Idiopathic tenosynovitis of the wrist with multiple rice bodies: A case report and review of literature.

BACKGROUND: Multiple rice bodies in the wrist is a rare disorder that requires surgery, and there are still many uncertainties regarding its diagnosis and treatment. CASE SUMMARY: We described a rare case of chronic idiopathic tenosynovitis with rice bodies of the wrist in a 71-year-old man and reviewed similar topics in the literature. A total of 43 articles and 61 cases were included in the literature review. Our case had a usual presentation: it was similar to those in the literature. The affected population was mainly older adults, with an average age of 59.43 (range, 3 to 90) years. The male-to-female ratio was 1.54:1 (37/24).Most of them showed limited swelling and pain, only 23.0% had carpal tunnel symptoms, and the average disease duration was 18.03 (0.5-60) mo. Wrist flexor tendon sheath involvement was the most common (95.1%, 58/61), and only 3 cases had extensor tendon sheath involvement.The main causes were tuberculosis (34.4%, 21/61), non-tuberculous mycobacteria (24.6%, 15/61), idiopathic tenosynovitis (31.1%, 19/61), and others (9.84%, 6/61). There were 10 patients with recurrences; in 6 of them, were due to non-tuberculous mycobacterial infections. CONCLUSION: We reported a case of wrist idiopathic tenosynovitis with rice body formation, and established a clinical management algorithm for wrist tenosynovitis with rice bodies, which can provide some reference for our clinical diagnosis and treatment. The symptoms of rice-body bursitis of the wrist are insidious, nonspecific, and difficult to identify. The aetiology is mainly idiopathic tenosynovitis and mycobacterial (tuberculosis or non-tuberculous) infections; the latter are difficult to treat and require long-duration systemic combination antibiotic therapies. Therefore, before a diagnosis of idiopathic tenosynovitis is made, we must exclude other causes, especially mycobacterial infections.

Comparison of organic acids supplementation on the growth performance, intestinal characteristics and morphology, and cecal microflora in broilers fed corn-soybean meal diet.

OBJECTIVE: The aim of this study was to compare the effects of three kinds of organic acid (OA) products on the growth performance, intestinal characteristics and morphology, and cecal microflora in broilers fed a corn-soybean meal meal diet. METHODS: A total of 420 one-day-old male Cobb 500 broilers with an average initial body weight of 49.11±1.02 g were used in this 42-day experiment. Birds were randomly allotted to one of five treatments (7 replicates with 12 birds per replicate). Treatments consisted of negative control (NC), basal diet; positive control (PC), basal diet+100 mg/kg of Aviramycin; OA1, basal diet+500 mg/kg of OA product 1; OA2, basal diet+1,000 mg/kg of OA product 2; and OA3, basal diet+1,200 mg/kg of OA product 3. RESULTS: The results indicated that OA product addition had no effect on growth performance parameters, such as body weight gain, feed intake, and feed conversion ratio, from days 1 to 14, 15 to 28, and 0 to 42, or on the pH values of the intestine, intestinal weight, or intestinal weight to body weight ratio. The intestinal morphology in terms of villus height and crypt depth were affected by dietary supplementation of OA products, respectively. Furthermore, dietary addition of OAs had positive influences on the maintenance of the cecal microflora based on the results of 16S rRNA analysis. CONCLUSION: Dietary inclusion of three kinds of OA products all benefit broilers, but the mode of action may be different. This study provides a basis for the application of OA products used in the poultry industry.

Crizotinib changes the metabolic pattern and inhibits ATP production in A549 non-small cell lung cancer cells.

