Incidence of surgical site infection in minimally invasive colorectal surgery.

BACKGROUND: Surgical site infection (SSI) is a common complication of colorectal surgery. Minimally invasive surgery notably reduces the incidence of SSI. This study aimed to compare the incidences of SSI after robot-assisted colorectal surgery (RACS) vs that after laparoscopic assisted colorectal surgery (LACS) and to analyze associated risk factors for SSI in minimally invasive colorectal surgery. AIM: To compare the incidences of SSI after RACS and LACS, and to analyze the risk factors associated with SSI after minimally invasive colorectal surgery. METHODS: Clinical data derived from patients who underwent minimally invasive colorectal surgery between October 2020 and October 2022 at the First Affiliated Hospital of Soochow University were collated. Differences in clinical characteristics and surgeryrelated information associated with RACS and LACS were compared, and possible risk factors for SSI were identified. RESULTS: A total of 246 patients (112 LACS and 134 RACS) were included in the study. Fortythree (17.5%) developed SSI. The proportions of patients who developed SSI were similar in the two groups (17.9% vs 17.2%, P = 0.887). Diabetes mellitus, intraoperative blood loss ≥ 100 mL, and incision length were independent risk factors for SSI. Possible additional risk factors included neoadjuvant therapy, lesion site, and operation time. CONCLUSION: There was no difference in SSI incidence in the RACS and LACS groups. Diabetes mellitus, intraoperative blood loss ≥ 100 mL, and incision length were independent risk factors for postoperative SSI.

HMGB1 promotes mitochondrial transfer between hepatocellular carcinoma cells through RHOT1 and RAC1 under hypoxia.

Mitochondrial transfer plays an important role in various diseases, and many mitochondrial biological functions can be regulated by HMGB1. To explore the role of mitochondrial transfer in hepatocellular carcinoma (HCC) and its relationship with HMGB1, field emission scanning electron microscopy, immunofluorescence, and flow cytometry were used to detect the mitochondrial transfer between HCC cells. We found that mitochondrial transfer between HCC cells was confirmed using tunnel nanotubes (TNTs). The transfer of mitochondria from the highly invasive HCC cells to the less invasive HCC cells could enhance the migration and invasion ability of the latter. The hypoxic conditions increased the mitochondrial transfer between HCC cells. Then the mechanism was identified using co-immunoprecipitation, luciferase reporter assay, and chromatin immunoprecipitation. We found that RHOT1, a mitochondrial transport protein, promoted mitochondrial transfer and the migration and metastasis of HCC cells during this process. Under hypoxia, HMGB1 further regulated RHOT1 expression by increasing the expression of NFYA and NFYC subunits of the NF-Y complex. RAC1, a protein associated with TNTs formation, promoted mitochondrial transfer and HCC development. Besides, HMGB1 regulated RAC1 aggregation to the cell membrane under hypoxia. Finally, the changes and significance of related molecules in clinical samples of HCC were analyzed using bioinformatics and tissue microarray analyses. We found that HCC patients with high HMGB1, RHOT1, or RAC1 expression exhibited a relatively shorter overall survival period. In conclusion, under hypoxic conditions, HMGB1 promoted mitochondrial transfer and migration and invasion of HCC cells by increasing the expression of mitochondrial transport protein RHOT1 and TNTs formation-related protein RAC1.

Inhibition of photosensitized degradation of organic contaminants by copper under conditions typical of estuarine and coastal waters.

Dissolved organic matter (DOM) driven-photochemical processes play an important role in the redox cycling of trace metals and attenuation of organic contaminants in estuarine and coastal ecosystems. In this study, we evaluate the effect of Cu on 4-carboxybenzophenone (CBBP) and Suwannee River natural organic matter (SRNOM)-photosensitized degradation of seven target contaminants (TCs) including phenols and amines under pH conditions and salt concentrations typical of those encountered in estuarine and coastal waters. Our results show that trace amounts of Cu(II) (25 -500 nM) induce strong inhibition of the photosensitized degradation of all TCs in solutions containing CBBP. The influence of TCs on the photo-formation of Cu(I) and the decrease in the lifetime of transformation intermediates of contaminants (TC•+/ TC•(-H)) in the presence of Cu(I) indicated that the inhibition effect of Cu was mainly due to the reduction of TC•+/ TC•(-H) by the photo-produced Cu(I). The inhibitory effect of Cu on the photodegradation of TCs decreased with the increase in Cl- concentration since less reactive Cu(I)-Cl complexes dominate at high Cl- concentrations. The impact of Cu on the SRNOM-sensitized degradation of TCs is less pronounced compared to that observed in CBBP solution since the redox active moieties present in SRNOM competes with Cu(I) to reduce TC•+/ TC•(-H). A detailed mathematical model is developed to describe the photodegradation of contaminants and Cu redox transformations in irradiated SRNOM and CBBP solutions.

