Shock index to predict outcomes in patients with trauma following traffic collisions: a retrospective cohort study.

PURPOSE: Taiwan, which has a rate of high vehicle ownership, faces significant challenges in managing trauma caused by traffic collisions. In Taiwan, traffic collisions contribute significantly to morbidity and mortality, with a high incidence of severe bleeding trauma. The shock index (SI) and the modified shock index (MSI) have been proposed as early indicators of hemodynamic instability. In this study, we aimed to assess the efficacy of SI and MSI in predicting adverse outcomes in patients with trauma following traffic collisions. METHODS: This retrospective cohort study was conducted at Chi Mei Hospital from January 2015 to December 2020. The comprehensive analysis included 662 patients, with data collected on vital signs and outcomes such as mortality, blood transfusion, emergent surgical intervention (ESI), transarterial embolization (TAE), and intensive care unit (ICU) admission. Optimal cutoff points for SI and MSI were identified by calculating the Youden index. Logistic regression analysis was used to assess outcomes, adjusting for demographic and injury severity variables. RESULTS: An SI threshold of 1.11 was associated with an increased risk of mortality, while an SI of 0.84 predicted the need for blood transfusion in the context of traffic collisions. Both SI and MSI demonstrated high predictive power for mortality and blood transfusion, with acceptable accuracy for TAE, ESI, and ICU admission. Logistic regression analyses confirmed the independence of SI and MSI as risk factors for adverse outcomes, thus, providing valuable insights into their clinical utility. CONCLUSIONS: SI and MSI are valuable tools for predicting mortality and blood transfusion needs in patients with trauma due to traffic collisions. These findings advance the quality of care for patients with trauma during their transition from the emergency room to the ICU, facilitating prompt and reliable decision-making processes and improving the care of patients with trauma.

Punicalagin is cytotoxic to human colon cancer cells by modulating cell proliferation, apoptosis, and invasion.

Purpose: The purpose of this study was to explore the anticancer effect of punicalagin, an abundant bioactive tannin compound isolated from Punica granatum L., on three colon cancer cell lines, namely, HCT 116, HT-29, and LoVo.Research Design: Normal and colon cancer cells were treated with different concentrations of punicalagin for different periods. Data Collection and Analysis: Cell viability was measured with a CCK-8 assay. Programmed cell death and invasion were analyzed using an annexin V and cell death kit and a cell invasion analysis kit. The expression of active caspase-3, MMP-2, MMP-9, Snail, and Slug were measured by Western blot.Results: The results of the cell viability analysis showed that punicalagin was cytotoxic to colon cancer cells, but it was not to normal cells in a dose- and time-dependent manner. Additionally, punicalagin induced apoptosis in colon cancer cells (shown by the cumulative percentage of colorectal cancer cells in early and late apoptosis). It was found that caspase-3 activity increased following punicalagin treatment. Western blot results also showed that punicalagin increased the expression of activated caspase-3. In contrast, punicalagin inhibited the invasion of colon cancer cells. Further, treatment of colon cancer cells with punicalagin suppressed the expression of MMP-2, MMP-9, Snail, and Slug. Conclusions: These results showed that the activation of caspase-3 and the inhibition of MMP-2, MMP-9, Snail and Slug were involved in the effects of punicalagin on colon cancer cells.

NCAPG deregulation indicates poor patient survival and contributes to colorectal carcinogenesis.

Colorectal cancer (CRC) is one of the types of cancers with a high incidence and is ranked the 3rd among men and 2nd among women worldwide. The purpose of this study was to investigate the correlation between non-SMC condensin I complex subunit G (NCAPG) and the prognosis of CRC and its function in CRC cells. The expression of NCAPG in colorectal tissues and cells was detected by immunoblotting and immunohistochemistry. Kaplan-Meier analysis was used to analyze the correlation between NCAPG and CRC prognosis. RNAi technology was used to investigate how NCAPG inhibition affected the proliferation and migration of CRC cells. Overexpression of NCAPG was positively correlated with several clinicopathologic characteristics, including T stage (P = 0.0198), M stage (P = 0.0005), and TNM stage (P < 0.0001). Kaplan-Meier analysis showed that the overexpression of NCAPG was also negatively correlated with disease-free survival and overall survival. In the culture of CRC cells, the knockdown of NCAPG inhibited the proliferation, migration, and invasion of the cells. Meanwhile, it was also found that NCAPG knockdown could interfere with G2/M-G1 transition in the cell cycle, resulting in the inhibition of cell proliferation. The overexpression of NCAPG may serve as a candidate biomarker for CRC prognosis. NCAPG is also a potential therapeutic target for CRC.

