NETs: an extracellular DNA network structure with implication for cardiovascular disease and cancer.

Cardiovascular (CV) diseases and tumors are best known for its high morbidity and mortality worldwide. There is a growing recognition of the association between CV diseases and tumorigenesis. In addition to CV damage caused by anti-tumor drugs and tumor-induced organ dysfunction, CV events themselves and their treatment may also have a role in promoting tumorigenesis. Therefore, Therefore, the diagnosis and treatment of the two kinds of diseases have entered the era of clinical convergence. Emerging evidence indicates significant biologic overlap between cancer and CV diseases, with the recognition of shared biologic mechanisms. Neutrophil extracellular traps (NETs) represent an immune mechanism of neutrophils promoting the development of tumors and their metastasis. It has been recently demonstrated that NETs exist in various stages of hypertension and heart failure, exacerbating disease progression. At present, most studies focus on the biological role of NETs in CV diseases and tumor respectively, and there are relatively few studies on the specific regulatory mechanisms and effects of NETs in cardiovascular diseases associated with tumors. In this narrative review, we summarize some recent basic and clinical findings on how NETs are involved in the pathogenesis of cardiovascular diseases associated with tumors. We also highlight that the development of treatments targeting NETs may be one of the effective ways to prevent and treat cardiovascular diseases associated with tumors.

Omadacycline for the Treatment of Severe Chlamydia psittaci Pneumonia Complicated with Guillain-Barre Syndrome.

Background: Chlamydia psittaci (C. psittaci) is a pathogen that is seldom implicated in community-acquired pneumonia and is rarely linked to severe pneumonia. Reports of severe C. psittaci pneumonia accompanied by Guillain-Barre syndrome (GBS) are scarce. Tetracyclines are the preferred therapeutic approach for psittacosis. Omadacycline, a novel tetracycline, demonstrates strong antibacterial efficacy against typical bacteria and atypical pathogens, including C. psittaci. However, its application in the treatment of psittacosis pneumonia remains constrained. Case Presentation: A 77-year-old female patient was admitted to the hospital presenting with symptoms of fever, low back pain, and headache. The diagnosis of C. psittaci was established through the utilization of metagenomic next-generation sequencing (mNGS). Initial administration of moxifloxacin, meropenem, piperacillin-tazobactam, and doxycycline proved to be ineffective. Subsequent omadacycline leaded to the successful resolution of fever and dyspnea. However, after the endotracheal tube was removed, the patient experienced a rapid decline in symmetrical limb strength, leading to a diagnosis of GBS based on clinical manifestations, cerebrospinal fluid analysis, and electromyography. Following a 5-day course of immunoglobulin therapy and nutritional nerve treatment, the patient's condition ameliorated, culminating in an uncomplicated discharge. Conclusion: This case provides evidence supporting the potential use of omadacycline as a therapeutic option for the treatment of severe C. psittaci pneumonia. The utilization of mNGS technology is of paramount importance in the prompt identification of uncommon pathogens, including C. psittaci. Nevertheless, the occurrence of GBS should be taken into consideration when C. psittaci pneumonia is accompanied by symmetrical limb weakness. These findings have important implications for the diagnosis, treatment, and management of patients with C. psittaci pneumonia.

Application of multidisciplinary in situ simulation training in the treatment of acute ischemic stroke: a quality improvement project.

