To observe the clinical efficacy and safety of the application of bromhexine hydrochloride injection combined with high-flow nasal cannula oxygen therapy in children with severe pneumonia complicated with type I respiratory failure.

Children with severe pneumonia complicated with type I respiratory failure who were treated in our hospital were collected and divided into control group and treatment group based on the treatment methods. The control group received conventional oxygen therapy on the basis of conventional treatment, while the treatment group was given bromhexine hydrochloride and glucose injection (2~4 mg each time, qd, intravenous drip) combined with high-flow nasal cannula oxygen therapy on the basis of conventional treatment. Both groups were treated for 7 days. The clinical efficacy, respiratory and circulatory indicators, and inflammatory indicators of the two groups were compared, and safety was evaluated.

A total of 94 children were included, including 49 in control group and 45 in treatment group. After treatment, the overall clinical response rates were 75.51% (37 cases/49 cases) in control group and 91.11% (41 cases /45 cases) in treatment group, demonstrating a statistically significant difference (P<0.05). After treatment, the arterial partial pressure of oxygen (PaO₂) levels of control group and treatment group were (75.43±7.71) and (80.35±8.63) mmHg, respectively; the percutaneous oxygen saturation (SpO₂) levels were (94.16±2.06)% and (95.31±2.33)%, respectively; the PaO₂/FiO₂ levels were 327.08±34.36 and 342.40±33.53, respectively; the respiratory rate (RR) levels were (30.16±3.39) and (28.33±3.03) time·min^-1, respectively; the lactate levels were (2.66±0.43) and (2.38±0.34) mmol·L^-1, respectively; the interleukin-6 (IL-6) levels were (14.45±3.37) and (12.64±3.31) pg·mL^-1, respectively; the white blood cell (WBC) levels were (7.94±2.13) and (7.07±1.87) ×10⁹·L^-1, respectively; the neutrophil percentage (NEUT%) levels were (55.36±8.25)% and (51.58±7.43)%, respectively; the procalcitonin (PCT) levels were (0.17±0.04) and (0.15±0.04) ng·mL^-1, respectively, all differences between the two groups were statistically significant (P<0.05, P<0.01). The main adverse drug reactions in control group were facial skin damage, nasal mucosa damage and abdominal distension; the main adverse drug reactions in treatment group were nausea, vomiting, facial skin damage and nasal mucosa damage. The total incidence of adverse drug reactions in control group and treatment group were 14.29% (7 cases/49 cases) and 11.11% (5 cases/45 cases), respectively, with no statistically significant difference (P>0.05).

The treatment plan of bromhexine hydrochloride and glucose injection combined with high-flow nasal cannula oxygen therapy for children with severe pneumonia complicated with type Ⅰ respiratory failure is effective. It can significantly improve clinical symptoms, shorten the time of symptom relief, improve respiratory and circulatory indicators, reduce inflammatory indicators, promote the absorption of pneumonia, improve treatment comfort, shorten hospital stay and has good safety.

To investigate the effects of celastrol (Cel) on airway remodeling factors, collagen synthesis and degradation in lung fibroblasts of chronic obstructive pulmonary disease (COPD) rats by regulating the neurogenic locus notch homolog protein (Notch) pathway.

A total of 30 rats were randomly divided into 3 groups: animal control group (normal feeding), animal model group (COPD rat model established by smoke exposure combined with lipopolysaccharide tracheal instillation) and animal experimental group (intraperitoneal injection of 0.01 mg·kg^-1 Cel after successful modeling). The bronchial fibroblasts (BF) cells were isolated from rats in the animal model group and randomly divided into cell control group (no treatment), cell experimental group (2 μmol·L^-1 Cel) and inhibitor group [1 mmol·L^-1 valproic acid (VPA)]. Pulmonary function was assessed in rats using invasive pulmonary function testing methods; Western blot was used to detect the expression of Notch signaling pathway-related proteins in each group of cells; real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect mRNA expression of airway remodeling-related factors; enzyme-linked immunosorbent assay (ELISA) was used to detect the contents of matrixmetalloproteinase-1 (MMP-1) and tissue inhibitors of metalloproteinase-1 (TIMP-1) in each group of cells.

