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Wildlife trade is a multi-billion-dollar sector that impacts a wide range of species, and thus is of significant research and conservation interest. Wildlife trade has also become a prominent topic in the public-facing media, where coverage has intensified following the outbreak of the global COVID-19 pandemic due to the potential connection between wildlife trade and the origin of the SARS Cov2 virus. Given the importance of the media in shaping public understanding and discourse of complex topics such as wildlife trade, this could impact the implementation of and public support for policy decisions. In this study, we followed a standardised protocol to extract wildlife trade-related discussion from 285 professional opinion pieces (NGO reports or articles in conservation-themed forums) and 107 scientific articles published in two time periods: "pre-COVID" (June 1-December 31, 2019) and "during-COVID" (January 1-May 31, 2020). We compared opinion pieces and scientific articles across the two time periods and to each other to investigate potential differences in the presentation of wildlife trade and associated speakers. We found a shift in the way that wildlife trade was discussed in professional opinion pieces between the periods, in that the discussion became less specific in terms of defining the legality and purpose of trade, and the animal groups involved in the "during-COVID" period. The generalised framing of wildlife trade in our dataset also coincided with an increased discussion of highly generalised management strategies, such as blanket bans on wildlife trade. We also found that publications included more quotes from researchers in the "during-COVID" period. In both professional opinion pieces and scientific articles, we found that quotations or research were often from speakers whose affiliation region was different to the geographic range of the trade they were speaking about. This highlights the importance of incorporating local knowledge and considering the diversity of speakers and interviewees in both research and the public-facing media about the wildlife trade., Competing Interests: The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Hannah S Mumby reports financial support was provided by Branco Weiss-Society In Science Fellowship. Hannah S Mumby reports financial support was provided by Association for the Study of Animal Behaviour., (© 2022 The Authors.)

The king scallop, Pecten maximus is a highly valuable seafood in Europe. Over the last few years, its culture has been threatened by toxic microalgae during harmful algal blooms, inducing public health concerns. Indeed, phycotoxins accumulated in bivalves can be harmful for human, especially paralytic shellfish toxins (PST) synthesized by the microalgae Alexandrium minutum. Deleterious effects of these toxic algae on bivalves have also been reported. However, its impact on bivalves such as king scallop is far from being completely understood. This study combined ecophysiological and proteomic analyzes to investigate the early response of juvenile king scallops to a short term exposure to PST producing A. minutum. Our data showed that all along the 2-days exposure to A. minutum, king scallops exhibited transient lower filtration and respiration rates and accumulated PST. Significant inter-individual variability of toxin accumulation potential was observed among individuals. Furthermore, we found that ingestion of toxic algae, correlated to toxin accumulation was driven by two factors: 1/ the time it takes king scallop to recover from filtration inhibition and starts to filtrate again, 2/ the filtration level to which king scallop starts again to filtrate after inhibition. Furthermore, at the end of the 2-day exposure to A. minutum, proteomic analyzes revealed an increase of the killer cell lectin-like receptor B1, involved in adaptative immune response. Proteins involved in detoxification and in metabolism were found in lower amount in A. minutum exposed king scallops. Proteomic data also showed differential accumulation in several structure proteins such as β-actin, paramyosin and filamin A, suggesting a remodeling of the mantle tissue when king scallops are subjected to an A. minutum exposure., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Sexual reproduction remains poorly characterized in dinoflagellates. This is especially the case at the molecular level. Here crossing experiments were performed among strains of the toxic dinoflagellate Alexandrium minutum belonging to two genetically divergent groups. Gene expression was compared between sexually compatible and incompatible crosses at the time of gamete fusion and resting cyst (~zygote) formation. Not a single transcript was identified as differentially expressed between compatible and incompatible crosses at these two crucial time points of the dinoflagellate life cycle. However, several thousands of transcripts displayed constitutive expression differences between strains. This was especially the case between the strains belonging to the genetically divergent groups. A few hundreds of transcripts were also identified as differentially expressed between strains belonging to opposite mating types. Some of these transcripts displayed homology with the SxtA protein, known to be involved in saxitoxin production in cyanobacteria, as well as with proteins potentially involved in mating in fungi., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Oregano essential oil has long been known for its health-promoting benefits. Here, we report its activity against viral replication. Oregano oil was found to specifically inhibit lentiviruses, such as human and simian immunodeficiency viruses (HIV and SIV), irrespective of virus tropism, but not hepatitis C virus, adenovirus 5 (ADV5), Zika virus, and influenza (H1N1) virus. Oregano oil's most abundant components, carvacrol and its isomer, thymol, were shown to block virus-target cell fusion while not perturbing other stages of the virus life cycle. We detected changes in virus particle density, suggesting that cholesterol depletion from the HIV-1 envelope membrane reduces virus entry. Furthermore, infection was rescued by adding exogenous cholesterol. The evolution of viral resistance to carvacrol supported this mechanism of action with the identification of mutations in the viral gp41 fusion protein that counteracted cholesterol depletion. In addition, resistance to carvacrol emerged later than typically observed for other clinically used drugs, strengthening its antiviral potential. Structure-activity relationship studies revealed key motifs of carvacrol and thymol required for HIV neutralization and identified previously unknown active analogs. Carvacrol was also shown to additively cooperate with antiretroviral therapy. In sum, oregano oil and improved carvacrol and thymol analogs could be considered to supplement current HIV therapeutics. IMPORTANCE Oregano essential oil has multiple benefits in traditional medicine, cosmetics, and food industries. Carvacrol and its analog, thymol, are well-described components of oregano oil. Here, we show that these compounds inhibit HIV-target cell fusion independently of viral tropism. Our results suggest that carvacrol and thymol alter the cholesterol content of the viral membrane, blocking HIV-1 entry into the target cell. Resistance to carvacrol has selected for viruses with mutations in the viral envelope glycoprotein, gp41. This protein is known for its interaction with cholesterol present in membrane lipid rafts. Together, these results demonstrate the potential of therapies targeting the viral envelope membrane, and oregano oil is a safe supplement to antiretrovirals, potentially delaying disease progression and resistance development., (Copyright © 2020 American Society for Microbiology.)

