The clinicopathological significance of TOP2A expression in malignant peritoneal mesothelioma.

BACKGROUND: Malignant peritoneal mesothelioma (MPM) is a rare malignant tumor with a high mortality rate and extremely poor prognosis. TOP2A expression is associated with cell proliferation and cell cycle progression. We aimed to demonstrate the expression profile of TOP2A in MPM and its correlation with clinicopathological features. METHODS: Clinicopathological information from 100 MPM cases was collected at Beijing Shijitan Hospital, Capital Medical University. Immunohistochemistry (IHC) was performed to evaluate TOP2A levels. The associations between TOP2A levels and clinicopathological features or prognosis were analyzed. Clinical follow-up data were reviewed to determine correlations among the pathological prognostic factors using the Kaplan-Meier estimator and univariate/multivariate Cox proportional hazards regression models. RESULTS: Among the 100 MPM patients, there were 48 males and 52 females, with a median age of 54 years (range: 24-72 years). The cutoff curve was used to find the boundary value of the TOP2A-positive rate. TOP2A positive rate ≥ 11.97 % accounted for 48 % in tumor tissue. The TOP2A-positive rate was not associated with sex, age, asbestos exposure, peritoneal carcinomatosis index (PCI) score, or completeness of cytoreduction (CC) score in MPM. Univariate analysis revealed survival-related pathological parameters, including asbestos exposure, CA125, histological type, PCI score, CC score, Ki-67 index, and TOP2A positive rate. Multivariate analysis identified that asbestos exposure history, PCI score, Ki-67 proliferation index and TOP2A positive rate in tissue are independent prognostic factors. CONCLUSIONS: High expression of TOP2A is linked to better prognosis of MPM.

In silico development and in vitro validation of a novel five-gene signature for prognostic prediction in colon cancer.

Colon cancer is one of the most common cancers in digestive system, and its prognosis remains unsatisfactory. Therefore, this study aimed to identify gene signatures that could effectively predict the prognosis of colon cancer patients by examining the data from the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) database. LASSO-Cox regression analysis generated a five-gene signature (DCBLD2, RAB11FIP1, CTLA4, HOXC6 and KRT6A) that was associated with patient survival in the TCGA cohort. The prognostic value of this gene signature was further validated in two independent GEO datasets. GO enrichment revealed that the function of this gene signature was mainly associated with extracellular matrix organization, collagen-containing extracellular matrix, and extracellular matrix structural constituent. Moreover, a nomogram was established to facilitate the clinical application of this signature. The relationships among the gene signature, mutational landscape and immune infiltration cells were also investigated. Importantly, this gene signature also reliably predicted the overall survival in IMvigor210 anti-PD-L1 cohort. In addition to the bioinformatics study, we also conducted a series of in vitro experiments to demonstrate the effect of the signature genes on the proliferation, migration, and invasion of colon cancer cells. Collectively, our data demonstrated that this five-gene signature might serve as a promising prognostic biomarker and shed light on the development of personalized treatment in colon cancer patients.

Retraction: a narrative review of long noncoding RNA: insight into neural ischemia/reperfusion mediated by two pathophysiological processes of injury and repair.

[This retracts the article DOI: 10.21037/atm-22-268.].

Prognosis-Related Nutritional Score for Cancer Patients (PRNS): a clinical nutritional score derived from a retrospective cohort study.

