Relationship between blood urea nitrogen to serum albumin ratio and short-term mortality among patients from the surgical intensive care unit: a population-based real-world study.

BACKGROUND: Patients admitted to the surgical intensive care unit (SICU) often suffer from multi-organ dysfunction and have a high mortality rate. Therefore, finding a simple but effective clinical indicator to predict the prognosis of patients is essential to improve their survival. The aim of this study was to investigate the relationship between blood urea nitrogen to serum albumin ratio (B/A) and short-term mortality among patients from the SICU. METHODS: All eligible adult patients admitted to the SICU from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database were recruited for this study. Participants were divided into a death group (n = 638) and a survival group (n = 2,048) based on the 90-day prognosis, and then grouped by B/A quartiles. We used restricted cubic splines (RCS) to visually analyze the correlation of B/A with 30- and 90-day risk of death. Cumulative survival rates were estimated using Kaplan-Meier survival curves according to B/A quartiles and evaluated using the log-rank test. Cox proportional risk models were developed and sensitivity analyses were performed to explore whether B/A was independently associated with short-term outcomes in SICU patients. Receiver operating characteristic (ROC) curves were analyzed to ascertain the value of B/A for prognosticating 90-day outcome. RESULTS: A total of 2686 participants were included in the final study, and their 30-day and 90-day all-cause mortality rates were 17.61% and 23.75%, respectively. The differences in 30-day and 90-day mortality rates were statistically significant among the four groups of patients (all p < 0.001). RCS curves showed that B/A was linearly associated with the risk of 30-day and 90-day all-cause mortality in SICU patients (χ2 = 0.960, p = 0.811; χ2 = 1.940, p = 0.584). Kaplan-Meier analysis showed that the 90-day cumulative survival rate gradually decreased as B/A increased, with patients in the highest quartile of B/A having the lowest survival rate (p < 0.001). Cox regression indicated that elevated B/A (> 9.69) was an independent risk factor for 30-day and 90-day all-cause mortality in SICU patients. The analysis of ROC curves demonstrated that B/A exhibited a significant predictive ability for 90-day mortality, with an optimal threshold of 6.587, a sensitivity of 56.9%, and a specificity of 64.8%. CONCLUSIONS: Elevated B/A (> 9.69) on admission was an independent risk factor for short-term mortality in SICU patients, and clinicians should pay more attention to this group of patients and intervene clinically at an early stage to reduce mortality.

Switch/Sucrose Non-Fermentable Complex-Deficient Rhabdoid Carcinoma of Stomach: A Rare Case Report and Literature Review.

Gastric undifferentiated/rhabdoid carcinoma is a rare highly invasive tumor of epithelial origin. Due to mutations in the switch/sucrose non-fermentable (SWI/SNF) complex, these tumor cells are usually dedifferentiated, presenting a characteristic rhabdoid profile. In this report, we present a gastric rhabdoid carcinoma in a 77-year-old man who presented with intermittent epigastric pain. Gastroscopy revealed a giant ulcer in the antrum, which proved to be a malignant tumor in the biopsy. Therefore, he was admitted to our hospital and underwent laparoscopic radical gastrectomy and D2 lymphadenectomy. The resected neoplasm contained a variety of rhabdoid cells that lacked well-differentiated elements. Immunohistochemical staining revealed that SMARCA4/BRG1 expression was absent in tumor cells. Finally, the patient was diagnosed with undifferentiated/rhabdoid carcinoma of the stomach. The patient was treated with tegafur-gimeracil-oteracil potassium capsules postoperatively. There were no signs of imaging changes observed at the 18-month follow-up. We reviewed similar cases in previous reports. These tumors are more likely to affect older male adults and usually lack typical symptoms. Histologically, most tumor cells are poorly cohesive and rhabdoid, and differentiated compositions of various degrees can occasionally be seen. Positive staining for vimentin was seen in all tumor cells. Epithelial markers are positive in the majority of tumors. SWI/SNF mutant tumors tend to be associated with a poor prognosis. In this review, more than half of the patients died within one year after surgery. The treatments for these diseases are still being explored.

Analysis of bacterial diversity and community structure in gastric juice of patients with advanced gastric cancer.