The forced vital capacity (FVC) of rats in animal control group, animal model group and animal experimental group were (6.74±0.87), (3.28±0.51) and (4.94±0.83) mL, respectively; the forced expiratory volume in 0.1 second (FEV0.1) were (3.94±0.45), (1.05±0.16) and (2.41±0.37) mL, respectively; the peak expiratory flow (PEF) were (28.09±4.60), (16.63±3.21) and (21.55±4.02) L·min^-1, respectively. Significant differences were observed in the above indicators between animal control group and animal model group, and between animal model group and animal experimental group (P<0.01, P<0.001). The relative expression levels of (Notch1) protein in cell control group, cell experimental group and inhibitor group were 1.00±0.19, 0.12±0.02 and 0.38±0.06, respectively; the relative expression levels of Notch1 receptor intracellular binding domain (NICD1) protein were 1.00±0.17, 0.72±0.12 and 0.85±0.13, respectively; the relative expression levels of serrated typical Notch ligand 1 (Jagged1) protein were 1.00±0.15, 0.71±0.11 and 0.84±0.12, respectively; the relative expression levels of hair and enhancer of split 1 (Hes1) protein were 1.00±0.11, 0.69±0.08 and 0.81±0.09, respectively; the relative expression levels of MMP-9 mRNA were 1.00±0.16, 0.59±0.08 and 0.73±0.11, respectively; the relative expression levels of type Ⅰ collagen(ColⅠ) mRNA were 1.00±0.14, 0.67±0.09 and 0.86±0.14, respectively; the relative expression levels of α-smoth muscle actin (α-SMA) mRNA were 1.00±0.16, 0.41±0.07 and 0.78±0.13, respectively; the relative expression levels of transforming growth factor-β (TGF-β) mRNA were 1.00±0.18, 0.53±0.09 and 0.75±0.14, respectively; the contents of MMP-1 were (1.19±0.17), (0.80±0.15) and (1.06±0.15) ng·mL^-1, respectively; the contents of tissue inhibitor of protease-1 (TIMP-1) were (219.78±30.24), (131.94±18.15) and (167.51±21.01) ng·mL^-1, respectively. There were all statistically significant differences in the above indicators between cell control group and cell experimental group, as well as between cell experimental group and inhibitor group (P<0.05, P<0.01, P<0.001).

Celastrol can effectively improve lung function and pulmonary pathological damage in COPD rats, reduce the levels of inflammatory cells and inflammatory factors, and improve the imbalance of airway remodeling-related factors and collagen synthesis/degradation in BF cells, which may be related to its inhibition of Notch signaling activation.

To evaluate the safety and bioequivalence of two formulations of agomelatine tablets in healthy Chinese subjects.

A randomized, open-label, two-treatment, four-period, two-sequence, fully replicated crossover bioequivalence study was conducted under both fasting and fed conditions. Each subject received a single 25 mg dose of the test (T) product or reference (R) product agomelatine tablet in both fasting and fed conditions. Plasma concentration of agomelatine was determined by the liquid chromatography-tandem mass spectrometry (LC-MS/MS) method. The main pharmacokinetic parameters were derived using WinNonlin 8.3 software.

A total of 128 subjects were enrolled, 64 in the fasting group and 64 in the fed group. The primary pharmacokinetic(PK) parameters of the test and reference formulations under fasting condition were as follows: C_max were (25.55±29.65) and (26.59±28.04) ng·mL^-1, AUC_0-t were (28.59±26.66) and (29.33±26.98) ng·h·mL^-1, AUC_0-∞ were (29.13±26.96) and (29.62±27.17) ng·h·mL^-1. The primary pharmacokinetic parameters of the test and reference formulations under fed condition were as follows: C_max were (26.26±23.29) and (28.97±34.82) ng·mL^-1, AUC_0-t were (35.75±27.67) and (36.91±32.59) ng·h·mL^-1, AUC_0-∞ were (36.15±27.89) and (37.14±32.69) ng·h·mL^-1. Under both fasting and post-meal conditions, the 90% confidence interval of the geometric mean ratio (GMR) of the main PK parameters of the test formulation of agomelatine tablets compared to the reference formulation fell within the range of 80%-125%.

