Obesity attenuates the beneficial effect of an intrauterine infusion of autologous platelet-rich plasma during in vitro fertilization.

OBJECTIVE: To assess how obesity, normal weight (NW) versus overweight/obese (OW/OB), impacts platelet-rich plasma's (PRP) effectiveness during in vitro fertilization and how obesity affects platelets during the menstrual cycle. METHODS: Endometrial mean thickness (EMT), embryo implantation, and clinical pregnancy were assessed using a self-controlled retrospective study that enrolled 59 patients with two failed cycles and treated with autologous PRP (three-dose scheme). The NHANES dataset was used to assess platelet changes during the menstrual cycle, using the mean platelet volume to platelet count ratio (MPR) index. The COSINOR packages for R were used to determine rhythmicity. RESULTS: PRP treatments significantly improved the EMT (2.5 ± 1.4 mm, P<0.001), unaffected by obesity. After the PRP treatment, one patient spontaneously became pregnant; therefore, 58 patients underwent embryo transfer (62 cycles), of which in 39 cycles the embryos implanted (63.9%). This was a significant improvement from their previous cycle (vs. 22.6%, P<0.001). Clinical pregnancy also improved with the PRP treatment over the previous cycle (57.4% vs. 16.1%, P<0.001). When stratified by obesity, there was an appreciable decrease in embryo implantation and clinical pregnancy rates for the OW/OB group; nevertheless, the PRP treatment significantly improved embryo implantation and clinical pregnancy (P<0.05). A rhythm was observed with the MPR index (P<0.05) only for the NW group, suggesting that the platelets normally fluctuate during the menstrual cycle. CONCLUSION: PRP improved embryo implantation and clinical pregnancy rates; however, these beneficial effects were attenuated by obesity. PRP presumptively promoted a change in the uterine environment to mimic the normal findings associated with normal-weight women.

[Association between metabolic syndrome, socioeconomic status and quality of life in mexicans]. / Asociación entre síndrome metabólico, nivel socioeconómico y calidad de vida en mexicanos.

Background: In Mexico there is little information regarding the link between metabolic syndrome (MetS), socioeconomic status (SES) and quality of life (QoL). Objective: To assess the association between subjects who are at high risk of developing MetS with SES and QoL. Material and methods: Patients attending UMF-2 IMSS or Centro Urbano-SSA Clínica-1 were asked to participate. Anthropometric measures were collected, the AMAI, SF12, and ESF-I questionnaire where apply for SES, QoL, and MetS, respectively. Association were determined by calculating Spearman's rho and the risk (odds ratio and 95% confidence-interval) was assessed using logistic regression. Results: The difference of SES (193 ± 53 vs. 124 ± 50) and QoL (86.3 ± 14.8 vs. 56.0±25.4) questionnaires were significantly between low-risk and high-risk groups, respectively (p < 0.001). There was a negative correlation between ESF-I and SES (rho = -0.623, p < 0.001) as well as the QoL (rho = -0.719, p < 0.001). MetS risk was augmented by decreasing SES (C+: OR = 6.4, 95%IC: 3.2-13.0; D: OR = 66.1, 95%IC: 23.2-188.3), whereas increasing QoL attenuated it (OR = 0.93, 95%CI: 0.91-0.94). However, QoL mitigated the effect of SES (C+: OR = 4.5, 95%IC: 2.1-9.6; D: OR = 11.9, 95%IC: 3.8-37.6). Conclusions: Lower QoL and SES increased the risk of MetS in Central Mexico; however, improving the QoL can mitigated the effect SES has on developing MetS.

