A case report of successful rescue using veno-arterial extracorporeal membrane oxygenation: managing cerebral-cardiac syndrome.

Introduction: The presence of cerebral-cardiac syndrome, wherein brain diseases coincide with heart dysfunction, significantly impacts patient prognosis. In severe instances, circulatory failure may ensue, posing a life-threatening scenario necessitating immediate life support measures, particularly effective circulatory support methods. The application of extracorporeal membrane oxygenation (ECMO) is extensively employed as a valuable modality for delivering circulatory and respiratory support in the care of individuals experiencing life-threatening circulatory and respiratory failure. This approach facilitates a critical temporal window for subsequent interventions. Consequently, ECMO has emerged as a potentially effective life support modality for patients experiencing severe circulatory failure in the context of cerebral-cardiac syndrome. However, the existing literature on this field of study remains limited. Case description: In this paper, we present a case study of a patient experiencing a critical cerebral-cardiac syndrome. The individual successfully underwent veno-arterial-ECMO (VA-ECMO) therapy, and the patient not only survived, but also received rehabilitation treatment, demonstrating its efficacy as a life support intervention. Conclusion: VA-ECMO could potentially serve as an efficacious life support modality for individuals experiencing severe circulatory failure attributable to cerebral-cardiac syndrome.

Case Report: Resuscitation of patient with tumor-induced acute pulmonary embolism by venoarterial extracorporeal membrane oxygenation.

Background: Pulmonary embolism is a condition of right cardiac dysfunction due to pulmonary circulation obstruction. Malignant tumor-induced pulmonary embolism, which has a poor therapeutic outcome and a significant impact on hemodynamics, is the cause of sudden death in patients with malignant tumors. Case description: A 38-year-old female patient, who had a medical history of right renal hamartoma, and right renal space-occupying lesion, was admitted to the hospital. During the procedure to resect the right renal malignancy, the blood pressure and end-tidal carbon dioxide level dropped, and a potential pulmonary embolism was considered as a possibility. After inferior vena cava embolectomy, the hemodynamics in the patient remained unstable. The successful establishment of venoarterial extracorporeal membrane oxygenation (VA-ECMO) resulted in the stabilization of her hemodynamics and ventilation. On Day 2 of VA-ECMO support, her respiration and hemodynamics were relatively stable, and ECMO assistance was successfully terminated following the "pump-controlled retrograde trial off (PCRTO)" test on Day 6. The patient improved gradually after the procedure and was discharged from the hospital after 22 days. Conclusion: VA-ECMO can be used as a transitional resuscitation technique for patients with massive pulmonary embolism. It is critical for the perfusion of vital organs and can assist with surgical or interventional treatment, lower right heart pressure, and hemodynamic stability. VA-ECMO has a significant impact on patient prognosis and can reduce the mortality rate.

Clinical Effect of Modified Ultrasound-Guided Subclavian Vein Puncture.

Objective: This study compared the effect of ultrasound-guided subclavian vein puncture with traditional blind puncture and the double-screen control method by evaluating the one-time puncture success and total success rates, the completion time for puncture and catheterization, and short-term complications. Methods: From January 2020 to January 2021, 72 patients with right subclavian venipuncture catheterization were collected, 12 of whom were excluded (including 3 cases of pneumothorax, 2 cases of hemothorax, 1 case of difficult positioning of thoracic deformity, 1 case of severe drug eruption, 3 cases of clavicle fracture, and 1 case of severe coagulation dysfunction). The remaining 60 cases were randomly divided into the traditional group (n = 30) and the improved group (n = 30). We record two sets of ultrasound localization time, puncture time, one-time puncture power, total puncture success rate, and short-term (24-hour) complications. Results: Compared with the traditional group, the ultrasound positioning time and puncture time in the improved group were significantly reduced and the puncture success rate was higher. There were no complications, such as incorrect arterial puncture and the occurrence of pneumothorax, in either group. Conclusion: The improved ultrasound-guided subclavian vein catheterization technique can greatly reduce the catheterization time and improve the success rate of puncture and catheterization. It can also reduce the occurrence of complications and damage to adjacent tissues. The operation is simple, fast, and easy to master, and it has a high popularization clinical value.

