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Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 has spread rapidly around the world and is a significant threat to global health. Patients in the Neonatal Surgery Department have rapidly progressing diseases and immature immunity, which makes them vulnerable to pulmonary infection and a relatively higher mortality. This means that these patients require multidisciplinary treatment including early diagnosis, timely transport, emergency surgery and intensive critical care. The COVID-19 pandemic poses a threat to carrying out these treatments. To provide support for the health protection requirements of the medical services in the Neonatal Surgery Department, we developed recommendations focusing on patient transport, surgery selection and protection requirements with the aim of improving treatment strategies for patients and preventing infection in medical staff during the current COVID-19 pandemic.

The Nrf2 (nuclear factor erythroid 2-related factor 2) plays a central role in cell protection against a wide variety of environmental stressors through the Nrf2-Keap1 (Kelch-like ECH-associated protein 1) pathway, but its involvement in modulation of antioxidant system of fish cell is still largely unexplored. The present study focused on the molecular cloning and silencing of the Nrf2 in the fathead minnow muscle cell line (FHM) in response to the oxidative stress induced by H2O2. A full-length cDNA of coding Nrf2 was cloned from FHM cells by RT-PCR and RACE approaches. The obtained cDNA covered 2578 bp with an open reading frame (1770 bp) of encoding 589 amino acids. Sequence alignment and phylogenetic analysis revealed a high degree of conservation (51–86%) among 16 fishes. Based on the cloned Nrf2 sequence, the siRNA-242 of targeting Nrf2 with the best knocking down efficiency was designed and detected. Then, the mRNA levels of Keap1, Nrf2, Maf (musculoaponeurotic fibrosarcoma oncogene), and HO-1 (haemoxygenase-1); the activities of T-SOD (total superoxide dismutase), CAT (catalase), and GSH-PX (glutathione peroxidase); the levels of GSH (glutathione) and MDA (malonaldehyde); and the cell cycle and apoptosis were analyzed to investigate the molecular responses after H2O2 exposure. These results showed a coordinated transcriptional regulation of Keap1, Maf, and HO-1 and antioxidants (T-SOD, GSH, CAT, and GSH-PX) and MDA levels after H2O2 exposure, leading to oxidative damage and apoptosis. These findings provided an insight to understand the mechanisms of Nrf2 against oxidative stress in fish.

Background Due to the particularity of patients with bone tumors, the risk of periprosthetic infection following megaprosthetic replacement is much higher than that of traditional total knee arthroplasty. Unfortunately, few studies specifically reported the risk factors for periprosthetic infection following megaprosthetic replacement. The purposes of the study were to (1) establish a nomogram model, which can provide a reference for clinicians, and patients to reduce the occurrence of periprosthetic infection (2) explore the risk factors for deep infection of megaprosthesis. Hypothesis A prediction model can be established and has favorable predictive accuracy. Patients and Methods One hundred and seventy-seven megaprostheses were identified. There were 61 female patients and 116 male patients with a mean age of 35 years. The following risk factors were analyzed: tumor site, sex, age, material for prosthetic stem, tumor type, smoking, diabetes, length of bone resection, operation time, chemotherapy, BMI, malignant tumor staging and hematoma formation. Finally, based on the multivariate analysis, the independent risk factors were used to develop a nomogram model. Results Univariate Cox regression analysis showed that the chemotherapy, longer operation time and hematoma formation were risk factors for periprosthetic infection. Multivariate Cox regression analysis showed that the chemotherapy, longer operation time and hematoma formation were significant risk factors for periprosthetic infection. The nomogram model was established using these significant risk factors, with a C-index of 0.766 and an acceptable consistency according to the internal validation, indicating that the prediction model had favorable predictive accuracy. Discussion This study has important implications for the future investigations of prevention of periprosthetic infection. The nomogram model identifies high-risk patients for whom attached prophylaxis measures are required. Future studies regarding reduction of incidence of periprosthetic infection should pay close attention to these high-risk patients. Level of evidence IV, retrospective, cohort study.

