RESUMEN
BACKGROUND: Pentraxin 3 is an acute inflammatory protein of the long pentraxin subfamily. A meta-analysis was performed to assess diagnostic accuracy of pentraxin 3 for respiratory tract infections. METHODS: We identify studies examining diagnostic value of pentraxin 3 for respiratory tract infections by searching Pubmed, Web of Knowledge, and Cochrane Library. The sensitivity, specificity, negative likelihood ratio (LR), positive LR, and diagnostic odds ratio were pooled. The area under the summary receiver operator characteristic (SROC) curve and Q point value (Q*) were calculated. RESULTS: A total of 8 studies with 961 individuals were eligible for this meta-analysis. The pooled sensitivity of pentraxin 3 in diagnosis of respiratory tract infections was 0.78, the pooled specificity was 0.73, the area under the SROC curve was 0.84, and the Q* was 0.77. The area under the SROC curve of serum and bronchoalveolar lavage fluid (BALF) pentraxin 3 was 0.85 and 0.89, respectively. Meta-regression analysis revealed that cutoff value was the source of heterogeneity among the included studies. The Deek funnel plot test suggested no evidence of publication bias. Subgroup analyses showed that the area under the SROC curve of pentraxin 3 in diagnosis of ventilator-associated pneumonia (VAP) was 0.89. CONCLUSION: Pentraxin 3 has a moderate accuracy for diagnosing respiratory tract infections and VAP. The overall diagnostic value of BALF level of pentraxin 3 is superior to its serum concentration.
Asunto(s)
Proteína C-Reactiva/análisis , Infecciones del Sistema Respiratorio/sangre , Infecciones del Sistema Respiratorio/diagnóstico , Componente Amiloide P Sérico/análisis , Biomarcadores , Líquido del Lavado Bronquioalveolar/química , Humanos , Oportunidad Relativa , Neumonía Asociada al Ventilador/sangre , Neumonía Asociada al Ventilador/diagnóstico , Valor Predictivo de las Pruebas , Curva ROCRESUMEN
Huntington's disease (HD) is a genetic and neurodegenerative disease, leading to motor and cognitive dysfunction in HD patients. At cellular level, this disease is caused by the accumulation of mutant huntingtin (HTT) in different cells, and finally results in the dysfunction of different cells. To clean these mutant proteins, ubiquitin-proteasome system (UPS) and autophagy system are two critical pathways in the brain; however, little is known in other peripheral tissues. As mutant HTT affects different tissues progressively and might influence the UPS and autophagy pathways at early stages, we attempted to examine two clearance systems in HD models before the onset. Here, in vitro results showed that the accumulation of UPS signals with time was observed obviously in neuroblastoma and kidney cells, not in other cells. In HD transgenic mice, we observed the impairment of UPS, but not autophagy, over time in the cortex and striatum. In heart and muscle tissues, disturbance of autophagy was observed, whereas dysfunction of UPS was displayed in liver and lung. These results suggest that two protein clearance pathways are disturbed differentially in different tissues before the onset of HD, and enhancement of protein clearance at early stages might provide a potential stratagem to alleviate the progression of HD.
Asunto(s)
Enfermedad de Huntington/genética , Enfermedad de Huntington/patología , Complejo de la Endopetidasa Proteasomal/genética , Ubiquitina/metabolismo , Animales , Autofagia/genética , Encéfalo/metabolismo , Encéfalo/patología , Línea Celular , Modelos Animales de Enfermedad , Proteínas Fluorescentes Verdes/genética , Proteínas Fluorescentes Verdes/metabolismo , Humanos , Proteína Huntingtina , Riñón/metabolismo , Riñón/patología , Hígado/metabolismo , Hígado/patología , Pulmón/metabolismo , Pulmón/patología , Ratones , Ratones Transgénicos , Músculos/metabolismo , Músculos/patología , Mutación/genética , Miocardio/metabolismo , Miocardio/patología , Proteínas del Tejido Nervioso/genética , Proteínas del Tejido Nervioso/metabolismo , Neuroblastoma/patología , Ubiquitina/genéticaRESUMEN
Liver diseases, which can be caused by alcohol abuse, chemical intoxication, viral hepatitis infection, and autoimmune disorders, are a significant health issue because they can develop into liver fibrosis and cirrhosis. Lactoferrin (LF), a siderophilic protein with 2 iron-binding sites, has been demonstrated to possess a multitude of biological functions, including antiinflammation, anticancer, and antimicrobial effects, as well as immunomodulatory-enhancing functions. In the current study, we induced hepatotoxicity in rats with dimethylnitrosamine (DMN) to establish a situation that would enable us to evaluate the hepatoprotective effects of LF against hepatic injury. Our results showed that DMN-induced hepatic pathological damage significantly decreased the body weight and liver index, increased the mRNA and protein levels of collagen α-1(I) (ColIα-1) and α-smooth muscle actin, and increased the hydroxyproline content. However, treatment with LF significantly increased body weight and liver index, decreased the mRNA and protein levels of ColIα-1 and α-smooth muscle actin, and suppressed the hydroxyproline content when compared with the DMN-treated group. Liver histopathology also showed that low-dose LF (100mg/kg of body weight) or high-dose LF (300 mg/kg of body weight) could significantly reduce the incidences of liver lesions induced by DMN. These results suggest that the LF exhibits potent hepatoprotection against DMN-induced liver damage in rats and that the hepatoprotective effects of LF may be due to the inhibition of collagen production and to stellate cell activation.
Asunto(s)
Lactoferrina/farmacología , Cirrosis Hepática/prevención & control , Animales , Peso Corporal/efectos de los fármacos , Dimetilnitrosamina/toxicidad , Modelos Animales de Enfermedad , Hidroxiprolina/análisis , Lactoferrina/uso terapéutico , Hígado/química , Hígado/diagnóstico por imagen , Hígado/patología , Cirrosis Hepática/inducido químicamente , Cirrosis Hepática/tratamiento farmacológico , Masculino , ARN Mensajero/genética , Ratas , Ratas Sprague-Dawley , UltrasonografíaRESUMEN
Treadmill running is a commonly used training method for patients with spasticity to improve functional performance. Botulinum toxin has been widely used therapeutically to reduce contraction force of spastic muscle. However, the effects of treadmill running in neuromuscular junction expression and motor unit physiology on muscle following botulinum toxin injection are not well established. To assess the effects of treadmill running on neuromuscular recovery of gastrocnemius following botulinum toxin A (BoNT-A) injection, we observed changes in gene expression. We hypothesized that the expression of acetylcholine receptor (AChR), myogenesis, and nerve plasticity could be enhanced. Twenty-four Sprague-Dawley rats received botulinum toxin injection in right gastrocnemius and were then randomly assigned into untrained control and treadmill running groups. The rats assigned to the treadmill running group were trained on a treadmill 3 times/week with a running speed of 15 m/min for 8 weeks. The duration of training was 20 min per session. Muscle strength and gene expression of AChR subunit (α, ß, δ, γ, and ε), MyoD, Myf-5, MRF4, myogenin, p21, IGF-1, GAP43, were analyzed. Treadmill running had no influence on gastrocnemius mass, but improved the maximal contraction force of the gastrocnemius in the treadmill running group (p < 0.05). Upregulation of GAP-43, IGF-1, Myo-D, Myf-5, myogenin, and AChR subunits α and ß were found following treadmill running. The expression of genes associated with neurite and AChR regeneration following treadmill exercise was upregulated, which may have contributed to enhanced recovery of gastrocnemius strength.