BACKGROUND: The occurrence and development of gastric cancer are related to microorganisms, which can be used as potential biomarkers of gastric cancer. OBJECTIVE: To screen the microbiological markers of gastric cancer from the microorganisms of gastric juice. METHODS: Gastric juice samples were collected from 61 healthy people and 78 patients with gastric cancer (48 cases of early gastric cancer and 30 cases of advanced gastric cancer). The bacterial 16 S rRNA V1-V4 region of gastric juice samples was sequenced. The Shannon index, Simpson index, Ace index and Chao index were used to analyze the diversity of gastric juice samples. The RDP classifier Bayesian algorithm was used to analyze the community structure of 97% OTU representative sequences with similar levels. Linear discriminant analysis and ST-test were used to analyze the differences. Six machine learning algorithms, including the logistic regression algorithm, random forest algorithm, neural network algorithm, support vector machine algorithm, Catboost algorithm and gradient lifting tree algorithm, were used to construct risk prediction models for gastric cancer and advanced gastric cancer. RESULTS: The microbiota diversity and the abundance of bacteria was different in the healthy group, early gastric cancer and advanced gastric cancer (P < 0.05). The top five abundant bacteria among the three groups were Streptococcus, Rhodococcus, Prevotella, Pseudomonas and Helicobacter. Bacterial flora such as Streptococcus, Rhodococcus and Ochrobactrum were significantly different between the healthy group and the gastric cancer group. The accuracy of the random forest prediction model is the highest (82.73% correct). The bacteria with the highest predictive value included Streptococcus, Lactobacillus and Ochrobactrum. The abundance of bacteria such as Fusobacterium, Capnocytophaga, Atopobium, Corynebacterium was high in the advanced gastric cancer group. CONCLUSION: Gastric juice bacteria can be used as potential biomarkers to predict the occurrence and development of gastric cancer.

Heterophyllin B inhibits the malignant phenotypes of gastric cancer cells via CXCR4.

Heterophyllin B (HB) is a cyclic lipopeptide that has been shown to have anticancer effects. This study intended to further explore the effects and modulatory mechanism of HB in gastric cancer (GC) cells. The binding relationship between HB and CXCR4 was investigated by network pharmacological analysis, molecular docking, and cellular thermal shift assay (CETSA)-WB assay. Cellular assays revealed that HB could restrain GC cell viability, proliferation, invasion and migration by binding to CXCR4. Further studies presented that HB could suppress PI3K/AKT signaling pathway via binding to CXCR4, thus repressing PD-L1 expression. In vivo experiments in nude mice demonstrated that HB constrained PI3K/AKT signaling pathway to suppress GC cell metastasis and PD-L1 expression. In summary, the key target of HB in GC treatment was CXCR4. Cell experiments were employed for the investigation of the mechanism by which HB repressed GC cells. The results confirmed that HB could constrain the malignant progression of GC by the binding of HB into CXCR4 and suppressed PD-L1 expression via hampering PI3K/AKT signaling pathway.

Analysis of Network Pharmacology and Molecular Docking on Radix Pseudostellariae for Its Active Components on Gastric Cancer.

Radix Pseudostellariae, a traditional Chinese medicine, functions in modulating human immunity and anti-tumor, but its pharmacological mechanism remained unclear. In this study, 8 active components and 91 targets of Radix Pseudostellariae were obtained from the Traditional Chinese Medicine Systems Pharmacology (TCMSP) database, and 225 genes related to gastric cancer (GC) were accessed from MalaCards. On the basis of these targets and GC-related genes, a protein-protein interaction (PPI) network was established. Random walk with restart (RWR) analysis was performed on the PPI network with the intersection of targets and GC-related genes as the seeds. The top 50 target genes with high affinity scores were obtained. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses showed that the enrichment of the top 50 genes was mostly presented in the cancer-related biological functions and signaling pathways, such as cellular response to oxidative stress, regulation of apoptotic signaling pathway, and P53 signaling pathway. A drug-component-target network was established, with the top 50 genes being used as key targets. Acacetin and luteolin were revealed to directly act on the core target TP53 in the network. Thus, SwissDock was used to simulate the molecular docking between TP53 protein and acacetin and luteolin. The results of docking simulation presented small estimated ΔG of two small molecules, which were suggested to be potential targets of TP53 protein. Subsequent cellular and molecular experiments confirmed this bioinformatics result. In conclusion, this study predicted the key anti-GC active components and corresponding targets of Radix Pseudostellariae through bioinformatics analysis. The findings underlie the anti-GC mechanism of Radix Pseudostellariae.