Hepatoid adenocarcinoma of the stomach with metastatic choriocarcinoma of the liver: A case report of a rare subtype of gastric cancer with a complex treatment course.

Gastric hepatoid adenocarcinoma and hepatic choriocarcinoma are rare diseases in clinical settings, and the case we report here is a combination of both. A 66-year-old woman presented with a chief complaint of abdominal discomfort. The patient was examined using gastroscopy and computed tomography (CT) scan, and these revealed an irregular surface ulcer on the wall of the gastric antrum. A mass, 2.0 cm in diameter, was found in the liver in April 2020. The endoscopic biopsy findings were consistent with a diagnosis of moderately to poorly differentiated hepatoid adenocarcinoma. She was then referred to our hospital for further treatment. Initially, neoadjuvant therapy was initiated for the patient. The CT scan showed that the liver metastases had progressed; hence, surgery was performed. Postoperative pathology showed that the gastric lesions were mostly hepatoid adenocarcinoma with no choriocarcinoma, while the liver lesions comprised approximately 10% hepatoid adenocarcinoma and 90% choriocarcinoma. One month later, the patient developed tumor recurrence in the liver as observed on CT imaging. Subsequently, a variety of chemotherapy regimens were tried with no obvious results. The patient eventually developed multiple organ metastasis and died in July 2021. The overall survival was 16 months. Based on findings from this case report, it appears that initial neoadjuvant therapy was not effective and radical surgery may be the best treatment for patients with hepatoid adenocarcinoma of the stomach.

Reversible Underwater Adhesion for Soft Robotic Feet by Leveraging Electrochemically Tunable Liquid Metal Interfaces.

Soft crawling robots have potential applications for surveillance, rescue, and detection in complex environments. Despite this, most existing soft crawling robots either use nonadjustable feet to passively induce asymmetry in friction to actuate or are only capable of moving on surfaces with specific designs. Thus, robots often lack the ability to move along arbitrary directions in a two-dimensional (2D) plane or in unpredictable environments such as wet surfaces. Here, leveraging the electrochemically tunable interfaces of liquid metal, we report the development of liquid metal smart feet (LMSF) that enable electrical control of friction for achieving versatile actuation of prismatic crawling robots on wet slippery surfaces. The functionality of the LMSF is examined on crawling robots with soft or rigid actuators. Parameters that affect the performance of the LMSF are investigated. The robots with the LMSF prove capable of actuating across different surfaces in various solutions. Demonstration of 2D locomotion of crawling robots along arbitrary directions validates the versatility and reliability of the LMSF, suggesting broad utility in the development of advanced soft robotic systems.

Nobiletin Inhibits Helicobacterium pylori Infection-Induced Gastric Carcinogenic Signaling by Blocking Inflammation, Apoptosis, and Mitogen-Activated Protein Kinase Events in Gastric Epithelial-1 Cells.