Delayed traumatic purulent pericarditis with cardiac tamponade - A rare case report.

Thoracic trauma often results in immediate or delayed hemorrhage. There are few cases of purulent pericarditis with pericardial tamponade reported in the literature. If a devastating complication develops several weeks following blunt thoracic trauma, the causal relationship with the thoracic trauma event is less evident. As such, accurate diagnosis and subsequent effective treatment implementation is likely to be delayed. Herein, we present the case of a 46-year-old male patient with delayed purulent pericarditis that led to cardiac tamponade 2 weeks after the initial trauma.

Adjuvant chemotherapy and survival outcomes in rectal cancer patients with good response (ypT0-2N0) after neoadjuvant chemoradiotherapy and surgery: A retrospective nationwide analysis.

Background: For rectal cancer, it remains unclear how to incorporate tumor response to neoadjuvant chemoradiotherapy (nCRT) when deciding whether to give adjuvant chemotherapy. In this study, we aim to determinate the survival benefit of adjuvant chemotherapy for rectal cancer patients with good response (ypT0-2N0) after nCRT and surgery. Methods: The study cohort included 720 rectal cancer patients who had good response (ypT0-2N0) after nCRT and surgery, who did or did not receive adjuvant chemotherapy between January 2007 and December 2017, from the Taiwan Cancer Registry and National Health Insurance Research database. The Kaplan-Meier method, log-rank tests, and Cox regression analysis were performed to investigate the effect of adjuvant chemotherapy on 5-year overall survival (OS) and disease-free survival (DFS). Results: Of 720 patients, 368 (51.1%) received adjuvant chemotherapy and 352 (48.9%) did not. Patients who received adjuvant chemotherapy were more likely to be female, younger (≤ 65), with advanced clinical T (3-4)/N (1-2) classification and ypT2 classification. No significant difference in 5-year OS (p=0.681) or DFS (p=0.942) were observed by receipt of adjuvant chemotherapy or not. Multivariable analysis revealed adjuvant chemotherapy was not associated with better OS (adjusted hazard ratio [aHR], 1.03; 95% Confidence Interval [CI], 0.88-1.21) or DFS (aHR, 1.05; 95% CI, 0.89-1.24). Stratified analysis for OS and DFS found no significant protective effect in the use of adjuvant chemotherapy, even for those with advanced clinical T or N classification. Conclusion: Adjuvant chemotherapy may be omitted in rectal cancer patients with good response (ypT0-2N0) after nCRT and surgery.

A novel mechanism driving poor-prognostic gastric cancer: overexpression of the transcription factor Krüppel-like factor 16 promotes growth and metastasis of gastric cancer through regulating the Notch pathway.

Gastric cancer (GC) is one of the most common malignant tumors worldwide and has high rates of morbidity and mortality. This study investigated the role of Krüppel-like factor 16 (KLF16) in GC. Real-time polymerase chain reaction, Western blotting, and immunohistochemistry were used to examine the expression of KLF16 in gastric cells and tissues. Gene overexpression and silencing were applied to study the involvement of KLF16 in GC cell growth and metastasis along with its underlying mechanism. The results indicate that KLF16 overexpression is significantly associated with nodal status, distant metastasis, staging, degree of differentiation, vascular invasion, and patient survival. Multivariate Cox proportional hazards regression model analysis revealed that the overexpression of KLF16 is an independent prognostic biomarker of GC. The in vitro study revealed that up-regulated KLF16 accelerates cell growth and metastasis, whereas the inhibition of KLF16 suppresses these cellular activities. The results of an animal study also indicated that the overexpression and silencing of KLF16 accelerate and repress xenograft proliferation and metastasis. Further studies of affected cell growth and metastasis revealed that KLF16 modulates the cell cycle and epithelial-mesenchymal transition through transcriptional regulation of microfibrillar-associated protein 5. Collectively, these results reveal that KLF16 overexpression is a potential prognostic biomarker and therapeutic target for the treatment of GC.

Novel signaling pathways regulate SARS-CoV and SARS-CoV-2 infectious disease.

