Recruitment limitation in three large‐seeded plant species in a tropical moist forest

Recruitment limitation—the failure of a species to establish recruits at an available site—is a potential determinant of plant communities’ structure, causing local communities to be a limited subset of the regional species pool. Recruitment limitation results from three mechanisms: (i) lack of seed sources (i.e., source limitation), (ii) failure of available seeds to reach recruitment sites (i.e., dispersal limitation), and (iii) failure of arrived seeds to establish at a location (i.e., establishment limitation). Here, we evaluated the relative importance of these mechanisms in three co-occurring tree species (Dipteryx oleifera, Attalea butyracea, and Astrocaryum standleyanum) that share seed dispersers/predators. The study was set up on Barro Colorado Island (Panama) at 62 one-ha sites with varying tree densities. Source limitation was estimated as the proportion of sites that would be reached by seeds if seeds were distributed uniformly. Dispersal limitation was estimated from the number of sites with seeds in the soil bank. Establishment limitation was evaluated by measuring germination and 1-year survival in seed addition experiments. The effect of conspecific and heterospecific densities on the mechanisms was evaluated at three spatial scales (1, 5, and 9 ha). For all species, seed predation was the most important recruitment component (~80% decrease in seed survival). Establishment varied among species and was affected by conspecific and heterospecific species densities across spatial scales. Given that species identity, distribution, and seed dispersal/predation affect recruitment at multiple scales, multiscale studies are required to understand how recruitment limitation determines community structure in tropical forests

Pathogenesis and Clinical Relevance of Candida Biofilms in Vulvovaginal Candidiasis

The ability of Candida spp. to form biofilms is crucial for its pathogenicity, and thus, it should be considered an important virulence factor in vulvovaginal candidiasis (VVC) and recurrent VVC (RVVC). Its ability to generate biofilms is multifactorial and is generally believed to depend on the site of infection, species and strain involved, and the microenvironment in which the infection develops. Therefore, both cell surface proteins, such as Hwp1, Als1, and Als2, and the cell wall-related protein, Sun41, play a critical role in the adhesion and virulence of the biofilm. Immunological and pharmacological approaches have identified the NLRP3 inflammasome as a crucial molecular factor contributing to host immunopathology. In this context, we have earlier shown that Candida albicans associated with hyphae-secreted aspartyl proteinases (specifically SAP4-6) contribute to the immunopathology of the disease. Transcriptome profiling has revealed that non-coding transcripts regulate protein synthesis post-transcriptionally, which is important for the growth of Candida spp. Other studies have employed RNA sequencing to identify differences in the 1,245 Candida genes involved in surface and invasive cellular metabolism regulation. In vitro systems allow the simultaneous processing of a large number of samples, making them an ideal screening technique for estimating various physicochemical parameters, testing the activity of antimicrobial agents, and analyzing genes involved in biofilm formation and regulation (in situ) in specific strains. Murine VVC models are used to study C. albicans infection, especially in trials of novel treatments and to understand the cause(s) for resistance to conventional therapeutics. This review on the clinical relevance of Candida biofilms in VVC focuses on important advances in its genomics, transcriptomics, and proteomics. Moreover, recent experiments on the influence of biofilm formation on VVC or RVVC pathogenesis in laboratory animals have been discussed. A clear elucidation of one of the pathogenesis mechanisms employed by Candida biofilms in vulvovaginal candidiasis and its applications in clinical practice represents the most significant contribution of this manuscript

Biomarkers of Inflammation in Obesity-Psoriatic Patients

Psoriasis is a common chronic inflammatory multisystemic disease with a complex pathogenesis consisting of genetic, immunological, and environmental components. It is associated with a number of comorbidities, including diabetes, metabolic syndrome, obesity, and myocardial infarction. In addition, the severity of psoriasis seems to be related to the severity of obesity. Patients with higher levels of obesity show poorer response to systemic treatments of psoriasis. Several studies have demonstrated that white adipose tissue is a crucial site of the formation of proinflammatory adipokines such as leptin, adiponectin, and resistin and classical cytokines such as interleukin- (IL-) 6 and tumour necrosis factor-alpha. In psoriasis, due to the proliferation of Th1, Th17, and Th22 cells, IL-22, among others, is produced in addition to the abovementioned cytokines. With respect to leptin and resistin, both of these adipokines are present in high levels in obese persons with psoriasis. Further, the plasma levels of leptin and resistin are related to the severity of psoriasis. These results strongly suggest that obesity, through proinflammatory pathways, is a predisposing factor to the development of psoriasis and that obesity aggravates existing psoriasis. Different inflammatory biomarkers link psoriasis and obesity. In this paper, the most important ones are described