BACKGROUND: Nutritional assessment and quality of life (QOL) have become important indices for therapeutic efficacy in patients with malignancies. We aim to develop and validate an easy-to-use questionnaire with prognostic value to assess nutritional status in hospitalized cancer patients. METHODS: A comprehensive survey focused on patient-generated subjective global assessment (PG-SGA) and 30-item European Organization for Research and Treatment of Cancer Core Quality of Life Questionnaire (EORTC QLQ-C30 Chinese version) was performed in a cohort of 22,776 patients derived from the INSCOC study. Among them, 1948 patients were followed for 3 years after admission. An observational, retrospective, cross-sectional cohort study was conducted in accordance with TRIPOD statement. Breiman's random forest model was applied to calculate variable importance (VIMP) for items in PG-SGA and EORTC QLQ-C30 (Chinese version) for nutritional recommendation. Cox regression model was employed to construct Prognosis-Related Nutritional Score for Cancer Patients (PRNS). Kaplan-Meier Survival curve, ROC and DCA were calculated to evaluate prognostic value of nutritional status categorized by PRNS, and compared with PG-SGA. RESULTS: Nutritional status was classified into 4 levels by PRNS scores: well nourished (≤ 4.5 points), mild malnourished (5-7.5 points), moderate malnourished (8-14.5 points), and severe malnourished (≥ 15 points). Significant median overall survival differences were found among nutritional status groups stratified by the PRNS (all Ps < 0.05). Compared with PG-SGA, PRNS had better prognostic value for survival stratified by nutritional status. The external, internal validity, test-retest reliability and rater reliability were satisfactory. CONCLUSIONS: We systematically developed and validated PRNS as a nutrition screening tool for cancer patients. Compared with PG-SGA, PRNS has better prognostic value and simpler operation. TRIAL REGISTRATION: Investigation on Nutrition Status and its Clinical Outcome of Common Cancers, ChiCTR1800020329. Registered 24 December 2018-Retrospectively registered, http://www.chictr.org.cn/showproj.aspx?proj=31813.

Association of differential body water composition by sex, measured using BIA, with survival in a real­world lung cancer cohort.

OBJECTIVE: The aim of this study was to evaluate the association of differential body water composition with survival in patients with lung cancer. METHODS: This retrospective cohort study included 1314 patients diagnosed with lung cancer in 80 Chinese institutions from May 2013 to August 2020. We calculated hazard ratios (HRs) to evaluate the associations of all-cause mortality with extracellular water (ECW) and intracellular water (ICW). Cox proportional risk regression models were adjusted for sociodemographic characteristics, tumor characteristics, treatment, body mass index (BMI), and body composition measures. We also evaluated cross-classification of the dichotomy of ECW and ICW with outcomes. The association among ECW, ICW, and survival was evaluated via Cox regression and the restricted cubic-spline model using a two-sided P value. RESULTS: The study included 819 (62%) men and 495 (28%) women. The HR of lung cancer mortality significantly decreased as ECW increased (HR, 0.96; 95% confidence interval [CI], 0.93-1.00) and ICW (HR, 0.97; 95% CI, 0.95-1.00) with cutoff values of 10.5 and 16.3 L, respectively. When patients were cross-classified into categories of sex, age, BMI, visceral fat index, pathology, tumor stage, tumor burden, total bilirubin, and neutrophil count, ICW and ECW were protective factors. Only sex interacted significantly with ICW or ECW. High ICW and ECW had significant protective effects, and women had a greater risk for death than men in the case of either poor ICW or poor ECW. Sensitivity analysis showed the protective effect of the higher dichotomy of ICW (HR, 0.52; 95% CI, 0.35-0.78) and ECW (HR, 0.45; 95% CI, 0.31-0.66) on female lung cancer patients by removing patients who died within 12 mo of diagnosis. CONCLUSION: Greater ICW and ECW, especially ICW, were independent predictors for better survival in patients with lung cancer. Female patients were more vulnerable to dehydration than male patients.

Remifentanil pretreatment attenuates brain nerve injury in response to cardiopulmonary bypass by blocking AKT/NRF2 signal pathway.

OBJECTIVE: This study aimed to explore the effect and mechanism of remifentanil on cardiopulmonary bypass (CPB)-induced cerebral nerve injury. METHODS: After pretreating with remifentanil, or dexmedetomidine (DEX), SD rats were subjected to the CPB for 2 h. The data of body temperature, blood gas and mean arterial pressure (MAP) and hematocrit (HCT) were recorded at different time points. The cerebral tissue water content of rats was determined and immunohistochemical (IHC) and H&E assays on the hippocampal CA1 region of rats was performed. The levels of interleukin (IL)-6, IL-10, soluble protein-100ß (S100ß) and neuron-specific enolase (NSE) were analyzed by ELISA, and those of the indexes for oxidative stress (malondialdehyde (MDA) and superoxide dismutase (SOD)) were detected by the commercial kits. Morris water maze was used to evaluate the learning and memory abilities. Western blot/qRT-PCR were used to detect the protein/mRNA expressions in hippocampus. RESULTS: CPB increased the levels/expressions of IL-6, IL-10, S100ß, NSE, MDA, cleaved caspase-3, Bax and decreased those of Bcl-2, SOD, p-AKT, HO-1, in serum and parietal cortex tissue, with increased brain water content, lesions in the hippocampal CA1 area, swimming distance, brain nerve injury and decreased escape latency, retention time on platform and times of crossing the platform of rats. The preconditioning of remifentanil or DEX partially attenuated CPB-induced injury and -decreased expressions on p-AKT and HO-1, while further promoting CPB-induced expression of nuclear Nrf2 expression and inhibiting that of cytoplasm Nrf2. CONCLUSION: This paper demonstrates that remifentanil preconditioning could partially attenuate CPB-induced brain nerve injury of rats.

