Adipose tissue dysfunction serum markers are associated with high density lipoprotein size and glycation in the early stages of type 2 diabetes.

BACKGROUND: High-density lipoproteins (HDLs) have antiatherogenic properties related to their chemical structure. Adipose tissue (AT) influences HDL reverse cholesterol transport and plasma HDL cholesterol levels. However, whether AT dysfunction affects HDL subpopulations and their glycation in early type 2 diabetes (T2D) is still unknown. OBJECTIVE: To investigate the association of inflammation and AT dysfunction serum markers with the size and glycation of HDLs in normoglycemic, prediabetes, and T2D subjects. METHODS: We assessed HDL particle size and advanced glycation end-product (AGE) content in HDLs isolated from normoglycemic (n = 17), prediabetes (n = 17), and recently T2D-diagnosed (n = 18) subjects. Insulin, adiponectin, and plasminogen activator inhibitor 1 (PAI-1) were determined using the Bio-Rad Multiplex Platform, and free fatty acids (FFAs) and high sensitivity C-reactive protein (hs-CRP) were determined by standard procedures. The AT insulin resistance (ATIR) index and ATIR/adiponectin and adiponectin/leptin ratios were calculated. RESULTS: HDL was progressively smaller (nm) and enriched with AGE (mg-BSA-AGE/mg protein) according to the glucose categories: 8.49 and 7.5 in normoglycemic subjects, 8.44 and 12.4 in prediabetic subjects, and 8.32 and 14.3 in T2D subjects (P = 0.033 and P = 0.009 for size and AGE, respectively). In multivariable regression analysis, the ATIR/adiponectin ratio was inversely associated with HDL size (ß = -0.257, P = 0.046), and the ATIR ratio was directly associated with HDL glycation (ß = 0.387, P = 0.036). In contrast, adiponectin and the adiponectin/leptin ratio were not associated with alterations in HDL particles. Furthermore, HDL size was associated with resistin (ß = -0.348, P = 0.007) and PAI-1 (ß = -0.324, P = 0.004). HDL and AGE were related to insulin concentrations (ß = 0.458, P = 0.015). Analyses were adjusted for age, sex, body mass index, triglycerides, and HDL-cholesterol. CONCLUSION: HDL size was significantly associated with the ATIR/adiponectin ratio and inflammation, whereas glycation was more strongly related to the ATIR index. These findings have important implications for the management and prevention of cardiovascular disease in T2D patients.

Autologous CXCR4+ Hematopoietic Stem Cells Injected into the Scar Tissue of Chronic Myocardial Infarction Patients Normalizes Tissue Contractility and Perfusion.

BACKGROUND: Chronic myocardial infarction (CMI), represents a public health and a financial burden. Since stem cell transplant is used to regenerate cardiac tissue after acute myocardial infarction. AIM OF THE STUDY: To determine if autologous CXCR4 stem cells could restore damaged myocardial tissue in patients with CMI lesions. METHODS: 20 NYHA grade III male patients with CMI defined by clinical, biochemical, ECG and echocardiographic parameters were included. Patients were treated with G-CSF for 6 d before isolating their autologous stem cells from PBMCs. Cell phenotyping was done by cytofluorometry using monoclonal antibodies (anti-CXCR4, -CD34, -48, -117, -133, -Ki67, -SDF1 and CXCR4); CXCR4 cell subpopulations isolated by sorting were adjusted to 1 × 108 cells by subpopulation and injected in a circular pattern into the cicatrix previously defined by echocardiography. RESULTS: Patients were followed for 6 and 12 months. Six months after cell implant improvements in left ventricle ejection fraction (from 33-50%), stress rate values (from -3/-9% to -18/-22%), stress tests (from 4-12 METS), and the quantity of left ventricle affected segments (3-9) disappeared according to the G-SPECT images. 12 months evaluations did not show significant differences. Interestingly, 3 months after cell implant the ECG showed normal electrical activity in 9 patients whereas after 6 months it was normal in all the patients. CONCLUSIONS: These results ratify that locally injected autologous CXCR4+ bone marrow-derived stem cells have a physiological and a clinical impact in patients with CMI.