Helicobacter pylori causes a Gram-negative bacterial infection that can increase the risk of gastric cancer. Consequently, meticulous prevention of an H. pylori infection is significant for averting gastric cancer in humans. Nobiletin, an important dietary polymethoxylated flavonoid in citrus fruits, possesses multidimensional pharmaceutical properties, including its ability to act as an anticancer, anti-inflammatory, antioxidative, cardiovascularly defensive, neuroprotective, and antimetabolic agent. Our study evaluates the role of nobiletin in inflammation-mediated gastric carcinogenic signaling of H. pylori-arbitrated coculture in the human gastric epithelial (GES)-1 cell line. Our results show that the culture system of H. pylori-tainted GES-1 cells demonstrates maximum fabrication of reactive oxygen species (ROS), mediating DNA injury and augmenting nuclear fragmentations. Treatment with nobiletin reduces ROS levels and apoptotic morphological changes by dual staining and decreases levels of lipid peroxides and glutathione content in H. pylori-infected GES-1 cells. Phosphatidylinositol-3 kinase (PI3K)/protein kinase B (AKT)/phosphatase and tensin homolog signaling have been implicated to affect cell endurance, inflammation, proliferation, and carcinogenic activity in gastric GES-1 cells. We find that nobiletin strongly impedes tumor necrosis factor-α, interleukin-6, cyclooxygenase-2, PI3K, AKT, and mitogen-activated protein kinase molecules, including p38, extracellular receptor kinase 1, and c-Jun amino-terminal expression in H. pylori-infected GES-1 cells. We conclude that nobiletin potentially impedes H. pylori infection and its related activation, likely preventing H. pylori infection-mediated gastric cancer.

Tumor-associated macrophage infiltration and prognosis in colorectal cancer: systematic review and meta-analysis.

BACKGROUND: Tumor-associated macrophages (TAMs) are key components of colorectal cancer (CRC) microenvironment, but their role in CRC prognosis is not fully defined. OBJECTIVE: This study aimed to evaluate prognostic value of different types and distribution of TAMs in CRC. METHODS: Total 27 studies with 6115 patients were searched from PubMed and Embase and analyzed to determine the association between TAMs, including distinct TAM subsets and infiltration location, and CRC survival. The prognostic impact of TAMs on CRC was further stratified by tumor type and mismatch repair system (MMR) status. RESULTS: A pooled analysis indicated that high density of TAMs in CRC tissue was significantly associated with favorable 5-year overall survival (OS) but not with disease-free survival (DFS). CD 68+ TAM subset correlated with better 5-year OS, while neither CD68+NOS2+ M1 subset nor CD163+ M2 subset was correlated with 5-year OS. Increased CD68+ TAM infiltration in tumor stroma but not in tumor islet predicted improved 5-year OS. Stratification by tumor type and MMR status showed that in colon cancer or MMR-proficient CRC, elevated TAM density was associated with better 5-year OS. CONCLUSIONS: High infiltration of CD68+ TAMs could be a favorable prognostic marker in CRC. Future therapies stimulating CD68+ TAM infiltration may be promising in CRC treatment.

The landscape and prognostic value of tumor-infiltrating immune cells in gastric cancer.

BACKGROUND: Gastric cancer (GC) is the fourth most frequently diagnosed malignancy and the second leading cause of cancer-associated mortality worldwide. The tumor microenvironment, especially tumor-infiltrating immune cells (TIICs), exhibits crucial roles both in promoting and inhibiting cancer growth. The aim of the present study was to evaluate the landscape of TIICs and develop a prognostic nomogram in GC. MATERIALS AND METHODS: A gene expression profile obtained from a dataset from The Cancer Genome Atlas (TCGA) was used to quantify the proportion of 22 TIICs in GC by the CIBERSORT algorithm. LASSO regression analysis and multivariate Cox regression were applied to select the best survival-related TIICs and develop an immunoscore formula. Based on the immunoscore and clinical information, a prognostic nomogram was built, and the predictive accuracy of it was evaluated by the area under the curve (AUC) of the receiver operating characteristic curve (ROC) and the calibration plot. Furthermore, the nomogram was validated by data from the International Cancer Genome Consortium (ICGC) dataset. RESULTS: In the GC samples, macrophages (25.3%), resting memory CD4 T cells (16.2%) and CD8 T cells (9.7%) were the most abundant among 22 TIICs. Seven TIICs were filtered out and used to develop an immunoscore formula. The AUC of the prognostic nomogram in the TCGA set was 0.772, similar to that in the ICGC set (0.730) and whole set (0.748), and significantly superior to that of TNM staging alone (0.591). The calibration plot demonstrated an outstanding consistency between the prediction and actual observation. Survival analysis revealed that patients with GC in the high-immunoscore group exhibited a poor clinical outcome. The result of multivariate analysis revealed that the immunoscore was an independent prognostic factor. DISCUSSION: The immunoscore could be used to reinforce the clinical outcome prediction ability of the TNM staging system and provide a convenient tool for risk assessment and treatment selection for patients with GC.