Utility of metagenomics next-generation sequencing in the diagnosis and treatment of severe infectious diseases in the intensive care unit.

BACKGROUND: Metagenomic next-generation sequencing (mNGS) is a new method that combines high-throughput sequencing and bioinformatics analysis. However, it has not become as popular due to the limited testing equipment and high costs and lack of family awareness with not much relevant intensive care unit (ICU) research data. OBJECTIVE: To explore the clinical use and value of metagenomics next-generation sequencing (mNGS) in patients with sepsis in the ICU. METHODS: We conducted a retrospective analysis of 102 patients with sepsis admitted to the ICU of Peking University International Hospital from January 2018 to January 2022. Based on whether mNGS was performed, the identified patients were divided into the observation group (n= 51) and the control group (n= 51), respectively. Routine laboratory tests, including routine blood test, C-reactive protein, procalcitonin, and culture of suspicious lesion specimens were performed in both groups within 2 hours after admission to the ICU, while mNGS tests were performed in the observation group. Patients in both groups were routinely given initial anti-infective, anti-shock, and organ support treatment. Antibiotic regimens were optimized in a timely manner according to the etiological results. Relevant clinical data were collected. RESULTS: The testing cycle of mNGS was shorter than that of the conventional culture (30.79 ± 4.01 h vs. 85.38 ± 9.94 h, P< 0.001), while the positive rate of mNGS was higher than that of the conventional culture (82.35% vs. 45.1%, P< 0.05), with obvious superiority in the detection of viruses and fungus. There were significant differences in the optimal time of antibiotics (48 h vs.100 h) and length of ICU stay (11 d vs. 16 d) between the observation group and control group (P< 0.01) respectively, with no difference in 28-day mortality (33.3% vs. 41.2%, P> 0.05). CONCLUSION: mNGS is useful in the detection of sepsis-causing pathogens in the ICU with the advantages of short testing time and high positive rate. There was no difference in the 28-day outcome between the two groups, which may be related to other confounding factors such as small sample size. Additional studies with extended sample size are needed.

Covalent Immobilization of Cellulase onto Amino and Graphene Oxide Functionalized Magnetic Fe2O3/Fe3O4@SiO2 Nanocomposites.

Magnetic Fe2O3/Fe3O4@SiO2 nanocomposites were prepared via the citric-alcohol solution combustion process. The obtained nanocomposites were characterized with SEM, XRD, VSM, TEM, EDS, HRTEM, and FTIR techniques. The results revealed that the magnetic Fe2O3/Fe3O4@SiO2 nanocomposites were successfully obtained with the average grain size of 87 nm and the saturation magnetization of 36 emu/g. After the surface of magnetic Fe2O3/Fe3O4@SiO2 nanocomposites was functionalized by amino group, the amino-functionalized Fe2O3/Fe3O4@SiO2-NH2 nanocomposites were loaded onto graphene oxide based on Mitsunobu reaction. Subsequently, the cellulase was immobilized onto Fe2O3/Fe3O4@SiO2-NH-GO nanocomposites by a glutaraldehyde-mediated Schiff base reaction. The immobilization conditions were optimized by adjusting the pH, temperature, and cellulase dose. The results revealed that optimized immobilization conditions were determined to be temperature of 50 °C, pH of 5, and cellulase solution of 0.1 mL. 97.3% cellulase were successfully immobilized under the optimal conditions. The catalytic performances of the immobilized cellulase were also evaluated. The maximum activity was achieved at pH 4, and 50 °C with cellulase solution of 0.4 mL.

An outbreak of Brucellosis via air-born transmission in a kitchen wastes disposing company in Lianyungang, China.

Brucellosis is a bacterial zoonotic disease caused by pathogenic Brucella spp. An outbreak caused by B. melitensis at Jinchi Biotechnological Company engaged in collecting and disposing of kitchen wastes from catering units in Lianyungang is reported here. An epidemiological investigation and serosurvey were conducted, and pathogen detection was performed. Three confirmed brucella cases, one probable case and two recessive infectors were found out; the attack rate was 33.3%, the screening positive rate by RBPT was 25.0%. The pathogen was B. melitensis identified from three patients: two for B. melitensis, biovars 1, and one for B. melitensis, biovars 2. The main symptoms included fever, sweating, headache, arthralgia, weakness and chill. The epidemiological investigation found that the transmission mode in this outbreak was air-born transmission through aerosols from the process of unloading the food residues and wastes into the feeding inlet. This outbreak of brucellosis was confirmed with patients' clinical symptoms, laboratory testing and epidemiological finds. The disinfection and personal protection were complemented by the kitchen wastes disposing company.