¿Qué son los inflamosomas? El NLRP3 como por ejemplo / What are inflammasomes? The NLRP3 as an example

Resumen Una de las prácticas médicas más concurridas en la actualidad es el uso indiscriminado de medicamentos con actividad inhibidora de la inflamación. Sin embargo la inflamación es un proceso de reparación biológica fuertemente controlado por complejos intracelulares, conocidos como inflamosomas, que actúan como sensores y mediadores de la misma. Los inflamosomas forman parte de la familia de receptores tipo NOD que está formada de 3 subfamilias: NOD (nucleotide-binding oligomerization domain), NLRC (NOD-like receptor CARD domain containing) y NLRP (NOD-like receptor Pyrin domain containing), que es la que se relaciona con la formación de inflamosomas. Existen 14 diferentes tipos de NLRP. Los miembros de la familia NLRP responden a señales exógenas mediadas por PAMPs (pathogen-associated molecular patterns) o a señales endógenas mediadas por DAMPs (damage-associated molecular patterns, [también conocidas como alarminas]). Los componentes de los inflamosomas tipo NLRP, una vez activado, se ensamblan de acuerdo a un patrón determinado y forman un complejo que activa a la caspasa-1 que activa a los precursores de IL-1b, IL-18 e IL-33, favoreciendo la secreción de estas citosinas hacia el espacio extracelular. La IL-1 y la IL-18 son miembros de la misma familia y se les reconoce como reguladores de la respuesta inmune innata y adaptativa, la IL-33 también es miembro de la familia de IL-1 y se le considera una alarmina. A manera de ejemplo, en el presente manuscrito describimos la estructura y formación del inflamosoma NLRP3 y mencionamos algunas de las enfermedades en las que se activa, enfatizando de manera muy particular su participación en la enfermedad de Alzheimer.

Abstract One highly common medical malpractice is the undiscriminatory use of inflammation inhibiting drugs. Inflammation is a biological repair process vastly controlled by intracellular complexes known as the inflammasome that act as sensors and mediators of the inflammation process. Inflammasomes are members of the NOD innate immune system family of receptors that consist of 3 closely related subfamilies: nucleotide-binding oligomerization domain (NOD), NOD-like receptor CARD domain containing (NLRC), and NOD-like receptor Pyrin domain containing (NLRP); the latter is the most directly related to the inflammasome. There are 14 different NLRPs all of which are activated by exogenous signals through pathogen-associated molecular patterns (PAMPs) or by endogenous signals via damage-associated molecular patterns, also known as alarmins, are endogenous molecules constitutively available and released upon tissue damage (DAMPs). Once activated, the components of the NLRP inflammasome begin an assembling process that follows a pre-established pattern so a caspase-1 activating complex is formed. This complex activates IL-1b, IL-18 and IL-33 precursors thus favoring the secretion of this cytokines to the extracellular milieu. IL-1 and IL-18 are members of the same cytokine family and their main function is to regulate the innate and adaptive immune response whereas IL-33, also a member of the IL-1 family of cytokines, is considered an alarmin. We emphasize the structure and formation of NLRP3, implicated on a host of inflammatory disorders, with special attention to its participation in Alzheimer´s diseases.

[Pathogenic molecular mechanisms in non-alcoholic steatohepatitis]. / Mecanismos moleculares patogénicos en la esteatohepatitis no alcohólica.

Non-alcoholic steatohepatitis is a chronic disease that occurs in persons without significative consumption of alcohol, characterized by macrovesicular steatosis, mixed inflammatory infiltrate, and diverse degrees of fibrosis. It can progress to cirrhosis and its evolution to hepatocellular carcinoma has been described. It principally occurs in patients with obesity, diabetes mellitus, and hyperlipidemia, and is at present considered a manifestation of metabolic syndrome with insulin resistance. In pathogenesis, diverse factors, fundamentally insulin resistance as a mechanism that determines hepatic steatosis, have been described. Later, alteration of signalling cascades, oxidative stress, and other mechanisms occur that lead to inflammation, necrosis, and finally to hepatic fibrosis, the details of which will be described in this review.

Seroprevalence of hepatitis B in pregnant women in Mexico.