There is a constant need to improve antiretrovirals against HIV since therapy is limited by cost, side effects and the emergence of drug resistance. Kudzu is a climbing vine from which the root extract (Pueraria lobata), rich in isoflavones and saponins, has long been used in traditional Chinese medicine for a variety of purposes, from weight loss to alcoholism prevention. Here we show that Kudzu root extract significantly inhibits HIV-1 entry into cell lines, primary human CD4 + T lymphocytes and macrophages, without cell-associated toxicity. Specifically, Kudzu inhibits the initial attachment of the viral particle to the cell surface, a mechanism that depends on the envelope glycoprotein gp120 but is independent from the HIV-1 cell receptor CD4 and co-receptors CXCR4/CCR5. This activity seems selective to lentiviruses since Kudzu inhibits HIV-2 and simian immunodeficiency virus, but does not interfere with Hepatitis C, Influenza, Zika Brazil and adenovirus infection. Importantly, depending on the dose, Kudzu can act synergistically or additively with the current antiretroviral cocktails against HIV-1 and can block   viruses resistant to the fusion inhibitor Enfuvirtide. Together our results highlight Kudzu's root extract value as a supplement to current antiretroviral therapy against HIV.

The perinucleolar compartment (PNC) is a subnuclear stucture forming predominantly in cancer cells; its prevalence positively correlates with metastatic capacity. Although several RNA-binding proteins have been characterized in PNC, the molecular function of this compartment remains unclear. Here we demonstrate that the cyclin-dependent kinase 13 (CDK13) is a newly identified constituent of PNC. CDK13 is a kinase involved in the regulation of gene expression and whose overexpression was found to alter pre-mRNA processing. In this study we show that CDK13 is enriched in PNC and co-localizes all along the cell cycle with the PNC component PTB. In contrast, neither the cyclins K and L, known to associate with CDK13, nor the potential kinase substrates accumulate in PNC. We further show that CDK13 overexpression increases PNC prevalence suggesting that CDK13 may be determinant for PNC formation. This result linked to the finding that CDK13 gene is amplified in different types of cancer indicate that this kinase can contribute to cancer development in human.

