Ten recent insights for our understanding of cooperation.
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ABSTRACT:
SUBMITTER: West SA
PROVIDER: S-EPMC7612052 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The field of microbial cooperation has grown enormously over the last decade, leading to improved experimental techniques and a growing awareness of collective behavior in microbes. Unfortunately, many of our theoretical tools and concepts for understanding cooperation fail to take into account the peculiarities of the microbial world, namely strong selection strengths, unique population structure, and non-linear dynamics. Worse yet, common verbal arguments are often far removed from the math involved, leading to confusion and mistakes. Here, we review the general mathematical forms of Price's equation, Hamilton's rule, and multilevel selection as they are applied to microbes and provide some intuition on these otherwise abstract formulas. However, these sometimes overly general equations can lack specificity and predictive power, ultimately forcing us to advocate for more direct modeling techniques.
| S-EPMC3176967 | biostudies-literature
Project description:BackgroundCareer prospects in academic medicine are strongly linked to scientific authorship and this marker has been widely used as an indicator of gender equity in academia. However, direct comparisons of medical disciplines regarding their proportion of female physicians (FP) in different countries are missing. This study examines the gender parity and gender cooperation using first authorships (FA) and senior authorships (SA) of scientific publications in five medical disciplines and six different OECD countries over a 10-year time-trend.MethodsArticles from three high-impact journals in each of the medical discipline radiology, urology, surgery, gynecology, and pediatrics from the years 2007/8 and 2017/18 were retrospectively reviewed. The gender and affiliation location of the FA and SA of original research articles and reviews were assigned and compared with the proportion of in each discipline for the United States of America, Canada, United Kingdom, France, Germany, and Japan. Mantel-Haenszel test and multinomial logistic regression models were used to calculate differences in proportions of women authors and FP and to assess trends and proportions of FA and SA.Results30,803 articles were evaluated. Equally, with rising proportions of FP in all disciplines, the number of women authors increased across years. The shares of women FAs were either significantly higher (urology/surgery/gynecology) or balanced (pediatrics/radiology) compared to the proportion of FP. In contrast, the shares of women SA were balanced only in disciplines with a low proportion of FP (urology and surgery) and otherwise reduced. Women same-gender cooperation was as common as men same-gender cooperation and preferred over a women-led mixed gender cooperation in disciplines where this seemed to be practicable due to the high proportions of FP.ConclusionIn contrast to FA, a significant disparity persists in SA, particularly in disciplines with a high proportion of FP. The discrepancy between FA and SA may reflect, among others, dropout from an academic career in early or mid-academic levels, for example, due to structural inequality; together with the findings on gender preference in authorship collaborations, this may inform future strategies for promoting equal career advancement for women physicians.
| S-EPMC9883917 | biostudies-literature
Project description:Vitiligo, an acquired depigmentation disorder, manifests as white macules on the skin and can cause significant psychological stress and stigmatization. Recent advances have shed light on key components that drive disease onset and progression as well as therapeutic approaches. Vitiligo can be triggered by stress to the melanin pigment-producing cells of the skin, the melanocytes. The triggers, which range from sunburn to mechanical trauma and chemical exposures, ultimately cause an autoimmune response that targets melanocytes, driving progressive skin depigmentation. The most significant progress in our understanding of disease etiology has been made on three fronts: (1) identifying cellular responses to stress, including antioxidant pathways and the unfolded protein response (UPR), as key players in disease onset, (2) characterizing immune responses that target melanocytes and drive disease progression, and (3) identifying major susceptibility genes. The current model for vitiligo pathogenesis postulates that oxidative stress causes cellular disruptions, including interruption of protein maturation in the endoplasmic reticulum (ER), leading to the activation of the UPR and expression of UPR-regulated chemokines such as interleukin 6 (IL-6) and IL-8. These chemokines recruit immune components to the skin, causing melanocytes to be targeted for destruction. Oxidative stress can further increase melanocyte targeting by promoting antigen presentation. Two key components of the autoimmune response that promote disease progression are the interferon (IFN)-?/CXCL10 axis and IL-17-mediated responses. Several genome-wide association studies support a role for these pathways, with the antioxidant gene NRF2, UPR gene XBP1, and numerous immune-related genes including class I and class II major histocompatibility genes associated with a risk for developing vitiligo. Novel approaches to promote repigmentation in vitiligo are being investigated and may yield effective, long-lasting therapies.
| S-EPMC5017284 | biostudies-other
Project description:Transcription factors (TFs) are a special class of DNA-binding proteins that orchestrate gene transcription by recruiting other TFs, co-activators or co-repressors. Their combinatorial interplay in higher organisms maintains homeostasis and governs cell identity by finely controlling and regulating tissue-specific gene expression. Despite the rich literature on the importance of cooperative TFs for deciphering the mechanisms of individual regulatory programs that control tissue specificity in several organisms such as human, mouse, or Drosophila melanogaster, to date, there is still need for a comprehensive study to detect specific TF cooperations in regulatory processes of cattle tissues. To address the needs of knowledge about specific combinatorial gene regulation in cattle tissues, we made use of three publicly available RNA-seq datasets and obtained tissue-specific gene (TSG) sets for ten tissues (heart, lung, liver, kidney, duodenum, muscle tissue, adipose tissue, colon, spleen and testis). By analyzing these TSG-sets, tissue-specific TF cooperations of each tissue have been identified. The results reveal that similar to the combinatorial regulatory events of model organisms, TFs change their partners depending on their biological functions in different tissues. Particularly with regard to preferential partner choice of the transcription factors STAT3 and NR2C2, this phenomenon has been highlighted with their five different specific cooperation partners in multiple tissues. The information about cooperative TFs could be promising: i) to understand the molecular mechanisms of regulating processes; and ii) to extend the existing knowledge on the importance of single TFs in cattle tissues.
