Idiopathic gingival fibromatosis and primary analysis of dominant bacteria in subgingival biofilm: a case report.

Idiopathic gingival fibromatosis (IGF), a rare fibroproliferative disease of unknown etiology, affects gingival tissue and has substantial adverse effects on patients. Therefore, the pathogenesis of IGF requires more extensive and in-depth research. In this case, a patient with confirmed IGF underwent initial nonsurgical periodontal therapy and gingivectomy, and the prognosis was good. The patient had no loss of periodontal attachment but had a history of swelling and bleeding of the gingiva prior to fibrous enlargement, which prompted further investigation. We explored the patient's subgingival microbiome and found a high abundance of periodontal pathogens. Gingival tissue biopsy revealed abundant fibrous tissue containing multiple inflammatory cell infiltrates. These results suggest that gingival inflammation secondary to periodontal pathogens can contribute to IGF onset.

Effect of Xuebijing injection on myocardium during cardiopulmonary bypass: A prospective, randomized, double blind trial.

BACKGROUND: Cardiopulmonary bypass (CPB) is an essential procedure for maintaining the blood supply to vital organs in patients undergoing cardiac surgery. However, perioperative cardiac injury related to CPB remains a severe complication in these patients. Cardiac protection is important for patients undergoing CPB. AIM: To evaluate the potential cardioprotective efficacy of the Chinese medicine preparation Xuebijing injection (XBJ) in patients undergoing CPB. METHODS: Sixty patients undergoing cardiac surgery with CPB were randomly allocated to the XBJ and control groups (saline). XBJ was administered intravenously three times: 12 h prior to surgery, at the beginning of the surgery, and 12 h after the second injection. Cardiac function was evaluated by echocardiography 48 h after surgery. Circulating inflammation- and oxidative-stress-related markers were measured. Clinical outcomes related to intensive care unit (ICU) stay were recorded. RESULTS: Compared to control treatment, XBJ was associated with improved PaO2/FiO2 and cardiac systolic function, but reduced troponin I and creatine kinase fraction after surgery (all P < 0.05). The circulating concentrations of tumor necrosis factor-α, interleukin (IL)-1ß and IL-8 in the XBJ group were significantly lower than those in the control group (all P < 0.05), whereas the circulating concentration of IL-10 was significantly higher in the XBJ group (P < 0.05). In addition, the lengths of ICU stay and hospitalization after surgery tended to be shorter in the XBJ group than in the control group, although the differences were not significant. CONCLUSION: Perioperative administration of XBJ was associated with attenuated cardiac injury during CPB, likely via anti-inflammatory and antioxidative mechanisms.

Ac2-26 Alleviates Brain Injury after Cardiac Arrest and Cardiopulmonary Resuscitation in Rats via the eNOS Pathway.

BACKGROUND: Brain injury is the leading cause of death following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). Ac2-26 and endothelial nitric oxide synthase (eNOS) have been shown to reduce neuroinflammation. This study is aimed at determining the mechanism by which Ac2-26 protects against inflammation during brain injury following CA and CPR. METHODS: Sixty-four rats were randomized into sham, saline, Ac2-26, and Ac2-26+L-NIO (endothelial nitric oxide synthase (eNOS) inhibitor) groups. Rats received Ac2-26, Ac2-26+L-NIO, or saline after CPR. Neurologic function was assessed at baseline, 24, and 72 hours after CPR. At 72 hours after resuscitation, serum and brain tissues were collected. RESULTS: Blood-brain barrier (BBB) permeability increased, and the number of surviving neurons and neurological function decreased in the saline group compared to the sham group. Anti-inflammatory and proinflammatory factors, neuron-specific enolase (NSE) levels, and the expression of eNOS, phosphorylated (p)-eNOS, inducible nitric oxide synthase (iNOS), and oxidative stress-related factors in the three CA groups significantly increased (P < 0.05). BBB permeability decreased, and the number of surviving neurons and neurological function increased in the Ac2-26 group compared to the saline group (P < 0.05). Ac2-26 increased anti-inflammatory and reduced proinflammatory markers, raised NSE levels, increased the expression of eNOS and p-eNOS, and reduced the expression of iNOS and oxidative stress-related factors compared to the saline group (P < 0.05). The effect of Ac2-26 on brain injury was reversed by L-NIO (P < 0.05). CONCLUSIONS: Ac2-26 reduced brain injury after CPR by inhibiting oxidative stress and neuroinflammation and protecting the BBB. The therapeutic effect of Ac2-26 on brain injury was largely dependent on the eNOS pathway.

