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Aims: This research explored the effect of exogenous abscisic acid (ABA) treatment on sugar metabolism in tomato fruits, and provided theoretical basis for the regulation of ABA on the growth and development of tomato fruits. Study Design: The whole tomato plant was treated by spraying with 50 mg·L-1 ABA. Spraying distilled water was as the control. Place and Duration of Study: College of Biological Science and Technology, between February 2019 and March 2020. Methodology: The contents of soluble sugar in tomato fruits were measured with HPLC (High performance liquid chromatography). The enzyme extraction and activities were followed the biochemical method. Results: Exogenous ABA treatment reduced the weight and transverse meridians of the fruit at the ripening stage, but increased the contents of fructose, glucose and sucrose in the fruit. At the same time, it also increased the activities of acid invertase, neutral invertase, and sucrose phosphate synthase at the ripening stage. Conclusions: Exogenous ABA treatment was beneficial to the accumulation of sugar in tomato fruit and improved tomato quality. Therefore, it could be applied to tomato production.
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Cutaneous lesions are observed in approximately 25% of patients with systemic sarcoidosis. Scar sarcoidosis is a rare but peculiar cutaneous form of sarcoidosis associated with trauma, surgery, tattoos and other types of damage. We present a 32-year-old male patient with a history of unilateral facial nerve palsy, nephrolithiasis and lung involvement. A chest CT revealed multiple bilateral hilar and mediastinal lymphadenopathy and PET-CT demonstrated an inflammatory response in multiple organs and regions. Recently, the patient had developed asymptomatic papulo-nodules scattered within the areas of tattoos and previous trauma. Histopathological examination of nodules from those different areas supported the diagnosis of sarcoidosis. The lesions almost cleared after systemic therapy with oral prednisone. It is worth remembering that skin lesions in areas of tattoos and trauma may be prominent symptoms of systemic sarcoidosis. Patients with systemic sarcoidosis should avoid tattooing.
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Background: To investigate the occurrence and risk factors of acute kidney injury (AKI) in organ donors. Methods: Clinical data of 153 donor patients who donated organs in our hospital from January 2016 to July 2018 were collected. Patients were divided into AKI group and non-AKI group according to AKI diagnostic criteria. Clinical indicators of patients in the two groups were compared, and the related risk factors were analyzed by unifactorial and multivariate logistic regression. Results: The incidence of donor patients complicated with AKI was 48.37%. Unifactorial analysis suggested that the SOFA score, positive rate of blood culture, hypothermia incidence and vasoactive drug dose in donor AKI group were larger than those in non-AKI group. Multivariate Logistic regression analysis showed that the dose of booster drugs (P=0.02, OR=3.53) and the positive rate of blood culture (P=0.01, OR=6.64) were independent risk factors for donor patients complicated with AKI. Conclusion: The incidence of acute kidney injury in organ donors is high, with the dose of booster drugs and the positive rate of blood culture as independent risk factors for evaluation basis to assess the incidence rate of donor patients complicated with AKI.
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Occupational noise-induced hearing loss (ONIHL) is a prevalent occupational disorder that impairs auditory function in workers exposed to prolonged noise. However, serum microRNA expression in ONIHL subjects has not yet been studied. We aimed to compare the serum microRNA expression profiles in male workers of ONIHL subjects and controls. MicroRNA microarray analysis revealed that four serum microRNAs were differentially expressed between controls (n=3) and ONIHL subjects (n=3). Among these microRNAs, three were upregulated (hsa-miR-3162-5p, hsa-miR-4484, hsa-miR-1229-5p) and one was downregulated (hsa-miR-4652-3p) in the ONIHL group (fold change >1.5 and Pbon value <0.05). Real time quantitative PCR was conducted for validation of the microRNA expression. Significantly increased serum levels of miR-1229-5p were found in ONIHL subjects compared to controls (n=10 for each group; P<0.05). A total of 659 (27.0%) genes were predicted as the target genes of miR-1229-5p. These genes were involved in various pathways, such as mitogen-activated protein kinase (MAPK) signaling pathway. Overexpression of miR-1229-5p dramatically inhibited the luciferase activity of 3′ UTR segment of MAPK1 (P<0.01). Compared to the negative control, HEK293T cells expressing miR-1229-5p mimics showed a significant decline in mRNA levels of MAPK1 (P<0.05). This preliminary study indicated that serum miR-1229-5p was significantly elevated in ONIHL subjects. Increased miR-1229-5p may participate in the pathogenesis of ONIHL through repressing MAPK1 signaling.