A narrative review of long noncoding RNA: insight into neural ischemia/reperfusion mediated by two pathophysiological processes of injury and repair.

Background and Objective: A thorough understanding of the role of long noncoding RNAs (lncRNAs) in cerebral ischemia/reperfusion injury (IRI) is conducive to a comprehensive understanding of the molecular regulatory network of IRI. Such an understanding could be of great significance for finding new biomarkers and therapeutic targets of IRI. Such findings could protect important tissues and organs and improve the clinical prognosis of patients. Methods: We conducted a literature search for published manuscripts on neural ischemia/reperfusion up to October 2021 in the PubMed, Web of Science, Cochrane Library, and EMBASE databases. Key Content and Findings: LncRNAs are a group of regulatory sequences that play a role at the transcriptional, posttranscriptional and epigenetic levels. LncRNAs are highly expressed in the central nervous system and play an important regulatory role in the development of the central nervous system and diseases. The mechanism of IRI is complex, and pathological injury processes, such as apoptosis, oxidative stress injury, neuroinflammation, excitatory amino acid toxicity, autophagy and impaired blood-brain barrier function, are mutually intertwined or promoted. These processes can aggravate the secondary injury of brain tissue after ischemia-reperfusion. Moreover, cerebral IRI can induce a large number of changes to the expression of lncRNAs in the brain, suggesting that lncRNAs are related to the complicated pathological process of cerebral IRI. Conclusions: In this narrative review, the roles of lncRNAs in cerebral IRI, apoptosis, anti-apoptosis, nerve regeneration, and repair after injury are reviewed. Additionally, possible future research directions for lncRNAs in ischemic stroke injury and repair are proposed.

A Four-Gene-Based Risk Score With High Prognostic Value in Gastric Cancer.

BACKGROUND: Gastric adenocarcinoma is an important contributor to cancer mortality and morbidity. This study aimed to explore the prognostic value of mutation patterns in gastric adenocarcinoma. MATERIALS AND METHODS: We extracted somatic mutation data for 437 gastric adenocarcinoma samples from The Cancer Genome Atlas (TCGA) Stomach Adenocarcinoma (STAD) cohort. Kaplan-Meier survival in the R package maftools was used to analyze associations between mutations and survival. Multivariate Cox proportional model was used to establish risk formula. A four-gene-based risk score was developed to predict the overall survival of patients with gastric adenocarcinoma. We used the Tianjin cohort dataset with survival information to further evaluate the clinical value of this mutation signature. RESULTS: Forty-five survival-related mutated genes were identified and verified, most of which were co-occurring in their mutation pattern and co-occurring with MLH3 and polymerase ϵ (POLE) mutations. Gastric adenocarcinoma samples with the 45 mutated genes had a significantly higher mutation count. Four-gene [UTRN, MUC16, coiled-coil domain-containing protein 178 (CCDC178), and HYDIN] mutation status was used to build a prognostic risk score that could be translated into the clinical setting. The association between the four-gene-based signature and overall survival remained statistically significant after controlling for age, sex, TNM stage, and POLE mutation status in the multivariate model [hazard ratio (HR), 1.88; 95% CI, 1.33-2.7; p < 0.001]. The prognostic significance of the four-gene-based risk score identified in TCGA cohort was validated in the Tianjin cohort. CONCLUSION: A four-mutated gene risk formula was developed that correlated with the overall survival of patients with gastric adenocarcinoma using a multivariable Cox regression model. In two independent genomic datasets from TCGA and Tianjin cohorts, low risk scores were associated with higher tumor mutation loads and improved outcome in patients with gastric adenocarcinoma. This finding may have implications for prognostic prediction and therapeutic guidance for gastric adenocarcinoma.

