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Objectives: We aimed to evaluate the association between the adipokines: Leptin, Adiponectin, Resistin, and high sensitive-C-reactive protein (hs-CRP) with clinical, radiographical and magnetic resonance imaging (MRI) assessment of knee osteoarthritis (OA) severity. Design: We performed a cross-sectional study in participants with earlier knee OA. Demographics, clinical (WOMAC), radiographical and MRI (BLOKS scoring) severity of knee OA were assessed. Serum leptin, adiponectin, resistin and hs-CRP were measured. Association of adipokines and hs-CRP with clinical, radiographic and MRI severity outcomes were evaluated using regression models with adjustment with age, sex, and body mass index (BMI). Results: 137 participants with earlier knee OA (82% women, mean â± âSD age: 55.5 â± â7.8 years) were included. Participants had moderate knee OA symptoms, mean WOMAC pain and function were 30.6 â± â18.0, and 31.7 â± â19.8 respectively. Mean BMI was 27.0 â± â5.9 âkg/m2. After adjustment with age, sex and BMI, serum leptin was positively associated with osteophyte size, cartilage integrity, infrapatellar synovitis and effusion. While hs-CRP was associated with meniscus extrusion and adiponectin was associated with WOMAC pain and function. Conclusion: Serum adipokines, particularly leptin was associated with severity of various structural defects of the knee joint on MRI beyond age, sex and BMI in earlier knee OA.
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Tuberculous pleural effusion is the second most common form of extrapulmonary tuberculosis, which is very difficult to rapidly distinguish from malignant pleural effusion in the clinical setting. A time-resolved fluoroimmunoassay (TRF) of CFP-10, a low molecular weight protein secreted by pathogenic Mycobacterium tuberculosis, was developed to differentiate tuberculous pleural effusion from malignant one. The measuring range was 0.3-187.5 ng/ml with the dose-response coefficient of 0.9998 and detection limit of 0.036 ng/ml. The intra-assay and inter-assay coefficients of variation were 3.6-9.2% and 10.0-12.4%, respectively. The concentration of CFP-10 in malignant pleural effusion was less than 0.8 ng/ml. The negative predictive value was 93.1% in malignant pleural effusion (n = 247) while the positive predictive value was 83.0% in tuberculous pleural effusion (n = 235). Moreover, there was a statistically significant difference in the CFP-10 concentration of pleural effusion between the groups before and after clinical therapy of tuberculosis (P < 0.001, n = 81). In addition, the stability of the diagnostic reagents lasted at least 1 year at 4 °C. Therefore, the TRF of CFP-10 may be used for the rapid diagnosis of tuberculous pleural effusion and further monitoring the clinical therapeutic efficacy of tuberculosis.
Asunto(s)
Proteínas Bacterianas/metabolismo , Fluoroinmunoensayo , Mycobacterium tuberculosis/metabolismo , Derrame Pleural/diagnóstico , Tuberculosis Pleural/diagnóstico , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Antituberculosos/uso terapéutico , Biomarcadores/metabolismo , Diagnóstico Diferencial , Femenino , Humanos , Masculino , Persona de Mediana Edad , Derrame Pleural/tratamiento farmacológico , Derrame Pleural/microbiología , Derrame Pleural Maligno/diagnóstico , Valor Predictivo de las Pruebas , Factores de Tiempo , Resultado del Tratamiento , Tuberculosis Pleural/tratamiento farmacológico , Tuberculosis Pleural/microbiología , Adulto JovenRESUMEN
Epidemiologic studies have provided solid evidence for the neurotoxic effect of lead for decades of years. In view of the fact that children are more vulnerable to the neurotoxicity of lead, lead exposure has been an urgent public health concern. The modes of action of lead neurotoxic effects include disturbance of neurotransmitter storage and release, damage of mitochondria, as well as induction of apoptosis in neurons, cerebrovascular endothelial cells, astroglia and oligodendroglia. Our studies here, from a novel point of view, demonstrates that lead specifically caused induction of COX-2, a well known inflammatory mediator in neurons and glia cells. Furthermore, we revealed that COX-2 was induced by lead in a transcription-dependent manner, which relayed on transcription factor NFAT, rather than AP-1 and NFκB, in glial cells. Considering the important functions of COX-2 in mediation of inflammation reaction and oxidative stress, our studies here provide a mechanistic insight into the understanding of lead-associated inflammatory neurotoxicity effect via activation of pro-inflammatory NFAT3/COX-2 axis.
