Optimising wound care for patients with cirrhosis: A study of the effect of combination therapy on wound healing.

Cirrhosis, a chronic liver disease, significantly impairs wound healing due to complex alterations in physiology, including compromised immune function, poor nutritional status and altered blood flow. This prospective observational cohort study aimed to evaluate the effectiveness of the multidimensional combination therapy approach in enhancing wound healing among patients diagnosed with cirrhosis. The study was conducted from February to November 2023 in Shanghai, China, including 248 patients with cirrhosis experiencing poor wound healing. The combination therapy consisted of tailored pharmacological treatments, advanced wound dressings, dietitian-directed dietary regimens and supplementary therapies like negative pressure wound therapy (NPWT), stem cell and hyperbaric oxygen therapy. The interventions were customised based on comprehensive initial assessments of liver function, nutritional status and wound characteristics. Follow-ups were conducted to monitor response and adjust treatments accordingly. The patient demographic was varied, predominantly 41-60 years old, with the slight male predominance. The study demonstrated that after 3 months of treatment, wound sizes decreased significantly across all cirrhosis severity levels: mild (2.4-1.7 cm2 ), moderate (4.1-2.6 cm2 ) and severe (6.2-4.4 cm2 ). Healing rates improved to 90% in mild, 75% in moderate and 45% in severe cases over 6 months. Albumin levels increased by the average of +0.3 g/dL to +0.4 g/dL post-treatment across the severity spectrum. However, complication rates escalated with severity: Mild cases had a 10% infection rate, while severe cases had up to 30% infection rate. Combination therapy significantly improved wound healing in cirrhosis patients, with the extent of improvement correlated with the severity of the condition. Tailored, multidisciplinary approaches are critical in managing the intricate wound healing process in cirrhosis, effectively reducing healing times and improving overall treatment outcomes. These findings advocate for personalised care strategies and highlight the potential of integrating various treatment modalities to address the complex needs of this population.

Evaluation of 18F-FAPI-04 Imaging in Assessing the Therapeutic Response of Rheumatoid Arthritis.

PURPOSE: Fibroblast activating protein (FAP) is highly expressed in the synovial tissues of rheumatoid arthritis (RA) patients. The aim of this study was to determine the feasibility of PET imaging with an Al[18F] F-NOTA-labeled FAP inhibitor 04(18F-FAPI-04) for the evaluation of arthritic progression and therapeutic response in experimental arthritis. METHODS: Fibroblast-like synoviocytes (FLSs) were obtained from patients with RA or osteoarthritis (OA), and the relationship between 18F-FAPI-04 uptake and the inflammatory activity of RA FLSs was investigated. Collagen-induce arthritis (CIA) mice models were established and treated with methotrexate (MTX) or etanercept (ETC). Then, PET imaging was performed 24 h following 18F-FAPI-04 injection. The imaging results were compared by assessing macroscopic arthritis scores and histological staining. RESULTS: 18F-FAPI-04 uptake was obvious in RA FLSs that characterizing FAP activation. The higher the uptake of 18F-FAPI-04, the more severity of the inflammatory phenotype in RA FLS. Furthermore, the uptake of 18F-FAPI-04 in inflamed joints could be found even before the deformity of the parental joints could be observed by histological examination. Both MTX and ETC were effective in inhibiting the progression of arthritis in CIA mice was confirmed by macroscopic, histological, and radiographic pathology scores. Importantly, 18F-FAPI-04 uptake declined accordingly in CIA models following MTX and ETC treatment. CONCLUSIONS: These findings suggest that PET imaging of 18F-FAPI-04 can be used to monitor treatment response in RA, and is more sensitive in disease speculation than macroscopic arthritis scoring.

Clinical Effect of Nursing Based on the Kano Model in Emergency Multiple Injuries.