MicroRNA-501-3p targeting TM4SF1 facilitates tumor-related behaviors of gastric cancer cells via EMT signaling pathway.

BACKGROUND: Increasing evidence shows that Transmembrane 4 L6 family member 1(TM4SF1) exerts a critical role in mediating the progression of various tumors. Nevertheless, the exact mechanism of TM4SF1 in gastric cancer (GC) remains unclear. METHODS: Bioinformatics analysis was utilized to analyze TM4SF1 expression in GC tissues. Also, MiRWalk and starBase databases were used to predict the upstream microRNAs which could regulate TM4SF1 expression. Gene set enrichment analysis (GSEA) for TM4SF1 was conducted to screen the potentially involved pathways. Dysregulation of microRNA-501-3p/TM4SF1 was implemented to investigate the regulatory roles of these genes in GC. qRT-PCR and western blot were employed to measure the expression changes of microRNA-501-3p, TM4SF1, and epithelial-mesenchymal transition (EMT) signaling pathway-associated proteins. CCK-8, colony formation, and transwell assays were introduced to examine the biological functions of GC cell lines. RESULTS: TM4SF1 presented a significantly low level in mRNA and protein in GC cells. MicroRNA-501-3p could target TM4SF1 and reduce its expression. Cell function experiments revealed that microRNA-501-3p facilitated cell proliferation, migration, and invasion, while inhibiting cell apoptosis in GC by targeting TM4SF1. EMT-associated proteins were altered by changing microRNA-501-3p/TM4SF1 axis. CONCLUSION: MicroRNA-501-3p regulated EMT signaling pathway by down-regulating TM4SF1 expression and therefore facilitated the malignant progression of GC, which may provide a new potential therapeutic target for the treatment of GC patients.

Knockdown of BATF3 Inhibits Gastric Cancer Cell Growth and Radioresistance via S1PR1/STAT3 Pathway.

OBJECTIVE: Gastric cancer is one of the most common and deadly cancers worldwide. Basic leucine zipper transcription factor ATF-like 3 (BATF3) plays a key role in tumor immunity. However, the function of BATF3 in gastric cancer remains unclear. Here, we demonstrated BATF3 positively regulated proliferation and radioresistance of gastric cancer cells by regulating S1PR1/STAT3 pathway. METHODS: The RNA-seq analyzed the gene expression by UALCAN web portal and Tumor Immune Estimation Resource. RT-qPCR and western blot was performed to verify BATF3 expression in gastric cancer cells. The assays of CCK-8, EdU incorporation and colony formation were used to analyze cell proliferation, and radioresistance in AGS and MKN45 cells. Flow cytometry was used to detect the cell apoptosis of AGS and MKN45 in treatment with si-BATF3 or radiation. Finally, western blot was performed to measure the expression of cell apoptosis-related modules including Bax, cleaved-caspase3, cleaved-PARP and assess the regulation of S1PR1/STAT3 pathway. RESULTS: BATF3 expression was upregulated in gastric cancer cells. Knockdown of BATF3 suppressed proliferation, radioresistance but promoted the radiation-induced apoptosis of gastric cancer cells through positively regulating S1PR1 expression and STAT3 phosphorylation. CONCLUSIONS: Knockdown of BATF3 inhibits gastric cancer cell growth and radioresistance via S1PR1/STAT3 pathway. BATF3 would become a potential diagnostic indicator for gastric cancer and target of therapeutic treatment.

Depletion of C12orf48 inhibits gastric cancer growth and metastasis via up-regulating Poly r(C)-Binding Protein (PCBP) 1.

BACKGROUND: Gastric cancer remains a major cause of cancer-related death worldwide. C12orf48, also named PARP1 binding protein, is over-expressed in several cancers. However, the expression profile and potential roles of C12orf48 in gastric cancer are largely unknown. METHODS: We used bioinformatics approaches and tissue microarray immunohistochemistry to analyze the expression profile of C12orf48 in gastric cancer tissues. Plasmid-mediated over-expression or knockdown were performed. CCK-8 assays and flow cytometry were employed to evaluate cellular proliferation and apoptosis respectively. Transwell assays were used to assess migrative and invasive abilities. The roles of C12orf48 were also evaluated in a xenograft tumor model. RESULTS: We found that C12orf48 was over-expressed in gastric cancer tissue, which associated with advanced stage and poor prognosis. In vitro and in vivo experiments showed depletion of C12orf48 attenuated cancer growth, while facilitated apoptosis. Further, the expression of Poly r(C)-Binding Protein (PCBP) 1 was found negatively regulated by C12orf48. Intended up-regulation of PCBP1 prevented C12orf48-mediated proliferation and rescued cells from apoptosis. Besides, C12orf48 promoted cellular migration and invasion, with E-cadherin down-regulated while vimentin and N-cadherin up-regulated, which was reversed by up-regulated PCBP1. CONCLUSIONS: Our findings indicate that depletion of C12orf48 inhibited gastric cancer growth and metastasis via up-regulating PCBP1. Targeting C12orf48-PCBP1 axis may be a potential therapeutic strategy.