Biomarkers of Inflammation in Obesity-Psoriatic Patients

Psoriasis is a common chronic inflammatory multisystemic disease with a complex pathogenesis consisting of genetic, immunological, and environmental components. It is associated with a number of comorbidities, including diabetes, metabolic syndrome, obesity, and myocardial infarction. In addition, the severity of psoriasis seems to be related to the severity of obesity. Patients with higher levels of obesity show poorer response to systemic treatments of psoriasis. Several studies have demonstrated that white adipose tissue is a crucial site of the formation of proinflammatory adipokines such as leptin, adiponectin, and resistin and classical cytokines such as interleukin-(IL-) 6 and tumour necrosis factor-In psoriasis, due to the proliferation of Th1, Th17, and Th22 cells, IL-22, among others, is produced in addition to the abovementioned cytokines. With respect to leptin and resistin, both of these adipokines are present in high levels in obese persons with psoriasis. Further, the plasma levels of leptin and resistin are related to the severity of psoriasis. These results strongly suggest that obesity, through proinflammatory pathways, is a predisposing factor to the development of psoriasis and that obesity aggravates existing psoriasis. Different inflammatory biomarkers link psoriasis and obesity. In this paper, the most important ones are described

Chitosan-G-Glycidyl Methacrylate/Au Nanocomposites Promote Accelerated Skin Wound Healing

Herein, we report the synthesis of Au nanoparticles (AuNPs) in chitosan (CTS) solution by chemically reducing HAuCl4. CTS was further functionalized with glycidyl methacrylate (chitosan-g-glycidyl methacrylate/AuNP, CTS-g-GMA/AuNP) to improve the mechanical properties for cellular regeneration requirements of CTS-g-GMA/AuNP. Our nanocomposites promote excellent cellular viability and have a positive effect on cytokine regulation in the inflammatory and anti-inflammatory response of skin cells. After 40 days of nanocomposite exposure to a skin wound, we showed that our films have a greater skin wound healing capacity than a commercial film (TheraForm®), and the presence of the collagen allows better cosmetic ave aspects in skin regeneration in comparison with a nanocomposite with an absence of this protein. Electrical percolation phenomena in such nanocomposites were used as guiding tools for the best nanocomposite performance. Our results suggest that chitosan-based Au nanocomposites show great potential for skin wound repair

Understanding the complex geomorphology of a deep sea area affected by continental tectonic indentation. The case of the Gulf of Vera (Western Mediterranean)

We present a multidisciplinary study of morphology, stratigraphy, sedimentology, tectonic structure, and physical oceanography to report that the complex geomorphology of the Palomares continental margin and adjacent Algerian abyssal plain (i.e., Gulf of Vera, Western Mediterranean), is the result of the sedimentary response to the Aguilas Arc continental tectonic indentation in the Eurasian–Africa plate collision. The indentation is imprinted on the basement of the margin with elongated metamorphic antiforms that are pierced by igneous bodies, and synforms that accommodate the deformation and create a complex physiography. The basement is partially covered by Upper Miocene deposits sealed by the regional Messinian Erosive Surface characterized by palaeocanyons that carve the modern margin. These deposits and outcropping basement highs are then covered and shaped by Plio-Quaternary contourites formed under the action of the Light Intermediate and Dense Deep Mediterranean bottom currents. Even though bottom currents are responsible for the primary sedimentation that shapes the margin, 97% of this region's seafloor is affected by mass-movements that modified contourite sediments by eroding, deforming, faulting, sliding, and depositing sediments. Mass-movement processes have resulted in the formation of recurrent mass-flow deposits, an enlargement of the submarine canyons and gully incisions, and basin-scale gravitational slides spreading above the Messinian Salinity Crisis salt layer. The Polopo, Aguilas and Gata slides are characterized by an extensional upslope domain that shapes the continental margin, and by a downslope contractional domain that shapes the abyssal plain with diapirs piercing (hemi)pelagites/sheet-like turbidites creating a seafloor dotted by numerous crests. The mass movements were mostly triggered by the interplay of the continental tectonic indentation of the Aguilas Arc with sedimentological factors over time. The indentation, which involves the progressively southeastward tectonic tilting of the whole land-sea region, likely generated a quasi-continuous oversteepening of the entire margin, thus reducing the stability of the contourites. In addition, tectonic tilting and subsidence of the abyssal plain favoured the flow of the underlying Messinian Salinity Crisis salt layer, contributing to the gravitational instability of the overlying sediments over large areas of the margin and abyssal plain