Strategies for expanding hematopoietic stem cells (HSCs) could have significant utility for transplantation-based therapies. However, deleterious consequences of such manipulations remain unknown. Here we examined the impact of HSC self-renewal divisions in vitro and in vivo on their subsequent regenerative and continuing ability to sustain blood cell production in the absence of telomerase. HSC expansion in vitro was obtained using a NUP98-HOXA10hd transduction strategy and, in vivo, using a serial transplant protocol. We observed ~ 10kb telomere loss in leukocytes produced in secondary mice transplanted with HSCs regenerated in primary recipients of NUP98-HOXA10hd-transduced and in vitro-expanded Tert(-/-) HSCs 6 months before. The second generation leukocytes also showed elevated expression of γH2AX (relative to control) indicative of greater accumulating DNA damage. In contrast, significant telomere shortening was not detected in leukocytes produced from freshly isolated, serially transplanted wild-type (WT) or Tert(-/-) HSCs, suggesting that HSC replication posttransplant is not limited by telomere shortening in the mouse. These findings document a role of telomerase in telomere homeostasis, and in preserving HSC functional integrity on prolonged self-renewal stimulation.

Gene therapy as well as methods capable of returning cells to a pluripotent state (iPS) have enabled the correction of genetic deficiencies in syngenic adult progenitors, reducing the need for immunosuppression in cell therapy approaches. However, in diseases involving mutations that lead to the complete lack of a protein, such as Duchenne muscular dystrophy, the main immunogens leading to rejection of transplanted cells are the therapeutic proteins themselves. In these cases even iPS cells would not circumvent the need for immunosuppression, and alternative strategies must be developed. One such potential strategy seeks to induce immune tolerance using hematopoietic stem cells originated from the same donor or iPS line from which the therapeutic progenitors are derived. However, donor hematopoietic stem cells (HSCs) are available in limiting numbers and embryonic stem (ES) cell-derived HSCs engraft poorly in adults. While these limitations have been circumvented by ectopic expression of HOXB4, overexpression of this protein is associated with inefficient lymphoid reconstitution. Here we show that adult HSCs expanded with a NUP98- HOXA10hd fusion protein sustain long-term engraftment in immunologically mismatched recipients and generate normal numbers of lymphoid cells. In addition, NUP98-HOXA10hd-expanded cells induce functional immune tolerance to a subsequent transplant of myogenic progenitors immunologically matched with the transplanted HSCs.

White adipose tissue (fat) is the primary organ for energy storage and its regulation has serious implications on human health. Excess fat tissue causes significant morbidity, and adipose tissue dysfunction caused by excessive adipocyte hypertrophy has been proposed to play a significant role in the pathogenesis of metabolic disease. Studies in both humans and animal models show that metabolic dysfunction is more closely associated with visceral than subcutaneous fat accumulation. Here, we show that in mice fed a high-fat diet, visceral fat (VAT) grows mostly by hypertrophy and subcutaneous fat (SAT) by hyperplasia, providing a rationale for the different effects of specific adipose depots on metabolic health. To address whether depot expansion is controlled at the level of stem/progenitor cells, we developed a strategy to prospectively identify adipogenic progenitors (APs) from both depots. Clonogenic assays and in vivo bromodeoxyuridine (BrdU) studies show that APs are eightfold more abundant in SAT than VAT, and that AP proliferation is significantly increased in SAT but not VAT in response to high-fat diet. Our results suggest that depot-specific differences in AP abundance and proliferation underlie whether a fat depot expands by hypertrophy or hyperplasia, and thus may have important implications on the development of metabolic disease. In addition, we provide the first evidence that dietary inputs can modulate the proliferation of adipogenic progenitors in adults.

The human immunodeficiency virus type 1 (HIV-1) Tat is a 14-kDa viral protein that acts as a potent transactivator by binding to the transactivation-responsive region, a structured RNA element located at the 5' end of all HIV-1 transcripts. Tat transactivates viral gene expression by inducing the phosphorylation of the C-terminal domain of RNA polymerase II through several Tat-activated kinases and by recruiting chromatin-remodeling complexes and histone-modifying enzymes to the HIV-1 long terminal repeat. Histone acetyltransferases, including p300 and hGCN5, not only acetylate histones but also acetylate Tat at lysine positions 50 and 51 in the arginine-rich motif. Acetylated Tat at positions 50 and 51 interacts with a specialized protein module, the bromodomain, and recruits novel factors having this particular domain, such as P/CAF and SWI/SNF. In addition to having its effect on transcription, Tat has been shown to be involved in splicing. In this study, we demonstrate that Tat interacts with cyclin-dependent kinase 13 (CDK13) both in vivo and in vitro. We also found that CDK13 increases HIV-1 mRNA splicing and favors the production of the doubly spliced protein Nef. In addition, we demonstrate that CDK13 acts as a possible restriction factor, in that its overexpression decreases the production of the viral proteins Gag and Env and subsequently suppresses virus production. Using small interfering RNA against CDK13, we show that silencing of CDK13 leads to a significant increase in virus production. Finally, we demonstrate that CDK13 mediates its effect on splicing through the phosphorylation of ASF/SF2.