The test formulations and reference formulations of agomelatine are bioequivalent under both fasting and fed conditions.

To investigate the clinical efficacy and safety of atorvastatin calcium tablets in patients with type 2 diabetes cardiomyopathy.

Patients with type 2 diabetic cardiomyopathy admitted to our hospital were divided into treatment group and control group according to the treatment methods. The control group received conventional therapy, while the treatment group was administered atorvastatin calcium tablets at 20 mg·d^-1, orally for 4 weeks. The heart function, blood lipids, blood glucose, autophagy-related proteins and the relative expression levels of phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway-related mRNA were compared between the two groups, along with a safety evaluation.

A total of 198 patients were included, with 104 in treatment group and 94 in control group. After 4 weeks of treatment, the total clinical effective rate of treatment group was 92.31% (96 cases/104 cases), significantly higher than control group’s 80.85% (76 cases/94 cases) (P<0.05). After treatment, the left ventricular end diastolic diameter of treatment group and control group were (54.41±3.87) and (58.62±3.44) mm, respectively; the left ventricular end diastolic volume were (115.63±8.06) and (121.53±9.88) mL, respectively; the left ventricular end systolic diameter were (30.34±3.52) and (34.84±3.46) mm, respectively; the left ventricular end systolic volume were (69.72±6.32) and (76.57±6.24) mL, respectively; the left ventricular ejection fraction were (52.30±5.53)% and (48.52±4.21)%, respectively; the total cholesterol were (4.48±1.32) and (5.92±1.76) mmol·L^-1, respectively; triglycerides were (1.75±0.52) and (2.38±0.57) mmol·L^-1, respectively; low-density lipoprotein cholesterol were (2.49±0.65) and (3.32±1.21) mmol·L^-1, respectively; high-density lipoprotein cholesterol were (1.02±0.26) and (0.80±0.21) mmol·L^-1, respectively; the levels of benzyl chloride 1 were (3.28±0.43) and (2.62±0.41) ng·mL^-1, respectively; the levels of autophagy related gene 7 were (6.38±1.07) and (4.60±0.86) ng· mL^-1, respectively; the relative expression levels of PI3K mRNA were 0.68±0.25 and 0.94±0.28, respectively; the relative expression levels of Akt mRNA were 0.58±0.27 and 0.95±0.30, respectively; the relative expression levels of mTOR mRNA were 0.66±0.31 and 0.98±0.32, respectively. The above indicators in treatment group were statistically significant compared with control group (all P<0.05). The adverse drug reactions in treatment group include liver dysfunction, gastrointestinal reactions and muscle pain; the control group had abnormal liver function and gastrointestinal reactions. The total incidence of adverse drug reactions in treatment group was 5.77% (6 cases/104 cases), while in control group was 3.19% (3 cases/94 cases). There was no statistically significant difference between the two groups (all P>0.05).

Atorvastatin tablets can significantly improve cardiac structure and function, and regulate blood lipid levels in patients with type 2 diabetic cardiomyopathy. Additionally, it exerts cardioprotective effects by promoting autophagosome formation and downregulating the activity of the PI3K/Akt/mTOR pathway.

To explore the potential mechanism of cinnamaldehyde in alleviating nerve injury in rats with traumatic brain injury (TBI).

Rats were randomly divided into sham group (only craniotomy), model group(TBI model), experimental-L group (TBI+25 mg·kg^-1 cinnamaldehyde), experimental-H group (TBI+75 mg·kg^-1 cinnamaldehyde), miR-NC group (TBI+miR-NC lentivirus+75 mg·kg^-1 cinnamaldehyde) and miR-27a-3p inhibitor group (TBI+miR-27a-3p inhibitor lentivirus+75 mg·kg^-1 cinnamaldehyde). After treatment, real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-27a-3p; the Morris water maze test was used to assess memory function; immunofluorescence assay was used to detect the expression of ionized calcium-binding adapter molecule 1 (Iba-1); Western blot was used to detect the expression of related proteins in brain tissues; and the dual-luciferase reporter gene assay was used to verify the binding of miR-27a-3p to BCL2/adenovirus E1B 19kDa interacting protein 3-like (BNIP3L).