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Humains , Mâle , Adulte , Adulte d'âge moyen , Exposition professionnelle/effets indésirables , Mitogen-Activated Protein Kinase 1/analyse , microARN/sang , Surdité due au bruit/sang , Maladies professionnelles/sang , Marqueurs biologiques/sang , Études cas-témoins , Régulation de l'expression des gènes , microARN/génétique , Réaction de polymérisation en chaine en temps réel , Gene Ontology , Surdité due au bruit/génétique , Maladies professionnelles/génétiqueRésumé
Ovarian cancer is one of the most common malignancies in women. Semaphorin 4D (sema 4D) is involved in the progress of multiple cancers. In the presence of estrogen-like ligands, estrogen receptors (ERα and ERβ) participate in the progress of breast and ovarian cancers by transcriptional regulation. The aim of the study was to investigate the role of sema 4D and elucidate the regulatory pattern of ERα and ERβ on sema 4D expression in ovarian cancers. Sema 4D levels were up-regulated in ovarian cancer SKOV-3 cells. Patients with malignant ovarian cancers had significantly higher sema 4D levels than controls, suggesting an oncogene role of sema 4D in ovarian cancer. ERα expressions were up-regulated in SKOV-3 cells compared with normal ovarian IOSE80 epithelial cells. Conversely, down-regulation of ERβ was observed in SKOV-3 cells. Forced over-expression of ERα and ERβ in SKOV-3 cells was manipulated to establish ERα+ and ERβ+ SKOV-3 cell lines. Incubation of ERα+ SKOV-3 cells with ERs agonist 17β-estradiol (E2) significantly enhanced sema 4D expression and rate of cell proliferation. Incubated with E2, ERβ+ SKOV-3 cells showed lower sema 4D expression and cell proliferation. Blocking ERα and ERβ activities with ICI182-780 inhibitor, sema 4D expressions and cell proliferation of ERα+ and ERβ+ SKOV-3 cells were recovered to control levels. Taken together, the data showed that sema 4D expression was positively correlated with the progress of ovarian cancer. ERα positively regulated sema 4D expression and accelerated cell proliferation. ERβ negatively regulated sema 4D expression and inhibited cell multiplication.
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Humains , Femelle , Récepteur alpha des oestrogènes/métabolisme , Récepteur bêta des oestrogènes/métabolisme , Tumeurs de l'ovaire/métabolisme , Sémaphorines/métabolisme , Marqueurs biologiques tumoraux/métabolisme , Prolifération cellulaire , Régulation négative , Sémaphorines/génétiqueRésumé
The aim of this study was to investigate whether exogenous retinoic acid (RA) can upregulate the mRNA and protein expression of growth-associated protein 43 (GAP-43), thereby promoting brain functional recovery in a rat distal middle cerebral artery occlusion (MCAO) model of ischemia. A total of 216 male Sprague Dawley rats weighing 300–320 g were divided into 3 groups: sham-operated group, MCAO+vehicle group and MCAO+RA group. Focal cortical infarction was induced with a distal MCAO model. The expression of GAP-43 mRNA and protein in the ipsilateral perifocal region was assessed using qPCR and immunocytochemistry at 1, 3, 7, 14, 21, and 28 days after distal MCAO. In addition, an intraperitoneal injection of RA was given 12 h before MCAO and continued every day until the animal was sacrificed. Following ischemia, the expression of GAP-43 first increased considerably and then decreased. Administration of RA reduced infarction volume, promoted neurological functional recovery and upregulated expression of GAP-43. Administration of RA can ameliorate neuronal damage and promote nerve regeneration by upregulating the expression of GAP-43 in the perifocal region after distal MCAO.