BACKGROUND: Ischemic stroke refers to a disorder in the blood supply to a local area of brain tissue for various reasons and is characterized by high morbidity, mortality, and disability. Early reperfusion of brain tissue at risk of injury is crucial for the treatment of acute ischemic stroke. The purpose of this study was to evaluate comfort levels in managing acute stroke patients with hypoxemia who required endotracheal intubation after multidisciplinary in situ simulation training and to shorten the door-to-image time. METHODS: This quality improvement project utilized a comprehensive multidisciplinary in situ simulation exercise. A total of 53 participants completed the two-day in situ simulation training. The main outcome was the self-reported comfort levels of participants in managing acute stroke patients with hypoxemia requiring endotracheal intubation before and after simulation training. A 5-point Likert scale was used to measure participant comfort. A paired-sample t-test was used to compare the mean self-reported comfort scores of participants, as well as the endotracheal intubation time and door-to-image time on the first and second days of in situ simulation training. The door-to-image time before and after the training was also recorded. RESULTS: The findings indicated that in situ simulation training could enhance participant comfort when managing acute stroke patients with hypoxemia who required endotracheal intubation and shorten door-to-image time. For the emergency management of hypoxemia or tracheal intubation, the mean post-training self-reported comfort score was significantly higher than the mean pre-training comfort score (hypoxemia: 4.53±0.64 vs. 3.62±0.69, t= -11.046, P<0.001; tracheal intubation: 3.98±0.72 vs. 3.43±0.72, t= -6.940, P<0.001). We also observed a decrease in the tracheal intubation and door-to-image time and a decreasing trend in the door-to-image time, which continued after the training. CONCLUSION: Our study demonstrates that the implementation of in situ simulation training in a clinical environment with a multidisciplinary approach may improve the ability and confidence of stroke team members, optimize the first-aid process, and effectively shorten the door-to-image time of stroke patients with emergency complications.

Biomechanical evaluation of reconstruction of the posterior complex in restorative laminoplasty with miniplates.

OBJECTIVE: To evaluate the biomechanical effects of different miniplates on restorative laminoplasty. METHODS: Assembled restorative laminoplasty models were developed based on 3D printed L4 lamina. Based on different internal fixations, the research was divided into H-shaped miniplates (HSMs) group, two-hole miniplates (THMs) group, and L-shaped miniplates (LSMs) group. The static and dynamic compression tests were analyzed to investigate the biomechanical effects of different internal fixations in restorative laminoplasty, until the failure and fracture of miniplates, or the collapse of miniplates. The static compression tests adopted the speed control mode, and the dynamic fatigue compression tests adopted the load control mode. RESULTS: The "door close" and the collapse of lamina occurred in THMs group and LSMs group, and plate break occurred in LSMs group. However, these phenomenon was absent in HSMs group, and only plate crack around a screw and looseness of a screw tail cap were found in HSMs group. The sustainable yield load of HSMs group was greater than that of THMs group and LSMs group (P < 0.05). No significant difference in yielding-displacement was found between HSMs group and LSMs group (P > 0.05), while both were much less than that of THMs (P < 0.05). Moreover, the compressive stiffness and the axial displacement under the same mechanical load were arranged as follows: HSMs group > LSMs group > THMs group (P < 0.05). The results of dynamic compression test revealed that the peak load of HSMs group could reached 873 N and was 95% of the average yield load of the static compression, and was better than that in THMs group and LSMs group (P < 0.05). Besides, according to the fatigue life-peak load diagram, the ultimate load of HSMs group was more than twice that of THMs group or LSMs group. CONCLUSIONS: The mechanical strength of H-shaped miniplates was superior to two-hole miniplates and L-shaped miniplates in maintaining spinal canal enlargement and spinal stability, and was more excellent in fatigue stability and ultimate load.

Trypsin inhibitor LH011 inhibited DSS-induced mice colitis via alleviating inflammation and oxidative stress.

Background: Ulcerative colitis (UC) is one type of inflammatory bowel disease, characterized by inflammation with infiltration and activation of macrophages in colonic tissue. LH011 is a trypsin inhibitor with potential anti-inflammatory effect. Purpose: Here, we aim to assay the effects of LH011 on UC and further investigate the potential mechanisms in vitro and in vivo. Methods: Dextran sulfate sodium (DSS, 3.5%, w/v) was used to induce UC, and lipopolysaccharide (LPS) was used to induce inflammation in RAW 264.7 cells. LH011 was administrated to mice in vivo or to RAW 264.7 cells in vitro at different concentrations. The cytokines (IL-1ß, IL-6, and TNF-α) and the changes of NF-κB and Nrf2 pathways were detected. Results: The results showed that LH011 improved DSS-induced mice colitis, including loss of weight, disease activity index (DAI), and colonic pathological damage. In addition, LH011 inhibited the expressions of IL-1ß, IL-6, and TNF-α and strengthened the anti-oxidative capacity. Mechanically, LH011 downregulated the nuclear localization of NF-κB p65 and upregulated the protein expression of Nrf2. Conclusion: These results demonstrated that LH011 alleviated inflammation and oxidative stress during UC by inhibiting TLR4/NF-κB and activating Nrf2/Keap1/HO-1 signaling pathways.