De-Ubiquitinating Enzymes USP21 Regulate MAPK1 Expression by Binding to Transcription Factor GATA3 to Regulate Tumor Growth and Cell Stemness of Gastric Cancer.

USP21 is a kind of deubiquitinating enzymes involved in the malignant progression of various cancers, while its role in gastric cancer (GC) and the specific molecular mechanism are still unclear. This study probed into the function of USP21 in vitro and in vivo, and discussed the regulatory mechanism of USP21 in GC in vitro. We reported that USP21 promoted GC cell proliferation, migration, invasion, and stemness in vitro, and regulated GC tumor growth and cell stemness in mice in vivo. USP21 stabilized the expression of GATA3 by binding to GATA3. Besides, GATA3 also regulated the expression of MAPK1 at the transcriptional level. A series of in vitro experiments testified that USP21 regulated the expression of MAPK1 by binding to transcription factor GATA3, thereby regulating the tumor growth and cell stemness of GC. Overall, this study identified a new USP21/GATA3/MAPK1 axis, which plays a pivotal role in promoting the malignant progression of GC and might provide a potential target for treatment.

Adjuvant albumin-bound paclitaxel combined with S-1 vs. oxaliplatin combined with capecitabine after D2 gastrectomy in patients with stage III gastric adenocarcinoma: a phase III multicenter, open-label, randomized controlled clinical trial protocol.

BACKGROUND: Surgery is the only treatment option for operable gastric cancer. The CLASSIC and ACTS-GC studies showed that the 5-year overall survival (OS) of patients with stage III gastric cancer undergoing D2 gastrectomy is still very low. Whether adjuvant nanoparticle albumin-bound paclitaxel (nab-paclitaxel) combined chemotherapy is more effective than the XELOX standard adjuvant chemotherapy in patients with stage III gastric cancer has not been confirmed. METHODS: This is a multicenter, open-label, phase III clinical study. In this trial, 616 patients with locally advanced stage III gastric cancer that underwent curative D2 radical surgery and achieved R0 are planned to be included. Patients will be randomized 1:1 to nab-paclitaxel combined with S-1 (AS) vs. oxaliplatin combined with capecitabine (XELOX). XELOX group: Patients assigned to the XELOX group received eight 3-week cycles of oral capecitabine (1000 mg/m2) twice daily on days 1-14 of each cycle plus intravenous oxaliplatin 130 mg/m2 on day 1 of each cycle. AS group: AS group received eight 3-week cycles of oral S-1 (80-120 mg) (< 1.25 m2, 40 mg; 1.25 to < 1.5 m2, 50 mg; and > 1.5 m2, 60 mg) twice daily on days 1-14 plus intravenous nab-paclitaxel 120 mg/m2 on days 1 and 8 of each cycle. The primary endpoint was the 3-year disease-free survival (3-year-DFS) defined as the time from randomisation to the time of recurrence of the original gastric cancer, development of a new gastric cancer, or death from any cause. The secondary endpoints were the overall survival, (defined as the time from the date of randomisation to date of death from any cause) and safety (any adverse event). DISCUSSION: Compared with previous studies, this study includes nab-paclitaxel based on S-1 adjuvant chemotherapy, which is expected to achieve better efficacy and lower toxicity than the standard treatment. This study is the first clinical study to evaluate the safety and efficacy of nab-paclitaxel combined with S-1 in patients with stage III gastric cancer after D2 radical resection. TRIAL REGISTRATION: This clinical trial has been registered with ClinicalTrials.gov, registration number: NCT04135781 , on October 20th, 2019.

Knockdown of RAP2A gene expression suppresses cisplatin resistance in gastric cancer cells.