ABSTRACT: Severe acute respiratory syndrome coronavirus (SARS-CoV)-2 induces severe infection, and it is responsible for a worldwide disease outbreak starting in late 2019. Currently, there are no effective medications against coronavirus. In the present study, we utilized a holistic bioinformatics approach to study gene signatures of SARS-CoV- and SARS-CoV-2-infected Calu-3 lung adenocarcinoma cells. Through the Gene Ontology platform, we determined that several cytokine genes were up-regulated after SARS-CoV-2 infection, including TNF, IL6, CSF2, IFNL1, IL-17C, CXCL10, and CXCL11. Differentially regulated pathways were detected by the Kyoto Encyclopedia of Genes and Genomes, gene ontology, and Hallmark platform, including chemokines, cytokines, cytokine receptors, cytokine metabolism, inflammation, immune responses, and cellular responses to the virus. A Venn diagram was utilized to illustrate common overlapping genes from SARS-CoV- and SARS-CoV-2-infected datasets. An Ingenuity pathway analysis discovered an enrichment of tumor necrosis factor- (TNF-) and interleukin (IL)-17-related signaling in a gene set enrichment analysis. Downstream networks were predicted by the Database for Annotation, Visualization, and Integrated Discovery platform also revealed that TNF and TNF receptor 2 signaling elicited leukocyte recruitment, activation, and survival of host cells after coronavirus infection. Our discovery provides essential evidence for transcript regulation and downstream signaling of SARS-CoV and SARS-CoV-2 infection.

The association between the composite quality measure "textbook outcome" and long term survival in operated colon cancer.

The aim of this study was to investigate the relationship between textbook outcome and survival in patients with surgically treated colon cancer. A total of 804 surgical cases were enrolled between June 1, 2010 and December 31, 2014. Textbook outcome was defined as patients who had colon cancer surgery and met the six healthcare parameters of surgery within 6 weeks, radical resection, lymph node (LN) yield ≥12, no ostomy, no adverse outcome and colonoscopy before/after surgery within 6 months. The effect of textbook outcome on 5-year disease-specific survival (DSS) was calculated using the Kaplan-Meier method. A Cox regression model was used to find significant independent variables and stratified analysis used to determine whether text-book outcome had a survival benefit. A textbook outcome was achieved in 59.5% of patients undergoing colon cancer surgery. Important obstacles to achieving textbook outcome were no stomy, no adverse outcome and LN yield ≥12. Patients with text-book outcome had statistically significant better 5-year DSS compared to those with-out (80.1% vs. 58.3%). Multivariate analyses indicated that colon cancer patients with textbook outcome had better 5-year DSS after adjusting for various confounders ([aHR], 0.44; 95% CI, 0.34-0.57). Thus, besides being an index of short-term quality of care, textbook outcomes could be used as a prognosticator of long-term outcomes, such as 5-year survival rates.

Increased expression of secreted frizzled related protein 1 (SFRP1) predicts ampullary adenocarcinoma recurrence.

Ampullary adenocarcinoma is a rare gastrointestinal cancer in which WNT signalling dysregulation has been previously reported. Secreted frizzled related protein 1 (SFRP1) is one of the extracellular ligands of WNT signalling. We performed bioinformatics analyses of SFRP1 expression in human cancer. Microarray analysis of SFRP1 in periampullary adenocarcinoma was obtained from the Gene Expression Omnibus GSE39409 dataset. SFRP1 expression in ampullary adenocarcinoma was detected by immunohistochemistry staining and correlated with patients' clinical outcomes. Our results showed that SFRP1 expression had different clinical applications in all types of human cancer. No detected alteration of SFPR1 gene and SFRP1 expression in ampullary adenocarcinoma was lower than that in other periampullary adenocarcinomas. However, high expression levels of SFRP1 protein were correlated with cancer recurrence, peritoneal carcinomatosis and poor patient prognosis. Gene set enrichment analysis showed downregulation of multiple WNT-related genes in primary culture cells from ampullary adenocarcinoma, but SFRP1 expression was increased. We found an interaction between WNT, bone morphogenetic protein and hedgehog signalling with SFRP1. Furthermore, a high expression of SFRP1 predicted poor prognosis for ampullary adenocarcinoma patients. Because it is a multifunctional protein, SFRP1 targeting serves as a potential therapy for ampullary adenocarcinoma patients.

Cancer-Derived Transforming Growth Factor-ß Modulates Tumor-Associated Macrophages in Ampullary Cancer.