OBJECTIVE: To determine the seroprevalence of hepatitis B in pregnant women from several regions of Mexico, as well as the risk factors associated with its occurrence. MATERIAL AND METHODS: A cross-sectional study was conducted between May and August 2000. It included 9,992 pregnant women attending the health services of the Mexican Institute of Social Security (Instituto Mexicano del Seguro Social-IMSS) in five cities: Tijuana, Ciudad Juarez, Acapulco, Cancun, and Mexico City (northeast and southeast regions). RESULTS: The overall prevalence for confirmed cases was 1.65% (165/9,992). The prevalences for individual cities were as follows: Tijuana, 1.27%; Ciudad Juarez, 1.46%; Acapulco, 2.47%; Cancun, 0.93%; northeastern Mexico City, 1.20%, and southeastern Mexico City, 2.52%. The risk factors found to be associated with HBsAg were: age, age at first sexual intercourse, city (Acapulco and southeastern Mexico City), and marital status (single or divorced). CONCLUSIONS: The prevalence of HBsAg in pregnant women (1.65%) was greater than that reported in previous studies and showed geographical differences. This high prevalence suggests that a considerable amount of cases of hepatitis B occurs perinatally and through contact with carriers in the general population. Vaccination of newborns of high-risk pregnant women should be considered.

Seroprevalence of hepatitis B in pregnant women in Mexico

OBJECTIVE: To determine the seroprevalence of hepatitis B in pregnant women from several regions of Mexico, as well as the risk factors associated with its occurrence. MATERIAL AND METHODS: A cross-sectional study was conducted between May and August 2000. It included 9 992 pregnant women attending the health services of the Mexican Institute of Social Security (Instituto Mexicano del Seguro Social-IMSS) in five cities: Tijuana, Ciudad Juarez, Acapulco, Cancun, and Mexico City (northeast and southeast regions). RESULTS: The overall prevalence for confirmed cases was 1.65 percent (165/9 992). The prevalences for individual cities were as follows: Tijuana, 1.27 percent; Ciudad Juarez, 1.46 percent; Acapulco, 2.47 percent; Cancun, 0.93 percent; northeastern Mexico City, 1.20 percent, and southeastern Mexico City, 2.52 percent. The risk factors found to be associated with HBsAg were: age, age at first sexual intercourse, city (Acapulco and southeastern Mexico City), and marital status (single or divorced). CONCLUSIONS: The prevalence of HBsAg in pregnant women (1.65 percent) was greater than that reported in previous studies and showed geographical differences. This high prevalence suggests that a considerable amount of cases of hepatitis B occurs perinatally and through contact with carriers in the general population. Vaccination of newborns of high-risk pregnant women should be considered

Respuesta inmune en la tuberculosis / Immune response in tuberculosis

La tuberculosis es una de las enfermedades infecciosas más antiguas que han afectado al hombre. En la actualidad, representa uno de los padecimientos más importantes como causa de muerte. En este trabajo se pretende discutir algunos aspectos recientemente identificados relacionados con la fisiopatogenia de la enfermedad y que incluyen la respuesta inmune del individuo y a la capacidad que posee para reconocer, adecuadamente, al agente etiológico. El conocimiento de esta enfermedad en el contexto del sistema de histocompatibilidad, representa un avance importante en la identificación oportuna de individuos o poblaciontes de alto riesgo de enfermedades, lo que permitirá contemplar alternativas de pronósticos y/o tratamiento

Sondas de DNA para el diagnóstico de tuberculosis: ¿utopía o realidad? / DNA probes for the diagnosis of tuberculosis: utopia or reality?

La tuberculosis sigue siendo un serio problema de salud pública. Tan sólo durante 1989/90 la taza de infección en el Continente Americano (exceptuando los Estados los Estados Unidos t Canadá) fue de 117 millones de personas. Esta traduce la dificultad de mantener un control efectivo sobre la población potencialmente infectada, debido entre otras razones, a la falta de técnica de diagnóstico que permitan una detección rápida y sensible del bacilo. Las técnicas comúnmente utilizadas implican el análisis microscópico de muestras de expectoración y/o el cultivo in vitro de los bacilos. A pesar de que ambas técnicas presentan una sensibilidad aceptable, requieren mucho tiempo para la obtención de los resultados. Es por esta razón que muchos investigadores se han abocado a la tarea de deseñar nuevas estrategias que permiten una detección rápida y sensible de este patógeno. En este contexto la utilización de sondas de este patógeno. En este contexto la utilización de sondas de DNA y la amplificación por PCR ha abierto nuevas esperanzas en la obtención de una técnica rápida y sensible, que puede ser utilizada como ayuda en el diagnóstico de la tuberculosis. Sin embargo, a pesar de las múltiples ventajas que conlleva su aplicación, en algunas ocaciones cabe ponderar su utulización como técnica diagnóstica.