Cisplatin (DDP) resistance is closely associated with the failure of chemotherapy to manage various different types of human cancer. The GTPase protein Ras-related protein Rap-2a (RAP2A) regulates cancer cell proliferation, migration and invasion; however, little is currently known regarding its role in cancer cell resistance to chemotherapy. The present study investigated the potential roles of the RAP2A gene in gastric cancer cell resistance to DDP treatment. The DDP half maximal inhibitory concentration (IC50) values for the proliferation inhibition of MGC803 and MGC803/DDP gastric cancer cells were determined by treating the cells with a DDP concentration gradient and measuring their survival rates using the Cell Counting Kit-8 (CCK-8) assay; cell viability was also assessed using the CCK-8 assay. Cell migration and invasion were assessed using Transwell Matrigel assays, and apoptosis and DNA damage were evaluated using flow cytometry and Hoechst staining. RAP2A expression was knocked down by siRNA transfection, and RAP2A protein levels were examined using western blotting. The DDP IC50 values for DDP-resistant MGC803/DDP cells were greater than those for MGC803 cells. Furthermore, MGC803/DDP cells exhibited increased levels of viability, migration and invasion, and decreased levels of apoptosis and DNA damage during DDP treatment. Knockdown of RAP2A expression significantly promoted MGC803/DDP cell apoptosis and DNA damage, and decreased the viability and invasion capabilities of these cells following treatment with DDP. The results of the present study revealed that RAP2A expression promotes DDP resistance in gastric cancer cells by increasing their viability, migration and invasion capacities, and by suppressing apoptosis and DNA damage.

The inhibitory role of recombinant P-selectin glycoprotein ligand immunoglobulin G on portal vein thrombosis based on a novel rat model.

The current study aimed to reveal a novel method for constructing a portal vein thrombosis (PVT) model in rats and to evaluate the inhibitory role of recombinant P-selectin glycoprotein ligand immunoglobulin G (rPSGL-Ig) on the formation of PVT. The PVT model was constructed in rats through intermittent portal vein obstruction (IPVO) combined with endangium destruction. A total of 4 mg/kg rPSGL-Ig was intraperitoneally pre-injected into rats 1 h prior to model construction. Changes in the thrombus size and vessel diameter were observed by B-scan ultrasonography. Histopathological changes in the portal vein, central hepatic vein and vasa intestini tenuis were observed using hematoxylin and eosin staining. Additionally, histopathological changes in the portal vein were observed by transmission electron microscopy. A total of 8 mg/kg rPSGL-Ig or 2×104 U/kg urokinase were used to compare the thrombolytic effects and thrombus sizes. The PVT model was successfully constructed in rats, and exhibited a significantly greater thrombus size and vessel diameter compared with the control group (P<0.05). Intervention with rPSGL-Ig significantly inhibited the formation of PVT, and resulted in a significantly lower thrombus size and vessel diameter compared with the model group (P<0.05). Additionally, histopathological changes in the portal vein, central hepatic vein and vasa intestini tenuis in PVT rats were considerably reversed following the intervention with rPSGL-Ig. rPSGL-Ig demonstrated a lower thrombolytic effect compared with that of URO. IPVO combined with endangium destruction effectively constructed a PVT model in rats. rPSGL-Ig effectively prevented PVT in rats. rPSGL-Ig may be used in future studies for the treatment of patients with PVT.

Hsa-miR-370 inhibited P-selectin-induced cell adhesion in human colon adenocarcinoma cells.

Sialyl Lewis x (sLex) is a minimal recognition motif for ligands of P-selectin and plays an important role in tumor cell adhesion and migration. Thus, targeting sLex could be an effective method to prevent tumor metastasis. In this study, we aimed to identify a microRNA (miRNA) which is capable to suppress the expression of sLex. MicroRNAs which may target ST3GAL4 were predicted by the online tools. Colo 320 HSR human colon adenocarcinoma cells were employed. The transcriptional and translational levels of ST3GAL4 were evaluated by western blotting and Real-time quantitative polymerase chain reaction. Cell adhesion and spread were assessed with or without hsa-miR-370 treatment. It was shown that hsa-miR-370 inhibited the expression of sLex in colo-320 cells, which repressed the binding of P-selectin, and led to reduced cell attachment and spread. Our results found that P-selectin-induced elevations of p-p38 and p-PI3K levels were significantly inhibited by hsa-miR-370, indicating that repressed sLex level is able to reduce the P-selectin binding and therefore eliminating the P-selectin-induced activation of p38 and PI3K signaling. In conclusion, we found that hsa-miR-370 specifically inhibits the expression of sLex, represses cell adhesion and spreading in colo-320 cells. Our study provides a possible effective treatment against tumor invasion.