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Animaux , Mâle , Protéine GAP-43/métabolisme , Expression des gènes/effets des médicaments et des substances chimiques , Infarctus du territoire de l'artère cérébrale moyenne/prévention et contrôle , Neuroprotecteurs/pharmacologie , Trétinoïne/pharmacologie , Régulation positive/effets des médicaments et des substances chimiques , Encéphalopathie ischémique/prévention et contrôle , Protéine GAP-43/génétique , Immunohistochimie , Infarctus du territoire de l'artère cérébrale moyenne/métabolisme , Infarctus du territoire de l'artère cérébrale moyenne/anatomopathologie , Répartition aléatoire , Rat Sprague-Dawley , Réaction de polymérisation en chaine en temps réel , Reproductibilité des résultats , Facteurs tempsRésumé
Human enterovirus 71 (EV71) is the major causative agent of hand, foot, and mouth disease (HFMD), particularly in infants and children below 4 years of age. Shikonin is a bioactive compound with anti-inflammatory, antiviral, and antibacterial activities derived from the roots of the Chinese medicinal herb Lithospermum erythrorhizon. This study aimed to examine the antiviral activity of PMM-034, a shikonin ester derivative, against EV71 in rhabdomyosarcoma (RD) cells. Cytotoxicity of PMM-034 on RD cells was determined using WST-1 assay. Dose- and time-dependent effects of PMM-034 on EV71 replication in RD cells were determined using plaque reduction assay. mRNA expression levels of EV71/VP1 and pro-inflammatory cytokines (IL-1β, IL-6, IL-8, and TNF-α) were determined by real-time RT-PCR, and EV71/VP1 and phospho-p65 protein expressions were determined by western blot analysis. PMM-034 exhibited only weak cytotoxicity against RD cells. However, PMM-034 exhibited significant antiviral activity against EV71 in RD cells with 50% inhibitory concentration of 2.31 μg/mL. The VP1 mRNA and protein levels were significantly reduced in cells treated with PMM-034. Furthermore, relative mRNA expression levels of IL-1β, IL-6, IL-8, and TNF-α significantly decreased in the cells treated with PMM-034, while the phospho-p65 protein expression was also significantly lower in the treated cells. These results indicated that PMM-034 suppressed the expressions of pro-inflammatory cytokines in RD cells, exhibiting antiviral activity against EV71, as evidenced by the reduced VP1 mRNA and protein levels in PMM-034-treated cells. Thus, PMM-034 is a promising candidate for further development as an EV71 inhibitor.
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Humains , Antiviraux/pharmacologie , Entérovirus humain A/effets des médicaments et des substances chimiques , Naphtoquinones/pharmacologie , Rhabdomyosarcome/virologie , Technique de Western , Lignée cellulaire tumorale , Cytokines/analyse , Relation dose-effet des médicaments , Réaction de polymérisation en chaine en temps réel , Tests de toxicité , Méthode des plages virales , Réplication virale/effets des médicaments et des substances chimiquesRésumé
Increasing evidence suggests that the cerebrospinal fluid-contacting nucleus (CSF-contacting nucleus) mediates the transduction and regulation of pain signals. However, the precise molecular mechanisms remain unclear. Studies show that release of fractalkine (FKN) from neurons plays a critical role in nerve injury-related pain. We tested the hypothesis that release of FKN from the CSF-contacting nucleus regulates neuropathic pain, in a chronic constriction injury rat model. The results show that FKN is expressed by neurons, via expression of its only receptor CX3CR1 in the microglia. The levels of soluble FKN (sFKN) were markedly upregulated along with the increase in FKN mRNA level in rats subjected to chronic constriction injury. In addition, injection of FKN-neutralizing antibody into the lateral ventricle alleviated neuropathic pain-related behavior followed by reduction in microglial activation in the CSF-contacting nucleus. The results indicate that inhibition of FKN release by the CSF-contacting nucleus may ameliorate neuropathic pain clinically.
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Animaux , Mâle , Rats , Noyau de la cellule/métabolisme , Liquide cérébrospinal/métabolisme , Seuil nociceptif/physiologie , Chimiokine CX3CL1/métabolisme , Douleur chronique/métabolisme , Névralgie/métabolisme , Régulation positive , Rat Sprague-Dawley , Modèles animaux de maladie humaine , Injections ventriculairesRésumé
We investigated the diagnostic value of the apparent diffusion coefficient (ADC) and fractional anisotropy (FA) of magnetic resonance diffusion tensor imaging (DTI) in patients with spinal cord compression (SCC) using a meta-analysis framework. Multiple scientific literature databases were exhaustively searched to identify articles relevant to this study. Mean values and standardized mean differences (SMDs) were calculated for the ADC and FA in normal and diseased tissues. The STATA version 12.0 software was used for statistical analysis. Of the 41 articles initially retrieved through database searches, 11 case-control studies were eligible for the meta-analysis and contained a combined total of 645 human subjects (394 patients with SCC and 251 healthy controls). All 11 studies reported data on FA, and 9 contained data related to the ADC. The combined SMDs of the ADC and FA showed that the ADC was significantly higher and the FA was lower in patients with SCC than in healthy controls. Subgroup analysis based on the b value showed higher ADCs in patients with SCC than in healthy controls at b values of both ≤500 and >500 s/mm2. In summary, the main findings of this meta-analysis revealed an increased ADC and decreased FA in patients with SCC, indicating that DTI is an important diagnostic imaging tool to assess patients suspected to have SCC.