Sea urchin is a classical research model system in developmental biology; moreover, the external fertilization and growth of embryos, their rapid division cycle, their transparency and the accessibility of these embryos to molecular visualization methods, made them good specimens to analyze the regulatory mechanisms of cell division. These features as well as the phylogenetic position of sea urchin, close to vertebrates but in an outgroup within the deuterostomes, led scientists working on this model to sequence the genome of the species S. purpuratus. The genome contains a full repertoire of cell cycle control genes. A comparison of this toolkit with those from vertebrates, nematodes, drosophila, as well as tunicates, provides new insight into the evolution of cell cycle control. While some gene subtypes have undergone lineage-specific expansions in vertebrates (i.e. cyclins, mitotic kinases,...), others seem to be lost in vertebrates, for instance the novel cyclin B identified in S. purpuratus. On the other hand, some genes which were previously thought to be vertebrate innovations, are also found in sea urchins (i.e. MCM9). To note is also the absence of cell cycle inhibitors of the INK type, which are apparently confined to vertebrates. The uncovered genomic repertoire of cell-cycle regulators will thus provide molecular tools that should further enhance future research on cell cycle control and developmental regulation in this model.

The human CDC2L5 gene encodes a protein of unknown physiological function. This protein is closely related to the cyclin-dependent kinase (Cdks) family and contains an arginine/serine-rich (RS) domain. The Cdks were first identified as crucial regulators of cell-cycle progression, more recently they were found to be involved in transcription and mRNA processing. RS domains are mainly present in proteins regulating pre-mRNA splicing, suggesting CDC2L5 having a possible role in this process. In this study, we demonstrate that CDC2L5 is located in the nucleoplasm, at a higher concentration in speckles, the storage sites for splicing factors. Furthermore, this localization is dependent on the presence of the N-terminal sequence including the RS domain. Then, we report that CDC2L5 directly interacts with the ASF/SF2-associated protein p32, a protein involved in splicing regulation. Overexpression of CDC2L5 constructs disturbs constitutive splicing and switches alternative splice site selection in vivo. These results argue in favor of a functional role of the CDC2L5 kinase in splicing regulation., (2006 Wiley-Liss, Inc.)

Intravenous cannula and administration set fixation is crucial for fluid resuscitation and intravenous administration of medications. Because conventional hospital fixations are insufficient for the military field scenario, two consecutive, prospective, randomized, clinical trials were performed in the Israel Defense Forces Medical School, to determine the most effective fixation method in the military arena. Gauze bandage, adhesive bandage, Coban wrap, and plastic wrap fixation methods were tested for field conditions and intravenous fluid flow. The results showed that plastic wrap is the fastest fixation method, withstands field conditions with minimal negative effects on the intravenous fluid flow, and is the most cost-effective.

Recent findings suggested that the role of cysteine proteases would not be limited to protein degradation in lysosomes but would also play regulatory functions in more specific cell mechanisms. We analyzed here the role of these enzymes in the control of cell cycle during embryogenesis. The addition of the potent cysteine protease inhibitor E64d to newly fertilized sea urchin eggs disrupted cell cycle progression, affecting nuclear as well as cytoplasmic characteristic events. Monitoring BrdU incorporation in E64d treated eggs demonstrated that DNA replication is severely disturbed. Moreover, this drug treatment inhibited male histones degradation, a step that is necessary for sperm chromatin remodeling and precedes the initiation of DNA replication in control eggs. This inhibition likely explains the DNA replication disturbance and suggests that S phase initiation requires cysteine protease activity. In turn, activation of the DNA replication checkpoint could be responsible for the consecutive block of nuclear envelope breakdown (NEB). However, in sea urchin early embryos this checkpoint doesn't control the mitotic cytoplasmic events that are not tightly coupled with NEB. Thus the fact that microtubule spindle is not assembled and cyclin B-cdk1 not activated under E64d treatment more likely rely on a distinct mechanism. Immunofluorescence experiments indicated that centrosome organization was deficient in absence of cysteine protease activity. This potentially accounts for mitotic spindle disruption and for cyclin B mis-localization in E64d treated eggs. We conclude that cysteine proteases are essential to trigger S phase and to promote M phase entry in newly fertilized sea urchin eggs., ((c) 2005 Wiley-Liss, Inc.)