Genome-Wide Analysis of Methylation-Driven Genes and Identification of an Eight-Gene Panel for Prognosis Prediction in Breast Cancer.

BACKGROUND: Aberrant DNA methylation is a crucial epigenetic regulator that is closely related to the occurrence and development of various cancers, including breast cancer (BC). The present study aimed to identify a novel methylation-based prognosis biomarker panel by integrally analyzing gene expression and methylation patterns in BC patients. METHODS: DNA methylation and gene expression data of breast cancer (BRCA) were downloaded from The Cancer Genome Atlas (TCGA). R packages, including ChAMP, SVA, and MethylMix, were applied to identify the unique methylation-driven genes. Subsequently, these genes were subjected to Metascape for GO analysis. Univariant Cox regression was used to identify survival-related genes among the methylation-driven genes. Robust likelihood-based survival modeling was applied to define the prognosis markers. An independent data set (GSE72308) was used for further validation of our risk score system. RESULTS: A total of 879 DNA methylation-driven genes were identified from 765 BC patients. In the discovery cohort, we identified 50 survival-related methylation-driven genes. Finally, we built an eight-methylation-driven gene panel that serves as prognostic predictors. CONCLUSIONS: Our analysis of transcriptome and methylome variations associated with the survival status of BC patients provides a further understanding of basic biological processes and a basis for the genetic etiology in BC.

Dexmedetomidine Exerts Brain-Protective Effects Under Cardiopulmonary Bypass Through Inhibiting the Janus Kinase 2/Signal Transducers and Activators of Transcription 3 Pathway.

Brain injury is a major complication resulted from cardiopulmonary bypass (CPB). Dexmedetomidine (DEX) has potential brain-protective effects; however, the mechanism is unclear. The aim of this study is to investigate the effect of DEX on brain injury in CPB rats and its mechanism. The levels of interleukin-6 (IL-6), interleukin-10 (IL-10), S100ß, and neuron-specific enolase (NSE) were measured by enzyme-linked immunosorbent assay. The hippocampus CA1 region in rats was observed by hematoxylin-eosin staining. Western blot and quantitative real-time polymerase chain reaction were performed to detect related proteins and mRNA expressions in the hippocampus tissues. We found that after CPB, the neuron cells in hippocampus CA1 region of rats were randomly arranged, and that the levels of IL-6, IL-10, S100ß, NSE, Cleaved Caspase-3, and Bax were upregulated, while Bal-2 level was downregulated. However, after DEX treatment, the neuron cells arranged in an orderly manner, and the levels of IL-6, IL-10, S100ß, NSE, Cleaved Caspase-3, and Bax were downregulated, but Bal-2 level was upregulated. DEX suppressed Janus kinase 2 (JAK2)/signal transducers and activators of transcription 3 (STAT3) pathway activated by CPB, ameliorated CPB-induced brain injury in rats by reducing inflammatory response, and inhibited neuronal apoptosis. The brain-protective effect of DEX may be related to the inhibition of the activation of JAK2/STAT3 pathway.

Corrigendum: NFκB/Orai1 Facilitates Endoplasmic Reticulum Stress by Oxidative Stress in the Pathogenesis of Non-alcoholic Fatty Liver Disease.

[This corrects the article DOI: 10.3389/fcell.2019.00202.].

NFκB/Orai1 Facilitates Endoplasmic Reticulum Stress by Oxidative Stress in the Pathogenesis of Non-alcoholic Fatty Liver Disease.

