Interannual variability of the Tropical Atlantic independent of and associated with ENSO: Part II. The South Tropical Atlantic

Two dominant ocean-atmosphere modes of variability on interannual timescales were defined in Part I of this work, namely, the North Tropical Atlantic (NTA) and South Tropical Atlantic (STA) modes. In this paper we focus on the STA mode that covers the equatorial and sub-tropical South Atlantic. We show that STA events occurring in conjunction with ENSO have a preference for the southern summer season and seem to be forced by an atmospheric wave train emanating from the central tropical Pacific and travelling via South America, in addition to the more direct ENSO-induced change in the Walker circulation. They are lagged by one season from the peak of ENSO. These events show little evidence for other-than-localised coupled ocean-atmosphere interaction. In contrast, STA events occurring in the absence of ENSO favour the southern winter season. They appear to be triggered by a Southern Hemisphere wave train emanating from the Pacific sector, and then exhibit features of a self-sustaining climate mode in the tropical Atlantic. The southward shift of the inter tropical convergence zone that occurs during the warm phase of such an event triggers an extra tropical wave train that propagates downstream in the Southern Hemisphere. We present a unified view of the NTA and STA modes through our observational analysis of the interannnual tropical Atlantic variability

Response to Maccio et al, - Multifactorial pathogenesis of COVID- 19- related coagulopathy: Can defibrotide have a role in the early phases of coagulation disorders?-

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/163392/2/jth15088_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/163392/1/jth15088.pd

Altered Gene Expression by Low-Dose Arsenic Exposure in Humans and Cultured Cardiomyocytes: Assessment by Real-Time PCR Arrays

Chronic arsenic exposure results in higher risk of skin, lung, and bladder cancer, as well as cardiovascular disease and diabetes. The purpose of this study was to investigate the effects on expression of selected genes in the blood lymphocytes from 159 people exposed chronically to arsenic in their drinking water using a novel RT-PCR TaqMan low-density array (TLDA). We found that expression of tumor necrosis factor-α (TNF-α), which activates both inflammation and NF-κB-dependent survival pathways, was strongly associated with water and urinary arsenic levels. Expression of KCNA5, which encodes a potassium ion channel protein, was positively associated with water and toe nail arsenic levels. Expression of 2 and 11 genes were positively associated with nail and urinary arsenic, respectively. Because arsenic exposure has been reported to be associated with long QT intervals and vascular disease in humans, we also used this TLDA for analysis of gene expression in human cardiomyocytes exposed to arsenic in vitro. Expression of the ion-channel genes CACNA1, KCNH2, KCNQ1 and KCNE1 were down-regulated by 1-μM arsenic. Alteration of some common pathways, including those involved in oxidative stress, inflammatory signaling, and ion-channel function, may underlay the seemingly disparate array of arsenic-associated diseases, such as cancer, cardiovascular disease, and diabetes

Metabolic effects of diets differing in glycaemic index depend on age and endogenous GIP

Aims/hypothesis High- vs low-glycaemic index (GI) diets unfavourably affect body fat mass and metabolic markers in rodents. Different effects of these diets could be age-dependent, as well as mediated, in part, by carbohydrate-induced stimulation of glucose-dependent insulinotrophic polypeptide (GIP) signalling. Methods Young-adult (16 weeks) and aged (44 weeks) male wild-type (C57BL/6J) and GIP-receptor knockout (Gipr −/− ) mice were exposed to otherwise identical high-carbohydrate diets differing only in GI (20–26 weeks of intervention, n = 8–10 per group). Diet-induced changes in body fat distribution, liver fat, locomotor activity, markers of insulin sensitivity and substrate oxidation were investigated, as well as changes in the gene expression of anorexigenic and orexigenic hypothalamic factors related to food intake. Results Body weight significantly increased in young-adult high- vs low-GI fed mice (two-way ANOVA, p < 0.001), regardless of the Gipr genotype. The high-GI diet in young-adult mice also led to significantly increased fat mass and changes in metabolic markers that indicate reduced insulin sensitivity. Even though body fat mass also slightly increased in high- vs low-GI fed aged wild-type mice (p < 0.05), there were no significant changes in body weight and estimated insulin sensitivity in these animals. However, aged Gipr −/− vs wild-type mice on high-GI diet showed significantly lower cumulative net energy intake, increased locomotor activity and improved markers of insulin sensitivity. Conclusions/interpretation The metabolic benefits of a low-GI diet appear to be more pronounced in younger animals, regardless of the Gipr genotype. Inactivation of GIP signalling in aged animals on a high-GI diet, however, could be beneficial

Exclusive electroproduction of K+ Lambda and K+ Sigma^0 final states at Q^2 = 0.030-0.055 (GeV/c)^2

Cross section measurements of the exclusive p(e,e'K+)Lambda,Sigma^0 electroproduction reactions have been performed at the Mainz Microtron MAMI in the A1 spectrometer facility using for the first time the Kaos spectrometer for kaon detection. These processes were studied in a kinematical region not covered by any previous experiment. The nucleon was probed in its third resonance region with virtual photons of low four-momenta, Q^2= 0.030-0.055 (GeV/c)^2. The MAMI data indicate a smooth transition in Q^2 from photoproduction to electroproduction cross sections. Comparison with predictions of effective Lagrangian models based on the isobar approach reveal that strong longitudinal couplings of the virtual photon to the N* resonances can be excluded from these models.Comment: 16 pages, 7 figure