Background Aseptic loosening has become the main cause of prosthetic failure in medium- to long-term follow-up. The objective of this study was to establish and validate a nomogram model for aseptic loosening after tumor prosthetic replacement around knee. Methods We collected data on patients who underwent tumor prosthetic replacements. The following risk factors were analyzed: tumor site, stem length, resection length, prosthetic motion mode, sex, age, extra-cortical grafting, custom or modular, stem diameter, stem material, tumor type, activity intensity, and BMI. We used univariate and multivariate Cox regression for analysis. Finally, the significant risk factors were used to establish the nomogram model. Results The stem length, resection length, tumor site, and prosthetic motion mode showed a tendency to be related to aseptic loosening, according to the univariate analysis. Multivariate analysis showed that the tumor site, stem length, and prosthetic motion mode were independent risk factors. The internal validation indicated that the nomogram model had acceptable predictive accuracy. Conclusions A nomogram model was developed for predicting the prosthetic survival rate without aseptic loosening. Patients with distal femoral tumors and those who are applied with fixed hinge and short-stem prostheses are more likely to be exposed to aseptic loosening.

Background Talc pleurodesis is an effective treatment for malignant pleural effusions (MPEs). This study was designed to estimate complication rates of thoracoscopic talc insufflation. Methods Literature search was conducted in electronic databases and studies were selected if they reported complication rates of thoracoscopic talc insufflation in cancer patients with MPEs. Meta-analyses of proportions were performed to obtain incidence rates of complications. Results Twenty-six studies (4482 patients; age 62.9 years [95% confidence interval (CI): 61.5, 64.4]; 50% [95% CI: 43, 58] females) were included. Intraoperative, perioperative, 30-day, and 90-day mortality rates were 0% [95% CI: 0, 1], 2% [95% CI: 0, 4], 7% [95% CI: 3, 13] and 21% [95% CI: 5, 43] respectively. Incidence rates [95% CI] of various complications were: pain (20% [1, 2]), fever (14% [3, 4]), dyspnea (13% [5, 6]), pneumothorax (6% [7, 8]) pneumonia (4% [0, 12]), emphysema (3% [3, 7]), prolonged air leakage (3% [0, 7]), prolonged drainage (3% [9, 10]), thromboembolism (3% [9, 11]), lung injury (2% [7, 12]), respiratory insufficiency (2% [0, 5]), re-expansion pulmonary edema (1% [0, 3]), empyema (1% [0, 2]), respiratory failure (0% [0, 1]), and acute respiratory distress syndrome (ARDS; 0% [0, 1]. Conclusions Whereas pain and fever were the most frequent complications of thoracoscopic talc insufflation, the incidence of ARDS was low. Pneumothorax, pneumonia, emphysema, prolonged air leakage, pulmonary embolism, arrythmia, re-expansion pulmonary edema, and empyema are important complications of thoracoscopic talc insufflation.

Background Capn4 and ZEB1 play important roles in the metastasis of several types of cancer. However, the roles and relationship of Capn4 and ZEB1 in esophageal squamous cell carcinoma (ESCC) remain unclear. Methods ESCC tumor tissues and corresponding normal esophageal epithelial tissues were obtained from 86 patients undergoing resection surgery at the Department of General Surgery, First Affiliated Hospital of Chinese PLA General Hospital from 2012 to 2017. Cell migration and invasion were examined via quantitative real-time PCR and Western blot assay. Results Our results indicate that both Capn4 and ZEB1 are significantly upregulated in ESCC tissues compared to corresponding adjacent tissues, and a positive correlation between expression and associated malignant characteristics was found. Silencing of Capn4 expression markedly inhibited ESCC invasion and metastasis in vitro and in vivo, and was accompanied by decreased ZEB1 expression. Furthermore, the anti-metastasis role of Capn4 silencing was reversed by ZEB1 overexpression, whereas knockdown of ZEB1 decreased ESCC metastasis driven by the upregulation of Capn4. Mechanistically, Capn4 regulated ZEB1 expression via activation of the Wnt/β-catenin signaling pathway in ESCC cells. Conclusion Overall, our results show that enhanced Capn4 expression activates the Wnt/β-catenin signaling pathway, resulting in increased ZEB1 expression and the promotion of ESCC cell metastasis.