Constrictive pericarditis caused by viral myocarditis in children: a brief report.

BACKGROUND: Constrictive pericarditis is more common in adults and has a low incidence in children. Here is a case of coxsackie virus induced myocarditis in children, resulting in constrictive pericarditis. CONCLUSION: Chronic inflammation of viral myocarditis can cause inflammatory changes of pericarditis and cause constrictive pericarditis.

M1 Macrophages Increase Endothelial Permeability and Enhance p38 Phosphorylation via PPAR-γ/CXCL13-CXCR5 in Sepsis.

PURPOSE: Vascular endothelial hyperpermeability and barrier disruption are involved in the initiation and development of sepsis. M1 macrophages promote inflammation in sepsis by releasing pro-inflammatory cytokines and chemokines. This study was designed to investigate the functional relationships between M1 macrophages and human umbilical vein endothelial cells (HUVECs), as well as the underlying molecular mechanisms. METHODS: HUVECs were co-cultured with THP-1-derived M1 macrophages pretreated with or without rosiglitazone (RSG), a peroxisome proliferator-activated receptor (PPAR)-γ agonist. C-X-C chemokine receptor type (CXCR)5 was knocked down by short hairpin RNA lentivirus. Cecal ligation and puncture were used to induce sepsis in a mouse model. Endothelial permeability was evaluated using transendothelial electrical resistance and fluorescein isothiocyanate (FITC)-dextran assays. RESULTS: Chemokine ligand (CXCL)13 was upregulated in M1 macrophages than M0 macrophages, as well as in the culture medium. In HUVECs co-cultured with M1 macrophages, transendothelial electrical resistance decreased, FITC-dextran flux increased, p38 phosphorylation was strengthened, and the expression of tight junction proteins (zonula occludens protein-1, occludin, and claudin-4) decreased. CXCR5 RNA interference or RSG pretreatment partially reversed these effects. A luciferase reporter assay revealed that CXCL13 was a direct target of PPAR-γ. RSG treatment decreased serum levels of creatinine, blood urea nitrogen, CXCL13, tumor necrosis factor-α, and interleukin-6, downregulated CXCL13 in peritoneal macrophages, and enhanced the survival rate of sepsis mice. CONCLUSION: M1 macrophages induced endothelial hyperpermeability and promoted p38 phosphorylation in sepsis by inhibiting PPAR-γ to increase CXCL13 production. PPAR-γ/CXCL13-CXCR5 signaling could be a promising novel therapeutic target for sepsis.

Coinfection with Hypervirulent Klebsiella pneumoniae and Aspergillus flavus in a Critically Ill Patient with Aspergillus Overlap Syndrome: A Case Report.