Crizotinib, an inhibitor of the hepatocyte growth factor receptor oncogene, has been studied extensively regarding its antitumor and clinically beneficial effects in non-small cell lung cancer (NSCLC). However, crizotinib's effects on cancer cell energy metabolism, which is linked with tumor proliferation and migration, in NSCLC are unclear. Therefore, the present study focused on crizotinib's effect on NSCLC glucose metabolism. Crizotinib's effects on glucose metabolism, proliferation, migration and apoptosis in A549 cells were explored. Several other inhibitors, including 2-DG, rotenone and MG132, were used to define the mechanism of action in further detail. Data showed that crizotinib treatment reduced A549 cell viability, increased glucose consumption and lactate production, while decreased mitochondrial transmembrane potential (Δψm) and ATP production. Crizotinib treatment, combined with rotenone and MG132 treatment, further inhibited ATP production and Δψm and increased reactive oxygen species content. However, crizotinib did not suppress cell proliferation, migration, ATP production, Δψm or mitochondrial-related apoptosis signals further following 2-DG-mediated inhibition of glycolysis. These results indicated that crizotinib induced low mitochondrial function and compensatory high anaerobic metabolism, but failed to maintain sufficient ATP levels. The alternation of metabolic pattern and insufficient ATP supply may serve important roles in the metabolic antitumor mechanism of crizotinib in A549 cells.

Author Correction: Eosinophil differentiation in the bone marrow is promoted by protein tyrosine phosphatase SHP2.

Since the publication of the article, the authors became aware that Figs. 1c, 5k and 6m contained errors in representative image and PAS score in control groups. The corrected Figs. 1c, 5k, and 6m are given below, and the figure legends are the same as original.

MTOR Suppresses Cigarette Smoke-Induced Epithelial Cell Death and Airway Inflammation in Chronic Obstructive Pulmonary Disease.

Airway epithelial cell death and inflammation are pathological features of chronic obstructive pulmonary disease (COPD). Mechanistic target of rapamycin (MTOR) is involved in inflammation and multiple cellular processes, e.g., autophagy and apoptosis, but little is known about its function in COPD pathogenesis. In this article, we illustrate how MTOR regulates cigarette smoke (CS)-induced cell death, airway inflammation, and emphysema. Expression of MTOR was significantly decreased and its suppressive signaling protein, tuberous sclerosis 2 (TSC2), was increased in the airway epithelium of human COPD and in mouse lungs with chronic CS exposure. In human bronchial epithelial cells, CS extract (CSE) activated TSC2, inhibited MTOR, and induced autophagy. The TSC2-MTOR axis orchestrated CSE-induced autophagy, apoptosis, and necroptosis in human bronchial epithelial cells; all of which cooperatively regulated CSE-induced inflammatory cytokines IL-6 and IL-8 through the NF-κB pathway. Mice with a specific knockdown of Mtor in bronchial or alveolar epithelial cells exhibited significantly augmented airway inflammation and airspace enlargement in response to CS exposure, accompanied with enhanced levels of autophagy, apoptosis, and necroptosis in the lungs. Taken together, these data demonstrate that MTOR suppresses CS-induced inflammation and emphysema-likely through modulation of autophagy, apoptosis, and necroptosis-and thus suggest that activation of MTOR may represent a novel therapeutic strategy for COPD.

Lentivirus-mediated disintegrin and metalloproteinase 17 RNA interference reversed the acquired resistance to gefitinib in lung adenocarcinoma cells in vitro.