Objective Femoral neck fracture is considered a difficult fracture to treat and often gives rise to unsatisfactory treatment results. Cannulated cancellous screws (CCS) or a sliding hip screw (SHS) are the mainstream internal fixations used for osteosynthesis of femoral neck fractures. There is a need to integrate existing data through a meta-analysis to investigate the safety and effectiveness of CCS and SHS in the treatment of femoral neck fractures. Method According to the Cochrane Handbook for Systematic Reviews of Interventions, we screened for the relevant studies by searching Google Scholar, the Cochrane Controlled Trials Register, the Cochrane Library, Web of Science, EMBASE, and PubMed. The PICOS criteria was used to make sure the included studies fulfilled the inclusion criteria. Results Pooled data showed that there were no significant differences between the SHS and CCS groups for the Harris Hip Score. Significant differences were found between the SHS and CCS groups in terms of union time, postoperative complications, blood loss, operation time, incision length and length of hospital stay. Conclusions Although the SHS and CCS groups showed similar functional recovery in treatment of femoral neck fracture in terms of the Harris Hip Score, the SHS group showed fewer postoperative complications and faster union time for patients with femoral neck fractures. Therefore, compared with CCS, the use of SHS may be a more effective treatment of femoral neck fractures.

Macrobrachium nipponense is a new aquaculture species with high market demand and is preferred as food by Asian consumers. However, its nutrient requirements and optimal dietary sources have not been fully evaluated. In the present study, we examined four common plant protein sources (soybean meal, cottonseed meal, rapeseed meal, and peanut meal) as partial replacement for 25% fishmeal protein in five isonitrogenous and isocaloric diets in M. nipponense for 8 weeks. The nutritional effects of the four plant protein sources were compared by means of growth performance, feed efficiency, histology, biochemical composition, oxidative stress, total hemocyte count, and in vitro digestion. Prawns fed the diets containing soybean (730.96 ± 33.50%) and cottonseed meals (672.32 ± 74.52%) had higher weight gain than those fed on rapeseed (503.71 ± 50.85%) and peanut (507.79 ± 52.10%) meal diets (p

// Hui Xia 1, 2, 3 , Wen Zhang 1 , Baoshi Zhang 1 , Yingnan Zhao 1 , Yunlong Zhao 1 , Shaojun Li 1 and Yang Liu 2 1 Department of Thoracic-Cardio Surgery, First Affiliated Hospital of PLA General Hospital, Beijing, China 2 Department of Thoracic Surgery, PLA General Hospital, Beijing, China 3 Medical School of PLA, Beijing, China Correspondence to: Hui Xia, email: 304xiahui@sina.com Yang Liu, email: China liuyangplats@126.com Keywords: miR-21, EZH2, lung cancer stem cells, radiotherapy, chemotherapy Received: November 10, 2016 Accepted: June 19, 2017 Published: August 07, 2017 ABSTRACT Non-small-cell lung cancer has a high mortality rate and poor prognosis. Therefore, novel therapeutic approaches are urgently needed to enhance patient survival rates. In this study, we investigated the effects of miR-21 and EZH2 on the biological behavior of human lung cancer stem cells in vitro . We found increased expression of EZH2 and miR-21 in LCSCs, and miR-21 overexpression increased EZH2 levels in LCSCs. In addition, EZH2 and miR-21 knockdown increased the sensitivity of LCSCs to chemo- and radiation therapy, and exogenous EZH2 expression rescued the effects of anti-miR-21. Cell proliferation was reduced by 39.2% and 69.7% in the presence of radio - or chemotherapy combined with anti-miR-21 transfection, respectively. The downstream molecules included Cdc2, cyclin B1, and Bcl-2, which are involved in the regulation of cell cycle and apoptosis and which could themselves be reduced or enhanced by changes in miR-21 and EZH2 levels in LCSCs. This study demonstrates the direct relationship between miR-21 and EZH2 which was increased by 43% after the application of the miR-21 mimic. Above data indicates that these two molecules can influence the biological behavior of LCSCs by altering their corresponding targets. Our findings support the potential roles of miR-21 and EZH2 in improving the therapeutic efficacy of clinical lung cancer treatments.