The combination of transversus abdominis plane block and rectus sheath block reduced postoperative pain after splenectomy: a randomized trial.

BACKGROUND: Splenectomy performed with a curved incision results in severe postoperative pain. The aim of this study was to evaluate the effect of transversus abdominis plane block and rectus sheath block on postoperative pain relief and recovery. METHODS: A total of 150 patients were randomized into the control (C), levobupivacaine (L) and levobupivacaine/morphine (LM) groups. The patients in the C group received only patient-controlled analgesia. The patients in the L and LM groups received transversus abdominis plane block and rectus sheath block with levobupivacaine or levobupivacaine plus morphine. The intraoperative opioid consumption; postoperative pain score; time to first analgesic use; postoperative recovery data, including the times of first exhaust, defecation, oral intake and off-bed activity; the incidence of postoperative nausea and vomiting and antiemetics use; and the satisfaction score were recorded. RESULTS: Transversus abdominis plane block and rectus sheath block reduced intraoperative opioid consumption. The patients in the LM group showed lower postoperative pain scores, opioid consumption, postoperative nausea and vomiting incidence and antiemetic use and presented shorter recovery times and higher satisfaction scores. CONCLUSIONS: The combination of transversus abdominis plane block and rectus sheath block with levobupivacaine and morphine can improve postoperative pain relief, reduce the consumption of analgesics, and partly accelerate postoperative recovery. TRIAL REGISTRATION: Chinese Clinical Trial Registry, ChiCTR 1,800,015,141, 10 March 2018.

Endothelial Progenitor Cells Attenuate Ventilator-Induced Lung Injury with Large-Volume Ventilation.

Ventilator-induced lung injury (VILI) is a common complication that results from treatment with mechanical ventilation (MV) in acute respiratory distress syndrome (ARDS) patients. The present study investigated the effect of endothelial progenitor cell (EPC) transplantation on VILI. Wistar rats were divided into three groups (n = 8): sham (S), VILI model (V) induced by tidal volume ventilation (17 mL/kg), and VILI plus EPC transplantation (VE) groups. The lung PaO2/FiO2 ratio, pulmonary wet-to-dry (W/D) weight ratio, number of neutrophils, total protein, neutrophil elastase level, and inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and serum were examined. Furthermore, the histological and apoptotic analysis, and lung tissue protein expression analysis of Bax, Bcl-2, cleaved caspase-3, matrix metalloproteinase (MMP)-9, total nuclear factor kappa B (total-NF-κB), phosphorylated NF-κB (phospho-NF-κB) and myosin light chain (MLC) were performed. The ventilation-induced decrease in PaO2/FiO2 ratio, and the increase in W/D ratio and total protein concentration were prevented by the EPC transplantation. The EPC transplantation (VE group) significantly attenuated the VILI-induced increased expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-8, MMP-9, phospho-NF-κB and MLC, neutrophil elastase levels and neutrophil counts in BALF. In addition, the anti-inflammatory factor IL-10 increased in the VE group. Furthermore, pulmonary histological injury and apoptosis (TUNEL-positive cells, increase in Bax and cleaved caspase-3) were considerably diminished by the EPC transplantation. The EPC transplantation ameliorated the VILI. The mechanism may be primarily through the improvement of epithelial permeability, inhibition of local and systemic inflammation, and reduction in apoptosis.

Ac2-26 ameliorates lung ischemia-reperfusion injury via the eNOS pathway.