OBJECTIVE: The aim of the study is to evaluate the effects of silencing a disintegrin and metalloproteinase 17 (ADAM17) gene expression by lentivirus-mediated RNA interference (RNAi) in the gefitinib-resistant lung adenocarcinoma cells, and then to explore whether the recombinant lentivirus mediated ADAM17 RNAi reversed the acquired resistance of lung adenocarcinoma to gefitinib in vitro. METHODS: The gefitinib-resistant RPC-9 cells were established and the mutations of EGFR were detected by gene sequencing. The ADAM17 shRNA expression vectors were constructed and packaged to recombinant lentivirus. The cell proliferation viability was detected by MTT, and cellular apotosis was analyzed by flow cytometry assay. The expression levels of ADAM17, EGFR and the phosphorylated EGFR were respectively detected by reverse transcription polymerase chain reaction and western blot. TGF-α production in the supernatant was detected by enzyme-linked immunosorbent assay. RESULTS: The gefitinib-resistant RPC-9 cells in which mutated EGFR (exon 20) carried 790T > T/M mutation were established. When the concentrations of gefitinib were less than 10µmol/L, there were no significant changes in the apoptosis and cellular proliferation of RPC-9 with the dose-escalation of gefitinib. The cell proliferation viability of RPC-9 was significantly decreased by lentivirus mediated ADAM17 RNAi (P < 0.05). Gefitinib did not inhibit ADAM17 expression in both the gefitinib-sensitive PC-9 and gefitinib-resistant RPC-9 cells (P > 0.05). Gefitinib had no significant effects on TGF alpha production in the supernatants (P > 0.05). Gefitinib did not inhibit EGFR expression in gefitinib-sensitive PC-9 and gefitinib-resistant RPC-9 cells (P > 0.05). The phosphorylation of EGFR in gefitinib-sensitive PC-9 cells was significantly inhibited by gefitinib (P < 0.05), but that in gefitinib-resistant RPC-9 could not be inhibited by gefitinib (P > 0.05). Lentivirus mediated ADAM17 RNAi significantly inhibited the mRNA and protein expression of ADAM17 in gefitinib-resistant RPC-9 cells (P < 0.05), as well as TGF alpha production in the supernatants (P < 0.05). Also, the phosphorylation of EGFR was significantly reduced in gefitinib-resistant RPC-9 cells by lentivirus mediated ADAM17 RNAi (P < 0.05); however, the mRNA and protein expression of EGFR could not be inhibited. CONCLUSION: Lentivirus mediated ADAM17 RNAi may reverse the acquired resistance of lung adenocarcinoma to gefitinib via inhibiting the upstream of EGFR signal pathway, which may provide a new therapeutic target to solve the acquired resistance to EGFR tyrosine kinase inhibitors in lung adenocarcinoma. © 2017 American Institute of Chemical Engineers Biotechnol. Prog., 34:196-205, 2018.

Efficacy and safety of benralizumab for eosinophilic asthma: A systematic review and meta-analysis of randomized controlled trials.

CONTEXT: Benralizumab is a humanized monoclonal antibody that targets the α chain of the IL-5 receptor (IL-5Rα) and is currently being assessed in clinical trials for asthma control. OBJECTIVE: Our systematic review and meta-analysis intends to evaluate the therapeutic efficacy and safety of benralizumab in patients with eosinophilic asthma. DATA SOURCES AND EXTRACTION: Literature searches of PubMed, Embase, and the Cochrane Library were performed to identify randomized controlled trials of benralizumab and clinic outcomes in asthmatics. RESULTS: In total, 7 articles with 2,321 subjects met our inclusion criteria. From this pooled analysis, we found that benralizumab significantly reduces exacerbations (RR: 0.63, 95% CI: 0.52-0.76, p < 0.00001; I2 = 52%, p = 0.06) compared to placebo in eosinophilic asthma. There was no statistical trend for improvement in forced expiratory volume in 1 second or asthma control indices such as Quality of Life Assessment (AQLQ) and Asthma Control Questionnaire score in benralizumab-treated patients. In addition, safety data indicated that benralizumab administration resulted no increasing incidence of adverse events and was well tolerated (RR: 1.00, 95% CI: 0.95-1.05, p = 0.96; I2 = 40%, p = 0.13). CONCLUSION: These results demonstrate the efficacy and safety of benralizumab for asthma patients with severe or uncontrolled symptoms and elevated eosinophils and provide support for benralizumab as an ideal option to treat asthma in this patient population.

Activating Transcription Factor 3 Is Essential for Cigarette Smoke-Induced Mucin Expression via Interaction with Activator Protein-1.

Mucus hypersecretion is an important pathologic feature of chronic obstructive pulmonary disease. Activating transcription factor 3 (ATF3) is an adaptive-response gene that participates in various cellular processes. However, little is known about its role in cigarette smoke (CS)-induced mucus hyperproduction. This study aimed to investigate the role and molecular mechanisms of ATF3 in CS-induced Mucin 5AC (MUC5AC) expression. ATF3 was elevated in lung tissues of mice exposed to CS for 12 weeks. Treatment with CS extract significantly induced ATF3 expression and MUC5AC production in human bronchial epithelial cells, NCI-H292, and mouse tracheal epithelial cells. Interference of ATF3 significantly attenuated CS-induced MUC5AC expression in NCI-H292 and human bronchial epithelial cells. Mouse tracheal epithelial cells isolated from Atf3-/- mice also exhibited less MUC5AC production in response to CS extract treatment. In vivo, the Atf3-/- mice also displayed a significantly reduced mucus production relative to wild-type controls in response to chronic CS exposure. Furthermore, a chromatin immunoprecipitation assay revealed increased ATF3 binding to the MUC5AC promoter after CS treatment, and this transcriptional binding was significantly inhibited by knockdown of JUN, a subunit of activator protein-1. These results demonstrate that ATF3 may be involved in activator protein-1 signaling and transcriptional promotion of CS-induced MUC5AC expression in airway epithelial cells.