SummaryAims Despite more than a century of research, spinal paralysis remains untreatable via biological means. A new understanding of spinal cord physiology and the introduction of membrane fusogens have provided new hope that a biological cure may soon become available. However, proof is needed from adequately powered animal studies. Methods and results Two groups of rats (n=9, study group, n=6 controls) were submitted to complete transection of the dorsal cord at T10. The animals were randomized to receive either saline or polyethylene glycol (PEG) in situ. After 4 weeks, the treated group had recovered ambulation vs none in the control group (BBB scores; P=.0145). One control died. All animals were studied with somatosensory-evoked potentials (SSEP) and diffusion tensor imaging (DTI). SSEP recovered postoperatively only in PEG-treated rats. At study end, DTI showed disappearance of the transection gap in the treated animals vs an enduring gap in controls (fractional anisotropy/FA at level: P=.0008). Conclusions We show for the first time in an adequately powered study that the paralysis attendant to a complete transection of the spinal cord can be reversed. This opens the path to a severance-reapposition cure of spinal paralysis, in which the injured segment is excised and the two stumps approximated after vertebrectomy/diskectomies.

Nrf2/Keap1 pathway is associated with oxidative stress. l-carnitine is currently under preclinical evaluation as a antioxidant, but the use of l-carnitine in aquaculture has been poorly evaluated and so far no mechanism has been demonstrated. Here, we explored the effects of l-carnitine in vitro and in vivo and discussed the possible molecular mechanisms involved. Firstly, Nrf2-siRNA significantly knocked down the mRNA level of Nrf2 in FHM cells. Thus, the activities of antioxidant enzymes (T-SOD, CAT, GSH-PX) and the level of antioxidant substance (GSH) and the level of MDA showed that Nrf2-siRNA pretreatment weakened the protective effect of l-carnitine. Moreover, the mRNA levels of Keap1, Nrf2, Maf and HO-1 indicated that l-carnitine regulated Nrf2/Keap1 activation. Furthermore, oxidized fish oil remarkably suppressed growth in Rhynchocypris lagowski Dybowski, and the lower antioxidant capacity was also observed in liver. According to the results of immune related indexes (the levels of IL-1β, TNF-α, LZM, AKP) in serum and the mRNA levels of immune related genes (NF-κB, IL-1β, TNF-α, IL-8, IL-10 and TGF-β) in liver, oxidized fish oil also induced inflammatory response in fish. Also, l-carnitine supplementation can relieve this bad condition. In conclusion, l-carnitine regulated Nrf2/Keap1 activation in vitro and in vivo and protected oxidized fish oil-induced inflammation response by inhibiting the NF-κB signaling pathway in Rhynchocypris lagowski Dybowski.