Clues to the nature of damped Lyman alpha systems from chemical evolution models

The evolution of the metallicity of damped Lyman alpha systems (DLAs) is investigated in order to understand the nature of these systems. The observational data on chemical abundances of DLAs are analysed with robust statistical methods, and the abundances are corrected for dust depletion. The results of this analysis are compared to predictions of several classes of chemical evolution models: one-zone dwarf galaxy models, multizone disk models, and chemodynamical models representing dwarf galaxies. We compare the observational data on the [alpha/Fe] and [N/alpha] ratios to the predictions from the models. In DLAs, these ratios are only partially reproduced by the dwarf galaxy one-zone model and by the disk model. On the other hand, the chemodynamical model for dwarf galaxies reproduces the properties of nearly all DLAs. We derive the formation epoch of dwarf galaxies, and we find that dwarf galaxies make a significant contribution to the total neutral gas density in DLAs, and that this contribution is more important at high redshifts (z > 2-3). We propose a scenario in which the DLA population is dominated by dwarf galaxies at high redshifts and by disks at lower redshifts. We also find that Lyman Break Galaxies (LBGs) may constitute a sequence rather than present a sharp dichotomy between the two populations. We also arise the possibility that we could be missing a whole population of high HI density column objects, with metallicities intermediate between those of DLAs and LBGs. Finally, we discuss the possibility that relying only on the observations of DLAs could lead to an underestimate of the metal content of the high redshift Universe.Comment: 23 pages, 19 figures. Accepted for publication in MNRA

Microcrystalline Tyrosine (MCT®): A Depot Adjuvant in Licensed Allergy Immunotherapy Offers New Opportunities in Malaria

Microcrystalline Tyrosine (MCT®) is a widely used proprietary depot excipient in specific immunotherapy for allergy. In the current study we assessed the potential of MCT to serve as an adjuvant in the development of a vaccine against malaria. To this end, we formulated the circumsporozoite protein (CSP) of P. vivax in MCT and compared the induced immune responses to CSP formulated in PBS or Alum. Both MCT and Alum strongly increased immunogenicity of CSP compared to PBS in both C57BL/6 and BALB/c mice. Challenge studies in mice using a chimeric P. bergei expressing CSP of P. vivax demonstrated clinically improved symptoms of malaria with CSP formulated in both MCT and Alum; protection was, however, more pronounced if CSP was formulated in MCT. Hence, MCT may be an attractive biodegradable adjuvant useful for the development of novel prophylactic vaccines

Effectiveness of rotavirus vaccination in Spain

With the aim of determining rotavirus vaccine effectiveness (RVVE) in Spain, from Oct-2008/Jun-2009, 467 consecutive children below 2 years old with acute gastroenteritis (AGE) were recruited using a pediatric research network (ReGALIP-www.regalip.org) that includes primary, emergency and hospital care settings. Of 467 enrolled children, 32.3% were rotavirus positive and 35.0% had received at least one dose of any rotavirus vaccine. RRVE to prevent any episode of rotavirus AGE was 91.5% (95% CI: 83.7%-95.6%). RVVE to prevent hospitalization by rotavirus AGE was 95.6% (85.6-98.6%). No differences in RVVE were found regarding the vaccine used. Rotavirus vaccines have showed an outstanding effectiveness in Spain

The Ubiquitin-Proteasome Reporter GFPu Does Not Accumulate in Neurons of the R6/2 Transgenic Mouse Model of Huntington's Disease

Impairment of the ubiquitin-proteasome system (UPS) has long been considered an attractive hypothesis to explain the selective dysfunction and death of neurons in polyglutamine disorders such as Huntington's disease (HD). The fact that inclusion bodies in HD mouse models and patient brains are rich in ubiquitin and proteasome components suggests that the UPS may be hindered directly or indirectly by inclusion bodies or their misfolded monomeric or oligomeric precursors. However, studies into UPS function in various polyglutamine disease models have yielded conflicting results, suggesting mutant polyglutamine tracts may exert different effects on the UPS depending on protein context, expression level, subcellular localisation and cell-type. To investigate UPS function in a well-characterised mouse model of HD, we have crossed R6/2 HD mice with transgenic UPS reporter mice expressing the GFPu construct. The GFPu construct comprises GFP fused to a constitutive degradation signal (CL-1) that promotes its rapid degradation under conditions of a healthy UPS. Using a combination of immunoblot analysis, fluorescence and immunofluorescence microscopy studies, we found that steady-state GFPu levels were not detectably different between R6/2 and non-R6/2 brain. We observed no correlation between inclusion body formation and GFPu accumulation, suggesting no direct relationship between protein aggregation and global UPS inhibition in R6/2 mice. These findings suggest that while certain branches of the UPS can be impaired by mutant polyglutamine proteins, such proteins do not necessarily cause total blockade of UPS-dependent degradation. It is therefore likely that the relationship between mutant polyglutamine proteins and the UPS is more complex than originally anticipated