The relative expression levels of miR-27a-3p in the sham group, model group, experimental-L group, experimental-H group, miR-NC group and miR-27a-3p inhibitor group were 1.00±0.08, 0.40±0.03, 0.52±0.08, 0.76±0.08, 0.73±0.09 and 0.18±0.02, respectively; the escape latency times were (11.19±0.75), (26.06±1.47), (23.59±1.39), (14.95±1.71), (15.37±0.77) and (24.91±1.96) s, respectively; the Iba-1 fluorescence intensities were (1 189.50±113.68), (2 958.70±279.29), (2 287.05±271.69), (1 916.55±205.44), (1 935.57±164.54) and (2 564.52±333.05) a.u., respectively; the relative expression levels of autophagy-related gene 5 (ATG5) protein were 0.32±0.03, 0.94±0.07, 0.71±0.09, 0.50±0.08, 0.53±0.07 and 0.85±0.09, respectively; the relative expression levels of Beclin-1 autophagy regulator (Beclin-1) protein were 0.35±0.03, 0.95±0.13, 0.75±0.12, 0.49±0.05, 0.48±0.07 and 0.73±0.10, respectively; the relative expression levels of Parkin RBR domain E3 ubiquitin protein ligase (Parkin) protein were 0.29±0.04, 0.64±0.08, 0.51±0.09, 0.41±0.04, 0.43±0.05 and 0.62±0.07, respectively. For the above indicators, there were all statistically significant differences when comparing the model group with the sham group, the experimental-L and experimental-H groups with the model group, and the miR-27a-3p inhibitor group with the miR-NC group (P<0.05, P<0.01, P<0.001). The dual-luciferase reporter gene assay confirmed the targeted binding of miR-27a-3p to BNIP3L.

Cinnamaldehyde may regulate autophagy through the miR-27a-3p/BNIP3L axis, improve neurological function, alleviate neuroinflammation and exert neuroprotective effects on TBI-induced brain injury.

To observe the clinical efficacy and safety of aripiprazole tablets combined with magnesium valproate sustained-release tablets in the treatment of patients with bipolar disorder (BD).

BD patients were divided into control group and treatment group according to treatment regimen. The control group was given oral magnesium valproate sustained-release tablets with an initial dose of 0.25 g per time, bid. After 1-2 weeks, the dose was adjusted to 0.75-1.5 g·d^-1 according to the patient’s condition. On the basis of the treatment for the control group, the treatment group was additionally given oral aripiprazole tablets, 5 mg per time, bid. After 2 weeks of medication, the dose was appropriately adjusted to 10 mg per time, bid, according to the patient’s tolerance. Both groups received treatment for 8 weeks. The efficacy, clinical symptom scores, cognitive function, sleep quality, 5-hydroxytryptamine(5-HT), quality of life and adverse drug reactions were compared between the two groups.

A total of 92 cases were enrolled, including 44 in the control group and 48 in the treatment group. After treatment, the clinical efficacy rates in the control group and treatment group were 72.73% (32 cases/44 cases) and 91.67% (44 cases/48 cases), respectively; the Hamilton depression rating scale (HAMD) scores were (7.07±1.38) and (6.38±1.35) points, respectively; the Bipolar disorder rating scale (BRMS) scores were (8.68±2.01) and (7.65±1.16) points, respectively; the positive and negative syndrome scale (PANSS) scores were (52.07±8.97) and (45.27±8.12) points, respectively; the Wisconsin card sorting test (WCST) scores were (51.57±5.66) and (54.13±5.43) points, respectively; the Hopkins Verbal learning test-revised (HVLT-R) scores were (26.27±3.64) and (28.02±3.50) points, respectively; the continuous performance test (CPT) scores were (1.86±0.63) and (2.13±0.57) points, respectively; sleep efficiency rates were (85.45±2.48)% and (89.17±1.17)%, respectively; wakefulness frequency were (3.39±0.81) and (2.92±0.77) times, respectively; 5-HT levels were (52.29±8.23) and (58.09±8.06) ng·L^-1, respectively. Comparisons between the two groups for all the aforementioned indicators showed statistically significant differences (P<0.05, P<0.01, P<0.001). The overall adverse drug reaction rates in the control group and treatment group were 11.36% (5 cases/44 cases) and 14.58% (7 cases/48 cases), respectively (P>0.05).

