Biological and fisheries data were analysed to assess the impact of fisheries mortality on a Critically Endangered subpopulation of <100 humpback dolphins Sousa chinensis in the eastern Taiwan Strait ...(ETS). Substantial interactions between ETS S. chinensis (hereafter Sousa) and fishing gear are known to cause dolphin mortality. In 2009, a total of 6318 motorised fishing vessels were operating from ports within Sousa habitats. An average of 32 fishing craft per kilometre was observed along a 200 km stretch of Sousa habitat. Based on a photo-identification catalogue, >30% of the ETS Sousa subpopulation exhibited injuries caused by fishing gear. Three individuals were photographed with fishing gear attached to their bodies, and 1 dolphin was found dead with fresh injuries caused by fishing gear. To ensure recovery of ETS Sousa, mortality due to human causes should be reduced to <1 individual every 7 yr. Fisheries bycatch is the most serious threat to these dolphins and needs to be eliminated as soon as possible to avoid extinction. Preventing the use of trammel nets, other gillnets and trawling throughout their habitat would be the single most effective conservation measure for ETS Sousa in the short term. Other fishing methods are available, and using the most selective, sustainable fishing methods available will benefit not only dolphins but also fish stocks, seabirds and other species, as well as the fishing industry, which depends on these species for its long-term viability. However, in the short term, there are costs associated with switching to more selective fishing gear.
Abstract
Background
Excessive activation of immune responses in coronavirus disease 2019 (COVID-19) is considered to be related to disease severity, complications, and mortality rate. The complement ...system is an important component of innate immunity and can stimulate inflammation, but its role in COVID-19 is unknown.
Methods
A prospective, longitudinal, single center study was performed in hospitalized patients with COVID-19. Plasma concentrations of complement factors C3a, C3c, and terminal complement complex (TCC) were assessed at baseline and during hospital admission. In parallel, routine laboratory and clinical parameters were collected from medical files and analyzed.
Results
Complement factors C3a, C3c, and TCC were significantly increased in plasma of patients with COVID-19 compared with healthy controls (P < .05). These complement factors were especially elevated in intensive care unit patients during the entire disease course (P < .005 for C3a and TCC). More intense complement activation was observed in patients who died and in those with thromboembolic events.
Conclusions
Patients with COVID-19 demonstrate activation of the complement system, which is related to disease severity. This pathway may be involved in the dysregulated proinflammatory response associated with increased mortality rate and thromboembolic complications. Components of the complement system might have potential as prognostic markers for disease severity and as therapeutic targets in COVID-19.
The complement system is persistently activated in hospitalized patients with coronavirus disease 2019 (COVID-19) and associated with disease severity and onset of thromboembolic complications. These findings support the potential use of complement inhibitors to treat severely ill patients with COVID-19.
We identified cellular and molecular mechanisms within the stem cell niche that control the activity of colonic epithelial progenitors (ColEPs) during injury. Here, we show that while WT mice ...maintained ColEP proliferation in the rectum following injury with dextran sodium sulfate, similarly treated Myd88(-/-) (TLR signaling-deficient) and prostaglandin-endoperoxide synthase 2(-/-) (Ptgs2(-/-)) mice exhibited a profound inhibition of epithelial proliferation and cellular organization within rectal crypts. Exogenous addition of 16,16-dimethyl PGE(2) (dmPGE(2)) rescued the effects of this injury in both knockout mouse strains, indicating that Myd88 signaling is upstream of Ptgs2 and PGE(2). In WT and Myd88(-/-) mice, Ptgs2 was expressed in scattered mesenchymal cells. Surprisingly, Ptgs2 expression was not regulated by injury. Rather, in WT mice, the combination of injury and Myd88 signaling led to the repositioning of a subset of the Ptgs2-expressing stromal cells from the mesenchyme surrounding the middle and upper crypts to an area surrounding the crypt base adjacent to ColEPs. These findings demonstrate that Myd88 and prostaglandin signaling pathways interact to preserve epithelial proliferation during injury using what we believe to be a previously undescribed mechanism requiring proper cellular mobilization within the crypt niche.
Referential signaling in a communally breeding bird LaPergola, Joshua B; Savagian, Amanda G; Smith, Maria G ...
Proceedings of the National Academy of Sciences - PNAS,
05/2023, Letnik:
120, Številka:
19
Journal Article
Recenzirano
Odprti dostop
Referential signaling, a complex form of communication in which specific signals are associated with external referents, was once thought to be limited to primates. Recent research has documented ...referential signaling in several other cooperative taxa, predominantly in kin-based societies. Here, we show that greater anis, communally nesting birds that breed in nonkin groups, give one type of alarm call in response to aerial threats (flying raptors) and another to more general threats (nonaerial predators). Observational data show that anis give these calls in response to different classes of threats, and playback experiments in the field confirmed that the alarm calls alone are sufficient to elicit appropriate behavioral responses even in the absence of an actual threat. Genetic data on a subset of groups confirmed that breeding groups are composed of nonkin, suggesting that referential alarm calls are often given in situations when no genetic relatives are present. These results suggest that complex referential communication can occur in social groups composed of nonrelatives, despite the absence of kin-selected fitness benefits.