Downregulation of STARD8 in gastric cancer and its involvement in gastric cancer progression.

OBJECTIVE: Rho-GTPases play a pivotal role in a wide variety of signal transduction pathways and are associated with a great number of human carcinomas. STARD8, which is a Rho-GTPase-activating protein, has been proposed as a tumor suppressor gene, but its role in gastric cancer remains elusive. In this study, we investigate the expression of STARD8 in gastric cancer and its association with gastric cancer progression. MATERIALS AND METHODS: One normal gastric mucosa cell line for example GES1 and six human gastric cancer cell lines such as AGS, MGC803, MKN45, SGC7901, HGC27 and BGC823 were utilized to analyze STARD8 mRNA and protein levels by reverse transcription polymerase chain reaction (RT-PCR) and Western blot. A total of 70 paired gastric tissues including corresponding nonmalignant gastric tissues and cancer tissues were utilized to analyze the protein expression of STARD8 using immunohistochemistry, and the correlation between STARD8 level and clinicopathological features was also evaluated. RESULTS: STARD8 was found to be downregulated in primary gastric cancer cells and tissues compared with the normal gastric mucosa cell line, GES1, and corresponding nonmalignant gastric tissues, while its decreased expression was significantly associated with TNM stage, lymph node metastasis and differentiation (p<0.05). CONCLUSION: There is significantly decreased expression of STARD8 in gastric cancer cells and tissues, and its expression may contribute to gastric tumorigenesis.

miR­145 inhibits human non­small-cell lung cancer growth by dual-targeting RIOK2 and NOB1.

Non-small cell lung cancer (NSCLC) is a leading cause of cancer-associated mortality worldwide. Right open reading frame kinase 2 (RIOK2) and nin one binding protein (NOB1) are important accessory factors in ribosome assembly. In our previous study, RIOK2 and NOB1 were revealed to be highly expressed in NSCLC, and were associated with the clinicopathological characteristics of patients with NSCLC, i.e. TNM clinical stage, lymph node metastasis and differentiation. In addition, RIOK2 expression was correlated with NOB1. To further explore the mechanism and the RIOK2 and NOB1 signaling pathway, microRNA (miR) regulation was analyzed. The tumor suppressor miR­145 has been reported to be lowly expressed in numerous types of human cancer; in the present study, the expression levels of miR­145 were decreased in patients with NSCLC. Furthermore, RIOK2 and NOB1 were predicted to be the direct targets of miR­145 using bioinformatics software; this was further validated using a dual luciferase reporter assay. In addition, the protein expression levels of RIOK2 and NOB1 were inhibited in response to miR­145 overexpression, thus resulting in the suppression of cell viability, migration and invasion. These results suggested that RIOK2 and NOB1 may be potential targets in the treatment of NSCLC, and miR­145 may be considered a therapeutic inhibitor of both genes.

DISC1 overexpression promotes non-small cell lung cancer cell proliferation.

Neuropsychiatric disorder-associated disrupted-in-schizophrenia-1 (DISC1) activates Wnt/ß-catenin signaling by inhibiting glycogen synthase kinase 3 beta (GSK3ß) phosphorylation, and may promote neural progenitor cell and pancreatic ß-cell proliferation. The present study found that DISC1 promotes non-small cell lung cancer (NSCLC) cell growth. Western blotting and immunohistochemistry analyses showed that DISC1 was highly expressed in NSCLC cell lines and patient tissues. DISC1 expression was negatively associated with phosphorylated (p-) GSK3ß, but positively correlated with a more invasive tumor phenotype and predicted poor NSCLC patient prognosis. siRNA-mediated DISC1 silencing increased p-GSK3ß expression and decreased expression of ß-catenin and Cyclin D1, while DISC1 upregulation produced the opposite results. DISC1 knockdown also reduced NSCLC cell proliferation rates in vitro. These results suggest that DISC1 promotes NSCLC growth, likely through GSK3ß/ß-catenin signaling, and that DISC1 may function as an oncogene and novel anti-NSCLC therapeutic target.