BACKGROUND: Lung ischemia-reperfusion injury (LIRI) is a major complication after lung transplantation. Annexin A1 (AnxA1) ameliorates inflammation in various injured organs. This study aimed to determine the effects and mechanism of AnxA1 on LIRI after lung transplantation. METHODS: Thirty-two rats were randomized into sham, saline, Ac2-26 and Ac2-26/L groups. Rats in the saline, Ac2-26 and Ac2-26/L groups underwent left lung transplantation and received saline, Ac2-26, and Ac2-26/L-NIO, respectively. After 24 h of reperfusion, serum and transplanted lung tissues were examined. RESULTS: The partial pressure of oxygen (PaO2) was increased in the Ac2-26 group compared to that in the saline group but was decreased by L-NIO treatment. In the Ac2-26 group, the wet-to-dry (W/D) weight ratios, total protein concentrations, proinflammatory factors and inducible nitric oxide synthase levels were notably decreased, but the concentrations of anti-inflammatory factors and endothelial nitric oxide synthase levels were significantly increased. Ac2-26 attenuated histological injury and cell apoptosis, and this improvement was reversed by L-NIO. CONCLUSIONS: Ac2-26 reduced LIRI and improved alveoli-capillary permeability by inhibiting oxygen stress, inflammation and apoptosis. The protective effect of Ac2-26 on LIRI largely depended on the endothelial nitric oxide synthase pathway.

Alpha 1-antitrypsin for treating ventilator-associated lung injury in acute respiratory distress syndrome rats.

Purpose: Mechanical ventilation (MV) is an essential life support tool for patients with acute respiratory distress syndrome (ARDS). However, MV for ARDS can result in ventilator-induced lung injury (VILI). This study aimed to assess whether alpha 1-antitrypsin (AAT) can reduce VILI in ARDS rats. Materials and Methods: Rats were randomly divided into five groups: the sham (S) group, MV (V) group, lipopolysaccharide (LPS) (L) group, MV/LPS (VL) group and MV/AAT (VA) group. Rats in the S group were anesthetized. The rats in the L group received LPS but not ventilation, the rats in the V group received only MV, and the rats in the VL and VA groups received LPS and MV. Additionally, the rats in the VA group were treated with AAT, and the other rats were injected with saline. The PaO2/FiO2 ratio and the wet/dry weight were assessed. The total protein and neutrophil elastase concentrations and the neutrophil and macrophage counts in bronchoalveolar lavage fluid (BALF) were evaluated. Proinflammatory factors in BALF and ICAM-1 and MIP-2 in serum were also tested. Furthermore, the oxidative stress response was detected, and histological injury and apoptosis were evaluated. Results: All the rats in the V, L and VL groups had significant lung injury, with the VL group exhibiting the most severe injury. Compared with the findings in the VL group, AAT significantly upregulated the PaO2/FiO2 ratio but decreased the wet/dry weight ratio and protein levels in BALF. AAT also reduced proinflammatory cytokine levels and inflammatory cell counts in BALF. Lung tissue injury and cell apoptosis were mitigated by AAT. Conclusions: AAT ameliorated VILI in ARDS rats. The protection conferred by AAT may be associated with the anti-inflammatory, antioxidative stress response and anti-apoptotic effects of AAT.

The effect of liraglutide on the proliferation, migration, and osteogenic differentiation of human periodontal ligament cells.