PURPOSE: Tumor-associated macrophages (TAMs) originate from monocytes and differentiate into mature macrophages. The interaction between cancer cells and TAMs promotes tumor growth and suppresses immunosurveillance. However, this phenomenon has seldom been observed in ampullary cancer. PATIENTS AND METHODS: TAMs in ampullary cancer were investigated using immunohistochemical (IHC) staining of cancer tissues. Bioinformatic analysis of data from the Gene Expression Omnibus (GEO) database revealed transforming growth factor-beta (TGF-ß) signaling in ampullary cancer. The complementary DNA microarray of cancer was compared with adjacent normal duodenum and enzyme-linked immunosorbent assay of serum was used to verify TGF-ß signaling in patients. The THP-1 cell line was activated in vitro to imitate M2 TAMs. ClueGo and CluePedia software were operated to simulate TGF-ß-related networks in ampullary cancer. RESULTS: The IHC study revealed that the majority of TAMs inside ampullary cancer were cluster of differentiation (CD)163+ cells and that the expression of mature CD68+ macrophages was correlated with advanced cancer stage. Bioinformatics analysis revealed that TGF-ß and its downstream signaling were significantly upregulated. To verify our bioinformatics-derived predictions, we performed several experiments and demonstrated that increased TGF-ß expression was detected in the cDNA microarray. Higher serum levels of TGF-ß were correlated with fewer CD68+ and more inducible nitric oxide synthase macrophages in ampullary cancer. Treatment with TGF-ß induced modulation of THP-1-derived macrophages. CONCLUSION: The present study demonstrates that TGF-ß modulates macrophage activity in ampullary cancer. Targeting TGF-ß could be an approach to activating immunosurveillance.

The Impact of High-Flow Nasal Cannula on the Outcome of Immunocompromised Patients with Acute Respiratory Failure: A Systematic Review and Meta-Analysis.

Background and objectives: High-flow nasal cannula (HFNC) can be used as a respiratory support strategy for patients with acute respiratory failure (ARF). However, no clear evidence exists to support or oppose HFNC use in immunocompromised patients. Thus, this meta-analysis aims to assess the effects of HFNC, compared to conventional oxygen therapy (COT) and noninvasive ventilation (NIV), on the outcomes in immunocompromised patients with ARF. The Pubmed, Embase and Cochrane databases were searched up to November 2018. Materials and Methods: Only clinical studies comparing the effect of HFNC with COT or NIV for immunocompromised patients with ARF were included. The outcome included the rate of intubation, mortality and length of stay (LOS). Results: A total of eight studies involving 1433 immunocompromised patients with ARF were enrolled. The pooled analysis showed that HFNC was significantly associated with a reduced intubation rate (risk ratio (RR), 0.83; 95% confidence interval (CI), 0.74-0.94, I2 = 0%). Among subgroup analysis, HFNC was associated with a lower intubation rate than COT (RR, 0.86; 95% CI, 0.75-0.95, I2 = 0%) and NIV (RR, 0.59; 95% CI, 0.40-0.86, I2 = 0%), respectively. However, there was no significant difference between HFNC and control groups in terms of 28-day mortality (RR, 0.78; 95% CI, 0.58-1.04, I2 = 48%), and intensive care unit (ICU) mortality (RR, 0.87; 95% CI, 0.73-1.05, I2 = 57%). The ICU and hospital LOS were similar between HFNC and control groups (ICU LOS: mean difference, 0.49 days; 95% CI, -0.25-1.23, I2 = 69%; hospital LOS: mean difference, -0.12 days; 95% CI, -1.86-1.61, I2 = 64%). Conclusions: Use of HFNC may decrease the intubation rate in immunocompromised patients with ARF compared with the control group, including COT and NIV. However, HFNC could not provide additional survival benefit or shorten the LOS. Further large, randomized controlled trials are needed to confirm these findings.

The impact of marital status on survival in patients with surgically treated colon cancer.

The aim of this study was to investigate the relationship between marital status and disease outcome in patients with surgically treated colon cancer. Between June 2010 and December 2015, a total of 925 patients with newly diagnosed colon cancer receiving curative resection were enrolled. The effect of marital status on 5-year disease-specific survival (DSS) was calculated using Kaplan-Meier method, and was compared by log-rank tests. A Cox regression model was used to find significant independent variables and determine whether marriage had a survival benefit in patients with colon cancer, using stratified analysis. Among these patients, 749 (80.9%) were married, and 176 (19.1%) were unmarried, including 42 (4.5%) never-married, 42 (4.5%) divorced/separated, and 93 (10.1%) widowed. There was no significant difference between the married and unmarried groups in cancer stage or adjuvant treatment. Married patients had better 5-year DSS compared with unmarried patients (69.1% vs 55.9%, P < .001). Uni- and multivariate analyses also indicated that unmarried patients had worse 5-year DSS after adjusting for various confounders (adjusted HR [aHR], 1.66; 95% CI, 1.24-2.22). Further stratified analysis according to demographic variables revealed that unmarried status was a significant negative factor in patients with the following characteristics: age >65 years, female sex, well/moderately differentiated tumor, and advanced tumor-node-metastasis (TNM) stage disease (III-IV). Thus, marriage has a protective effect, and contributes to better survival in patients with surgically treated colon cancer. Additional social support for unmarried colon cancer patients may lead to improve outcomes.