The exosome-mediated PI3k/Akt/mTOR signaling pathway in cervical cancer.

BACKGROUND: Cervical cancer is the second most common cancer and one of the leading causes of cancer deaths among women worldwide. OBJECTIVE: To evaluate the clinical significance of the PI3k/Akt/mTOR signaling pathway in cancer tissues and exosomes extracted from vaginal secretions. METHODS: Immunohistochemical staining was used to detect the protein expression of PI3k, Akt, and mTOR in tissue samples from the control group, the CIN (cervical intraepithelial neoplasia) group, and the cervical cancer group. qPCR (quantitative PCR) was used to detect the expressions of PI3k, Akt, and mTOR in cervical cancer tissues, the corresponding adjacent tissues, and exosomes extracted from vaginal secretions. RESULTS: Compared with those of healthy people and CIN, the PI3k/Akt/mTOR protein levels in extracts from tissues were higher in the cervical cancer patients. The PI3k/Akt/mTOR gene and protein levels increased in the cervical cancer tissues with the increase in the degree of malignancy of the cancer. There was no significant difference in PI3k/Akt/mTOR gene expression between the cervical cancer tissues and the exosomes extracted from vaginal secretions, but both were significantly higher than the expressions of the corresponding adjacent tissues. CONCLUSIONS: The PI3k/Akt/mTOR signaling pathway mediated by exosomes extracted from vaginal secretions may provide candidate diagnostic biomarkers or potential therapeutic targets.

TM4SF1 inhibits apoptosis and promotes proliferation, migration and invasion in human gastric cancer cells.

Gastric cancer (GC) is associated with poor patient prognosis, and so it crucial to investigate the molecular mechanisms underlying the progression of GC. The aim of the present study was to investigate the role of transmembrane-4 L6 family member 1 (TM4SF1) in the progression of GC. TM4SF1 small interfering RNA (siRNA) and TM4SF1-expressing plasmids were employed to regulate TM4SF1 expression. In vitro experiments were performed to determine the effect of TM4SF1 on the expression of apoptosis-associated molecules and determine the role of TM4SF1 in apoptosis, proliferation, migration and invasion using human GC cell lines MGC803 and MKN45. The data of the present study demonstrated that TM4SF1 may regulate the expression of apoptosis-associated molecules at the mRNA and protein levels. TM4SF1 silencing reduced B-cell lymphoma 2 (Bcl2) expression, whilst caspase-3 and Bcl2-associated X expression increased, and upregulating TM4SF1 reversed these changes in GC cells. Furthermore, TM4SF1 knockdown promoted apoptosis while inhibiting the proliferation, migration and invasion of GC cells. Rescue experiments demonstrated that TM4SF1 upregulation reversed the changes induced by transfection with TM4SF1 siRNA. In summary, TM4SF1 is an anti-apoptosis protein associated with the progression of GC. Additional in vivo experiments and clinical trials are required to confirm the possible use of TM4SF1 in tumor therapy.

P-Selectin Level at First and Third Day After Portal Hypertensive Splenectomy for Early Prediction of Portal Vein Thrombosis in Patients With Cirrhosis.

We aimed to investigate the changes in p-selectin (p-sel), thrombus precursor protein, and D-dimer (D-D) in patients with cirrhosis after portal hypertensive splenectomy and explore its values on the prediction of postoperative portal vein thrombosis (PVT) formation. A total of 144 patients with cirrhosis with portal hypertension who underwent portal hypertensive splenectomy from January 2009 to December 2016 were enrolled in this study and divided into the thrombus and nonthrombus groups. The levels of p-sel, thrombus precursor protein (TpP), and D-D were measured by flow cytometry, enzyme-linked immunosorbent assay, and immunoturbidimetry, respectively. Sensitivity, specificity, and other values for p-sel, TpP, and D-D were calculated. The linear discriminant, logistic regression, and decision tree methods were used to analyze the p-sel value on the prediction of PVT formation. Seventy-nine patients were confirmed having postoperative PVT, with the incidence rate of 54.86%. No significant differences were observed in the p-sel, TpP, and D-D between the thrombus and nonthrombus groups before surgery, but these 3 indexes were obviously elevated in the thrombus group after operation (P < .01). P-selectin level on first day showed the highest positive predictive value (91.0%) and diagnostic coincidence rate (83.3%), while negative expected value (76.6%) was lower than those of TpP and D-D. Multiple analyses showed the prediction accuracy of PVT was 61.1% (P = .023), 97.2% (P < .001), and 97.2% (P < .001), respectively. P-selectin has a significant value in predicting PVT. P-selectin level on first and third day is valuable and feasible for the early prediction of PVT.