| S-EPMC6522001 | biostudies-literature
Project description:The definition of cholangiocarcinoma (CCA) encompasses all tumors originating in the epithelium of the bile ducts, including the intrahepatic bile ducts (ICCA) and extrahepatic bile ducts (ECCA). The incidence of ICCA and ECCA has increased in the last few decades, and molecular advances in both entities have brought understanding of their differences and allowed treatment advances aimed at personalized therapy. In this review, we discuss recent progress in the molecular landscape of CCAs, emerging treatment biomarker-guided strategies, and future insights into the management of advanced disease.
| S-EPMC7886064 | biostudies-literature
Project description:Many traits that are sexually dimorphic, appearing either differently or uniquely in one sex, are also sensitive to an organism's condition. This phenomenon seems to have evolved to limit genetic conflict between traits that are under different selective pressures in each sex. Recent work has shed light on the molecular and developmental mechanisms that govern this condition sensitive growth, and this work has now expanded to encompass both sexual dimorphism as well as conditionally plastic growth, as it seems the two phenomena are linked on a molecular level. In all cases studied the gene doublesex, a conserved regulator of sex differentiation, controls both sexual dimorphism as well as the condition-dependent plastic responses common to these traits. However, the advent of next-generation -omics technologies has allowed researchers to decipher the common and diverged mechanisms of sexually dimorphic plasticity and expand investigations beyond the foundation laid by studies utilizing beetle weapons.
| S-EPMC5880310 | biostudies-literature
Project description:Exonic circular RNAs (circRNAs) have been discovered in all kingdoms of life. In many cases, the details of circRNA function and their involvement in cellular processes and diseases are not yet fully understood. However, the past few years have seen significant developments in bioinformatics and in experimental protocols that advance the ongoing research in this still-emerging field. Sophisticated methods for circRNA generation in vitro and in vivo have been developed, allowing model studies into circRNA function and application. We here review the ongoing circRNA research, giving special attention to recent progress in the field.
| S-EPMC7324948 | biostudies-literature
Project description:By definition, congenital myopathy typically presents with skeletal muscle weakness and hypotonia at birth. Traditionally, congenital myopathy subtypes have been predominantly distinguished on the basis of the pathological hallmarks present on skeletal muscle biopsies. Many genes cause congenital myopathies when mutated, and a burst of new causative genes have been identified because of advances in gene sequencing technology. Recent discoveries include extending the disease phenotypes associated with previously identified genes and determining that genes formerly known to cause only dominant disease can also cause recessive disease. The more recently identified congenital myopathy genes account for only a small proportion of patients. Thus, the congenital myopathy genes remaining to be discovered are predicted to be extremely rare causes of disease, which greatly hampers their identification. Significant progress in the provision of molecular diagnoses brings important information and value to patients and their families, such as possible disease prognosis, better disease management, and informed reproductive choice, including carrier screening of parents. Additionally, from accurate genetic knowledge, rational treatment options can be hypothesised and subsequently evaluated in vitro and in animal models. A wide range of potential congenital myopathy therapies have been investigated on the basis of improved understanding of disease pathomechanisms, and some therapies are in clinical trials. Although large hurdles remain, promise exists for translating treatment benefits from preclinical models to patients with congenital myopathy, including harnessing proven successes for other genetic diseases.
| S-EPMC6290972 | biostudies-literature
Project description:Frontotemporal degeneration (FTD) is a heterogeneous spectrum of neurodegenerative disorders characterized by diverse clinical presentations, neuropathological characteristics, and underlying genetic causes. In the last few years, several advances in the knowledge of clinical and biological aspects have been accomplished and three major scenarios have emerged that will represent the core issues in the FTD scene over the next few years. Foremost, the development of cerebrospinal fluid and blood biomarkers as well as neuroimaging techniques will aid the pursuit of new diagnostic and prognostic markers able to identify the ongoing proteinopathy and predict disease progression, which is key in identifying and stratifying patients for enrolment in clinical trials as well as evaluating response to treatment. On the other hand, current research has focused on the first attempts to slow down or revert disease progression, with the identification of disease modulators associated with disease onset and the ongoing development of the first pharmacological treatments for both sporadic and genetic FTD. Future research will certainly improve our knowledge of FTD and possibly open up a new era of disease-modifying therapies for this still-orphan disorder.
| S-EPMC6913220 | biostudies-literature
Project description:Antiphospholipid syndrome (APS), also known as Hughes Syndrome, is a systemic autoimmune disease characterized by thrombosis and/or pregnancy morbidity in the presence of persistently positive antiphospholipid antibodies. A patient with APS must meet at least one of two clinical criteria (vascular thrombosis or complications of pregnancy) and at least one of two laboratory criteria including the persistent presence of lupus anticoagulant (LA), anticardiolipin antibodies (aCL), and/or anti-b2 glycoprotein I (anti-b2GPI) antibodies of IgG or IgM isotype at medium to high titres in patient's plasma. However, several other autoantibodies targeting other coagulation cascade proteins (i.e. prothrombin) or their complex with phospholipids (i.e. phosphatidylserine/prothrombin complex), or to some domains of ?2GPI, have been proposed to be also relevant to APS. In fact, the value of testing for new aPL specificities in the identification of APS in thrombosis and/or pregnancy morbidity patients is currently being investigated.
| S-EPMC5224683 | biostudies-literature