46 research outputs found

    Saharan hot and dry sirocco winds drive extreme fire events in Mediterranean Tunisia (North Africa)

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    With hot and dry summers, the Mediterranean basin is affected by recurrent fires. While drought is the major driver of the seasonal and inter-annual fire distribution in its northern and mildest climate conditions, some extreme fire events are also linked to extreme winds or heat waves. The southern part of the Mediterranean basin is located at the driest range of the Mediterranean bioclimate and is influenced by Saharan atmospheric circulations, leading to extreme hot and dry episodes, called Sirocco, and potentially acting as a major contributor to fire hazard. The recently created fire database for Tunisia was used to investigate the +/- 10-day pre- and post-fire timeframe of daily weather conditions associated with fire events over the 1985-2006 period. Positive anomalies in minimum and maximum temperatures, negative anomalies in air relative humidity, and a preferential south-eastern wind during fire events were identified, which were characteristic of Sirocco winds. +7 degrees C anomalies in air temperature and -30% in relative air humidity were the critical thresholds for the most extreme fire conditions. In addition, meteorological anomalies started two days before fire events and lasted for three days after for large fires >400 ha, which suggests that the duration of the Sirocco event is linked with fire duration and final fire size. Lastly, the yearly number of intense Sirocco events better explained the inter-annual variability of burned area over the 1950-2006 period than summer drought based on Standardized Precipitation Evaporation Index (SPEI) indices

    PhLP3 modulates CCT-mediated actin and tubulin folding via ternary complexes with substrates.

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    International audienceMany ATP-dependent molecular chaperones, including Hsp70, Hsp90, and the chaperonins GroEL/Hsp60, require cofactor proteins to regulate their ATPase activities and thus folding functions in vivo. One conspicuous exception has been the eukaryotic chaperonin CCT, for which no regulator of its ATPase activity, other than non-native substrate proteins, is known. We identify the evolutionarily conserved PhLP3 (phosducin-like protein 3) as a modulator of CCT function in vitro and in vivo. PhLP3 binds CCT, spanning the cylindrical chaperonin cavity and contacting at least two subunits. When present in a ternary complex with CCT and an actin or tubulin substrate, PhLP3 significantly diminishes the chaperonin ATPase activity, and accordingly, excess PhLP3 perturbs actin or tubulin folding in vitro. Most interestingly, however, the Saccharomyces cerevisiae PhLP3 homologue is required for proper actin and tubulin function. This cellular role of PhLP3 is most apparent in a strain that also lacks prefoldin, a chaperone that facilitates CCT-mediated actin and tubulin folding. We propose that the antagonistic actions of PhLP3 and prefoldin serve to modulate CCT activity and play a key role in establishing a functional cytoskeleton in vivo

    Alpha-synuclein research: defining strategic moves in the battle against Parkinson’s disease

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    With the advent of the genetic era in Parkinson’s disease (PD) research in 1997, α-synuclein was identified as an important player in a complex neurodegenerative disease that affects >10 million people worldwide. PD has been estimated to have an economic impact of $51.9 billion in the US alone. Since the initial association with PD, hundreds of researchers have contributed to elucidating the functions of α-synuclein in normal and pathological states, and these remain critical areas for continued research. With this position paper the authors strive to achieve two goals: first, to succinctly summarize the critical features that define α-synuclein’s varied roles, as they are known today; and second, to identify the most pressing knowledge gaps and delineate a multipronged strategy for future research with the goal of enabling therapies to stop or slow disease progression in PD. © 2021, The Author(s)

    Usher syndrome IIIA gene clarin-1 is essential for hair cell function and associated neural activation†