Remote ischemia preconditioning (RIPC) is a convenient and effective method for alleviating cerebral ischemia-reperfusion injury (CIRI). However, to date, the underlying mechanism has not been fully elucidated. The aim of this research was to explore the protective mechanism of RIPC on the brain after CIRI. Four groups of rats were included in this experiment: the sham group, the middle cerebral artery occlusion (MCAO) group, the RIPC group, and the AG490 group. As an inhibitor of Janus kinase 2 (JAK2), AG490 was used after MCAO in the AG490 group to explore the role of JAK2/signal transducers and activators of transcription 3 (STAT3) after CIRI. Brain tissue was collected for evaluation after 2 h of ischemia and 24 h of reperfusion. ELISA for interleukin (IL)-6, IL-1β and tumor necrosis factor-α, western blot for phosphorylated-JAK2 and phosphorylated-STAT3, the neurological severity score and Longa scoring system for neurological deficit evaluation, triphenyltetrazolium chloride staining for cerebral infarction, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining for apoptotic cells in the brain tissue were performed. Neurological function in the RIPC group was notably better than that in the MCAO group. There were smaller infarction sizes and fewer apoptotic cells in the ischemic area in the RIPC group than in the MCAO group. In the RIPC group, the expression levels of IL-1β, tumor necrosis factor-α, IL-6, and phosphorylated-JAK2 and phosphorylated-STAT3 were significantly lower than those in the MCAO group. The findings in the RIPC and AG490 groups were similar. The inflammatory response and apoptosis are two important processes involved in brain dysfunction after CIRI. The JAK2/STAT3 signaling pathway has an underlying relationship with these two processes. These findings suggest that RIPC can alleviate the damage to brain tissue by CIRI by regulating the JAK2/STAT3 signaling pathway negatively.

Metabotropic glutamate receptor 1 (mGlu1 receptor) is expressed in many cancer cell types as compared to normal counterparts underscoring its potential role in tumor behavior. The aim of present study was to test the role of mGlu1 receptor in experimental non-small cell lung cancer (NSCLC). First, protein expression of mGlu1 receptor was higher in human NSCLC cell lines, including both adenocarcinoma and squamous carcinoma subtypes, when compared to normal bronchial epithelial cells. Inhibition of mGlu1 receptor by BAY36-7620 (an mGlu1 receptor-specific inhibitor) inhibited tumor growth and prolonged survival of mice with tumors of A549 or H1299. Treatment with BAY36-7620 suppressed AKT phosphorylation in A549 tumors and pre-treatment with BAY36-7620 blocked the L-quisqualate (a potent mGlu1 receptor agonist)-induced AKT phosphorylation in A549 cells. Treatment with BAY36-7620 reduced cellular proliferation of A549 cells. Treatment with BAY36-7620 enhanced cleaved PARP levels and reduced protein expression of bcl-2, HIF-1α, and VEGF. In contrast, treatment with L-quisqualate reduced cleaved PARP levels and enhanced protein expression of bcl-2, HIF-1α, VEGF, and IL-8, which was reversed by co-incubation with MK2206 (an AKT inhibitor). Pre-treatment with BAY36-7620 blocked the VEGF-induced AKT phosphorylation in HUVECs. Treatment of HUVECs with L-quisqualate resulted in enhancement of capillary tube formation, which was reversed by co-incubation with MK2206. Furthermore, mGlu1 receptor knockdown suppressed tumor growth and prolonged survival of mice with tumors of A549 or H1299. Collectively, inhibition of mGlu1 receptor suppressed tumor growth and angiogenesis in experimental NSCLC.