Activation of the nuclear factor erythroid 2-related factor 2-antioxidant response element signal in rats with diffuse axonal injury.

Oxidative stress is a critical mechanism underlying secondary injury during diffuse axonal injury (DAI), and nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) is an important element in the antioxidative stress pathway. This study investigated changes in Nrf2-ARE expression in rats with DAI to provide a basis for studying the DAI mechanism and a guide for clinical practice. The rat traumatic brain injury (TBI) model was established by a speeding rotation device and confirmed by neural scoring and silver staining. Nrf2 protein expression at 1, 6, 24, 48, and 72 h after TBI was measured by western blot analysis. Nrf2, heme oxygenase-1 (HO-1), and NAD(P)H:quinone oxidoreductase 1 gene expression was measured by RT-PCR. The in-situ expression of Nrf2 and HO-1 was detected by immunohistochemistry analysis. Nrf2 protein expression was significantly higher in TBI rats than in sham rats (P<0.01). The change in Nrf2 expression was time dependent, peaking at 24 h and remaining high for 72 h. RT-PCR analysis indicated that HO-1 and NAD(P)H:quinone oxidoreductase 1 mRNA expression was increased in TBI rats compared with that in sham rats (P<0.05). Immunohistochemistry analysis indicated that the Nrf2 and HO-1 expression in the nuclei and cytoplasm of neurons and glial cells was significantly increased in TBI rats compared with that in sham rats (P<0.05). The Nrf2-ARE signaling pathway may be involved in the endogenous response to DAI.

CircRNA circPDSS1 promotes the gastric cancer progression by sponging miR-186-5p and modulating NEK2.

The aim of this study is to investigate the regulatory mechanism of circPDSS1/miR-186-5p/NEK2 axis on the viability and proliferation in gastric cancer (GC) cell line. Differentially expressed circRNAs, miRNAs, and mRNAs in GC tissues and paracarcinoma tissues were analyzed using gene chips GSE83521, GSE89143, and GSE93415. Then, the expression of circPDSS1, miR-186-5p, and NEK2 was analyzed via quantitative real-time polymerase chain reaction (qRT-PCR). Survival analysis was adopted to explore the association between the circPDSS1 expression and the prognosis of GC. The effect of circPDSS1 on GC cell cycle and apoptosis was verified with the flow cytometry. Targeting relationships among circPDSS1, miR-186-5p, and NEK2 were predicted via bioinformatics analysis and demonstrated by the dual-luciferase reporter assay. Our results showed that circPDSS1 and NEK2 were high-expressed whereas miR-186-5p was low-expressed in GC tissues and cells. CircPDSS1 promoted GC cell cycle and inhibited apoptosis by sponging miR-186-5p, while miR-186-5p inhibited cell cycle and promoted apoptosis by targeting NEK2. Thus, circPDSS1 acts as a tumor promoter by regulating miR-186-5p and NEK2, which could be a potential biomarker and therapeutic target for the management of GC.

MicroRNA-19a regulates the proliferation, migration and invasion of human gastric cancer cells by targeting CUL5.

Gastric cancer is one of the prevalent types of cancers and despite improvements in its treatment, the overall survival is still far from descent. The dearth of efficient biomarkers, chemotherapeutic agents and therapeutic targets form a major hurdle in the treatment of the gastric cancer. Accumulating evidences suggest that MicroRNAs (miRs) may prove important therapeutic targets/agents for the management of cancers including gastric cancer. Herein, we examined the expression of miR-19a by qRT-PCR in gastric cancer and attempted to explore its potential role. It was found that the expression of miR-19a is significantly (p < 0.05) enhanced in the gastric cancer tissues as well as the gastric cancer cell lines. Inhibition of miR-19a in gastric cancer cells suppressed the proliferation migration and invasion of the gastric cancer cells. Bioinformatic analysis revealed CUL5 to be the potential target of miR-19a. Contrary, to the expression of miR-19a, the expression of CUL5 was significantly (p < 0.05) downregulated in all the gastric cancer tissues and cell lines. However, inhibition of miR-19a in SNU-16 gastric cancer cells could cause upsurge of CUL5 expression. Overexpression of CUL-5 was found to exhibit similar effects on the proliferation, migration and invasion of the SNU-16 gastric cancer cells as that of miR-19a suppression. Additionally, overexpression of CUL5 could at least partially abolish the effects of miR-19a suppression on the proliferation, migration and invasion of SNU-16 gastric cancer cells. Finally, overexpression of miR-19a caused inhibition of the xenografted tumors in vivo indicating the potential of miR-19a as therapeutic target for gastric cancer.