OBJECTIVE: Liraglutide (LIRA) is a novel antidiabetic therapy that may have anti-inflammatory and bone protective effects. Thus, we studied the potential therapeutic effect of LIRA on periodontitis by assessing the effects of LIRA on the proliferation, migration, inflammation, and osteogenic differentiation of human periodontal ligament cells (hPDLCs) after LPS stimulation. MATERIAL AND METHODS: The expression of glucagon like-peptide 1 receptor (GLP-1R) was measured using qRT-PCR. HPDLCs proliferation after LIRA were analyzed using MTT assays. Cell migration was quantified using a wound-healing assay. The expression of inflammatory (IL-6 and TNF-α) was measured by qRT-PCR and ELISA in hPDLCs. The effect of LIRA on the mineralization potential of hPDLCs was assessed by alizarin red S staining. Furthermore, the expression of Runx2 and ALP was measured by qRT-PCR and Western blot in hPDLCs. RESULTS: GLP-1R mRNA was present on hPDLCs, and LIRA increased the expression of GLP-1R mRNA. When cultured with 25, 50, 75, 100 and 125 nM LIRA for 24 h, hPDLCs proliferation was enhanced in a dose-dependent manner (P < 0.05), and 100 nM was optimal. LIRA promoted hPDLCs migration in a time-dependent manner. LPS significantly increased the expression of IL-6 and TNF-α (P < 0.01), decreased the formation of mineralization nodes (P < 0.01), and inhibited the expression of ALP and Runx2 (P < 0.05). LIRA treatment blocked the expression of IL-6 and TNF-α (P < 0.01), increased the formation of mineralization nodes (P < 0.01), and enhanced the expression of ALP and Runx2 (P < 0.05). CONCLUSION: LIRA can enhance the proliferation, migration, and osteogenic differentiation of hPDLCs and inhibit the inflammatory response. Thus, LIRA may have potential therapeutic use as an adjuvant treatment for human periodontitis, and this effect is independent of hypoglycemic activity.

Endothelial Colony-forming Cells Attenuate Ventilator-induced Lung Injury in Rats with Acute Respiratory Distress Syndrome.

BACKGROUND: Mechanical ventilation (MV) can cause ventilator-induced lung injury (VILI). AIM OF THE STUDY: This study investigated whether endothelial colony-forming cells (ECFC) could inhibit VILI in a rat model of acute respiratory distress syndrome (ARDS). METHODS: Male Wistar rats received the femoral artery and venous cannulation (sham group) or were injected intravenously with 500 µg/kg lipopolysaccharide to induce ARDS. The ARDS rats were subjected to MV. Immediately after the MV, the rats were randomized and injected intravenously with vehicle (ARDS group) or ECFC (ECFC group, n = 8 per group). The oxygen index, lung wet-to-dry weight (W/D) ratios, cytokine protein levels in serum or bronchoalveolar lavage fluid (BALF), neutrophil counts, neutrophil elastase and total protein levels in BALF, histology and cell apoptosis in the lung were detected. The protein levels of endothelin-1, inducible nitric oxide synthase (iNOS), endothelial NOS, matrix metalloproteinase (MMP)-9, Bax, Bcl-2, gelsolin, cleaved caspase-3, phosphorylated NF-κBp65 and myosin light chain (MLC) in the lung were analyzed. RESULTS: Compared with the ARDS group, treatment with ECFC significantly increased the oxygen index, and decreased the lung W/D ratios and injury, and the numbers of apoptotic cells in the lungs, neutrophils counts, total protein and elastase concentrations in BALF of rats. ECFC treatment significantly minimized the protein levels of pro-inflammatory cytokines in BALF and serum, but increased interleukin 10 in rats. Furthermore, ECFC treatment significantly reduced the protein levels of endothelin-1, iNOS, Bax, Gelsolin, MMP-9, cleaved caspase-3, phosphorylated NF-κBp65 and MLC, but enhanced eNOS and Bcl-2 in the lungs of rats. CONCLUSIONS: Therefore, ECFC attenuated inflammation, cell apoptosis and VILI in ARDS rats.

[Apoptosis and Ca~(2+) balance disorder of BV-2 cells induced by polychlorinated biphenyl].