Fish oil can not only provide energy for the growth and development of fish, but also constitute a variety of tissue and cellular structural components of fish. However, fish oil is easily oxidized in the process of feed processing, treatment and storage, which reduces the feed quality and threatens the health of fish. Therefore, the purpose of this study was to investigate the effects of different degrees of oxidation of fish oil in feed on fatty acid composition and lipid metabolism in hepatopancreas of Rhynchocypris lagowski Dybowski. Five diets containing five oxidation levels (0, 100, 200, 300 and 400 meq/kg) of fish oil were formulated and fed to 525 healthy R. lagowski (4.48 ± 0.14 g) that were randomly divided into 15 glass aquariums. After 8 weeks, hepatopancreas samples were taken for fatty acid composition, and biochemical analysis. The results showed that the content of Polyunsaturated fatty acid (PUFA) in muscle of R. lagowski increased significantly with the increase of oxidation degree of fish oil (P < 0.05), but there were no changes in Saturated fatty acid (SFA), Monounsaturated fatty acid (MUFA), EPA (C20:5n3), and ∑n-6 (P>0.05). Compared with the control group, the contents of SFA, MUFA and EPA in hepatopancreas were significantly increased (P < 0.05), while DHA (C22:6n3), ∑n-3, ∑n-6, and PUFA were decreased (P < 0.05). Feeding with OFO increased hepatopancreas total cholesterol (TC), triacylglycerol (TG), HDL/LDL ratio, FAS, and ACCα that involved in lipid synthesis enzymes (P < 0.05), while reduced liver esterase (HL), fatty acyl-CoA synthetase (ACS), carnitine palmitoyltransferase (CPT-1) and hormone-sensitive triglyceride lipase α (HSLα) enzyme activity and gene expression that associated with lipid decomposition (P < 0.05). It is suggested that the adverse effects of dietary oxidized oil may be achieved by promoting fatty acid synthesis, inhibiting fatty acid oxidation, increasing fatty acid uptake by hepatopancreas and reducing the ability of TG to transport from hepatopancreas to extrahepatic tissues, thus inducing fat accumulation in hepatopancreatic cells and further affecting lipid metabolism in hepatopancreas.

Aim: Although, miR-218 has been implicated in epithelial-to-mesenchymal transition process, the detailed mechanisms of miR-218 involvement in epithelial-to-mesenchymal transition in human lung adenocarcinoma cell are still unclear. Materials & methods: miR-218 function assays and its target gene analysis were performed. Results: miR-218 suppresses human lung adenocarcinoma cell migration and invasion and inhibits its target gene, Ecop and Robo1 expression, which subsequently suppresses NF-κB activity and its downstream targets. Conclusion: miR-218 inhibits human lung adenocarcinoma cell migration and invasion via the suppression of Ecop and Robo1 expression, thus suggesting that miR-218 could serve as a potential therapeutic target.

Supplemental Digital Content is available in the text, Objective: The aim of this study was to evaluate the immediate effects of lateral wedge arch support insoles (LWAS) on reducing the knee joint load in patients with medial knee osteoarthritis (OA) compared with an appropriate control. Methods: Databases including Medline, EMBASE, Web of Science, Wiley Online Library, Cochrane library, and Google Scholar were searched with no limits on study date or language, from the earliest available date to October 31, 2016. The included studies had to have the aim of reducing knee load and have an appropriate control. The main measured values were the first and second peak external knee adduction moments (EKAM) and the knee adduction angular impulse (KAAI). The random-effects model was used for analyzing the eligible studies. Results: Nine studies met the inclusion criteria with a total of 356 participants of whom 337 received LWAS treatment. The risk of methodological bias scores (quality index) ranged from 21 to 27 of 32. Treatment with LWAS resulted in statistically significant reductions in the first peak EKAM (P = .005), the second peak EKAM (P = .01), and the KAAI (P = .03). However, among trials in which the control treatment was control shoes, the LWAS showed no associations on the first peak EKAM (P = .10) or the KAAI (P = .06); among trials in which the control treatment was neutral insoles, the LWAS showed no associations on the second peak EKAM (P = .21) or the KAAI (P = .23). At the same time, the LWAS showed no statistically significant reduction on the first peak EKAM (P = .39) when compared with flat insoles. Conclusion: Although meta-analysis outcomes of all studies indicated statistically significant associations between LWAS and reductions of the first peak EKAM, second peak EKAM and KAAI in people with medial knee OA while walking, different results existed in subgroups using various control conditions for comparison. These findings do not support the use of LWAS insoles for reducing knee load. An optimal LWAS treatment should provide the appropriate height of arch support and amount of lateral wedging. Further research should investigate the best combination of these 2 parameters to achieve efficacy without altered comfort.