Pulmonary aspergillosis is generally categorized into three groups: allergic bronchopulmonary aspergillosis, chronic pulmonary aspergillosis and invasive pulmonary aspergillosis. Aspergillus overlap syndromes (AOS) defined as the occurrence of more than one form of aspergillus disease in a single individual is not common. We present a 62-year-old-male patient with tachypnea, hypoxemia and shock after 4 weeks of cough, expectoration and intermittent hemoptysis, and 2 days of hyperpyrexia. Cardiac arrest occurring during tracheal intubation was resuscitated successfully. Laboratory examination showed acute kidney failure and severe myelosuppression with leukopenia and thrombocytopenia. Chest computed tomography (CT) scan showed the cavity with aspergilloma in the right upper lung lobe, a mass of consolidation in the right lower lung lobe and hyperdense shadow bronchiectasis in the left lower lobe. Bronchoscopy showed lots of sputum occluding the opening of the right airway bronchus. Laboratory examination showed significantly increased C-reactive protein (CRP) and procalcitonin concentration, serum (1,3)-ß-D-glucan (BDG) and aspergillus immunoglobulin G (IgG) levels were also elevated. The metagenomic next-generation sequencing and sputum cultures revealed Klebsiella pneumoniae and Aspergillus flavus infection. Pulmonary aspergillosis, invasive aspergillosis infection and severe pneumonia were diagnosed. Initial caspofungin and meropenem followed by piperacillin-tazobactam sodium and voriconazole were administrated in combination. Continuous renal replacement therapy and mechanical ventilation were also performed. The patient's condition gradually recovered. Oral antifungal therapy was continued for 1 year after discharge and CT images gradually improved. Coinfections with K. pneumoniae and A. flavus in a patient with AOS will complicate clinical conditions. A search of PubMed showed few reports of similar cases. Clinicians should pay enough attention to the polymicrobial interactions and improve clinical management strategies, especially in critically ill patient with AOS.

Progress in research and development of particle electrodes for three-dimensional electrochemical treatment of wastewater: a review.

A three-dimensional (3D) electrochemical technology is regarded as a very effective industrial wastewater treatment method as it has high treatment efficiency, high current efficiency, and low energy consumption, and especially can completely mineralize nonbiodegradable organic pollutants. The core of the 3D electrochemical technology is a particle electrode, and the particle electrode plays several important roles for removing pollutants during the electrochemical reaction process. Many types of particle electrodes have been developed and used for different types of wastewater treatment. In this paper, a comprehensive review on the research and development of particle electrodes of the 3D electrochemical reactors for wastewater treatment is conducted. Specifically, the role that the particle electrode plays during the 3D electrochemical treatment of wastewater is thoroughly investigated and systematized. In addition, the different types of particle electrodes used in the 3D electrochemical wastewater treatment are classified into several types according to the presence or absence of a catalyst and the main components of the particle electrode or carrier. Also, focusing on the recent research results, the structural characteristics, performance, advantages and defects, and the role of catalyst components of each particle electrodes are evaluated. Finally, the direction and prospect of future research on the particle electrode is presented.

Progress of research on disease-modifying osteoarthritis drugs / 中国药科大学学报

@#Osteoarthritis (OA) is a common chronic joint disease,whose main pathological changes are the degeneration of articular cartilage and secondary bone hyperplasia.The limitation of current treatment methods including pain relief and joint replacement surgery is that they cannot fundamentally improve the damage of articular cartilage.The emergence of disease-modifying osteoarthritis drugs (DMOAD) may break the above limitations.They fundamentally inhibit the structural degeneration of articular cartilage by participating in the regulation of cartilage metabolic balance, regulation of subchondral bone remodeling,and control of local inflammation.Thereby,OA patients will get symptom improvement including pain relief and joint function restoration,delay the artificial joint replacement surgery, and improve the quality of life. There are still no DMOAD drugs widely available on the market worldwide.This paper reviews the background of R&D,the classification of mechanisms of action and research progress of representative drugs under different inechanisms so as to provide reference for future research.

[Role and mechanism of endoplasmic reticulum stress response induced by wear particles in osteolysis].

