Objective To analyze the influencing factors of hospitalization costs of obstructive hydronephrosis and explore the optimal grouping of diagnosis-intervention packet (DIP), so as to provide a basis for hospitals to strengthen the cost control of diseases, improve the level of refined management, and improve the compensation mechanism of DIP expenses by medical insurance departments. Methods The homepage data of medical records of Pingshan District People’s Hospital of Shenzhen City from January 2019 to December 2021 were collected, and the information of the discharged patients with the International Classification of Diseases-10th revision code as N13.2 was selected. The factors affecting hospitalization costs were analyzed by single factor analyses and multiple stepwise linear regression, the main surgical methods, number of other operations, and influencing factors of expenses were used as classification nodes, and the decision tree model was used to group and predict costs. Results A total of 1319 patients were included, the median inpatient expense was 10889.59 yuan, and the interquartile range was 10943.89 yuan. The case classification, days of hospitalization, condition of admission, whether it was hospitalized for the first time, whether clinical pathway was implemented, the way of discharge, the number of other diagnoses, and admission path were important factors affecting the inpatient expenses, and 12 groups of case mixes and corresponding expense standards were formed. The reduction in variance was 86.10%, the maximum coefficient of variation was 0.33, and the cost analysis ratio was 96.25%. Conclusions Combining the DIP grouping principle and the multi-factor grouping strategy of diagnosis-related groups, the grouping of obstructive hydronephrosis cases constructed by decision tree model is reasonable and the cost standard is close to reality. The case mixes and cost criteria can provide data support and decision-making reference for hospitals and medical insurance institutions.
ObjectiveTo investigate the effect of Gasdermin D(GSDMD) gene knockout on lung injury and reactive oxygen species (ROS)/nod-like receptor protein 3 (NLRP3)/cysteinyl aspartate specific proteinase-1(caspase-1) pyroptosis pathway of pneumonia mice. Methods20 wild-type (WT) male C57BL/6J mice were randomly divided into WT control group and WT model group. 20 GSDMD gene knockout (KO) mice were randomly divided into KO control group and KO model group, each group consisted of 10 animals. The pneumonia model was induced by puncturing the nasal mucosa with a sterile needle and slowly instilling Streptococcus pneumoniae suspension in WT model group and KO model group. Serum and bronchoalveolar lavage fluid (BALF) were collected 7 days after modeling, and the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected; the lung tissues were collected and the dry wet ratio (W/D), pathological changes, the levels of malondialdehyde (MDA), total antioxidant capacity (T-AOC), superoxide dismutase (SOD), ROS activity, and the protein expression levels of GSDMD, GSDMD-N, NLRP3, Caspase-1 were detected. ResultsThe lung tissue of WT model group showed cell infiltration with alveolar septal thickening, the ratio of W/d in lung tissue, the levels of IL-1β, IL-6 and TNF-α in serum and BALF, the levels of MDA, ROS, NLRP3 and Caspase-1 in lung tissue were all higher than those in WT control group, the levels of T-AOC and SOD in lung tissue were lower than those in WT control group (P<0.05), and the levels of serum, BALF and lung tissue in KO control group were not significantly different from those in WT control group (P>0.05) There was no expression of GSDMD-N in the lung tissue of KO model group, lung tissue w/d ratio, serum and BALF levels of IL-1β, IL-6, TNF-α, MDA, ROS activity, GSDMD-N, NLRP3 and Caspase-1 protein expression were lower than those in WT model group, the levels of T-AOC and SOD in lung tissue were higher than those in WT Model Group (P<0.05). ConclusionGSDMD gene knockout attenuates lung injury and inhibits ROS/NLRP3/Caspase-1 pathway in pneumonia mice.