SummaryAims A successful cephalosomatic anastomosis (“head transplant”) requires, among others, the ability to control long-term immune rejection and avoidance of ischemic events during the head transference phase. We developed a bicephalic model of head transplantation to study these aspects. Methods and Results The thoracic aorta and superior vena cava of a donor rat were anastomosed with the carotid artery and extracorporeal veins of a recipient rat by vascular grafts. Before thoracotomy in the donor rat, the axillary artery and vein of the donor were connected to the carotid and the extracranial vein of the third rat through a silicone tube. The silicone tube was passed through a peristaltic pump to ensure donor brain tissue blood supply. There is no ischemia reperfusion injury in donor brain tissue analyzed by electroencephalogram. Postoperative donor has pain reflex and corneal reflex. Conclusions Peristaltic pump application can guarantee the blood supply of donor brain tissue per unit time, while the application of temperature change device to the silicone tube can protect the brain tissue hypothermia, postoperative experimental data show that there is no brain tissue ischemia during the whole operation. The application of vascular grafting can also provide the possibility of long-term survival of the model.

Five isonitrogenous and isolipidic diets containing fresh fish oil and four degrees of oxidized fish oil (POV:100; 200; 300; 400) were formulated to investigate the effects of dietary oxidized fish oil on growth performance, the antioxidation function of Rhynchocypris lagowski Dybowski. After an 8-week feeding trial, fish fed oxidized oil diets obtained significantly lower weight gain and specific growth rate due to their lower feed efficiency and protein efficiency. With the increasing of fish oil oxidation level, MDA level of the liver significantly increased, the antioxidant enzymes (T-SOD, CAT, GSH-PX) activities and GSH content of the liver were significantly decreased, and CAT, CuZn-SOD and GSH-PX mRNA levels of the liver showed the same change trend. Further analysis showed that, Keap1 mRNA level of the liver was increased, and the Nrf2, Maf, HO-1 mRNA levels of the liver were significantly decreased. However, some parameters showed a reverse trend after the 4-week feeding. In conclusion, by checking indicators of growth performance, the main antioxidant parameters, the related genes mRNA levels, the present study showed that dietary oxidized fish oil can induce oxidative damage in R. lagowski Dybowski.

Background: A superficial abdominal surgical incision elicits cardioprotection against cardiac ischemia–reperfusion (I/R) injury in mice. This process, called remote preconditioning of trauma (RPCT), has both an early and a late phase. Previous investigations have demonstrated that early RPCT reduces cardiac infarct size by 80% to 85%. We evaluated the cardioprotective and molecular mechanisms of late-phase RPCT in a murine I/R injury model. Methods: Wild-type mice, bradykinin (BK) 2 receptor knockout mice, 3M transgenic mice (nuclear factor κB [NF-κb] repressor inhibitor of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha [IκBα(S32A, S36A, Y42F)]), and inducible nitric oxide synthase (iNOS) knockout mice were analyzed using a previously established I/R injury model. A noninvasive abdominal surgical incision was made 24 hours prior to I/R injury and the infarct size was determined at 24 hours post-I/R injury. Results: The results indicated that a strong cardioprotective effect occurred during late-phase RPCT (58.42% ± 1.89% sham vs 29.41% ± 4.00% late RPCT, mean area of the infarct divided by the mean area of the risk region; P ≤ .05; n = 10). Furthermore, pharmacological intervention revealed the involvement of neurogenic signaling in the beneficial effects of late RPCT via sensory and sympathetic thoracic nerves. Pharmacological experiments in transgenic mice-implicated BK receptors, β-adrenergic receptors, protein kinase C, and NF-κB but not iNOS signaling in the cardioprotective effects of late RPCT. Conclusion: Late RPCT significantly decreased myocardial infarct size via neurogenic transmission and various other signaling pathways. This protective mechanism differentiates late and early RPCT. This study describes a new cardiac I/R injury prevention method and refines the concept of RPCT.