⅰ (LC3-Ⅰ) protein were 0.29±0.03, 0.31±0.03, 0.86±0.10, 0.84±0.09 and 0.43±0.05, respectively; the relative expression levels of Beclin-1 protein were 0.18±0.02, 0.20±0.02, 0.74±0.08, 0.78±0.09 and 0.35±0.04, respectively; the relative expression levels of sequestosome-1 (P62) protein were 0.93±0.12, 0.89±0.10, 0.51±0.06, 0.54±0.06 and 0.86±0.10, respectively; the 48 h cell mobility was (62.87±7.26)%, (59.23±6.89)%, (24.13±3.49)%, (26.14±4.72)% and (40.11±5.71)%, respectively; the relative expression levels of phospho- (p-) PI3K/PI3K protein were 0.67±0.12, 0.64±0.10, 0.32±0.06, 0.35±0.06 and 0.74±0.09, respectively. The above indexes of miR-183-5p inhibitor+si-RBMS1 group were compared with those of miR-183-5p inhibitor+si-NC group, and those of miR-183-5p inhibitor group were compared with those of NC inhibitor group, and the differences were statistically significant (all P<0.05).

Inhibition of miR-183-5p expression can promote autophagy and inhibit cell migration in MCF-7 cells, while down-regulation of RBMS1 has the opposite effect, which is related to the PI3K/Akt/mTOR pathway.

To investigate the regulatory effects of aloperin on bladder cancer cell growth and endoplasmic reticulum stress-dependent mitochondrial pathway.

253J cells were randomly divided into control group, experimental-L group (25.0 μmoL·L^-1 aloperin), experimental-M group (50.0 μmoL·L^-1 aloperin), experimental-H group (100.0 μmoL·L^-1 aloperin), 4-PBA group [100.0 μmoL·L^-1 aloperin+20 μmoL·L^-1 4-phenylbutyric acid (4-PBA)], si-NC (transfected with si-NC+100.0 μmoL·L^-1 aloperin), si-CHOP group [transfected with si-CCAAT-enhancer-binding protein homologous protein (CHOP)+100.0 μmoL·L^-1 aloperin]. Cell proliferation was detected by 5-ethynyl-2′-deoxyuridine (EdU) assay; protein expression was detected by Western blot assay; apoptosis was detected by flow cytometry; mitochondrial membrane potential (MMP) was detected by JC-1 assay.

The EdU positive cell rates in control group, experimental-L group, experimental-M group and experimental-H group were (37.51±2.98)%, (29.52±2.19)%, (23.10±2.58)% and (12.94±2.52)%, respectively; the expression levels of C/EBP homologous protein (CHOP) were 0.29±0.04, 0.53±0.05, 0.71±0.08, 0.90±0.12, respectively. The apoptosis rates in control group, experimental-H group and 4-PBA group were (4.79±0.62)%, (23.01±2.03)% and (13.75±1.14)%, respectively. The expressions of CHOP protein in control group, experimental-H, si-NC and si-CHOP groups were 0.30±0.03, 0.92±0.08, 0.91±0.11 and 0.20±0.02, respectively; the apoptosis rates were (4.39±0.30)%, (22.11±1.82)%, (22.65±2.40)% and (15.32±1.19)%, respectively; mitochondrial cytochrome C (Cyto-C) protein levels were 0.78±0.07, 0.43±0.05, 0.42±0.05 and 0.65±0.06; cytoplasmic Cyto-C protein levels were 0.51±0.06, 0.91±0.10, 0.88±0.05 and 0.61±0.04; MMP levels were (100.00±2.79)%, (57.49±3.34)%, (54.09±4.32)% and (69.91±6.81)%, respectively. The above indexes in the experimental-L, -M, -H groups were compared with the control group, the above indexes in the 4-PBA group were compared with the experimental-H group, and the above indexes in the si-CHOP group were compared with the si-NC group, the differences were statistically significant (all P<0.01).

Aloperin can inhibit the proliferation of 253J cells by up-regulating the endoplasmic reticulum stress-dependent mitochondrial apoptosis pathway mediated by CHOP.

To study the effect of tazemetostat on the stemness of diffuse large B-cell lymphoma and the related mechanism of action.

OCI-LY3 cells were divided into blank group, tazemetostat group and microRNA-378a-3p (miR-378a-3p) mimics group. Blank group cell conventional culture; tazemetostat group was treated with 5 μmol·L^-1 tazemetostat; miR-378a-3p mimics group was transfected with miR-378a-3p mimics. The relative expression level of miR-378a-3p was detected by fluorescence in situ hybridization. mRNA expression levels of dryness related factors were detected by quantitative real time polymerase chain reaction; the expression of signal pathway-related proteins was detected by Western blot.

The relative expression levels of miR-378a-3p in blank group and tazemetostat group were 1.00±0.14 and 0.52±0.08, respectively, the difference was statistically significant (P<0.001). The relative expression of octamer binding transcription factor 4 mRNA in blank group, tazemetostat group and miR-378a-3p mimics group were 1.00±0.16, 0.21±0.06 and 0.49±0.08, respectively; the relative expression of sex determining region Y box protein 2 mRNA were 1.00±0.09, 0.39±0.05 and 0.85±0.11, respectively; the relative expression of Nanog homeobox mRNA were 1.00±0.13, 0.17±0.03 and 0.65±0.10, respectively; the relative expressions of Kruppel like factor 4 mRNA were 1.00±0.10, 0.28±0.05 and 0.86±0.14, respectively; the relative expressions of Yes associated protein were 1.00±0.19, 3.46±0.52 and 2.14±0.36, respectively; the relative expression of transcriptional coactivator with PDZ-binding motif protein were 1.00±0.14, 1.90±0.35 and 1.51±0.33, respectively. The above indexes of tazemetostat group were compared with those of blank group, and the above indexes of miR-378a-3p mimics group were compared with those of tazemetostat group, the differences were statistically significant (P<0.001, P<0.05).

Tazemetostat can inhibit the stemness of OCI-LY3 cells by down-regulating the level of miR-378a-3p, which may be achieved through the Yes associated protein/transcriptional coactivator with PDZ-binding motif signaling pathway.