Introducción: en México existe escasa información respecto al vínculo entre el síndrome metabólico (MetS), el nivel socioeconómico (NSE) y la calidad de vida (CdV) de la población. Objetivo: evaluar la asociación entre sujetos que tienen alto riesgo de desarrollar MetS con NSE y CdV. Material y métodos: se invitó a participar a pacientes de la UMF-2 del IMSS y del Centro Urbano-SSA Clínica-1. Se recolectaron medidas antropométricas y se aplicaron los cuestionarios AMAI, SF12 y ESF-I para NSE, CdV y MetS, respectivamente. La asociación se determinó calculando rho de Spearman. El riesgo se evaluó mediante regresión logística (razon de momios e intervalo de confianza del 95%). Resultados: la diferencia entre NSE (193 ± 53 frente a 124 ± 50) y CdV (86.3 ± 14.8 frente a 56.0 ± 25.4) fue significativa entre los grupos de bajo y alto riesgo, respectivamente (p < 0.001). Hubo una fuerte correlación negativa entre las puntuaciones de la ESF-I y NSE (rho = -0.623, p < 0.001) así como con la CdV (rho = -0.719, p < 0.001). El riesgo de MetS aumentó al disminuir el NSE (C+: OR = 6.4, IC95%: 3.2 - 13.0; D: OR = 66.1, IC95%: 23.2 - 188.3), mientras que el aumento de la CdV lo atenuó (OR = 0.93, IC95%: 0.91 - 0.94). Interesantemente, la CdV mitigó el efecto del NSE (C+: OR = 4.5, IC95%: 2.1 - 9.6; D: OR = 11.9, IC95%: 3.8 - 37.6). Conclusión: Una menor CdV y NSE aumentan el riesgo de MetS en la región centro de México; sin embargo, el aumento en la CdV podría disminuir el efecto que tiene el NSE en el desarrollo de MetS.

Asociación entre síndrome metabólico, nivel socioeconómico y calidad de vida en mexicanos / Association between metabolic syndrome, socioeconomic status and quality of life in mexicans

Introducción: en México existe escasa información respecto al vínculo entre el síndrome metabólico (MetS), el nivel socioeconómico (NSE) y la calidad de vida (CdV) de la población. Objetivo: evaluar la asociación entre sujetos que tienen alto riesgo de desarrollar MetS con NSE y CdV. Métodos: se invitó a participar a pacientes de la UMF-2 del IMSS y del Centro Urbano-SSA Clínica-1. Se recolectaron medidas antropométricas y se aplicaron los cuestionarios AMAI, SF12 y ESF-I para NSE, CdV y MetS, respectivamente. La asociación se determinó calculando rho de Spearman. El riesgo se evaluó mediante regresión logística (razon de momios e intervalo de confianza del 95%). Resultados: la diferencia entre NSE (193  53 frente a 124  50) y CdV (86.3  14.8 frente a 56.0  25.4) fue significativa entre los grupos de bajo y alto riesgo, respectivamente (p < 0.001). Hubo una fuerte correlación negativa entre las puntuaciones de la ESF-I y NSE (rho = -0.623, p < 0.001) así como con la CdV (rho = -0.719, p < 0.001). El riesgo de MetS aumentó al disminuir el NSE (C+: OR = 6.4, IC95%: 3.2 - 13.0; D: OR = 66.1, IC95%: 23.2 - 188.3), mientras que el aumento de la CdV lo atenuó (OR = 0.93, IC95%: 0.91 - 0.94). Interesantemente, la CdV mitigó el efecto del NSE (C+: OR = 4.5, IC95%: 2.1 - 9.6; D: OR = 11.9, IC95%: 3.8 - 37.6). Conclusión: Una menor CdV y NSE aumentan el riesgo de MetS en la región centro de México; sin embargo, el aumento en la CdV podría disminuir el efecto que tiene el NSE en el desarrollo de MetS.

Background: In Mexico there is little information regarding the link between metabolic syndrome (MetS), socioeconomic status (SES) and quality of life (QoL) Objective: To assess the association between subjects who are at high risk of developing MetS with SES and QoL. Methods: Patients attending UMF-2 IMSS or Centro Urbano-SSA Clínica-1 were asked to participate. Anthropometric measures were collected, the AMAI, SF12, and ESF-I questionnaire where apply for SES, QoL, and MetS, respectively. Association were determined by calculating Spearman's rho and the risk (odds ratio and 95% confidence-interval) was assessed using logistic regression. Results: The difference of SES (193  53 vs. 124  50) and QoL (86.3  14.8 vs. 56.025.4) questionnaires were significantly between low-risk and high-risk groups, respectively (p < 0.001). There was a negative correlation between ESF-I and SES (rho = -0.623, p < 0.001) as well as the QoL (rho = -0.719, p < 0.001). MetS risk was augmented by decreasing SES (C+: OR = 6.4, 95%IC: 3.2-13.0; D: OR = 66.1, 95%IC: 23.2-188.3), whereas increasing QoL attenuated it (OR = 0.93, 95%CI: 0.91-0.94). However, QoL mitigated the effect of SES (C+: OR = 4.5, 95%IC: 2.1-9.6; D: OR = 11.9, 95%IC: 3.8-37.6).