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Humains , Syndrome de compression médullaire/diagnostic , Imagerie par résonance magnétique de diffusion/méthodes , Imagerie par tenseur de diffusion/méthodes , Études cas-témoins , Anisotropie , Biais de publication , Diagnostic précoce , Exactitude des donnéesRésumé
Bipolar disorder (BD) is a common psychiatric mood disorder affecting more than 1-2% of the general population of different European countries. Unfortunately, there is no objective laboratory-based test to aid BD diagnosis or monitor its progression, and little is known about the molecular basis of BD. Here, we performed a comparative proteomic study to identify differentially expressed plasma proteins in various BD mood states (depressed BD, manic BD, and euthymic BD) relative to healthy controls. A total of 10 euthymic BD, 20 depressed BD, 15 manic BD, and 20 demographically matched healthy control subjects were recruited. Seven high-abundance proteins were immunodepleted in plasma samples from the 4 experimental groups, which were then subjected to proteome-wide expression profiling by two-dimensional electrophoresis and matrix-assisted laser desorption/ionization-time-of-flight/time-of-flight tandem mass spectrometry. Proteomic results were validated by immunoblotting and bioinformatically analyzed using MetaCore. From a total of 32 proteins identified with 1.5-fold changes in expression compared with healthy controls, 16 proteins were perturbed in BD independent of mood state, while 16 proteins were specifically associated with particular BD mood states. Two mood-independent differential proteins, apolipoprotein (Apo) A1 and Apo L1, suggest that BD pathophysiology may be associated with early perturbations in lipid metabolism. Moreover, down-regulation of one mood-dependent protein, carbonic anhydrase 1 (CA-1), suggests it may be involved in the pathophysiology of depressive episodes in BD. Thus, BD pathophysiology may be associated with early perturbations in lipid metabolism that are independent of mood state, while CA-1 may be involved in the pathophysiology of depressive episodes.
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Adolescent , Adulte , Femelle , Humains , Mâle , Jeune adulte , Apolipoprotéine A-I/sang , Apolipoprotéines/sang , Trouble bipolaire/sang , Carbonic anhydrase I/sang , Troubles du métabolisme lipidique/métabolisme , Lipoprotéines HDL/sang , Protéomique , Trouble bipolaire/complications , Trouble bipolaire/diagnostic , Bases de données de protéines , Diagnostic différentiel , Évolution de la maladie , Régulation négative , Trouble dépressif majeur/diagnostic , Électrophorèse bidimensionnelle sur gel , Immunotransfert , Immunoprécipitation , Troubles du métabolisme lipidique/complications , Spectrométrie de masse/méthodesRésumé
Hormesis is an adaptive response to a variety of oxidative stresses that renders cells resistant to harmful doses of stressing agents. Caffeic acid (CaA) is an important antioxidant that has protective effects against DNA damage caused by reactive oxygen species (ROS). However, whether CaA-induced protection is a hormetic effect remains unknown, as is the molecular mechanism that is involved. We found that a low concentration (10 μM) of CaA increased human liver L-02 cell viability, attenuated hydrogen peroxide (H2O2)-mediated decreases in cell viability, and decreased the extent of H2O2-induced DNA double-strand breaks (DSBs). In L-02 cells exposed to H2O2, CaA treatment reduced ROS levels, which might have played a protective role. CaA also activated the extracellular signal-regulated kinase (ERK) signal pathway in a time-dependent manner. Inhibition of ERK by its inhibitor U0126 or by its specific small interfering RNA (siRNA) blocked the CaA-induced improvement in cell viability and the protective effects against H2O2-mediated DNA damage. This study adds to the understanding of the antioxidant effects of CaA by identifying a novel molecular mechanism of enhanced cell viability and protection against DNA damage.
