New molecular approaches in adipogenesis regulation: The connexin 43 role

Indexación: Scopus; Redalyc.La prevalencia de la obesidad a nivel mundial se ha incrementado rápidamente durante los últimos años debido principalmente a los cambios en el estilo de vida de la población con un aumento significativo en el consumo de energía y disminución de los niveles de actividad física. Es por esto que la comunidad científica está interesada en comprender de forma más profunda los mecanismos que regulan la fisiopatología de la obesidad. Dentro de los diferentes blancos de estudio se encuentra la adipogénesis, cuyo entendimiento es fundamental para comprender el desarrollo de la obesidad y las patologías asociadas a esta. Recientemente ha surgido importantes evidencias que involucran a la proteína de canales de “Gap Junction” conexina 43 (Cx43) en la regulación de los procesos relacionados con adipogénesis, cuyo papel es básicamente anti-adipogénico, sin embargo, nuevas funciones de Cx43 en la regulación de la formación del tejido adiposo siguen descubriéndose.The global prevalence of obesity has been increased rapidly over the past few years mainly due to changes in the lifestyle of the population with a significant increase in energy consumption and decreased levels of physical activity. As a result, the scientific community is interested in a deeper understanding of the mechanisms that regulate the pathophysiology of obesity. In this context, adipogenesis process is an important target of study to understand the obesity and associated pathologies. Recently has been emerged important evidence that involve gap junction channel protein connexin 43 (Cx43) in the regulation of processes related to adipogenesis, whose role is fundamentally anti-adipogenic. However, new functions of Cx43 in the regulation of adipose tissue function also continued to emerge.http://www.redalyc.org/articulo.oa?id=5594990800

Origins of the Ambient Solar Wind: Implications for Space Weather

The Sun's outer atmosphere is heated to temperatures of millions of degrees, and solar plasma flows out into interplanetary space at supersonic speeds. This paper reviews our current understanding of these interrelated problems: coronal heating and the acceleration of the ambient solar wind. We also discuss where the community stands in its ability to forecast how variations in the solar wind (i.e., fast and slow wind streams) impact the Earth. Although the last few decades have seen significant progress in observations and modeling, we still do not have a complete understanding of the relevant physical processes, nor do we have a quantitatively precise census of which coronal structures contribute to specific types of solar wind. Fast streams are known to be connected to the central regions of large coronal holes. Slow streams, however, appear to come from a wide range of sources, including streamers, pseudostreamers, coronal loops, active regions, and coronal hole boundaries. Complicating our understanding even more is the fact that processes such as turbulence, stream-stream interactions, and Coulomb collisions can make it difficult to unambiguously map a parcel measured at 1 AU back down to its coronal source. We also review recent progress -- in theoretical modeling, observational data analysis, and forecasting techniques that sit at the interface between data and theory -- that gives us hope that the above problems are indeed solvable.Comment: Accepted for publication in Space Science Reviews. Special issue connected with a 2016 ISSI workshop on "The Scientific Foundations of Space Weather." 44 pages, 9 figure

ALPK1 missense pathogenic variant in five families leads to ROSAH syndrome, an ocular multisystem autosomal dominant disorder

Purpose: To identify the molecular cause in five unrelated families with a distinct autosomal dominant ocular systemic disorder we called ROSAH syndrome due to clinical features of retinal dystrophy, optic nerve edema, splenomegaly, anhidrosis, and migraine headache. Methods: Independent discovery exome and genome sequencing in families 1, 2, and 3, and confirmation in families 4 and 5. Expression of wild-type messenger RNA and protein in human and mouse tissues and cell lines. Ciliary assays in fibroblasts from affected and unaffected family members. Results: We found the heterozygous missense variant in the ɑkinase gene, ALPK1, (c.710C>T, [p.Thr237Met]), segregated with disease in all five families. All patients shared the ROSAH phenotype with additional low-grade ocular inflammation, pancytopenia, recurrent infections, and mild renal impairment in some. ALPK1 was notably expressed in retina, retinal pigment epithelium, and optic nerve, with immunofluorescence indicating localization to the basal body of the connecting cilium of the photoreceptors, and presence in the sweat glands. Immunocytofluorescence revealed expression at the centrioles and spindle poles during metaphase, and at the base of the primary cilium. Affected family member fibroblasts demonstrated defective ciliogenesis. Conclusion: Heterozygosity for ALPK1, p.Thr237Met leads to ROSAH syndrome, an autosomal dominant ocular systemic disorder

Evaluation of family health history collection methods impact on data and risk assessment outcomes

10.1016/j.pmedr.2020.101072Preventive Medicine Reports1810107

Association of the rs1801133 variant in the MTHFR gene and sporadic Parkinson's disease

The MTHFR gene has been reported as a susceptibility locus for sporadic Parkinson's disease (sPD). The functional variant rs1801133 has been linked to hyperhomocysteinemia and dopaminergic cell death. Among different populations, Mexican-Mestizos (most present-day Mexicans) have the highest frequency of this variant. Therefore, we sought to determine a possible association of rs1801133 with SPD. In total, 356 individuals were included: 140 pa tients with PD, diagnosed according to the Queen Square Brain Bank criteria, and 216 neurologically healthy controls. Genotyping was performed using TaqMan probes for rs1801133 and real-time PCR. Logistic regression analysis with adjustment for smoking and gender was used to test for an association between genotype and SPD. The CC genotype was associated with SPD; exp(?) = 2.06; 95% CI: 1.101-3.873, p = 0.024. No association with age at onset, cognitive impairment or gender was found in our study group. Our data suggest an important role of MTHFR gene variants in SPD