The polyunsaturated aldehydes are highly reactive products of fatty acid peroxidation and combustion of organic materials, and they have been documented to have diverse cyctotoxic and genotoxic effects. The alpha,beta,gamma,delta-unsaturated aldehyde 2-trans-4-trans-decadienal is produced by marine microalgae, and it is known to inhibit cell proliferation and induce apoptosis in several different cell types. However, the molecular basis for the cell cycle arrest is not fully understood. We used sea urchin embryos to examine how some of the key events of the mitotic cell division were influenced by this polyunsaturated aldehyde. We found that cell divisions in embryos of Sphaerechinus granularis were inhibited by 2-trans-4-trans-decadienal in a dose dependent manner with an EC50 of 1.3 microM. Mitotic events in the nondividing eggs were characterized using immunofluorescent staining. DNA labelling revealed that pronuclear migration was inhibited, and a total absence of incorporation of the DNA-base analogue 5-bromo-2-deoxyuridine indicated that no DNA replication had occurred. Staining of alpha-tubulin subunits showed that tubulin-polymerization was disrupted and aberrations were induced in mitotic spindles. Furthermore, we monitored the activity of the G2-M promoting complex cyclin B-Cdk1 in newly fertilized sea urchin eggs, and found that this complex was not activated in embryos treated with 2-trans-4-trans-decadienal despite the accumulation of cyclin B.

The experiments reported here were motivated by our interest to express in stably-transfected cells large amounts of recombinant rat GABAA receptors. For this, we developed an original two step selection strategy, in which the first step consisted of transfecting HEK 293 cells with rat GABAA receptor alpha and beta subunits. G 418 resistant colonies isolated at this step were screened for [3H] muscimol binding to select for those that coexpressed alpha- and beta-subunits. The best alpha and beta subunit expressing colony was then supertransfected with a plasmid coding for the gamma rat GABAA receptor subunit and a mutant DHFR gene. After a second round of selection, this time in presence of methotrexate, those colonies that coexpressed ternary alpha beta gamma GABAA receptor combinations were distinguished using [3H] flumazenil as a probe. This strategy was applied to the isolation of 3 GABAA receptor clones, alpha 1 beta 2 gamma 2s, alpha 3 beta 2 gamma 2s and alpha 5 beta 3 gamma 2s, that expressed relatively high levels of these proteins. These 3 cell lines exhibited pharmacological and functional properties similar to cells transiently-transfected with equivalent subunit combinations. These cell lines therefore provide attractive models with which to evaluate the intrinsic activity and potency of compounds at recombinant GABAA receptor subtypes.

Oculomotor apraxia may be idiopathic or a symptom of a variety of diseases. In Gaucher disease, oculomotor deficit is characterized by a failure of volitional horizontal gaze with preservation of vertical movements. We present 2 sisters, 6 1/2 and 5 1/2 years of age, in whom the presenting sign was oculomotor apraxia. Oculomotor apraxia has not been previously reported as the presenting manifestation of Gaucher disease.

A rare syndrome comprising midfacial hypoplasia, lack of anterior nasal spine, and malocclusion is described. To the best of our knowledge, only sporadic cases with a similar cluster of defects have been reported, usually with the appellation of Binder syndrome. We describe an affected mother and daughter, thus suggesting a dominant mode of inheritance.

Three antenatal monitoring tests--fetal movement acceleration test (FMAC-test), fetal heart rate-nonstress test (FHR-NST), and daily fetal movement recording (DFMR) were evaluated in 212 high risk pregnant women. While in 196 cases all three tests were normal, in 16 patients one to three tests showed pathological results. In the latter group, there was a significantly higher incidence of perinatal mortality, low Apgar score and growth retardation. Since false positives are known to occur in these tests, at least two should be pathological to warrant delivery in am attempt to prevent fetal death in utero. The sequence in which the pathology appears in the deteriorating fetus is as follows: the first to become non-reactive is the FMAC-test, followed by decreased fetal movements till cessation, and, finally, severe changes in the FHR-NST take place. The importance of this sequence of events is discussed.