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Humains , Antioxydants/pharmacologie , Acides caféiques/pharmacologie , Survie cellulaire/effets des médicaments et des substances chimiques , Altération de l'ADN/effets des médicaments et des substances chimiques , Extracellular Signal-Regulated MAP Kinases/effets des médicaments et des substances chimiques , Espèces réactives de l'oxygène/analyse , Analyse de variance , Technique de Western , Cellules cultivées , Lignée cellulaire/effets des médicaments et des substances chimiques , Extracellular Signal-Regulated MAP Kinases/antagonistes et inhibiteurs , Foie , Stress oxydatif/effets des médicaments et des substances chimiques , Reproductibilité des résultats , Facteurs tempsRésumé
The present study investigated the effect of silibinin, the principal potential anti-inflammatory flavonoid contained in silymarin, a mixture of flavonolignans extracted from Silybum marianum seeds, on palmitate-induced insulin resistance in C2C12 myotubes and its potential molecular mechanisms. Silibinin prevented the decrease of insulin-stimulated 2-NBDG (2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-D-glucose) uptake and the downregulation of glutamate transporter type 4 (GLUT4) translocation in C2C12 myotubes induced by palmitate. Meanwhile, silibinin suppressed the palmitate-induced decrease of insulin-stimulated Akt Ser473 phosphorylation, which was reversed by wortmannin, a specific inhibitor of phosphatidylinositol-3-kinase (PI3K). We also found that palmitate downregulated insulin-stimulated Tyr632 phosphorylation of insulin receptor substrate 1 (IRS-1) and up-regulated IRS-1 Ser307 phosphorylation. These effects were rebalanced by silibinin. Considering several serine/threonine kinases reported to phosphorylate IRS-1 at Ser307, treatment with silibinin downregulated the phosphorylation of both c-Jun N-terminal kinase (JNK) and nuclear factor-κB kinase β (IKKβ), which was increased by palmitate in C2C12 myotubes mediating inflammatory status, whereas the phosphorylation of PKC-θ was not significantly modulated by silibinin. Collectively, the results indicated that silibinin prevented inhibition of the IRS-1/PI3K/Akt pathway, thus ameliorating palmitate-induced insulin resistance in C2C12 myotubes.
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Adulte , Sujet âgé , Humains , Adulte d'âge moyen , État de porteur sain/épidémiologie , État de porteur sain/microbiologie , Staphylococcus aureus résistant à la méticilline/isolement et purification , Infections à staphylocoques/diagnostic , Répartition par âge , Canal anal/microbiologie , Infection croisée/prévention et contrôle , Infections à VIH/microbiologie , Analyse multifactorielle , Muqueuse nasale/microbiologie , Facteurs de risque , Sensibilité et spécificité , Singapour/épidémiologie , Peau/microbiologie , Infections à staphylocoques/prévention et contrôleRésumé
Necrotizing enterocolitis (NEC) is one of the most common acquired diseases of the gastrointestinal tract in preterm infants. Some randomized, controlled trials (RCTs) have indicated that probiotics may potentially lower the incidence of NEC and mortality. However, debate still remains about the safety of probiotics and their influence on normal infant growth. We performed this meta-analysis to assess the safety and benefits of probiotic supplementation in preterm infants. We searched in PubMed, Embase, and Cochrane databases for English references, and in Wanfang, VIP, and CNKI databases for Chinese references. Ultimately, 27 RCTs (including 9 Chinese articles) were incorporated into this meta-analysis. Relative risk (RR) and weighted mean difference (WMD) were calculated using a random-effects or fixed-effects model, depending on the data type and heterogeneity. A total of 6655 preterm infants, including the probiotic group (n=3298) and the placebo group (n=3357), were eligible for inclusion in this meta-analysis. For Bell stage ≥I and gestational age <37 weeks, risk of NEC incidence was significantly lower in the probiotic group [RR=0.35, 95% confidence interval (CI)=0.27-0.44, P<0.00001]. For Bell stage ≥II or gestational age <34 weeks, there were likewise significant differences between the probiotic and placebo groups concerning NEC incidence (RR=0.34, 95%CI=0.25-0.48, P<0.00001; and RR=0.39, 95%CI=0.27-0.56, P<0.00001). Risk of death was significantly reduced in the probiotic group (RR=0.58, 95%CI=0.46-0.75, P<0.0001). In contrast, there was no significant difference concerning the risk of sepsis (RR=0.94, 95%CI=0.83-1.06, P=0.31). With respect to weight gain and the age at which infants reached full feeds, no significant differences were found between the probiotic and placebo groups (WMD=1.07, 95%CI=−0.21-2.34, P=0.10; and WMD=−1.66, 95%CI=−3.6-0.27, P=0.09). This meta-analysis has shown that, regardless of gestational age and NEC stage, probiotic supplementation could significantly reduce the risk of NEC in preterm infants. Analysis also indicated that such supplementation did not increase the incidence risk of sepsis or of mortality. Finally, the study showed that probiotic supplementation may have no adverse effect on normal feeding and growth.