OBJECTIVE: To analyze the role of endoplasmic reticulum stress response in the development of osteoblast apoptosis and osteolysis in osteolytic bone tissue, and to explore the causes of artificial joint loosening, so as to provide new ideas and theoretical basis for the prevention and treatment of artificial joint loosening. METHODS: The animal model of osteolysis induced by wear particles was established by mouse skull, and randomly divided into 4 groups, 7 rats in each group:group 1, blank control group;group 2, wear particles tial6v4 nano alloy powder (TiNPs) group;group 3, endoplasmic reticulum stress response positive control (TiNPs+Tg) group; group 4, endoplasmic reticulum stress response inhibitor (TiNPs+4-PBA) group. The pathological changes of osteolysis were observed by toluidine blue staining, HE staining and ALP staining;the expression of endoplasmic reticulum stress response marker protein was detected by Western Blotting;the apoptosis of osteoblasts in osteolytic skull tissue was detected by TUNEL and Caspase-3 immunohistochemistry. RESULTS: Wear particles TiNPs can induce osteolysis in vitro, aggravate the infiltration of inflammatory cells and inhibit the differentiation and maturation of osteoblasts. At the same time, wear particles can also up regulate the markers of endoplasmic reticulum stress response and promote the apoptosis of osteoblasts in osteolytic bone tissue. After adding 4-PBA, an inhibitor of endoplasmic reticulum stress (4-PBA), on the basis of wear particles TiNPs, the symptoms of osteolysis were significantly relieved, bone erosion and inflammatory infiltration were significantly reduced, the differentiation and maturation of osteoblasts were improved, the number of apoptotic osteoblasts decreased sharply, and the expression of endoplasmic reticulum stress marker protein gradually decreased. CONCLUSION: Endoplasmic reticulum stress is involved in the formation of osteolysis and plays an important role in the occurrence and development of osteolysis. At the same time, endoplasmic reticulum stress can be used as a new therapeutic target to provide new ideas and methods for clinical reversal or treatment of osteolysis and aseptic loosening.

CXCL13 Is Involved in the Lipopolysaccharide-Induced Hyperpermeability of Umbilical Vein Endothelial Cells.

Sepsis is a disease that is characterized by a severe systemic inflammatory response to microbial infection and lipopolysaccharide (LPS) and is a well-known inducer of sepsis, as well as endothelial cell hyperpermeability. In the present study, we confirm the elevation of CXC chemokine ligand 13 (CXCL13) in sepsis patients. We also show that LPS exposure increases the release of CXCL13, as well as the mRNA and protein expression of CXCL13 and its receptor, CXC chemokine receptor 5 (CXCR5) in human umbilical vein endothelial cells (HUVECs) in a dose- and time-dependent manner. We also examined the effects of CXCL13 knockdown on LPS-mediated endothelial hyperpermeability and tight junction (TJ) protein expression in HUVECs. Our results show that HUVECs exposed to LPS result in a significant decrease in transendothelial electrical resistance (TER) and TJ protein (Zonula occluden-1, occludin, and claudin-4) expression, and a notable increase in fluorescein isothiocyanate (FITC)-dextran flux and p38 phosphorylation, which was partially reversed by CXCL13 knockdown. Recombinant CXCL13 treatment had a similar effect as LPS exposure, which was attenuated by a p38 inhibitor, SB203580. Moreover, the CXCL13-neutralizing antibody significantly increased the survival rate of LPS-induced sepsis mice. Collectively, our results show that CXCL13 plays a key role in LPS-induced endothelium hyperpermeability via regulating p38 signaling and suggests that therapeutically targeting CXCL13 may be beneficial for the treatment of sepsis.

Association between C-reactive protein gene variant and treatment efficacy of etanercept in ankylosing spondylitis patients receiving hip arthroplasty.

BACKGROUND: C-reactive protein (CRP) level is one of the most widely used parameters to assess ankylosing spondylitis (AS), since CRP is associated with poor radiographic progression of AS patients. Recent studies have investigated the association between CRP gene variants and AS risk, but with conflicting findings. MATERIAL AND METHODS: We enrolled 232 AS cases and 314 controls in this case-control study. Next, we assessed the association of CRP gene rs3091244 polymorphism with the efficacy of etanercept for AS. Genotyping was done using a custom-by-design 48-Plex SNP scanTM Kit. RESULTS: CRP gene rs3091244 polymorphism was associated with an increased risk of AS in this Chinese population. Clinical indicators of AS patients including morning stiffness time, Bath AS function index (BASFI), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Visual Analogue Scale (VAS), erythrocyte sedimentation rate (ESR), and CRP were significantly decreased after 12 weeks of etanercept treatment. Furthermore, AA genotype carriers showed higher values of VAS, BASDAI, BASFI, and CRP before etanercept treatment. AA genotype or A allele of rs3091244 polymorphism was associated with Ankylosing Spondylitis Assessment Study group response criteria 20 scores (ASAS20) and Assessment in SpondyloArthritis international Society 40 response (ASAS40) improvement. In addition, AA genotype carriers showed significantly higher CRP levels compared with genotype GG carriers (16.3 vs 8.8 mg/L). CONCLUSION: CRP gene rs3091244 polymorphism is associated with an increased risk of AS. Additionally, rs3091244 polymorphism could serve as a biomarker for good response to etanercept treatment in AS.