OBJECTIVE: To study the neurotoxicity and mechanism of polychlorinated biphenyl( PCB) in BV-2 cells. METHODS: The experiment was divided into control group and PCB118, 138, 153, 180 treated group, the dosages were 0. 000, 0. 015, 0. 030, 0. 050, 0. 100, 0. 150 µmol/L. Through the statistical analysis of the survival rate of the cells, the final dose was divided into low, middle and high dose levels. Among them, the high dose group except PCB118 was 0. 15 µmol/L, the PCB138, 153, 180 concentration was 0. 015, 0. 05 and 0. 1 µmol/L for the low, medium and high dose groups. In vitro culture of mouse microglia cells with different doses of PCB after exposure, CCK-8 method to detect cell growth and viabilities; FITC Annexin V/PI method to detect cell apoptosis rate; detection of lactate dehydrogenase( LDH) release by ELISA kit; fluorescence probe method( Fluo-4 AM) to detect the intracellular calcium content changes. RESULTS: CCK-8 and FITC Annexin V/PI double staining experiments showed that PCB118, 138, 153, 180 could inhibit cell activity, and with the increase in dose, cell survival rate decreased, apoptosis rate increased. PCB118 dose in 0. 15 µmol/L toxicity increased, cytoactive was reduced to( 66. 56 ± 0. 10) %, apoptosis rate increased to( 27. 39 ± 1. 80) %; PCB138, 153 in 0. 1 µmol/L cell survival rate reached( 66. 66 ± 0. 10) % and( 67. 17 ± 0. 12) %, apoptosis rate reached( 48. 77 ± 2. 43) % and( 56. 42 ± 3. 59) %; PCB180 dose of 0. 015µmol/L cell survival rate reached( 92. 07 ± 0. 38) %, cell apoptosis rate was( 6. 82 ±0. 51) %, significantly higher than that of the control group, the difference was statistically significant( P < 0. 05). LDH assay showed that the release amount of LDH was proportional to the dose of PCB. The lactate dehydrogenase amounts of PCB118, 138, 153 and 180 were( 523. 78 ± 13. 58) U/L, ( 430. 37 ± 22. 03) U/L, ( 540. 58 ± 13. 08)U/L, ( 411. 88 ± 21. 92) U/L, which were significantly higher than those in the control group, the difference was statistically significant( P < 0. 05). The result of Fluo-4 and AM showed that the average fluorescence intensity of intracellular calcium( Ca~(2+)) in PCB exposed group increased obviously. The average fluorescence intensity of Ca~(2+) in the PCB118, 138, 153 and 180 groups was( 10. 14 ± 2. 36), ( 32. 47 ± 1. 56), ( 16. 54 ± 0. 97)and( 40. 46 ± 2. 19) when the dose was 0. 015 µmol/L, significantly higher than that of the control group, the difference was statistically significant( P < 0. 05). CONCLUSION: PCB could cause neurotoxicity damage, increase LDH, destroy cell membrane integrity, induce the balance disorder of cell calcium and lead to the cell apoptosis.

Effects of Yangzheng Sanjie Decoction-containing serum mediated by microRNA-7 on cell proliferation and apoptosis in gastric cancer.

Gastric cancer (GC) is one of the most common types of cancer and a leading cause of cancer-associated mortality. MicroRNAs (miRNAs/miRs) are demonstrated to function as oncomiRs or tumor-suppressor-miRs in GC. miR-7 has been identified to be a tumor suppressor of GC by targeting epidermal growth factor receptor (EGFR). In our previous study, Yangzheng Sanjie Decoction (YZSJD), a traditional Chinese formula, was identified to be effective in alleviating the symptoms and even postponing turnover of precancerous lesions. To elucidate the mechanism of YZSJD, the present study evaluated the effects of YZSJD of the GC MKN-45 cell line and investigated the underlying molecular mechanisms using YZSJD-containing serum (YCS). The expression of miR-7 in GC, normal and adjacent tissue samples was examined. The results demonstrated that YCS inhibited proliferation by inducing cell cycle arrest at the S phase, and significantly induced apoptosis compared with the control group. miR-7 was significantly downregulated in GC tissues compared with the matched ones. Using reverse transcription-quantitative polymerase chain reaction and western blot analysis, the expression of miR-7 was inversely associated with EGFR. This indicates that YCS inhibits proliferation and induces apoptosis of GC cells mediated by miR-7 targeting EGFR, which may be one of the mechanisms whereby YZSJD exerts its effects on GC.

Yangzheng Sanjie decoction regulates proliferation and apoptosis of gastric cancer cells by enhancing let-7a expression.

