MicroRNA-425-5p modulates osteoporosis by targeting annexin A2

The disease (COVID-19) novel coronavirus pandemic has so far infected millions resulting in the death of over a million people as of Oct 2020. More than 90% of those infected with COVID-19 show mild or no symptoms but the rest of the infected cases show severe symptoms resulting in significant mortality. Age has emerged as a major factor to predict the severity of the disease and mortality rates are significantly higher in elderly patients. Besides, patients with underlying conditions like Type 2 diabetes, cardiovascular diseases, hypertension, and cancer have an increased risk of severe disease and death due to COVID-19 infection. Obesity has emerged as a novel risk factor for hospitalization and death due to COVID-19. Several independent studies have observed that people with obesity are at a greater risk of severe disease and death due to COVID-19. Here we review the published data related to obesity and overweight to assess the possible risk and outcome in Covid-19 patients based on their body weight. Besides, we explore how the obese host provides a unique microenvironment for disease pathogenesis, resulting in increased severity of the disease and poor outcome.

     

Microarray analysis of brain RNA in mice with methylenetetrahydrofolate reductase deficiency and hyperhomocysteinemia

Methylenetetrahydrofolate reductase (MTHFR) deficiency is the most common genetic cause of hyperhomocysteinemia, which is associated with increased risk for cardiovascular disease, stroke and possibly other neurological disorders. Microarray analysis of brain RNA from day 14 Mthfr(-/-) mice revealed several genes with altered expression. Expression changes in inositol 1,4,5-triphosphate receptor, type 1 (Itpr1), proteolipid protein (Plp), neurogenic differentiation factor 1 (Neurod1), S100 calcium binding protein A8 (S100a8), and methylenetetrahydrofolate dehydrogenase (NAD+ dependent), methenyltetrahydrofolate cyclohydrolase (Mthfd2) were confirmed by RT-PCR. We propose that neuronal damage by hyperhomocysteinemia may involve disruption of intracellular calcium.     

Gene structure of human and mouse methylenetetrahydrofolate reductase (MTHFR)

Methylenetetrahydrofolate reductase (MTHFR) catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a co-substrate for homocysteine remethylation to methionine. A human cDNA for MTHFR, 2.2 kb in length, has been expressed and shown to result in a catalytically active enzyme of approximately 70 kDa. Fifteen mutations have been identified in the MTHFR gene: 14 rare mutations associated with severe enzymatic deficiency and 1 common variant associated with a milder deficiency. The common polymorphism has been implicated in three multifactorial diseases: occlusive vascular disease, neural tube defects, and colon cancer. The human gene has been mapped to chromosomal region 1p36.3 while the mouse gene has been localized to distal Chromosome (Chr) 4. Here we report the isolation and characterization of the human and mouse genes for MTHFR. A human genomic clone (17 kb) was found to contain the entire cDNA sequence of 2.2 kb; there were 11 exons ranging in size from 102 bp to 432 bp. Intron sizes ranged from 250 bp to 1.5 kb with one exception of 4.2 kb. The mouse genomic clones (19 kb) start 7 kb 5′ exon 1 and extend to the end of the coding sequence. The mouse amino acid sequence is approximately 90% identical to the corresponding human sequence. The exon sizes, locations of intronic boundaries, and intron sizes are also quite similar between the two species. The availability of human genomic clones has been useful in designing primers for exon amplification and mutation detection. The mouse genomic clones will be helpful in designing constructs for gene targeting and generation of mouse models for MTHFR deficiency. Received: 28 January 1998 / Accepted: 9 April 1998     

Change in the Green-Up Dates for Quercus mongolica in Northeast China and Its Climate-Driven Mechanism from 1962 to 2012

The currently available studies on the green-up date were mainly based on ground observations and/or satellite data, and few model simulations integrated with wide coverage satellite data have been reported at large scale over a long time period (i.e., > 30 years). In this study, we combined phenology mechanism model, long-term climate data and synoptic scale remote sensing data to investigate the change in the green-up dates for Quercus mongolica over 33 weather stations in Northeast China and its climate-driven mechanism during 1962-2012. The results indicated that the unified phenology model can be well parameterized with the satellite derived green-up dates. The optimal daily mean temperature for chilling effect was between -27°C and 1°C for Q. mongolica in Northeast China, while the optimal daily mean temperature for forcing effect was above -3°C. The green-up dates for Q. mongolica across Northeast China showed a delayed latitudinal gradient of 2.699 days degree^-1, with the earliest date on the Julian day 93 (i.e., 3^th April) in the south and the latest date on the Julian day 129 (i.e., 9^th May) in the north. The green-up date for Q. mongolica in Northeast China has advanced 6.6 days (1.3 days decade^-1) from 1962 to 2012. With the prevailing warming in autumn, winter and spring in Northeast China during the past 51 years, the chilling effect for Q. mongolica has been weakened, while the forcing effect has been enhanced. The advancing trend in the green-up dates for Q. mongolica implied that the enhanced forcing effect to accelerate green-up was stronger than the weakened chilling effect to hold back green-up while the changes of both effects were caused by the warming climate.     

Climate warming alters the relative importance of plant root and microbial community in regulating the accumulation of soil microbial necromass carbon in a Tibetan alpine meadow

Climate warming is predicted to considerably affect variations in soil organic carbon (SOC), especially in alpine ecosystems. Microbial necromass carbon (MNC) is an important contributor to stable soil organic carbon pools. However, accumulation and persistence of soil MNC across a gradient of warming are still poorly understood. An 8-year field experiment with four levels of warming was conducted in a Tibetan meadow. We found that low-level (+0–1.5°C) warming mostly enhanced bacterial necromass carbon (BNC), fungal necromass carbon (FNC), and total MNC compared with control treatment across soil layers, while no significant effect was caused between high-level (+1.5–2.5°C) treatments and control treatments. The contributions of both MNC and BNC to soil organic carbon were not significantly affected by warming treatments across depths. Structural equation modeling analysis demonstrated that the effect of plant root traits on MNC persistence strengthened with warming intensity, while the influence of microbial community characteristics waned along strengthened warming. Overall, our study provides novel evidence that the major determinants of MNC production and stabilization may vary with warming magnitude in alpine meadows. This finding is critical for updating our knowledge on soil carbon storage in response to climate warming.