Curcumin attenuates myocardial ischemia-reperfusion injury.

BACKGROUND: Cardiovascular diseases (CVDs) are at a badly high-risk of morbidity and mortality in the world. METHODS: Our study was attempted to investigate the cardioprotective role of curcumin. Hearts injury was assessed in isolated hearts and the rats of coronary artery ligated. RESULTS AND CONCLUSIONS: The inhibition of pro-inflammatory cytokines was observed by curcumin in coronary artery ligated rats. ST segment was also reduced by curcumin. Triphenyltetrazolium chloride staining (TTC) staining and pathological analysis were also showed that curcumin could dramatically alleviate myocardial injury. Besides, the results in vitro also demonstrated that curcumin could improved the function of isolated hearts. Besides, the expressions of inflammation-related pathway in both rats and isolated hearts treated with curcumin were significantly decreased. The present study investigated the protective effects of curcumin on myocardial injury and its mechanism.

High Expression of RIOK2 and NOB1 Predict Human Non-small Cell Lung Cancer Outcomes.

Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related mortality worldwide. However, there is a shortage of suitable diagnostic markers for early stages of NSCLC, and therapeutic targets are limited. Right open reading frame (Rio) kinase 2 (RIOK2) and Nin one binding (NOB1) protein are important accessory factors in ribosome assembly and are highly expressed in malignant tumours; moreover, they interact with each other. However, the RIOK2 expression profile and its clinical significance as well as NOB1's mechanism in NSCLC remain unknown. In this study, NSCLC cell lines and 15 NSCLC tumour tissues (paired with adjacent normal lung tissues) were collected for a real-time quantitative PCR (RT-qPCR) analysis. In addition, 153 NSCLC cases and 27 normal lung tissues were used in an immunohistochemical analysis to evaluate the RIOK2 and NOB1 expression profiles, their clinicopathological factors in NSCLC and their correlations with prognoses. RIOK2 and NOB1 were highly expressed in NSCLC cells and tissues, and their expression profiles were significantly associated with the Tumour Node Metastasis (TNM) clinical stage, lymph node metastasis, and differentiation. RIOK2 expression was correlated with NOB1. The results suggested that simultaneously determining the expression of RIOK2 and NOB1 will improve the diagnostic rate in early stages of NSCLC. Moreover, RIOK2 and NOB1 might be potential targets for NSCLC therapy.

NDRG1 Controls Gastric Cancer Migration and Invasion through Regulating MMP-9.

The purpose of this study is to detect the clinical significance of NDRG1 and its relationship with MMP-9 in gastric cancer metastatic progression. 101 cases of gastric cancer specimens were utilized to identify the protein expression of NDRG1 and MMP-9 by immunohistochemistry, their clinical significance was also analyzed. The suppression by siRNA-NDRG1 was employed to detect the role of NDRG1 in gastric cancer progression and its relationship with MMP-9. NDRG1 expression was correlated inversely with the degree of tumor cell differentiation (p < 0.01), invasion depth (p < 0.05), lymph node metastasis (p < 0.05) and TNM stage (p < 0.05), whereas MMP-9 was positive correlated with the degree of tumor cell differentiation (p < 0.01), lymph node metastasis (p < 0.05) and TNM stage (p < 0.05), but not correlated with invasion depth (p>0.05). Furthermore, cell proliferation and invasion effect were remarkably enhanced when NDRG1 was silencing, but MMP-9 expression was increased. NDRG1 silencing enhances gastric cancer cells progression through upregulating MMP-9. It suggests that NDRG1 may inhibit the metastasis of gastric cancer via regulating MMP-9.

NDRG1 expression is related to the progression and prognosis of gastric cancer patients through modulating proliferation, invasion and cell cycle of gastric cancer cells.