MicroRNA profiling of diabetic atherosclerosis in a rat model.

OBJECTIVE: The incidence of diabetic atherosclerosis (DA) is increasing worldwide. The study aim was to identify differentially expressed microRNAs (DE-miRs) potentially associated with the initiation and/or progression of DA, thereby yielding new insights into this disease. METHODS: Matched iliac artery tissue samples were isolated from 6 male rats with or without DA. The Affymetrix GeneChip microRNA 4.0 Array was used to detect miRs. Differential expression between atherosclerotic group and non-atherosclerotic group samples was analyzed using the Gene-Cloud of Biotechnology Information platform. Targetscan and miRanda were then used to predict targets of DE-miRs. Functions and pathways were identified for significantly enriched candidate target genes and a DE-miR functional regulatory network was assembled to identify DA-associated core target genes. RESULTS: A total of nine DE-miRs (rno-miR-206-3p, rno-miR-133a-5p, rno-miR-133b-3p, rno-miR-133a-3p, rno-miR-325-5p, rno-miR-675-3p, rno-miR-411-5p, rno-miR-329-3p, and rno-miR-126a-3p) were identified, all of which were up-regulated and together predicted to target 3349 genes. The target genes were enriched in known functions and pathways related to lipid and glucose metabolism. The functional regulatory network indicated a modulatory pattern of these metabolic functions with DE-miRs. The miR-gene network suggested arpp19 and MDM4 as possible DA-related core target genes. CONCLUSION: The present study identified DE-miRs and miRNA-gene networks enriched for lipid and glucose metabolic functions and pathways, and arpp19 and MDM4 as potential DA-related core target genes, suggesting DE-miRs and/or arpp19 and MDM4 could act as potential diagnostic markers or therapeutic targets for DA.

Long non-coding RNA MIF-AS1 promotes gastric cancer cell proliferation and reduces apoptosis to upregulate NDUFA4.

Long non-coding RNA MIF-AS1 (lncMIF-AS1) has been found to be upregulated in the tumor tissues of gastric cancer; however, its importance for the progression of gastric cancer remains unknown. Thus, the present study was designed to determine the role of the lncMIF-AS1-based signal transduction pathway in mediating the proliferation and apoptosis of gastric cancer cells. Differentially expressed lncRNAs and mRNAs were screened out using microarray analysis, based on the published data (GSE63288), and validated using quantitative RT-PCR. Target relationships between lncRNA-micro RNA (miRNA) and miRNA-mRNA were predicted by bioinformatics analysis and verified by dual-luciferase reporter assay. Protein expression of NDUFA4, COX6C and COX5B was detected by western blot. Cell proliferation, cell cycle and apoptosis were determined using colony formation assay and flow cytometry analysis. Oxidative phosphorylation in gastric cancer cells was assessed by levels of oxygen consumption and ATP synthase activity. Expression of lncMIF-AS1 and NDUFA4 were upregulated in gastric cancer tissues and cells as compared with non-cancerous gastric tissues and cells (P < .05). MiR-212-5p was identified as the most important miRNA linker between lncMIF-AS1 and NDUFA4, which was negatively regulated by lncMIF-AS1 and its depletion is the main cause of NDUFA4 overexpression (P < .01). The upregulated expression of NDUFA4 then greatly promoted the proliferation and decreased the apoptosis of gastric cancer cells through activation of the oxidative phosphorylation pathway. Taken together, the present study implies that inhibition of lncMIF-AS1/miR-212-5p/NDUFA4 signal transduction may provide a promising therapeutic target for the treatment of gastric cancer.