AIM: To explore the let-7a-mediated anti-cancer effect of Yangzheng Sanjie decoction (YZSJD) in gastric cancer (GC) cells. METHODS: YZSJD-containing serum (YCS) was prepared using traditional Chinese medicine serum pharmacology methods. After YCS treatment, cell proliferation and apoptosis were assessed by cell counting kit-8 assay and flow cytometry, respectively, and miRNA expression profiles were determined using qPCR arrays. Let-7a expression was examined by in situ hybridization in GC tissues and by qPCR in GC cells. c-Myc protein expression was detected by immunohistochemistry in GC tissues, and by Western blot in cell lines. RESULTS: YZSJD significantly inhibited proliferation and induced apoptosis in AGS and HS-746T GC cells. After treatment with YCS, the miRNA expression profiles were altered and the reduced let-7a levels in both cell lines were up-regulated, accompanied by a decrease in c-Myc expression. Moreover, decreased let-7a expression and increased c-Myc expression were observed during the progression of gastric mucosa cancerization. CONCLUSION: YZSJD inhibits proliferation and induces apoptosis of GC cells by restoring the aberrant expression of let-7a and c-Myc.

Characterization of plasma metal profiles in Alzheimer's disease using multivariate statistical analysis.

The exact cause of Alzheimer's disease (AD) and the role of metals in its etiology remain unclear. We have used an analytical approach, based on inductively coupled plasma mass spectrometry coupled with multivariate statistical analysis, to study the profiles of a wide range of metals in AD patients and healthy controls. AD cannot be cured and the lack of sensitive biomarkers that can be used in the early stages of the disease may contribute to this treatment failure. In the present study, we measured plasma levels of amyloid-ß1-42(0.142±0.029µg/L)and furin(2.292±1.54µg/L), together with those of the metalloproteinases, insulin-degrading enzyme(1.459±1.14µg/L) and neprilysin(0.073±0.015µg/L), in order to develop biomarkers for AD. Partial least squares discriminant analysis models were used to refine intergroup differences and we discovered that four metals(Mn, Al, Li, Cu) in peripheral blood were strongly associated with AD. Aberration in homeostasis of these metals may alter levels of proteinases, such as furin, which are associated with neurodegeneration in AD and can be a used as plasma-based biomarkers.

Synthesis of Luminescent Graphene Quantum Dots with High Quantum Yield and Their Toxicity Study.

High fluorescence quantum yield graphene quantum dots (GQDs) have showed up as a new generation for bioimaging. In this work, luminescent GQDs were prepared by an ameliorative photo-Fenton reaction and a subsequent hydrothermal process using graphene oxide sheets as the precursor. The as-prepared GQDs were nanomaterials with size ranging from 2.3 to 6.4 nm and emitted intense green luminescence in water. The fluorescence quantum yield was as high as 24.6% (excited at 340 nm) and the fluorescence was strongest at pH 7. Moreover, the influences of low-concentration (12.5, 25 µg/mL) GQDs on the morphology, viability, membrane integrity, internal cellular reactive oxygen species level and mortality of HeLa cells were relatively weak, and the in vitro imaging demonstrated GQDs were mainly in the cytoplasm region. More strikingly, zebrafish embryos were co-cultured with GQDs for in vivo imaging, and the results of heart rate test showed the intake of small amounts of GQDs brought little harm to the cardiovascular of zebrafish. GQDs with high quantum yield and strong photoluminescence show good biocompatibility, thus they show good promising for cell imaging, biolabeling and other biomedical applications.

[Catalytic removal of NO on modified precious catalyst].

The streams of waste gases containing NO from industries would cause seriously pollution on the environment if they are directly discharged without further purification. The property of removal of NO from the waste gas at lower temperature performed on platinum catalyst by reduction with NH3 was investigated. Experimental study showed that the precious catalyst, platinum, had good activity at low temperature and high selectivity of catalytic removal of NO from the waste gas by ammonia. However, its performance was affected by the sulfur compound, SO2, which was present in the waste gas. Results indicated that the performance of platinum supported catalyst could be improved with addition of lanthanides on it. The suitable compositions of the modified catalyst were 1:3.78:3.56 molar ratio of Pt:La:Ce in the experiment.