α7nAChR Deletion Aggravates Myocardial Infarction and Enhances Systemic Inflammatory Reaction via mTOR-Signaling-Related Autophagy.

Alpha7 nicotinic acetylcholine receptor (α7nAChR) has been previously reported to play an alleviative role in myocardial infarction (MI). In this study, we investigated its specific mechanism. α7nAChR-/- mice and its control (α7nAChR+/+) were used for the study of α7nAChR. Left anterior descending coronary artery occlusion was conducted for the creation of mice MI model and lipopolysaccharide (LPS) was used as inflammatory stressor in murine peritoneal macrophages. Triphenyltetrazolium chloride (TTC) staining and echocardiography was used for the detection of infarct size and cardiac function, respectively. Western blot was conducted for the testing of autophagy-related proteins and enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (RT-PCR) was used for the testing of proinflammatory cytokines. Rapamycin was used for the induction of autophagy through inhibiting mammalian target of rapamycin (mTOR)-related signaling. We found that knocking out α7nAChR enhanced the cardiac infarct size and damaged cardiac function in MI. α7nAChR deficiency increased the levels of several proinflammatory cytokines in serum and spleen from MI mice as well as murine macrophages under inflammatory stress. α7nAChR deletion decreased the level of autophagy in spleen from MI mice and macrophages under inflammatory stress. Rapamycin alleviated the cardiac function and systemic inflammatory reaction in MI mice as well as inflammatory reaction in macrophages under inflammatory stress, which was attenuated by knocking out α7nAChR. Our current study investigated the mechanism of α7nAChR-mediated cardio-protective and anti-inflammatory effect related to mTOR-related autophagy, which might provide a novel insight in the treatment of MI.

The association between MMP-1 gene rs1799750 polymorphism and knee osteoarthritis risk.

Matrix metalloproteinase 1 (MMP-1) degrades cartilage, which may result in osteoarthritis (OA) development. Several studies have explored the association between MMP-1 gene rs1799750 polymorphism and OA in different populations. However, the results are inconsistent. The aim of this case-control study was to investigate the association between MMP-1 gene rs1799750 polymorphism and knee OA in a Chinese population. The present study included 308 cases and 404 controls. Genotyping was performed using standard polymerase chain reaction and restriction fragment length polymorphism. The present study found that 2G2G genotype (2G2G vs 1G1G: OR & 95% CI, 2.28 (1.47-3.53), P<0.001; 2G2G + 1G2G vs 1G1G: OR & 95% CI, 1.61 (1.15-2.24), P=0.005; 2G2G vs 1G2G + 1G1G: OR & 95% CI, 1.84 (1.26-2.68), P=0.002) or 2G allele carriers (2G vs 1G: OR & 95% CI, 1.48 (1.20-1.83), P<0.001) of MMP-1 gene rs1799750 polymorphism increased the risk of OA. In conclusion, this case-control study confirms that MMP-1 gene rs1799750 polymorphism increases the risk of knee OA in Chinese Han population.

Clinical relevance of cleaved RAGE plasma levels as a biomarker of disease severity and functional outcome in aneurysmal subarachnoid hemorrhage.