[Catheter directed thrombolysis for early left lower extremity deep venous thrombosis without vena cava filters protection].

OBJECTIVE: To investigate the indications, safety and efficacy of catheter directed thrombolysis for early left lower extremity deep venous thrombosis (DVT) without vena cava filters protection. METHODS: Clinical data of 54 cases of early left lower extremity DVT received catheter directed thrombolysis without vena cava filters from July 2008 to June 2010 were retrospectively analyzed. The thrombosis was entire without free floating clots and no thrombosis in vena cava detected with ultrasound scan. Twenty-five patients were male and 29 were female with the average age of 52.8 years. Fifty-one of which were iliofemoral and popliteal, the other 3 were iliofemoral. The course were ≤ 7 d in 45 cases and these were 8 to 30 d in 9 cases. Urokinase of 300 000 U was infused through catheters per 2 h twice a day. Meanwhile 4000 U of low weight heparin was administered subcutaneously per 12 h, or heparin infusion at dosage of 18 U×kg(-1)×h(-1). RESULTS: The procedure technically succeeded in all patients. In total cases venous score decreased to 4.6 ± 2.1 post 6 to 10 d of thrombolysis from 10.8 ± 1.0 with thrombolysis rate of 58% ± 18% which was not significantly different between groups of ≤ 7 d and 8 to 30 d (t = 1.02, P = 0.34). On 14(th) day, 11 patients (20.4%) completely recovered, 35 cases (64.8%) experienced large improvement, 8 patients (14.8%) had mild improvement and nobody was failed, resulting in total efficacy of 100%. No patient developed clinical symptomatic pulmonary embolism. SpO2 did not alter markedly post thrombolysis [(91.0 ± 2.6)% vs. (90.8 ± 2.4)%, t = 2.03, P = 0.05]. No patients suffered from cerebral hemorrhage and haemoturia, and catheter induced inflammation occurred in 4 cases (7.41%). There was mild bleeding in puncture sites in 11 patients (20.4%) during the course. There were 36 patients (66.7%) had been followed up with the time of 6 to 21 months. In which 31 cases had no lower extremity edema or had mild edema after activities. Two patients developed serious edema after activities for deep venous insufficiency. Three cases combined with malignant tumor or renal failure recurred. CONCLUSIONS: For early left extremity DVT which is entire without free floating clots and no thrombosis in vena cava, catheter directed thrombolysis without filter protection maybe administered with safety, efficiency and lower expense.

[Treatment on post-operational complications of aortic endovascular grafting exclusion].

OBJECTIVE: To investigate the post-operative complications of aortic endovascular grafting exclusion (EVGE) and its reasons and treatments. METHODS: Clinical data of 82 cases received aortic endovascular grafting exclusion from January 2002 to October 2008 were retrospectively analyzed. Seventy-one cases were male and 11 cases were female with the age of 33 to 78 years and the average age of 49.2 years. There were 66 cases of thoracic aortic dissecting aneurysms and 16 cases of abdominal aortic aneurysm. The effect, post-operational complications and its treatment were investigated. RESULTS: There were 90.1% patients had been followed up with the time of 3 to 78 months with technical success of 90.3%, clinical success of 94.1%, peri-operational mortality of 2.4%, total mortality of 6.1% and mortality associated with EVGE of 2.4%. Twenty-one cases underwent complications including type I endoleak (13 cases), abdominal aortoduodenal fistula (1 case), narrow true lumen (2 cases), reverse Stanford A dissection (2 cases), post EVGE syndrome (12 cases), delayed healing of inguinal incision (5 cases), constipation (3 cases), cerebral infarction (1 case). No paraplegia, left subclavian artery ischemia, contrast media associated nephrosis, ischemic colitis, ischemic neurologic injury, and artery embolism occurred. Post operation 4 cases had the second intervention including 2 type I endoleak and 2 narrow true lumen. CONCLUSIONS: The technique-related complications still hinder the long-term effect of EVGE. It needs to be further investigated on technique improvement and treatment standardization.