Differential effects of the methylenetetrahydrofolate reductase polymorphisms (C677T and A1298C) on hematological malignancies among Latinos: a meta-analysis.

Our objective was to determine the association between the methylenetetrahydrofolate reductase polymorphisms (C677T and A1298C) and the risk of developing acute lymphoblastic leukemia (ALL), chronic myeloid leukemia (CML), acute myeloid leukemia (AML), and multiple myelomas (MM) in Latinos. PubMed, SCOPUS, EBSCO, LILACS, and other Latin-specific databases were searched for case-control studies that investigated the association between these polymorphisms and hematologic malignancies until November 2017. Genotype distributions were extracted and either fixed-effects or random-effects models were used to calculate the pooled crude odds ratios (ORs) for the heterozygous, homozygous, dominant, recessive, and allelic genetic models. No publication bias was detected by the Begg-Mazumdar's test and Egger's test. From 290 publications, we identified 15 studies on the C677T polymorphism and 13 studies on the A1298C polymorphism. We observed a significant decrease in risk for the C677T polymorphism (OR range=0.54-0.75, p<0.01) and a significant increase in risk for the A1298C polymorphism (OR range=1.28-2.52, p<0.05) in developing ALL for all genetic models. No associations were determined for CML, AML, or MM for either polymorphism. This meta-analysis demonstrated that the A1298C polymorphism was associated with an increased risk of developing ALL, whereas the C677T polymorphism was associated with a decreased risk (protective factor) in the Latino population.

Distinct contribution of protein kinase Cδ and protein kinase Cε in the lifespan and immune response of human blood monocyte subpopulations.

Monocytes, key components of the immune system, are a heterogeneous population comprised of classical monocytes (CD16(-) ) and non-classical monocytes (CD16(+) ). Monocytes are short lived and undergo spontaneous apoptosis, unless stimulated. Dysregulation of monocyte numbers contribute to the pathophysiology of inflammatory diseases, yet the contribution of each subset remains poorly characterized. Protein kinase C (PKC) family members are central to monocyte biology; however, their role in regulating lifespan and immune function of CD16(-) and CD16(+) monocytes has not been studied. Here, we evaluated the contribution of PKCδ and PKCε in the lifespan and immune response of both monocyte subsets. We showed that CD16(+) monocytes are more susceptible to spontaneous apoptosis because of the increased caspase-3, -8 and -9 activities accompanied by higher kinase activity of PKCδ. Silencing of PKCδ reduced apoptosis in both CD16(+) and CD16(-) monocytes. CD16(+) monocytes express significantly higher levels of PKCε and produce more tumour necrosis factor-α in CD16(+) compared with CD16(-) monocytes. Silencing of PKCε affected the survival and tumour necrosis factor-α production. These findings demonstrate a complex network with similar topography, yet unique regulatory characteristics controlling lifespan and immune response in each monocyte subset, helping define subset-specific coordination programmes controlling monocyte function.

Metallothionein-1 and nitric oxide expression are inversely correlated in a murine model of Chagas disease

Chagas disease, caused by Trypanosoma cruzi, represents an endemic among Latin America countries. The participation of free radicals, especially nitric oxide (NO), has been demonstrated in the pathophysiology of seropositive individuals with T. cruzi. In Chagas disease, increased NO contributes to the development of cardiomyopathy and megacolon. Metallothioneins (MTs) are efficient free radicals scavengers of NO in vitro and in vivo. Here, we developed a murine model of the chronic phase of Chagas disease using endemic T. cruzi RyCH1 in BALB/c mice, which were divided into four groups: infected non-treated (Inf), infected N-monomethyl-L-arginine treated (Inf L-NAME), non-infected L-NAME treated and non-infected vehicle-treated. We determined blood parasitaemia and NO levels, the extent of parasite nests in tissues and liver MT-I expression levels. It was observed that NO levels were increasing in Inf mice in a time-dependent manner. Inf L-NAME mice had fewer T. cruzi nests in cardiac and skeletal muscle with decreased blood NO levels at day 135 post infection. This affect was negatively correlated with an increase of MT-I expression (r = -0.8462, p < 0.0001). In conclusion, we determined that in Chagas disease, an unknown inhibitory mechanism reduces MT-I expression, allowing augmented NO levels.