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    Usher syndrome 3A (USH3A) is an autosomal recessive disorder characterized by progressive loss of hearing and vision due to mutation in the clarin-1 (CLRN1) gene. Lack of an animal model has hindered our ability to understand the function of CLRN1 and the pathophysiology associated with USH3A. Here we report for the first time a mouse model for ear disease in USH3A. Detailed evaluation of inner ear phenotype in the Clrn1 knockout mouse (Clrn1−/−) coupled with expression pattern of Clrn1 in the inner ear are presented here. Clrn1 was expressed as early as embryonic day 16.5 in the auditory and vestibular hair cells and associated ganglionic neurons, with its expression being higher in outer hair cells (OHCs) than inner hair cells. Clrn1−/− mice showed early onset hearing loss that rapidly progressed to severe levels. Two to three weeks after birth (P14–P21), Clrn1−/− mice showed elevated auditory-evoked brainstem response (ABR) thresholds and prolonged peak and interpeak latencies. By P21, ∼70% of Clrn1−/− mice had no detectable ABR and by P30 these mice were deaf. Distortion product otoacoustic emissions were not recordable from Clrn1−/− mice. Vestibular function in Clrn1−/− mice mirrored the cochlear phenotype, although it deteriorated more gradually than cochlear function. Disorganization of OHC stereocilia was seen as early as P2 and by P21 OHC loss was observed. In sum, hair cell dysfunction and prolonged peak latencies in vestibular and cochlear evoked potentials in Clrn1−/− mice strongly indicate that Clrn1 is necessary for hair cell function and associated neural activation

    Effectiveness of a stunting recovery program for children treated in a specialized center

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    BACKGROUND: Stunting is still very prevalent in many poor and developing regions in the world. This study assessed the effectiveness of a stunting recovery program in children and its associated factor. METHODS: The retrospective study was conducted in a center of stunting recovery. There, children stayed in a day hospital system (9h per day5 days per week), and received five meals per day, pioviding 80% of their energetic daily needs. The main outcome was the stunting recovery rate (i.e., the child present a height for age index (HAZ) > - 1.0 at the time of data collection). A total of 75 children treated for at least 24 months, aged between 6 and 48 months and with an HAZ 24 months" (prevalence rate (PR) = 0.39, 95% confidence interval (Cl): 0.15-0.99P = 0.04) and the variable "Household crowding index" (PR = 0.65, 95% Cl: 0.44-0.95, P = 0.03) were associated with the success of the treatment. CONCLUSION: The environmental conditions in which the children live in their households and late admission to the center negatively influenced the success of stunting recovery, even with an intensive treatment.Univ Fed Alagoas, Fac Nutr, Ctr Recuperacao & Educ Nutr, Cidade Univ, Maceio, BrazilUniv Fed Sao Paulo, Dept Fisiol, Sao Paulo, BrazilUniv Fed Sao Paulo, Dept Fisiol, Sao Paulo, BrazilWeb of Scienc

    Methylation silencing and mutations of the p14ARF and p16INK4a genes in colon cancer.

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    The INK4a-ARF locus encodes two tumor suppressor proteins involved in cell-cycle regulation, p16INK4a and p14ARF, whose functions are inactivated in many human cancers. The aim of this study was to evaluate p14ARF and p16INK4a gene inactivation and its association with some clinocopathological parameters in colon cancer. The mutational and methylation status of the p14ARF and p16INK4a genes was analyzed in 60 primary colon carcinomas and 8 colon cancer cell lines. We have identified the first two reported mutations affecting exon 1beta of p14ARF in the HCT116 cell line and in one of the primary colon carcinomas. Both mutations occur within the N-terminal region of p14ARF, documented as important for nucleolar localization and interaction with Mdm2. Tumor-specific methylation of the p14ARF and p16INK4a genes was found in 33% and 32% of primary colon carcinomas, respectively. Methylation of the p14ARF was inversely correlated with p53 overexpression (p = 0.02). p14ARF and p16INK4a gene methylation was significantly more frequent in right-sided than in left-sided tumors (p = 0.02). Methylation of the p14ARF gene occurred more frequently in well-differentiated adenocarcinomas (p = 0.005), whereas the p16INK4a gene was more often methylated in poorly differentiated adenocarcinomas (p = 0.002). The present results underline the role of p14ARF and p16INK4a gene inactivation in the development of colon carcinoma. They suggest that the methylation profile of specific genes, in particular p14ARF and p16INK4a, might be related to biologically distinct subsets of colon carcinomas and possibly to different tumorigenic pathways
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