BACKGROUND: Cleaved receptor for advanced glycation end-products (cRAGE) has been introduced as a new inflammatory marker. We clarified the associations between cRAGE levels, disease severity and functional outcome in aneurysmal subarachnoid hemorrhage (aSAH). METHODS: In this prospective, observational study, plasma levels of total soluble RAGE (sRAGE) and endogenous secretory RAGE (esRAGE) were quantified in 108 aSAH patients and 108 controls. The level of cRAGE was calculated by subtracting the level of esRAGE from that of sRAGE. World Federation of Neurological Surgeons (WFNS) score, modified Fisher score, and Hunt Hess (HH) score were recorded to assess aSAH severity. Relationship between plasma cRAGE levels and 6-month poor outcome (Glasgow Outcome Scale score of 1-3) was assess using multivariate analysis. RESULTS: Plasma cRAGE levels were significantly higher in patients than in controls. Its levels were significantly correlated with WNFS score, modified Fisher score and HH score of patients. Plasma cRAGE emerged as an independent predictor for 6-month poor outcome. Area under receiver operating characteristic curve (AUC) of this biomarker was similar to those of WNFS score, modified Fisher score and HH score. Moreover, it significantly improved AUCs of WNFS score, modified Fisher score and HH score. CONCLUSIONS: Plasma cRAGE levels are highly associated with the severity and poor prognosis in aSAH.

Acute Hemodynamic Effects of Remote Ischemic Preconditioning on Coronary Perfusion Pressure and Coronary Collateral Blood Flow in Coronary Heart Disease.

BACKGROUND: The aim of this study was to assess the acute hemodynamic effects of remote ischemic preconditioning (RIPC) on coronary perfusion pressure and coronary collateral blood flow. METHODS: A total of 17 patients with coronary heart disease with severe (70%-85%) stenosis in one or two vessels confirmed by angiography were enrolled into this study. They were randomly divided into the RIPC group (9 patients) and the control group (8 patients). Distal pressure of coronary artery stenosis before balloon dilation (non-occlusive pressure, Pn-occl) and distal coronary artery occlusive pressure (Poccl) during balloon dilation occlusion were measured in all patients. The patients in the RIPC group received three cycles of lower limb ischemia-reperfusion preconditioning (5 minutes inflation of a blood pressure cuff, followed by 5 minutes reperfusion). For controls, the cuff was not inflated. After this process, Pn-occl and Poccl were measured again in each patient. RESULTS: There were no significant differences in angiographic characteristics between the two groups (all p > 0.05). Troponin I (TNI) levels after percutaneous coronary intervention (PCI) were lower in the RIPC group than in the control group (p = 0.004). In the RIPC group, mean Pn-occl and Poccl were significantly increased after RIPC compared to before RIPC [(72.78 ± 10.10) mmHg vs. (79.67 ± 9.79) mmHg, p = 0.002, (20.89 ± 8.61) mmHg vs. (26.78 ± 10.73) mmHg, p = 0.001, respectively]. CONCLUSIONS: RIPC can improve distal coronary perfusion pressure and rapidly increase distal coronary occlusive pressure thereby improving coronary collateral blood flow.

A single nucleotide polymorphism of AIRE gene located in the 21q22.3 increases the risk of rheumatoid arthritis.

Several studies addressed the association of autoimmune regulator (AIRE) gene polymorphism with the risk of rheumatoid arthritis (RA); however, their conclusions were inconsistent. For better investigating the effects of this polymorphism on the risk of RA, we conducted this study to evaluate the role of AIRE rs2075786 polymorphism in the risk of RA. Four eligible studies involving 6,755 cases and 7,970 controls were identified by searching the databases of PubMed, CNKI and EMBASE up to February 2017. Our study revealed that AIRE rs2075786 polymorphism was associated with an increased risk of RA under all genetic models. In the subgroup analysis, AIRE rs2075786 polymorphism contributed to RA susceptibility among Asians, but not among Caucasians. To summarize,, this meta-analysis confirms that AIRE rs2075786 polymorphism may play a significant role in increasing the risk of RA. Stratification analysis by ethnicity reveals that AIRE rs2075786 polymorphism is associated with an increased risk of RA among Asians, but not among Caucasians. These findings need further validation in the large multicenter case-control studies.