Multiple injury refers to the injury of two or more anatomical parts of the body caused by mechanical injury factors. Even if only one injury exists alone, it can endanger limbs or lives. Therefore, nursing plays an important role in its treatment. Here, we investigated the application and clinical effect of nursing based on the Kano model in emergency multiple injuries. A case-control study was designed, where 48 patients with multiple injuries in the emergency department were divided into the control group to perform routine care and 48 patients were divided into the study group to carry on nursing based on the Kano model. The first-aid indexes, success rate of rescue, inflammatory response indicators, satisfaction rate of nursing, incidence of adverse events, and prognosis were compared between the two groups. A monofactor analysis showed that the emergency response time, admission time, and emergency department rescue time were shorter in the study group than those in the control group, indicating a higher success rate of rescue with nursing based on the Kano model. For the immunity of patients, the scores of mental states and the serum levels of inflammatory factors were lower in the study group than those in the control group. In addition, the rate of nursing satisfaction and good prognosis in the study group was significantly higher than those in the control group, and the incidence of adverse events was significantly lower than that in the control group. These results indicated that nursing based on the Kano model in patients with emergency multiple injuries can reduce the body inflammatory reaction, reduce the risk of adverse events, improve the prognosis of patients, and obtain high patient satisfaction.

Danshensu alleviates bleomycin-induced pulmonary fibrosis by inhibiting lung fibroblast-to-myofibroblast transition via the MEK/ERK signaling pathway.

Pulmonary fibrosis (PF) is a chronic pulmonary interstitial disease, and its pathological process is closely related to fibroblast-myofibroblast differentiation. Danshensu (DSS) has been reported to exert an anti-fibrotic effect in heart and liver. However, it is unknown whether DSS has an equally anti-fibrotic effect on lungs. To evaluate the effect of DSS on PF and demonstrate its possible molecular mechanisms, we established an in vitro model on TGF-ß1 (5 ng/mL)-stimulated NIH3T3 cells and in vivo model on bleomycin (BLM) (5 mg/kg)-induced PF mice. In vitro, our results revealed that 50 µM DSS effectively inhibited the fibroblast proliferation, migration and differentiation into myofibroblast. In vivo, our results showed that DSS (28 and 56 mg/kg) reduced damaged lung structures, infiltrated inflammatory cells and accumulated areas of collagen deposition. Moreover, we showed that DSS decreased the fibroblast-specific protein 1 (FSP-1) - and α-SMA-positive areas. Meanwhile, we indicated that DSS reduced the expression of TGF-ß1, α-SMA and COL-I in the lung tissues of mice. To further explore the mechanism of DSS on alleviating PF, we detected the MEK/ERK signaling pathway. Our results showed that DSS reduced the phosphorylation of MEK1/2 and ERK1/2, indicating that DSS might inhibit the MEK/ERK signaling pathway. Taken together, these results demonstrated that DSS could suppress lung fibroblast proliferation, migration and differentiation to myofibroblasts, possibly through suppressing the MEK/ERK signaling pathway, which suggested that DSS might be a potential therapeutic drug for PF treatment.

RNA interference remarkably suppresses bcl-2 gene expression in cancer cells in vitro and in vivo.

Bcl-2 is an anti-apoptotic protein. If the level of Bcl-2 protein can be reduced sufficiently in tumors using RNA interference (RNAi) to target the gene message, the apoptosis of tumor cells may be promoted. In this study, we synthesized 19 nucleotides (nts) small interference RNA (siRNA) constructs suppressing bcl-2 gene expression in human tumor cells (HeLaB2 and BGC-823 cell lines) in vitro. The bcl-2 gene expression levels were significantly reduced when these siRNA were transfected into experimental two tumor cells for 72 hours. The apoptosis process was also examined in the tumor cells. Here we synthesized siRNA from a DNA template under the control of the RNA polymerase III promoter in transfected tumor cells. Using this DNA vector-based approach, we found that the siRNA efficiently and specifically inhibited the synthesis of protein encoded by the bcl-2 gene in HeLaB2 and BGC-823 tumor cells. Tumor growth was inhibited by 66.5% with 2mg/kg pSilencer 3.1H1-bcl-2 in mouse liver tumor-bearing BALB/c mice. This approach may prove to be a valuable clinical technique for the analysis of specific gene functions and gene therapy of malignant tumors that utilize the bcl-2 gene via RNA interference.