N-myc downstream-regulated gene 1 (NDRG1) has been proposed as a tumor suppressor gene in many different types of tumors, but its potential function and corresponding mechanism are not yet fully elucidated. This study aims to detect the possible function of NDRG1 in gastric cancer progression. In this study, 112 paired gastric cancer tissues and corresponding nonmalignant gastric tissues were utilized to identify the differential protein expression of NDRG1 by immunohistochemistry and its clinical significance was analyzed. Furthermore, 49 of 112 paired gastric specimens were used to detect the differential mRNA expression by real-time PCR. The over expression of NDRG1 in human gastric cancer cell line AGS by PcDNA3.1-NDRG1 transfection was utilized to detect the role of NDRG1 in regulating the biological behavior of gastric cancer. NDRG1 expression was significantly decreased in primary gastric cancer tissues, compared with its corresponding nonmalignant gastric tissues (p < 0.05), and its decreased expression was significantly associated with lymph node metastasis (p < 0.01), invasion depth (p < 0.01) and differentiation (p < 0.05). Additionally, the overall survival rate of gastric cancer patients with high expression of NDRG1 was higher than those with low expression during the follow-up period. NDRG1 overexpression suppressed cells proliferation, invasion and induced a G1 cell cycle arrest in gastric cancer. Furthermore, the down-regulation of NDRG1 in gastric cancer metastatic progression was correlated to E-cadherin and MMP-9. Our results verify that NDRG1 acts as a tumor suppressor gene and may play an important role in the metastasis progression and prognosis of gastric cancer.

Expression of ADAMTS1 and its correlation with angiogenesis in primary gastric cancer and lymph node metastasis.

BACKGROUND: A disintegrin and metallopeptidase with thrombospondin motif type 1 (ADAMTS1) is a recently discovered metalloproteinase with antiangiogenic activity. The function of ADAMTS1 in gastric cancer remains unknown. Therefore, we were interested in examining ADAMTS1 expression in human gastric cancer, as well as its possible correlation with angiogenesis. METHODS: The mRNA and protein expression of ADAMTS1, thrombospondin type I (TSP1), and vascular endothelial growth factor (VEGF) was evaluated by RT-PCR and immunohistochemistry, respectively, in 56 paired tumor and normal tissue samples, and corresponding metastatic lymph nodes (n = 42). Microvessel density (MVD) was also evaluated by immunohistochemistry. RESULTS: ADAMTS1 mRNA and protein levels were significantly lower in primary tumors than in corresponding normal tissues, and were significantly higher in metastatic lymph nodes compared to their matched primary tumors. High ADAMTS1 mRNA and protein expression was found to be significantly associated with lymph node metastasis in primary tumors. There was a negative correlation between ADAMTS1 and VEGF mRNA and protein expression in primary gastric tumors and normal tissues. A negative correlation was also found between ADAMTS1 protein expression and MVD in primary gastric tumors. In contrast, no correlation was detected between ADAMTS1 and TSP1 mRNA and protein expression in primary gastric tumors, normal tissues, and metastatic lymph nodes. CONCLUSIONS: These findings suggest that ADAMTS1 expression is altered in primary gastric cancer and paired lymph node metastasis. In addition, ADAMTS1 has angioinhibitory effects in primary gastric cancer due to its low expression and negative correlation with VEGF and MVD. However, it appears to lose its anti-angiogenic activity in metastatic lymph nodes in gastric cancer.

DNA methylation of NDRG2 in gastric cancer and its clinical significance.

BACKGROUND: Gastric cancer is one of the most common digestive malignancies worldwide. N-myc downstream-regulated gene 2 (NDRG2) is a differentiation-related gene that is considered to be a metastasis suppressor gene. In this study, we examined the expression and DNA methylation of NDRG2 in gastric cancer cell lines and tissues, as well as its clinical significance. METHODS: Six gastric cancer cell lines and 42 paired normal and gastric cancer tissue samples were used to assess NDRG2 mRNA expression using RT-PCR. NDRG2 DNA methylation status was evaluated by methylation-specific PCR (MSP) in gastric cancer cell lines and tissues. The suppression of NDRG2 in BGC823 cells by siRNA transfection was utilized to detect the role of NDRG2 in gastric cancer progression. RESULTS: NDRG2 mRNA was down-regulated in gastric cancer cell lines and tissues, and its expression was just related to lymph node metastasis (p = 0.032). MSP showed methylation of NDRG2 in 54.0 % (47/87) of primary gastric cancer specimens and in 20.0 % (16/80) of corresponding nonmalignant gastric tissues. NDRG2 methylation was related to depth of tumor invasion, Borrmann classification and TNM stage (p < 0.05). Upon treatment with 5-aza-2'-deoxycytidine and trichostatin A, NDRG2 expression was upregulated in HGC27 cells, and demethylation of the highly metastatic cell line, MKN45, inhibited cell invasion. Furthermore, the suppression of NDRG2 by siRNA transfection enhanced BGC823 cells invasion. CONCLUSIONS: Our results suggest that the aberrant methylation of NDRG2 may be mainly responsible for its downregulation in gastric cancer, and may play an important role in the metastasis of gastric cancer.