Primary ovarian small cell carcinoma of pulmonary type with coexisting endometrial carcinoma in a breast cancer patient receiving tamoxifen: A case report and literature review.

RATIONALE: Small cell carcinoma of the ovary (SCCO) is a rare and aggressive extra-pulmonary variant of small cell tumors of uncertain histogenesis. The pathogenesis and optimal treatment of SCCO is unclear. We present a very rare case of a synchronous primary ovarian small cell carcinoma and endometrioid adenocarcinoma of the uterus in a patient after 2 years of tamoxifen treatment for breast cancer. This is the first such report in the English literature. PATIENT CONCERNS: A 46-year-old woman had a history of left breast cancer that was treated with a simple mastectomy and sentinel lymph node biopsy in 2013. The post-operative pathology was invasive ductal carcinoma of the left breast. she had been taking tamoxifen for 2 years. The patient underwent an exploratory laparotomy to reduce the tumor burden, improve bowel compression symptoms, and promote defecation in 2015. The post-operative pathology revealed a rare, simultaneous occurrence of two tumors (endometrial adenocarcinoma and SCCO [pulmonary type]). DIAGNOSES: Primary ovarian small cell carcinoma of pulmonary type with coexisting endometrial carcinoma in a breast cancer patient. INTERVENTIONS: The patient received 3 courses of chemotherapy after operation. The effect was not apparent and the general health status was poor. OUTCOMES: The patient died of progressive disease 7 months post-operatively. LESSONS: The present case suggests that tamoxifen use might be among many etiologic factors in SCCO development. Despite its rarity, SCCO requires a high degree of attention in clinical work because it is an aggressive tumor that has a poor prognosis.

Structural and functional analysis of two novel somatostatin receptors identified from topmouth culter (Erythroculter ilishaeformis).

In the present study, we cloned and characterized two somatostatin (SS) receptors (SSTRs) from topmouth culter (Erythroculter ilishaeformis) designated as EISSTR6 and EISSTR7. Analysis of EISSTR6 and EISSTR7 signature motifs, 3D structures, and homology with the known members of the SSTR family indicated that the novel receptors had high similarity to the SSTRs of other vertebrates. EISSTR6 and EISSTR7 mRNA expression was detected in 17 topmouth culter tissues, and the highest level was observed in the pituitary. Luciferase reporter assay revealed that SS14 significantly inhibited forskolin-stimulated pCRE-luc promoter activity in HEK293 cells transiently expressing EISSTR6 and EISSTR7, indicating that the receptors can be activated by SS14. We also identified phosphorylation sites important for the functional activity of EISSTR6 and EISSTR7 by mutating Ser23, 43, 107, 196, 311 and Ser7, 29, 61, 222, 225 residues, respectively, to Ala, which significantly reduced the inhibitory effects of SS14 on the CRE promoter mediated by EISSTR6 and EISSTR7. Furthermore, treatment of juvenile topmouth culters with microcystin-LR or 17ß-estradiol significantly affected EISSTR6 and EISSTR7 transcription in the brain, liver and spleen, suggesting that these receptors may be involved in the pathogenic mechanisms induced by endocrine disruptors. Our findings should contribute to the understanding of the structure-function relationship and evolution of the SSTR family.

Laparoscopic ligation of proximal splenic artery aneurysm with splenic function preservation.

Splenic artery aneurysm is one of the most common visceral aneurysms, and patients with this type of aneurysm often present without symptoms. However, when rupture occurs, it can be a catastrophic event. Although most of these aneurysms can be treated with percutaneous embolization, some located in uncommon parts of the splenic artery may make this approach impossible. We present a patient with an aneurysm in the proximal splenic artery, close to the celiac trunk, which was treated by laparoscopic ligation only, without resection of the aneurysm, and with long-term preservation of splenic function.