Metallothionein-1 and nitric oxide expression are inversely correlated in a murine model of Chagas disease.

Chagas disease, caused by Trypanosoma cruzi, represents an endemic among Latin America countries. The participation of free radicals, especially nitric oxide (NO), has been demonstrated in the pathophysiology of seropositive individuals with T. cruzi. In Chagas disease, increased NO contributes to the development of cardiomyopathy and megacolon. Metallothioneins (MTs) are efficient free radicals scavengers of NO in vitro and in vivo. Here, we developed a murine model of the chronic phase of Chagas disease using endemic T. cruzi RyCH1 in BALB/c mice, which were divided into four groups: infected non-treated (Inf), infected N-monomethyl-L-arginine treated (Inf L-NAME), non-infected L-NAME treated and non-infected vehicle-treated. We determined blood parasitaemia and NO levels, the extent of parasite nests in tissues and liver MT-I expression levels. It was observed that NO levels were increasing in Inf mice in a time-dependent manner. Inf L-NAME mice had fewer T. cruzi nests in cardiac and skeletal muscle with decreased blood NO levels at day 135 post infection. This affect was negatively correlated with an increase of MT-I expression (r = -0.8462, p < 0.0001). In conclusion, we determined that in Chagas disease, an unknown inhibitory mechanism reduces MT-I expression, allowing augmented NO levels.

Trypanosoma cruzi strains isolated from human, vector, and animal reservoir in the same endemic region in Mexico and typed as T. cruzi I, discrete typing unit 1 exhibit considerable biological diversity.

In this study, three strains of Trypanosoma cruzi were isolated at the same time and in the same endemic region in Mexico from a human patient with chronic chagasic cardiomyopathy (RyC-H); vector (Triatoma barberi) (RyC-V); and rodent reservoir (Peromyscus peromyscus) (RyC-R). The three strains were characterized by multilocus enzyme electrophoresis, random amplified polymorphic DNA, and by pathological profiles in experimental animals (biodemes). Based on the analysis of genetic markers the three parasite strains were typed as belonging to T. cruzi I major group, discrete typing unit 1. The pathological profile of RyC-H and RyC-V strains indicated medium virulence and low mortality and, accordingly, the strains should be considered as belonging to biodeme Type III. On the other hand, the parasites from RyC-R strain induced more severe inflammatory processes and high mortality (> 40%) and were considered as belonging to biodeme Type II. The relationship between genotypes and biological characteristics in T. cruzi strains is still debated and not clearly understood. An expert committee recommended in 1999 that Biodeme Type III would correspond to T. cruzi I group, whereas Biodeme Type II, to T. cruzi II group. Our findings suggest that, at least for Mexican isolates, this correlation does not stand and that biological characteristics such as pathogenicity and virulence could be determined by factors different from those identified in the genotypic characterization.

Trypanosoma cruzi strains isolated from human, vector, and animal reservoir in the same endemic region in Mexico and typed as T. cruzi I, discrete typing unit 1 exhibit considerable biological diversity

In this study, three strains of Trypanosoma cruzi were isolated at the same time and in the same endemic region in Mexico from a human patient with chronic chagasic cardiomyopathy (RyC-H); vector (Triatoma barberi) (RyC-V); and rodent reservoir (Peromyscus peromyscus) (RyC-R). The three strains were characterized by multilocus enzyme electrophoresis, random amplified polymorphic DNA, and by pathological profiles in experimental animals (biodemes). Based on the analysis of genetic markers the three parasite strains were typed as belonging to T. cruzi I major group, discrete typing unit 1. The pathological profile of RyC-H and RyC-V strains indicated medium virulence and low mortality and, accordingly, the strains should be considered as belonging to biodeme Type III. On the other hand, the parasites from RyC-R strain induced more severe inflammatory processes and high mortality (> 40 percent) and were considered as belonging to biodeme Type II. The relationship between genotypes and biological characteristics in T. cruzi strains is still debated and not clearly understood. An expert committee recommended in 1999 that Biodeme Type III would correspond to T. cruzi I group, whereas Biodeme Type II, to T. cruzi II group. Our findings suggest that, at least for Mexican isolates, this correlation does not stand and that biological characteristics such as pathogenicity and virulence could be determined by factors different from those identified in the genotypic characterization