The combination therapy regimen of aripiprazole tablets and magnesium valproate sustained-release tablets can effectively alleviate clinical symptoms in patients with BD, improve cognitive function and sleep quality, enhance overall quality of life and demonstrate good safety profiles.

To explore the mechanism of action by which icariin regulates the loss of immune tolerance to immune thrombocytopenia (ITP) through the microRNA (miRNA)-98-5p-mediated adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)/Unc-51-like autophagy-activating kinase 1 (ULK1) signaling pathway.

The ITP model was established by intraperitoneal injection of guinea pig anti-mouse platelet serum into mice. Another 12 normal mice were taken as the control group. The mice with successful modeling were divided into model group, the experimental-low group, the experimental-high group and the positive drug group. The experimental-low and experimental-high groups and the positive drug group were gavaged with 1.25, 5.00 mg·kg^-1 icariin and 9.1 mg·kg^-1 prednisone acetate, respectively, after the mice were modeled. The levels of platelets (PLT) and hemoglobin (Hb) were detected by automatic blood analyzer; the levels of thrombopoietin (TPO) and inflammatory factors were detected by enzyme-linked immunosorbent assay; the pathological damage of spleen tissue was detected by hematoxylin-eosin staining; megakaryocytes were observed with sternum bone marrow smears; the relative expression level of miRNA-98-5p was detected by real-time fluorescence quantitative polymerase chain reaction; and the protein relative expression levels of the AMPK/mTOR/ULK1 signaling pathway was detected by Western blotting.

The PLT levels in control group, model group, experimental-low group, experimental-high group and positive drug group were (1 504.56±166.99), (752.68±80.33), (862.95±98.33), (1 212.35±134.23) and (1 363.23±155.33)×10·L^-1, respectively; the Hb levels were (151.33±18.96), (124.11±13.56), (138.32±14.02), (145.33±16.88) and (149.22±16.02) g·L^-1, respectively; the TPO levels were (12.05±1.33), (5.86±0.78), (6.62±0.96), (7.85±0.92) and (9.66±0.89) pg·mL^-1, respectively; the levels of interleukin-6 (IL-6) were (18.96±2.33), (44.33±5.39), (39.25±4.46), (32.32±4.33) and (22.98±3.78) ng·L^-1, respectively; the levels of IL-10 were (42.15±6.48), (23.12±3.56), (26.89±3.99), (31.02±4.65) and (33.66±4.86) ng·L^-1, respectively; the levels of tumor necrosis factor-α(TNF-α) were (31.02±4.65), (77.36±8.98), (67.65±7.88), (60.52±7.34) and (40.56±5.99) ng·L^-1, respectively; the levels of interferon-gamma (IFN-γ) were (4.33±0.68), (8.33±0.96), (7.35±0.89), (6.02±0.81) and (5.86±0.75) ng·L^-1, respectively; the relative expression levels of miRNA-98-5p were 1.00±0.16, 1.78±0.21, 1.51±0.18, 1.22±0.16 and 1.15±0.15, respectively; the relative expression levels of phosphorylated (p)-AMPK/AMPK were 1.00±0.14, 1.81±0.28, 1.60±0.19, 1.31±0.16 and 1.25±0.21, respectively; the relative expression levels of p-mTOR/β-actin were 1.00±0.16, 0.48±0.07, 0.59±0.09, 0.79±0.12 and 0.82±0.14, respectively; the relative expression levels of p-ULK1/β-actin were 1.00±0.15, 0.42±0.06, 0.53±0.09, 0.89±0.14 and 0.93±0.16, respectively. There were statistically significant differences when comparing the above indicators of model group with those of control group, and also when comparing the above indicators of the experimental-low, experimental-high groups and positive drug group with those of model group (P<0.05, P<0.01, P<0.001).