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Humains , Nouveau-né , Entérocolite nécrosante/prévention et contrôle , Prématuré/croissance et développement , Probiotiques/usage thérapeutique , Bases de données bibliographiques , Entérocolite nécrosante/mortalité , Sécurité des aliments , Âge gestationnel , Biais de publication , Probiotiques/effets indésirables , Essais contrôlés randomisés comme sujet , Sepsie/étiologie , Sepsie/prévention et contrôle , Prise de poidsRésumé
SRY-related high-mobility-group box 9 (Sox9) gene is a cartilage-specific transcription factor that plays essential roles in chondrocyte differentiation and cartilage formation. The aim of this study was to investigate the feasibility of genetic delivery of Sox9 to enhance chondrogenic differentiation of human umbilical cord blood-derived mesenchymal stem cells (hUC-MSCs). After they were isolated from human umbilical cord blood within 24 h after delivery of neonates, hUC-MSCs were untreated or transfected with a human Sox9-expressing plasmid or an empty vector. The cells were assessed for morphology and chondrogenic differentiation. The isolated cells with a fibroblast-like morphology in monolayer culture were positive for the MSC markers CD44, CD105, CD73, and CD90, but negative for the differentiation markers CD34, CD45, CD19, CD14, or major histocompatibility complex class II. Sox9 overexpression induced accumulation of sulfated proteoglycans, without altering the cellular morphology. Immunocytochemistry demonstrated that genetic delivery of Sox9 markedly enhanced the expression of aggrecan and type II collagen in hUC-MSCs compared with empty vector-transfected counterparts. Reverse transcription-polymerase chain reaction analysis further confirmed the elevation of aggrecan and type II collagen at the mRNA level in Sox9-transfected cells. Taken together, short-term Sox9 overexpression facilitates chondrogenesis of hUC-MSCs and may thus have potential implications in cartilage tissue engineering.
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Humains , Différenciation cellulaire/génétique , Chondrogenèse/génétique , Sang foetal/cytologie , Cellules souches mésenchymateuses/cytologie , Facteur de transcription SOX-9/génétique , Agrécanes/biosynthèse , Technique de Western , Cartilage/métabolisme , Prolifération cellulaire/génétique , Chondrocytes/métabolisme , Collagène de type II/biosynthèse , Cytométrie en flux , Protéines à fluorescence verte , Régulation de l'expression des gènes/physiologie , Cellules endothéliales de la veine ombilicale humaine/cytologie , Immunohistochimie , Immunophénotypage , Culture de cellules primaires , RT-PCR , Ingénierie tissulaire , TransfectionRésumé
INTRODUCTION: Angiogenesis plays an important role in the biology of ovarian cancer. The clinical efficacy and side effects of bevacizumab, the vascular endothelial growth factor inhibitor, on survival and toxicity in women with this ovarian cancer, was not conclusive. We performed this systematic review and meta‑analysis in order to clarify the efficacy of bevacizumab combined with chemotherapy in the treatment of ovarian cancer. MATERIALS AND METHODS: We searched the electronic database of MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials and CNKI for clinical controlled trials of comparing bevacizumab combined with chemotherapy and chemotherapy alone in the treatment of ovarian cancer. The primary outcomes of eligible studies included median progression‑free survival (PFS), overall survival (OS), and toxicities such as enterobrosis, hypertension, albuminuria, congestive heart failure (CHF), neutrophils, thrombosis, and bleeding. The Hazard ratio (HR) and relative risk were used for the meta‑analysis and were expressed with 95% confidence intervals (CIs). All the statistical analyses were carried out by Stata 11.0 software (http://www.stata.com; Stata Corporation, College Station, TX, USA). RESULTS: We included 5 studies with 1798 cases in the bevacizumab combined with the chemotherapy group and 1810 subjects in the chemotherapy alone group. The pooled results showed that bevacizumab + chemotherapy compared with chemotherapy alone can significant prolong the median PFS (HR, 0.64; 95% CI, 0.46–0.82; P < 0.05) but not the OS (HR, 0.84; 95% CI, 0.59–10.9; P > 0.05); the toxicity analysis showed that the enterobrosis, hypertension, albuminuria, neutrophils, thrombosis, and bleeding were significantly increased in the bevacizumab + chemotherapy group compared with chemotherapy alone (Pall < 0.05). But the CHF risk between the two groups was not statistical different (P > 0.05). CONCLUSION: Bevacizumab combined with chemotherapy prolonged the median PFS in patients with ovarian cancer but also increase the risk of developing enterobrosis, hypertension, albuminuria, neutrophils, thrombosis, and bleeding.