Protective effect of higenamine ameliorates collagen-induced arthritis through heme oxygenase-1 and PI3K/Akt/Nrf-2 signaling pathways.

Existing in Ranunculaceae Aconitum and tomato, with the chemical name 1-phydroxybenzyl-1,2,3,4-tetrahy-droisoquinoline, higenamine is widely distributed in China. Higenamine's anti-inflammatory, antioxidant and anti-apoptotic effects have been identified in previous studies. The present study attempted to determine the protective effect of higenamine against collagen-induced arthritis through heme oxygenase-1 (HO-1) and PI3K/Akt/Nrf-2 signaling pathways. A type II collagen (CII)-induced arthritis (CIA) model was established and clinical arthritis scores were used to appraise the curative effect of higenamine. Inflammatory reactions, oxidative damage and caspase-3/9 activation were detected using specific ELISA kits. In addition, western blotting was used to evaluate the expression of HO-1, Akt and Nrf-2 protein in CII-induced CIA mice. In CII-induced CIA mice, the clinical arthritis scores, inflammatory reactions, oxidation damage and caspase-3/9 activation were increased and activated. The results demonstrated that treatment with higenamine significantly reduced the elevation of clinical arthritis scores (P<0.01), and suppressed the promotion of inflammatory reactions, oxidation damage and caspase-3/9 activation. Furthermore, higenamine significantly increased HO-1 protein expression (P<0.01) and upregulated the PI3K/Akt/Nrf-2 signal pathway in CII-induced CIA mice. Collectively, it is concluded that higenamine protects against CII-induced CIA through the induction of HO-1 and the upregulation of the PI3K/Akt/Nrf-2 signaling pathway. In conclusion, higenamine may be a beneficial drug for protecting against CIA.

[The impact of perioperative function exercises on hidden blood loss in elderly patients with total hip replacement].

OBJECTIVE: To investigate the effects of initiative and passive perioperative function exercises on hidden blood loss (HBL). METHODS: Two hundreds and thirty elderly patients with hip fractures aging from 67 to 87 years (average age of 73.6 years) who underwent total hip replacement were included. By the intensity and the manner of perioperative function exercises, patients were divided into four groups: little initiative function exercises group (group A, n=51), little initiative and passive function exercises group (group B, n=54), normal initiative function exercises group (group C, n=65), normal initiative and passive function exercises group (group D, n=60). The true total blood loss, HBL and their proportion on the original blood volume and total blood loss was calculated depending on height, weight, intra-operative blood loss, post-operative blood loss, pre- and post-operative hematocrit, and blood transfused. According to the proportion of mean HBL on total blood loss, patients were divided into low HBL group and high HBL group. The data were analyzed by t test. RESULTS: The mean HBL was 517 ml, 41.9% of the total blood loss. Thereinto, the mean HBL was 695 ml in group A, 49.3% of the total blood loss, the prevalence of high HBL was 66.7% (34/51); the mean HBL was 625 ml in group B, 46.9% of the total blood loss, the prevalence of high HBL was 59.3% (32/54); the mean HBL was 446 ml in group C, 38.4% of the total blood loss, the prevalence of high HBL was 30.8% (20/65); the mean HBL was 346 ml in group D, 32.3% of the total blood loss, the prevalence of high HBL was 20.0% (12/60). Mean HBL, mean HBL/total blood loss, prevalence of high HBL were lower in group C than that in group A and group B (all P<0.05); and were lower in group D than that in group C (all P<0.05). The prevalence was 57.4% (132 cases) in low HBL group, and 42.6% (98 cases) in high HBL. The proportion of little initiative function exercises patients in high HBL group was obviously higher than that in low HBL group (P<0.05). CONCLUSIONS: The intensity and the manner of perioperative function exercises are strongly associated with the HBL in elderly patients with total hip replacement. The initiative combined with the passive function exercises could be effectively prevent and reduce the incidence of high HBL.