Icariin regulates the loss of immune tolerance in rats with ITP, inhibits autophagy, and thus elevates platelet levels by down-regulating the expression of miRNA-98-5p and modulating the AMPK/mTOR/ULK1 signaling pathway.

To investigate the mechanism of peiminine (PEI) affects pain and cartilage injury in rats with knee osteoarthritis (KOA) by regulating the peroxisome proliferator-activated receptor gamma (PPARγ)/cellular sloan kettering institute(c-SKI) signaling pathway through a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS-5).

The KOA model was established in rats by intra-articular injection of sodium iodoacetate. The rats were divided into control group, model group, experimental group (intraperitoneal injection of 3.5 mg·kg^-1 PEI) and ADAMTS-5 overexpression group (tail vein injection of oe-ADAMTS-5 plasmid). The pain threshold of rats was measured using the mechanical stimulation method; the pathological injury of the rat knee joint was examined by hematoxylin-eosin (HE) staining; the protein levels of ADAMTS-5, matrix metalloproteinase (MMP)-3, MMP-13 and proteins in the PPARγ/c-SKI signaling pathway in rat knee joint tissues were detected by Western blot; the protein level of collagen type Ⅱ alpha 1 chain (Col2α1) in rat knee joint tissues was determined by immunohistochemistry; the levels of inflammatory factors in rat serum were measured using corresponding commercial kits.

The pain thresholds in control group, model group and experimental group were (19.15±2.87), (7.10±1.03) and (13.69±1.27) g, respectively; the relative expression levels of ADAMTS-5 were 1.00±0.16, 1.77±0.21 and 1.35±0.18, respectively; Col2α1 levels in control, model, experimental, and ADAMTS-5 overexpression groups were 1.00±0.10, 0.28±0.04, 0.76±0.13 and 0.58±0.06, respectively; the relative expression levels of MMP-3 were 1.00±0.15, 2.11±0.36, 1.62±0.22 and 1.83±0.25, respectively; the relative expression levels of MMP-13 were 1.00±0.18, 1.98±0.28, 1.27±0.16 and 1.45±0.19, respectively; the tumor necrosis factor-alpha (TNF-α) levels were (62.74±6.93), (159.37±26.40), (98.08±14.09) and (124.43±17.79) pg·mL^-1, respectively; the interleukin (IL)-4 levels were (75.62±11.54), (19.56±2.59), (53.28±6.34) and (41.67±5.31) pg·mL^-1, respectively; IL-6 levels were (42.65±9.77), (133.84±13.22), (84.19±11.71) and (105.24±18.19) pg·mL^-1, respectively; IL-10 levels were (98.06±24.50), (23.42±10.61), (64.72±20.96) and (38.09±12.86) pg·mL^-1, respectively; the relative expression levels of PPARγ were 1.00±0.13, 0.39±0.07, 0.73±0.09 and 0.51±0.08, respectively; the relative expression levels of c-SKI were 1.00±0.17, 0.32±0.05, 0.86±0.15 and 0.44±0.09, respectively. The above indicators in model group were statistically significantly different from those in control group, those in experimental group were statistically significantly different from those in model group, and those in ADAMTS5 overexpression group were statistically significantly different from those in experimental group (all P<0.05).

PEI inhibits inflammatory cytokine levels, alleviates bone fibrosis, and improves bone injury in KOA rats, thereby relieving joint pain, possibly by downregulating ADAMTS-5 expression to activate the PPARγ/c-SKI signaling pathway.

To construct a clinical pharmacist intervention strategy for tislelizumab injection in the treatment of advanced non-small cell lung cancer (NSCLC) and evaluate its practical effects.

Patients with advanced NSCLC admitted to our hospital were divided into control group and treatment group. The control group received routine pharmaceutical care, while the treatment group received a clinical pharmacist intervention strategy. Therapeutic efficacy, incidence of immune-related adverse events (irAEs), incidence of grade ≥3 irAEs, treatment-related drug withdrawal rate, medication adherence, quality of life and satisfaction with pharmaceutical care were compared between the two groups.