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OBJECTIVE: This study aims to explore the chemokine receptor 7 (CCR7) expression of spleen dendritic cells (DCs) and their role in the changes of migration and activity of spleen DCs in multiple-organ dysfunction syndrome (MODS). METHODS: The MODS model of mice was reproduced. The mice were randomly assigned to the following groups: normal, three-hour to six-hour, 24-hour to 48-hour, and 10-day to 12-day postzymosan injection. CD11c and CD205 were analysed by immunohistochemistry; the expressions of CD86 and CCR7 of DCs were studied using flow cytometry analyses. RESULTS: In normal mice, many DCs were found at the margin between the red and white pulp. In the three-hour to six-hour and 24- to 48-hour group, DC effectively upregulated CD86 and CCR7, and they were distributed in T-cell areas. In the 10-day to 12-day group, DCs were distributed at the margin by the immature form. CONCLUSION: The CCR7 expression level of DCs had close correlations with the migration of DCs. Chemokine receptor 7 can be used to evaluate the migration and functional activity of DCs in MODS.
OBJETIVO: Este estudio persigue explorar la expresión del receptor de la quimiocina 7 (CCR7) de células dendríticas del bazo (CD), y su papel en los cambios de la migración y la actividad del las células DC del bazo en el síndrome de disfunción orgánica múltiple (SDOM). MÉTODOS: Se reprodujo el modelo SDOM de los ratones. Los ratones fueron asignados aleatoriamente a los siguientes grupos de inyección de post-zymosan: hora normal, tres a seis horas, 24 horas a 48 horas, y de 10 a 12 días. CD11c y CD205 fueron analizados mediante inmunohistoquímica. Las expresiones de CD86 y CCR7 de CD se estudiaron mediante análisis de citometría de flujo. RESULTADOS: En los ratones normales, muchas células CD fueron encontradas en el margen entre la pulpa roja y la blanca. En el grupo de tres a seis horas y el grupo de 24 a 48 horas, CD86y CCR7 fueron efectivamente sobre-regulados en CD, y distribuidos en las áreas de células T. En el grupo de 10 a 12 días, las CDs fueron distribuidas en el margen por la forma inmadura. CONCLUSIÓN: El nivel de expresión CCR7 de las CDs tuvo estrecha correlación con la migración de las CDs. El receptor de la quimiocina de tipo 7 puede utilizarse para evaluar la migración y la actividad funcional de las CDs en SDOM.
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Animaux , Mâle , Souris , Rate/cytologie , Cellules dendritiques/immunologie , Récepteurs aux chimiokines/immunologie , Défaillance multiviscérale/anatomopathologie , Immunohistochimie , Mouvement cellulaire , Modèles animaux de maladie humaine , Souris de lignée C57BL , Défaillance multiviscérale/immunologieRésumé
To find Epstein-Barr virus (EBV) strains with genetic variations of EBV latent membrane protein 1 (EBV-LMP1) from nasopharyngeal carcinoma (NPC), the full-length DNA of LMP1 genes from 21 NPC biopsies obtained in Hunan province in southern China was amplified and sequenced. Our sequences were compared to those previously reported by the Clustal V method. Results showed that all 21 sequences displayed two amino acid changes most frequently in LMP1 of CD4+ T cell epitopes at codons 144 (F arrow right I, 21/21) and 212 (G arrow right S, 19/21) or (G arrow right N, 2/21). We also show that type A EBV strain is prevalent in the cases of NPC from Hunan province with a 30-bp 18/21 deletion, and we highlight that this deletion resulted in loss of one of the CD4+ T cell-restricted epitopes. The other 3 sequences without this deletion all had a change at codon 344 (G arrow right D). Furthermore, in the major epitope sequence of CD8+ T cells restricted by HLA-A2, all 21 sequences showed changes at codons 126 (L arrow right F) and 129 (M arrow right I). Our study discovered that one of the 21 sequence variations harbored a new change at codon 131 (W arrow right C), and 5/21 specimens showed another novel change at codon 115 (G arrow right A) in the major epitope sequence of CD8+ T cells restricted by HLA-A2. Our study suggests that these sequence variations of NPC-derived LMP1 may lead to a potential escape from host cell immune recognition, protecting latent EBV infection and causing an increase in tumorigenicity.