Autophagy plays an essential role in cigarette smoke-induced expression of MUC5AC in airway epithelium.

Mucus hypersecretion is a common pathological feature of chronic airway inflammatory diseases including chronic obstructive pulmonary disease (COPD). However, the molecular basis for this condition remains incompletely understood. We have previously demonstrated a critical role of autophagy in COPD pathogenesis through mediating apoptosis of lung epithelial cells. In this study, we aimed to investigate the function of autophagy as well as its upstream and downstream signals in cigarette smoke-induced mucus production in human bronchial epithelial (HBE) cells and in mouse airways. Cigarette smoke extract (CSE), as well as the classical autophagy inducers starvation or Torin-1, significantly triggered MUC5AC expression, and inhibition of autophagy markedly attenuated CSE-induced mucus production. The CSE-induced autophagy was mediated by mitochondrial reactive oxygen species (mitoROS), which regulated mucin expression through the JNK and activator protein-1 pathway. Epidermal growth factor receptor (EGFR) was also required for CSE-induced MUC5AC in HBE cells, but it exerted inconsiderable effects on the autophagy-JNK signaling cascade. Airways of mice with dysfunctional autophagy-related genes displayed a markedly reduced number of goblet cells and attenuated levels of Muc5ac in response to cigarette smoke exposure. These results altogether suggest that mitoROS-dependent autophagy is essential for cigarette smoke-induced mucus hyperproduction in airway epithelial cells, and reemphasize autophagy inhibition as a novel therapeutic strategy for chronic airway diseases.

Parallel microscope-based fluorescence, absorbance and time-of-flight mass spectrometry detection for high performance liquid chromatography and determination of glucosamine in urine.

A parallel microscope-based laser-induced fluorescence (LIF), ultraviolet-visible absorbance (UV) and time-of-flight mass spectrometry (TOF-MS) detection for high performance liquid chromatography (HPLC) was achieved and used to determine glucosamine in urines. First, a reliable and convenient LIF detection was developed based on an inverted microscope and corresponding modulations. Parallel HPLC-LIF/UV/TOF-MS detection was developed by the combination of preceding Microscope-based LIF detection and HPLC coupled with UV and TOF-MS. The proposed setup, due to its parallel scheme, was free of the influence from photo bleaching in LIF detection. Rhodamine B, glutamic acid and glucosamine have been determined to evaluate its performance. Moreover, the proposed strategy was used to determine the glucosamine in urines, and subsequent results suggested that glucosamine, which was widely used in the prevention of the bone arthritis, was metabolized to urines within 4h. Furthermore, its concentration in urines decreased to 5.4mM at 12h. Efficient glucosamine detection was achieved based on a sensitive quantification (LIF), a universal detection (UV) and structural characterizations (TOF-MS). This application indicated that the proposed strategy was sensitive, universal and versatile, and it was capable of improved analysis, especially for analytes with low concentrations in complex samples, compared with conventional HPLC-UV/TOF-MS.

Nuclear erythroid 2 p45-related factor-2 Nrf2 ameliorates cigarette smoking-induced mucus overproduction in airway epithelium and mouse lungs.