Non-esterified fatty acids (NEFAs) promote de novo lipogenesis, which caused abnormal hepatic lipid accumulation, by the NFκB-Orai1 pathway. Oxidative stress and endoplasmic reticulum (ER) stress have been recognized as key mechanisms in non-alcoholic fatty liver disease (NAFLD) pathogenesis. Whether Orai1 facilitates ER stress by oxidative stress remains unknown. The rat model of NAFLD was constructed by feeding high-fat diet (HFD). BRL-3A cells were treated with NEFAs, Orai1inhibtor BTP2, NFκB inhibitor wogonin, or small interfering Orai (siOrai) 1, respectively. The content of intracellular reduced glutathione (GSH) and malondialdehyde (MDA), indicating oxidative stress, was measured by a spectrophotometer. ER stress major proteins PERK, IRE1, ATF6, CHOP, and GRP78 were quantified using Western blot and qRT-PCR analyses. For the intracellular location of reactive oxygen species (ROS) and Orai1 were measured by Western blot and immunofluorescence, and cytosolic Ca2+ was measured by flow cytometry. As we expected, the liver of rats with NAFLD showed lipid droplets in HE and Oil Red O. The decreased GSH and increased MDA were found in rats fed with HFD. ER stress major proteins PERK, IRE1, ATF6, GRP78, and CHOP were significantly increased in the HFD group. In BRL-3A cells, GSH content dramatically decreased from 1 h, MDA content dramatically increased from 3 h, and expression levels of ER stress significantly increased from 3 h by NEFA treatment. Furthermore, cytosolic Ca2+ increased from 0.5 h by NEFAs treated in BRL-3A cells. It indicated that NEFAs increased cytosolic Ca2+ to induce oxidative stress, thus ER stress. The content of oxidative stress and ER stress proteins showed the same trends by NEFAs treated in BRL-3A cells. These effects were reversed by the Orai1 inhibitor BTP2 and the NFκB inhibitor wogonin. Moreover, siOrai1 abrogated NEFAs' influence in BRL-3A cells. Last, ROS was found by NEFAs treated in BRL-3A cells, and NEFA treatment enhanced the nuclear localization of NF-κB p65 and ORAI1. It was considered that high NEFAs increased cytosolic Ca2+ and enhanced NFκB-dependent SOCE and its moiety protein Orai1 to decrease GSH and thus induced oxidative stress at earlier stages and furthermore tempted ER stress in the pathologic progress of NAFLD.

Loss of PTPN4 activates STAT3 to promote the tumor growth in rectal cancer.

Colorectal cancer (CRC) is one of the most common types of malignant tumor. Many genetic factors have been proved to show high association with the occurrence and development of CRC and many mutations are detected in CRC. PTPN4/PTP-MEG1 is a widely expressed non-receptor protein tyrosine phosphatase. Over the past three decades, PTPN4 has been demonstrated in the literature to participate in many biological processes. In this study, we identified a nonsense mutation of PTPN4 with a mutation ratio of 90.90% from 1 case of rectal cancer, leading to loss of function in PTPN4 gene. Several somatic mutations occurred in 5/137 rectal cancer samples from The Cancer Genome Atlas Rectum Adenocarcinoma (TCGA READ) database. Interestingly, we found that PTPN4 negative cytoplasm staining was more prone to lymphatic metastasis (N = 50, P = 0.0153) and low expression of PTPN4 in rectal cancer was highly associated with poor prognosis. Overexpression of PTPN4 suppressed the cell growth, and moreover, the loss of PTPN4 accelerated cell growth and boosted clonogenicity of CRC cells. Furthermore, we revealed that the deletion of PTPN4 promoted the tumor formation of NCM460 cells in vivo. In terms of the molecular mechanism, we demonstrated that PTPN4 dephosphorylates pSTAT3 at the Tyr705 residue with a direct interaction and suppresses the transcriptional activity of STAT3. In summary, our study revealed a novel mechanism that the tumorigenesis of colorectal cancer might be caused by the loss of PTPN4 through activating STAT3, which will broaden the therapy strategy for anti-rectal cancer in the future.

A 5-serum miRNA panel for the early detection of colorectal cancer.