Sujets)
Adulte , Femelle , Humains , Mâle , Adulte d'âge moyen , Déterminants antigéniques des lymphocytes T/génétique , Variation génétique , /génétique , Tumeurs du rhinopharynx/virologie , Protéines de la matrice virale/génétique , Séquence d'acides aminés , Biopsie , Déterminants antigéniques des lymphocytes T/analyse , Génotype , Réaction de polymérisation en chaîne , Analyse de séquence d'ADNRésumé
BACKGROUND & OBJECTIVES: The goal of the present study was to improve and simplify the diagnosis of Streptococcus agalactiae (group B Streptococcus, GBS) infection for routine clinical practice. METHODS: A total of 71 clinical samples were tested by microbiologic culture, counter immunoelectrophoresis (CIE) and PCR described in the literature. Southern hybridization was accomplished with the Enzo(TM) "DNA Labeling and Detection Kit", Roche (Germany). The computer techniques were used for selection of the specific primers and for analysis of the sizes of PCR products. RESULTS: The primers for the regions around the 51 bp deletion in C5a peptidase gene (scpB) of GBS were selected. PCR analysis revealed the 255 bp amplification fragment in GBS, 306 bp fragment in groups A and G streptococci (GAS, GGS) and did not reveal any fragments in other bacterial species. Among 71 urine and serum clinical samples tested, none were found to be GBS positive by microbiologic culture, 16 samples by CIE, 36 by PCR. The specificity of amplification was confirmed by Southern hybridization. INTERPRETATION & CONCLUSION: The 51 bp deletion in scpB gene in comparison with scpA and scpG genes can be used as a diagnostic tool for identification of GBS. The 51 bp deletion based PCR proved to be faster and more reliable test than microbiologic culture or CIE.
Sujets)
Adhésines bactériennes/génétique , Séquence nucléotidique , Amorces ADN , Endopeptidases/génétique , Femelle , Gènes bactériens , Humains , Réaction de polymérisation en chaîne/méthodes , Grossesse , Infections à streptocoques/diagnostic , Streptococcus agalactiae/génétiqueRésumé
Allergic rhinitis is a common disease in children, and antihistamines are the key medication. However, traditional tablets are not convenient and lead to low compliance in young children. The aim of this double-blind, placebo-controlled, parallel, randomized study was to evaluate the effectiveness and safety of loratadine syrup for the treatment of children aged 3 to 12 years with allergic rhinitis. Sixty children with allergic rhinitis due to dust mites were enrolled. They were randomized into 2 parallel groups: one group received loratadine syrup 5 mg or 10 mg daily for 3 weeks, and the other group received placebo. The patients returned to special clinics for symptoms evaluation at day 7 and day 21, and the parents were requested to record disease severity daily. Both evaluations, physician's and parents', were recorded with a 4-point scale for 5 symptoms: sneezing, rhinorrhea, nasal congestion, nasal itching and ocular symptoms. Forty-six patients completed the study, 22 in the loratadine group and 24 in the placebo group. At the initial visit, the total symptom score (TSS) in both groups was not significantly different (p = 0.39). The TSS of the loratadine syrup group at day 7 and day 21 was lower than those of the placebo group (p = 0.003, p = 0.06). The daily card scores in the experimental group were also significantly lower than those of the placebo group (week 1, p = 0.014; week 2, p = 0.029; week 3, p = 0.014). No adverse reactions were recorded in both groups. This study revealed that loratadine syrup 5 mg or 10 mg once a day improved symptom scores of children with allergic rhinitis effectively and safely.