BACKGROUND AND OBJECTIVE: Nuclear erythroid 2 p45-related factor-2 (Nrf2) is known to play important roles in airway disorders, whereas little has been investigated about its direct role in airway mucus hypersecretion. The aim of this study is to determine whether this factor could protect pulmonary epithelium and mouse airway from cigarette-induced mucus overproduction. METHODS: Using genetic approaches, the role of Nrf2 on cigarette smoking extracts (CSE) induced MUC5AC expression was investigated in lung A549 cells. Nrf2 deficiency mice were smoked for various periods, and the airway inflammation and mucus production was characterized. RESULTS: Acute smoking exposure induced expression of MUC5AC and Nrf2 in both A549 cells and mouse lungs. Genetic ablation of Nrf2 augmented, whereas overexpression of this molecule ameliorated CSE-induced expression of MUC5AC. Nrf2 knockout mice, after exposure to cigarette smoking, displayed enhanced airway inflammation and mucus production. CONCLUSION: Nrf2 negatively regulated smoking-induced mucus production in vitro and in vivo, suggesting therapeutic potentials of this factor in airway diseases with hypersecreted mucus.

Balance of apoptotic cell death and survival in allergic diseases.

Allergic diseases result from over-reaction of the immune system in response to exogenous allergens, where inflammatory cells have constantly extended longevity and contribute to an on-going immune response in allergic tissues. Here, we review disequilibrium in the death and survival of epithelial cells and inflammatory cells in the pathological processes of asthma, atopic dermatitis, and other allergic diseases.

[Effect and mechanism of ropivacaine on the isolated human umbilical artery].

OBJECTIVE: To investigation the effect of ropivacaine on the contraction of the isolated human umbilical artery and the mechanisms involved. METHODS: Endothelium-denuded human umbilical artery rings obtained from healthy full-term parturients were prepared. Using isometric force transducers and a fluorometer, the effect of ropivacaine in cumulative concentration on the contraction response induced by KCl in the presence or absence of verapamil, or verapamil plus ruthenium red or verapamil plus heparin was observed. Furthermore, the effect of ropivacaine on the contraction response of the artery rings incubated in different concentrations of extracellular Ca(2+) was also observed. RESULTS: Ropivacaine induced a dose-dependent biphasic contractile response of human umbilical artery rings: increasing at concentrations of 1.0 x 10(-5) to 1.0 x 10(-4) mol/L and decreasing from 3.0 x 10(-4) to 3.0 x 10(-3) mol/L, which was inhibited by verapamil, or verapamil plus ruthenium red, or verapamil plus heparin. No difference was found between pre-treatment of verapamil, verapamil plus ruthenium red and verapamil plus heparin. Ropivacaine induced no contractile response in Ca(2+)-free solution and a extracellular Ca(2+) dose-dependent increasing contractile response (1.0 x 10(-4) to 3.0 x 10(-2) mol/L). CONCLUSION: Ropivacaine induced a dose-dependent biphasic contractile response of human umbilical artery rings. The increase in intracellular Ca(2+) concentrations by the extracellular Ca(2+) influx, not by the release from the sarcoplasmic reticulum, is involved in ropivacaine-induced vasoconstriction of human umbilical artery smooth muscle.

[Research on detection of Vibrio comma and Vibro parahaemolyticus from foodstuffs using MPCR methods].

OBJECTIVE: To establish a set of multi-PCR (MPCR) methods to detect Vibrio comma O1 serogroup (EVC) and O139 serogroup, and Vibrio parahaemolyticus rapidly and sensitively from foodstuffs. METHODS: Using T139 (specific gene of O139 serogroup), ctxB and tcpA genes from V. comma, and tdh gene from V. parahaemolyticus as target sequences, we detected the anticipative amplified bands, whose sizes were relatively 417bp, 564bp, 471bp and 202bp. RESULTS: Excellent specificity of the amplified products could be found from both standard and wild strains of EVC, O139VC and V. parahaemolyticus. It also means that no amplified band was detected from total 35 strains of other bacilli, including salmonella, comma bacillus which do not belong to O1 and O139 serogroups. The detection limits of artificial contaminated samples such as tilapia flesh, oyster and mixture of tilapia intestines and gills were proved to be 22cfu/g in EVC, 50cfu/g in O139 and 65cfu/g in V. parahaemolyticus. Besides, it took only 8-10 hours to finish the whole process. CONCLUSION: Experiment results show that MPCR is a sensitive, convenient and time saving method suitable for detection.