OBJECTIVE: The study aimed to screen microRNAs (miRNAs) that can be used for the early detection of colorectal cancer (CRC) based on differential expression of miRNA in serum. MATERIALS AND METHODS: A three-stage study was designed with a total of 217 CRCs, 168 colorectal adenomas (CRAs), and 190 healthy controls (HCs). A quantitative reverse transcription polymerase chain reaction was performed in three stages. We screened 528 miRNA expression profiles in the sera of 40 patients (CRC n=20, CRA n=10, and HC n=10) for candidate miRNAs, then 210 serum samples (CRC n=90, CRA n=60, and HC n=60) were used for screening of candidate miRNAs. Three hundred and twenty-five independent individual samples (CRC n=107, CRA n=98, and HC n=120) were used to validate the most differentially-expressed miRNAs in the screening stage, and binary logistic regression was used in the validation stage. A receiver operating characteristic curve was drawn to evaluate the diagnostic accuracy. RESULTS: A 5-serum miRNA panel (miRNA-1246, miRNA-202-3p, miRNA-21-3p, miRNA-1229-3p, and miRNA-532-3p) effectively distinguished CRCs from HCs with 91.6% sensitivity and 91.7% specificity. The area under the curve (AUC) was 0.960 (95% confidence interval [CI]: 0.937-0.983). In addition, the panel also accurately distinguished CRCs from CRAs with 94.4% sensitivity and 84.7% specificity. The AUC was 0.951 (95% CI: 0.922-0.980). CONCLUSION: Our 5-serum miRNA panel accurately distinguished CRCs from CRAs and HCs with high sensitivity and specificity. The 5-serum miRNA panel may be a promising prospect for application as a nonintrusive and inexpensive method for the early detection of CRC.

Phosphate and ammonium adsorption of sesame straw biochars produced at different pyrolysis temperatures.

The adsorption of [Formula: see text] and [Formula: see text] by sesame straw biochars (C-300, C-500, and C-700) prepared under different temperatures (300, 500, and 700 °C) was investigated in this study. The physicochemical properties of the biochars were characterized using Brunauer-Emmett-Teller method, X-ray diffraction, scanning electron microscopy, and Fourier transform infrared spectrometry. In batch experiments, C-300 showed the best [Formula: see text] adsorption capacity of 3.45 mg/g because of its abundant surface functional groups at low pyrolysis temperature. C-700 achieved the optimal [Formula: see text] adsorption capacity of 34.17 mg/g because of its high Ca, Mg, and Al contents and high surface area at high pyrolysis temperature. The isothermal study showed that the Langmuir-Freundlich model could sufficiently describe the [Formula: see text] and [Formula: see text] adsorption values, indicating the multiple adsorption processes of nutrients on biochars. The maximum [Formula: see text] adsorption capacity was 93.61 mg/g on C-300, whereas the maximum [Formula: see text] adsorption capacity was as high as 116.58 mg/g on C-700. Kinetic study showed that [Formula: see text] adsorption on C-300 was mainly controlled by intraparticle diffusion, and the pseudo-second-order model could well describe [Formula: see text] adsorption on C-700.

Dexmedetomidine reduces the neuronal apoptosis related to cardiopulmonary bypass by inhibiting activation of the JAK2-STAT3 pathway.

Cardiopulmonary bypass (CPB) constitutes one of the primary methodologies pertaining to cardiac surgery. However, this form of surgery can cause damage to the body. Many studies have reported that dexmedetomidine confers cerebral protection. In this study, we aimed to investigate the effect and mechanism of dexmedetomidine on neuronal apoptosis caused by CPB. Here, rats were treated with different doses of dexmedetomidine by intravenous infusion 2 hours after CPB. We observed that dexmedetomidine treatment to rats reduces the S100ß, NSE levels in plasma, and neuronal apoptosis following CPB in a dose-dependent manner. Furthermore, we observed that the beneficial effect of dexmedetomidine treatment following CPB was associated with a reduction in IL6, an inflammatory cytokine in plasma and cortex. Our results suggest that dexmedetomidine provides neuroprotective effects by inhibiting inflammation and reducing neuronal apoptosis. There was a correlation between the protective effect on the brain and the dose of dexmedetomidine. In addition, dexmedetomidine administration inhibits phosphorylation of JAK2 and STAT3 proteins in the hippocampus of rats 2 hours after CPB. Therefore, we speculate that the JAK2-STAT3 pathway plays an important role in the neuroprotective effects of dexmedetomidine following brain injury induced by CPB.

Biochar as an adsorbent for inorganic nitrogen and phosphorus removal from water: a review.

