Correlation between Balthazar CT grading, CECT necrosis volume, attenuation value, and prognosis of patients with acute necrotizing pancreatitis.

To analyze the correlation between Balthazar CT grading and contrast-enhanced CT necrosis volume and attenuation value and prognosis of patients with acute necrotizing pancreatitis. Ninety-two patients with acute necrotizing pancreatitis who were treated in the hospital were selected between June 2019 and June 2021, and they were divided into the poor prognosis group and the good prognosis group according to the clinical prognosis at 6 months of follow-up. Balthazar CT, contrast-enhanced CT necrosis volume, and attenuation value were compared between the 2 groups. Multivariate logistic regression analysis was used to analyze the influencing factors. Receiver operating characteristic curve was adopted to analyze the predictive value. Among the 92 participants, there were 28 cases with good prognosis (30.43%) and 64 cases with poor prognosis (69.57%). The Acute Physiology and Chronic Health Evaluation II score, C-reactive protein, urea nitrogen, Balthazar CT, necrotic volume, and average attenuation value of the poor prognosis group were significantly higher than those of the good prognosis group (all P values <.05). The results of the multivariate logistic analysis showed that Balthazar CT grade, necrotic volume, and average attenuation value were independent risk factors for poor prognosis in patients with acute necrotizing pancreatitis (all P values <.05). The area under the curve of Balthazar CT grade, necrotic volume, average attenuation value, and the joint detection in predicting the prognosis of patients with acute necrotizing pancreatitis were 0.765, 0.624, 0.764, and 0.861, respectively. The Balthazar CT grading, necrosis volume, and average attenuation value are significantly higher among patients with acute necrotizing pancreatitis complicated with poor prognosis, and they are also independent risk factors for poor prognosis in patients with acute necrotizing pancreatitis, and can help clinically predict the prognosis of patients with acute necrotizing pancreatitis, and the combined detection has better application effects.

Bacteria-responsive programmed self-activating antibacterial hydrogel to remodel regeneration microenvironment for infected wound healing.

There is still an urgent need to develop hydrogels with intelligent antibacterial ability to achieve on-demand treatment of infected wounds and accelerate wound healing by improving the regeneration microenvironment. We proposed a strategy of hydrogel wound dressing with bacteria-responsive self-activating antibacterial property and multiple nanozyme activities to remodel the regeneration microenvironment in order to significantly promote infected wound healing. Specifically, pH-responsive H2O2 self-supplying composite nanozyme (MSCO) and pH/enzyme-sensitive bacteria-responsive triblock micelles encapsulated with lactate oxidase (PPEL) were prepared and encapsulated in hydrogels composed of L-arginine-modified chitosan (CA) and phenylboronic acid-modified oxidized dextran (ODP) to form a cascade bacteria-responsive self-activating antibacterial composite hydrogel platform. The hydrogels respond to multifactorial changes of the bacterial metabolic microenvironment to achieve on-demand antibacterial and biofilm eradication through transformation of bacterial metabolites, and chemodynamic therapy enhanced by nanozyme activity in conjunction with self-driven nitric oxide (NO) release. The composite hydrogel showed 'self-diagnostic' treatment for changes in the wound microenvironment. Through self-activating antibacterial therapy in the infection stage to self-adaptive oxidative stress relief and angiogenesis in the post-infection stage, it promotes wound closure, accelerates wound collagen deposition and angiogenesis, and completely improves the microenvironment of infected wound regeneration, which provides a new method for the design of intelligent wound dressings.

Better survival and prognosis in SCLC survivors after combined second primary malignancies: A SEER database-based study.

With recent advances in treatment modalities, the survival time for patients with small cell lung cancer (SCLC) has increased, along with the likelihood of recurrence of a second primary tumor. However, patient treatment options and prognosis remain uncertain. This research evaluated the survival rates of patients with SCLC with a second malignancy, aiming to provide new insights and statistics on whether to proceed with more active therapy. SCLC patients were selected based on the Surveillance, Epidemiology, and End Results (SEER) database, updated on April 15, 2021. We defined those with SCLC followed by other cancers (1st of 2 or more primaries) in the sequence number as S-second primary malignant cancer (S-SPM). Those who had other cancers followed by SCLC (2nd of 2 or more primaries) were defined as OC-SCLC. We performed Kaplan-Meier survival analysis, life table analysis, univariate analysis, stratified analysis, and multiple regression analysis of patient data. We considered the difference statistically meaningful at P < .05. After selection, data for 88,448 participants from the SEER database was included in our analysis. The mean survival time for patients with S-SPM was 69.349 months (95% confidence interval [CI]: 65.939, 72.759), and the medium duration of survival was 34 months (95% CI: 29.900, 38.100). Univariate analysis showed that for overall survival, the hazard ratio (HR) of S-SPM was 0.367 (95% CI: 0.351, 0.383), which was 0.633 lower than that of patients with solitary SCLC and 0.606 lower than that of patients with OC-SCLC. For cancer-specific survival (CSS), the HR of S-SPM was 0.285 (95% CI: 0.271, 0.301), which was 0.715 lower than for patients with solitary SCLC and 0.608 lower than that for patients with OC-SCLC. Multiple regression analysis showed that the HR values of S-SPM were lower than those of patients with single SCLC and those with OC-SCLC, before and after adjustment for variables. Kaplan-Meier survival curves showed that patients with S-SPM had significantly better survival times than the other groups. The survival time and prognosis of patients with S-SPM were clearly superior to those with single SCLC and OC-SCLC.

LINC01207 promotes prostate cancer progression by sponging miR-1182 to upregulate AKT3.

Prostate cancer (PC) is recognized as a common malignancy in male patients. Long non-coding RNA (lncRNA) has been implicated in the development of PC. Recently, long intergenic non-protein coding RNA 1207 (LINC01207) has been reported to regulate the carcinogenesis of multiple cancer types. However, its role in the progression of PC remains to be determined. The aim of the present study was to investigate the expression profile, clinicopathological implication and molecular mechanism of action of LINC01207 in the progression of PC. LINC01207 expression levels were compared between PC tumor and paired normal tissue samples from The Cancer Genome Atlas. The expression of LINC01207 was further analyzed in PC cell lines and a normal prostatic cell line. The role of LINC01207 in proliferation, migration and invasion of PC cells was examined using small interfering RNA-mediated silencing. Western blot analysis was used to investigate the changes in protein levels underlying the mechanism of action of LINC01207. The role of LINC01207 in tumorigenesis was evaluated in a xenograft model. LINC01207 was upregulated in PC tumor samples from TCGA data compared with paired normal tissue. LINC01207 expression was significantly increased in PC cells and tumor tissues compared with in normal prostate cells (RWPE1) and normal prostate tissues, respectively. Furthermore, LINC01207 silencing inhibited PC cell proliferation and colony formation and induced apoptosis. Mechanistic experiments showed that LINC01207 promoted carcinogenesis by sponging miR-1182 to regulate the protein levels of AKT3 in PC cell lines. Thus, the findings of the present study indicated that LINC01207 might play a role in the tumorigenesis of PC and may serve as a therapeutic target for PC treatment.