Association of NDRG1 gene promoter methylation with reduced NDRG1 expression in gastric cancer cells and tissue specimens.

NDRG1 (N-myc downstream-regulated gene 1) plays a role in cell differentiation and suppression of tumor metastasis. This study aims to determine the expression of NDRG1 mRNA and protein in gastric cancer cell lines and tissue specimens and then assess the possible cause of its aberrant expression. Six gastric cancer cell lines and 20 pairs of normal and gastric cancer tissue samples were used to assess NDRG1 expression using Real-time PCR and Western blot. High-resolution melting analysis (HRM) and methylation-specific PCR (MSP) were performed to detect gene mutation and methylation, respectively, in cell lines and tissues samples. Expression of NDRG1 mRNA and protein was downregulated in gastric cancer cell lines and tissues. Specifically, expression of NDRG1 mRNA and protein was lower in all six gastric cancer cell lines than that of normal gastric cells, while 15 out of 20 cases of gastric cancer tissues had the reduced levels of NDRG1 mRNA and protein. HRM data showed that there was no mutation in NDRG1 gene, but MSP data showed high levels of NDRG1 gene promoter methylation in the CpG islands in both cell lines and tissue samples. Moreover, treatment with the DNA methyltransferase inhibitor 5-Aza-2'-deoxycytidine upregulated NDRG1 expression in gastric cancer HGC27 cells, but not in the histone deacetylase inhibitor trichostatin A-treated HGC27 cells. In conclusion, this study has shown that expression of NDRG1 mRNA and protein was reduced in gastric cancer cell lines and tissues, which is due to methylation of NDRG1 gene promoter. Further study will unearth the clinical significance of the reduced NDRG1 protein in gastric cancer.

Down-regulation of CXCL12 by DNA hypermethylation and its involvement in gastric cancer metastatic progression.

BACKGROUND: Chemokine receptors are now known to play an important role in cancer growth and metastasis. However, there is little information regarding chemokine expression in gastric cancer. In this study, we examined CXCL12 expression in gastric cancer and also evaluated whether the down-regulation of CXCL12 is due to aberrant methylation of the gene. METHODS: CXCL12 expression was examined using real-time reverse-transcription polymerase chain reaction (RT-PCR), immunofluorescence, flow cytometry, and immunohistochemistry, and the methylation status of the gene was evaluated by methylation-specific PCR (MSP) in normal gastric and gastric cancer cell lines and 35 primary gastric carcinomas and corresponding nonmalignant gastric tissues. RESULTS: The down-regulation of CXCL12 was observed in gastric cancer cell lines and primary gastric carcinomas, while decreased expression of CXCL12 protein was significantly associated with lymph node metastasis and histological grade. And this down-regulation was found to be in accordance with aberrant methylation of the gene. Hypermethylation of the gene was observed in 65.7% (23 of 35) of the primary gastric carcinomas, while it was found in only 11.4% (4/35) of the corresponding nonmalignant tissues. Furthermore, CXCL12 expression was restored in gastric cancer cell lines after treatment with the demethylating agent, 5-aza-2'-deoxycytidine (5-Aza-dC), and demethylation of the highly metastatic cells SGC-7901 induced invasion suppression of the cells. For two CXCL12 receptors, CXCR4 and CXCR7, the mRNA levels remained almost unchanged with the 5-Aza-dC treatment. CONCLUSIONS: Collectively, our results suggest that the aberrant methylation of CXCL12 frequently occurs in the down-regulation of CXCL12 in gastric cancers and that it may play a role in the metastasis of gastric cancer.