Asunto(s)
Ciclooxigenasa 2/biosíntesis , Intoxicación del Sistema Nervioso por Plomo/etiología , Plomo/toxicidad , FN-kappa B/metabolismo , Factores de Transcripción NFATC/metabolismo , Neuroglía/efectos de los fármacos , Factor de Transcripción AP-1/metabolismo , Animales , Ciclooxigenasa 2/genética , Relación Dosis-Respuesta a Droga , Células Endoteliales/efectos de los fármacos , Células Endoteliales/enzimología , Inducción Enzimática , Mediadores de Inflamación/metabolismo , Intoxicación del Sistema Nervioso por Plomo/enzimología , Intoxicación del Sistema Nervioso por Plomo/genética , Ratones , Factores de Transcripción NFATC/genética , Células-Madre Neurales/efectos de los fármacos , Células-Madre Neurales/enzimología , Neuroglía/enzimología , Neuronas/efectos de los fármacos , Neuronas/enzimología , Células PC12 , ARN Mensajero/biosíntesis , Ratas , Transducción de Señal/efectos de los fármacos , Factores de Tiempo , Transcripción Genética/efectos de los fármacos , Transfección , Regulación hacia ArribaRESUMEN
OBJECTIVE: To investigate alpha- and beta-thalassemia (alpha- and beta-thal) gene frequencies and gene mutation spectrum in the population of Sihui City. METHODS: The umbilical cord blood samples from 1 007 neonates and peripheral blood samples from 1 524 apparently healthy adults for pre-marriage health check in Sihui city were collected for molecular epidemiologic study of alpha- and beta-thal respectively. The diagnostic standard for alpha-thal was the presence of Hb Bart's, and that for beta-thal was both the decrease of mean corpuscular volume (MCV<80 fl) and the increase of Hb A(2) level (> or = 3.5%). The samples of identified subjects with positive thal genotypes were further examined with PCR-based DNA analysis for determining the alpha- or beta-globin gene genotype, while those from subjects with positive genotypes but without mutations known to Chinese subjects were subjected to DNA sequence analysis of beta-globin gene. In addition, the alpha-thal alleles, -alpha(3.7) and -alpha(4.2) were examined in all umbilical cord blood samples. RESULTS AND CONCLUSION: Of all the 1 007 umbilical cord blood samples, 110 were identified as from alpha-thal gene carriers, 3 from patients Hb H disease and 1 from patients with hydrops fetalis, which meant an alpha-thal gene frequency of 11.72% (118/1 007). Three types of alpha-gene deletion were identified in this cohort, with the frequency of 53.4% (--SEA)), 34.7% (-alpha(3.7)) and 11.9% (-alpha(4.2)) respectively. By examining the peripheral venous blood samples from the 1,524 healthy adult subjects, 59 subjects were found to be beta-thal gene carriers with a rate of 3.87% (59/1,524), whose genotypes were determined and from whom 7 beta-thal mutations were identified. Of these 59 beta-thal gene carriers, 11 were diagnosed as having heterozygotes compound for beta- and alpha-thal genes with the deletion of the --(SEA) in 7 cases and -alpha(3.7) in 4 cases respectively, showing an incidence of 0.72% (11/1,524). The three commonest point mutations, beta CD41-42 (-CTTT) frameshift mutation, beta IVS2-654(C-->T) aberrant splicing mutation and beta-28 (A-->G) transcription mutation occurred with a total frequency of 84.75% among subjects with beta-thal allele mutations. In addition, a novel mutation, beta-globin gene promoter -90 (C-->T) allele was detected for the first time in Chinese subjects.