Biochar is the solid product of biomass pyrolysis that can be used for carbon sequestration, soil amendment, and pollution remediation. The use of biochar as an adsorbent for the removal of water contaminants has elicited increasing interest due to the multifunctional properties of this material. The application of biochar in the adsorption of inorganic nutrients from eutrophic water has not been reviewed. This review focuses on recent research on the use of biochar for the adsorption of inorganic nitrogen (ammonium and nitrate) and phosphorus (phosphate) from water, especially for the main influence factors and mechanisms for nitrogen and phosphorus adsorption on biochar.

Cold blood versus crystalloid cardioplegia for myocardial protection in adult cardiac surgery: a meta-analysis of randomized controlled studies.

OBJECTIVE: The purpose of this article was to systematically review randomized controlled trials in which cold blood cardioplegia was compared with cold crystalloid cardioplegia for cardiac surgery. DESIGN: Correlation studies were searched independently in the EMBASE, MEDLINE and Cochrane library databases. The primary endpoints of interest were spontaneous sinus rhythm (SSR) after declamping, perioperative myocardial infarction (MI) and mortality (within 30 days). SETTING: A hospital. PARTICIPANTS: Randomized controlled trials. INTERVENTION: A meta-analysis of 12 studies. MEASUREMENTS AND MAIN RESULTS: The 12 included trials recruited a total of 2866 participants; 1357 patients received cold crystalloid cardioplegia, and 1509 patients received cold blood cardioplegia. The pooled analysis showed no significant difference favoring either cold crystalloid cardioplegia or cold blood cardioplegia in terms of spontaneous sinus rhythm (SSR) after declamping (789/1028 [76.75%] v 773/1025 [75.41%], relative risk (RR) = 0.92 [0.76, 1.13], p = 0.43 with 6 studies included), mortality (within 30 days) (20/1335 [1.50%] v 24/1469 [1.63%], relative risk (RR) = 1.09 [0.62, 1.91], p = 0.77 with 11 studies included), atrial fibrillation (AF) (329/1043 [31.54%] v 365/1040 [35.10%], RR =0.90 [0.80, 1.01], p = 0.08 with 6 studies included) or stroke (45/1114 [4.04%] v 20/1240 [1.61%], RR = 2.18 [0.69, 6.93], p = 0.19 with 4 studies included). The aggregate data showed that the incidence of perioperative myocardial infarction was lower in patients who received cold blood cardioplegia (CB) (32/1310 [2.44%] v 17/1434 [1.19%], RR = 2.30 [1.33, 3.98], p = 0.003 with 11 studies included). CONCLUSIONS: Cold blood cardioplegia reduced perioperative myocardial infarction when compared with cold crystalloid cardioplegia. No differences in the overall incidence rates of spontaneous sinus rhythm, mortality (within 30 days), atrial fibrillation or stroke were observed.

Association of apolipoprotein A1 -75 G/A polymorphism with susceptibility to the development of acute lung injury after cardiopulmonary bypass surgery.

INTRODUCTION: Apolipoprotein A1 (apoA1) is the major apoprotein constituent of high density lipoprotein (HDL) which exerts innate protective effects in systemic inflammation. However, its role in the acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) has not been well studied. The objective of this study was to investigate the potential association between APOA1 -75 G/A polymorphism and the development of ALI after cardiopulmonary bypass (CPB) surgery. MATERIALS AND METHODS: A hospital-based case-control study was conducted in patients with ALI (n = 300), patients without ALI (n = 300) and healthy controls (n = 300). Polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) assay was applied to assess the APOA1 -75 G/A genotypes. RESULTS: Patients with ALI had a significantly higher frequency of APOA1 -75 AA genotype [odds ratio (OR) =1.75, 95% confidence interval (CI) = 1.04, 2.92; P = 0.03] than patients without ALI. APOA1 -75 AA genotype (OR =3.47, 95% CI = 1.60, 7.52; P = 0.002) and A allele (OR =1.92, 95% CI = 1.24, 2.96; P = 0.003) were the significant independent prognostic factors for the 30-day survival rate of patients with ALI after CPB surgery. CONCLUSION: Our study suggested that APOA1 -75 AA genotype was associated with a higher ALI risk after CPB surgery. Patients with the APOA1 -75 AA genotype and A allele had higher 30-day mortality of ALI after CPB surgery. Additional studies are needed to confirm this finding.