Metabolic networks perform some of the most fundamental functions in living cells, including energy transduction and building block biosynthesis. While these are the best characterized networks in ...living systems, understanding their evolutionary history and complex wiring constitutes one of the most fascinating open questions in biology, intimately related to the enigma of life's origin itself. Is the evolution of metabolism subject to general principles, beyond the unpredictable accumulation of multiple historical accidents? Here we search for such principles by applying to an artificial chemical universe some of the methodologies developed for the study of genome scale models of cellular metabolism. In particular, we use metabolic flux constraint-based models to exhaustively search for artificial chemistry pathways that can optimally perform an array of elementary metabolic functions. Despite the simplicity of the model employed, we find that the ensuing pathways display a surprisingly rich set of properties, including the existence of autocatalytic cycles and hierarchical modules, the appearance of universally preferable metabolites and reactions, and a logarithmic trend of pathway length as a function of input/output molecule size. Some of these properties can be derived analytically, borrowing methods previously used in cryptography. In addition, by mapping biochemical networks onto a simplified carbon atom reaction backbone, we find that properties similar to those predicted for the artificial chemistry hold also for real metabolic networks. These findings suggest that optimality principles and arithmetic simplicity might lie beneath some aspects of biochemical complexity.
Pilocytic astrocytoma is the most common childhood brain tumor, characterized by constitutive MAPK activation. MAPK signaling induces oncogene-induced senescence (OIS), which may cause unpredictable ...growth behavior of pilocytic astrocytomas. The senescence-associated secretory phenotype (SASP) has been shown to regulate OIS, but its role in pilocytic astrocytoma remains unknown.
The patient-derived pilocytic astrocytoma cell culture model, DKFZ-BT66, was used to demonstrate presence of the SASP and analyze its impact on OIS in pilocytic astrocytoma. The model allows for doxycycline-inducible switching between proliferation and OIS. Both states were studied using gene expression profiling (GEP), Western blot, ELISA, and cell viability testing. Primary pilocytic astrocytoma tumors were analyzed by GEP and multiplex assay.
SASP factors were upregulated in primary human and murine pilocytic astrocytoma and during OIS in DKFZ-BT66 cells. Conditioned medium induced growth arrest of proliferating pilocytic astrocytoma cells. The SASP factors IL1B and IL6 were upregulated in primary pilocytic astrocytoma, and both pathways were regulated during OIS in DKFZ-BT66. Stimulation with rIL1B but not rIL6 reduced growth of DKFZ-BT66 cells and induced the SASP. Anti-inflammatory treatment with dexamethasone induced regrowth of senescent cells and inhibited the SASP. Senescent DKFZ-BT66 cells responded to senolytic BCL2 inhibitors. High
and SASP expression in pilocytic astrocytoma tumors was associated with favorable progression-free survival.
We provide evidence for the SASP regulating OIS in pediatric pilocytic astrocytoma, with IL1B as a relevant mediator. SASP expression could enable prediction of progression in patients with pilocytic astrocytoma. Further investigation of the SASP driving the unpredictable growth of pilocytic astrocytomas, and its possible therapeutic application, is warranted.
Biodiesel is obtained from a renewable source and has been used as an alternative to fossil fuels. It has unsaturated fatty acid methyl esters that can degrade due to oxidation of the double bonds. ...The instability of biodiesel during storage may cause problems regarding the maintenance and operation of motors. This work evaluated the effect of several variables on the storage conditions of biodiesel:diesel blends. The study was performed using an experimental design, and the variables were water content in biodiesel (0.01, 0.05 and 0.09%), biodiesel content in diesel (5.0, 7.5 and 10.0%), time (15, 30 and 45 days) and temperature (30, 40 and 50 °C). The levels simulated actual Brazilian storage conditions. The degradation was evaluated based on direct measurement of methyl linoleate and methyl oleate in the blends by gas chromatography-mass spectrometry. These unsaturated fatty acid methyl esters are target compounds in the oxidation process. All experiments were carried out in sealed flasks. The results suggest that the restriction of oxygen limited the degradation of biodiesel in blends with higher percentage of the biofuel. The variables temperature, time and water content in biodiesel individually did not affect the degradation process within the range investigated at 95% confidence interval.
BRAF
V600 mutations occur in a wide range of tumor types and RAF inhibition has become standard in several of these cancers. Despite this progress,
BRAF
V600 mutations have historically been ...considered a clear demonstration of tumor lineage context-dependent oncogene addiction, based predominantly on the insensitivity of RAF inhibition in colorectal cancer. However, the true broader activity of RAF inhibition pan-cancer remains incompletely understood. To address this, we conducted a multi-cohort ‘basket’ study of the BRAF inhibitor vemurafenib in non-melanoma BRAF V600 mutation-positive solid tumors. In total, 172 patients with 26 unique cancer types were treated, achieving an overall response rate of 33% and median duration of response of 13 months. Responses were observed in 13 unique cancer types, including historically treatment-refractory tumors such as cholangiocarcinoma, sarcoma, glioma, neuroendocrine carcinoma, and salivary gland carcinomas. Collectively, these data demonstrate that single-agent BRAF inhibition has broader clinical activity than previously recognized.
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