A total of 106 patients were included, including 53 in control group and 53 in treatment group. After treatment, the objective response rates (ORR) of treatment group and control group were 47.17% and 28.30%, respectively; the disease control rates (DCR) were 60.38% and 39.62%, respectively. The above indicators in treatment group were statistically significantly higher than those in control group (all P<0.05). The incidences of irAEs in treatment group and control group were 39.62% and 60.38%, respectively; the incidences of irAEs≥grade 3 were 13.21% and 30.19%, respectively; the treatment-related discontinuation rates were 9.43% and 24.53%, respectively. The above indicators in treatment group were statistically significantly lower than those in control group (all P<0.05). After treatment, the European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire–lung cancer 13 (EORTC QLQ-LC13) scores for treatment group and control group were (50.15±9.06) and (53.94±7.19) points, respectively, with treatment group statistically significantly lower than control group (P<0.05). The satisfaction rate of pharmaceutical services in treatment group was 90.57%, statistically significantly higher than control group’s 75.47% (P<0.05).

The clinical pharmacist intervention strategy can improve medication adherence to tislelizumab injection, reduce immune-related adverse events and treatment interruption, improve quality of life, and enhance satisfaction with pharmaceutical care, thereby contributing to better clinical outcomes.

To observe the clinical efficacy and safety of budesonide/glycopyrrolate bromide/formoterol fumarate inhalation aerosol combined with theophylline sustained-release tablets in patients with severe chronic obstructive pulmonary disease (COPD) complicated by bronchiectasis (BE).

Patients with BE complicated with severe COPD admitted to our hospital were divided into control group and treatment group based on the treatment method. The control group received theophylline sustained-release tablets (oral, twice daily, 0.1 g per dose), while the treatment group received budesonide/glycopyrrolate/formoterol fumarate aerosol (oral inhalation, twice daily, two puffs per dose) combined with theophylline sustained-release tablets (oral, twice daily, 0.1 g per dose). Both groups were treated for 12 weeks. Inflammatory factor levels, pulmonary ventilation function indicators and clinical efficacy were compared between the two groups, and safety was evaluated.

A total of 133 patients were enrolled, including 71 in treatment group and 62 in control group. Propensity score matching (PSM) was performed at 1∶1 ratio, resulting in 50 patients in each group. After treatment, the total clinical effective rates in control group and treatment group were 80.00% (40 cases/50 cases) and 92.00% (46 cases /50 cases), respectively, with statistically significant difference (P<0.05). After treatment, the levels of C-reactive protein (CRP) in treatment group and control group were (13.85±2.43) and (27.54±3.71) mg·L^-1, respectively; tumor necrosis factor-alpha (TNF-α) levels were (50.54±4.28) and (59.37±4.61) pg·mL^-1, respectively; interleukin-6 (IL-6) levels were (42.30±4.71) and (56.42±5.24) pg·mL^-1, respectively; interleukin-8 (IL-8) levels were (15.71±2.63) and (17.88±3.11) pg·mL^-1, respectively; interleukin-18 (IL-18) levels were (59.42±6.25) and (78.62±7.09) pg·mL^-1, respectively. Differences in the above indicators between the two groups were statistically significant (all P<0.05). After treatment, the forced expiratory volume in 1 second (FEV₁) in treatment group and control group were (2.64±0.37) and (2.06±0.32) L, respectively; forced vital capacity (FVC) were (2.82±0.30) and (2.04±0.27) L, respectively; FEV₁/FVC were (65.68±5.94)% and (54.83±5.55)%, respectively. Differences in the above indicators between the two groups were statistically significant (all P<0.05). The main adverse drug reactions in treatment group were nausea, headache, rash and gastrointestinal discomfort; those in control group were nausea, insomnia, gastrointestinal discomfort and rash. The total incidence of adverse drug reactions was 10.00% in treatment group and 8.00% in control group, with no statistically significant difference (P>0.05).

For patients with BE combined with severe COPD, the regimen of budesonide/glycopyrronium bromide/formoterol fumarate inhalation aerosol combined with theophylline sustained-release tablets demonstrates favorable clinical advantages. It can effectively reduce inflammatory factors in patients and improve their ventilation function.