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The physics-biology continuum relies on the fact that life emerged from prebiotic molecules. Here, I argue that life emerged from the coupling between nucleic acid and protein synthesis during which proteins (or proto-phenotypes) maintained the physicochemical parameter equilibria (or proto-homeostasis) in the proximity of their encoding nucleic acids (or proto-genomes). This protected the proto-genome physicochemical integrity (i.e., atomic composition) from environmental physicochemical constraints, and therefore increased the probability of reproducing the proto-genome without variation. From there, genomes evolved depending on the biological activities they generated in response to environmental fluctuations. Thus, a genome maintaining homeostasis (i.e., internal physicochemical parameter equilibria), despite and in response to environmental fluctuations, maintains its physicochemical integrity and has therefore a higher probability to be reproduced without variation. Consequently, descendants have a higher probability to share the same phenotype than their parents. Otherwise, the genome is modified during replication as a consequence of the imbalance of the internal physicochemical parameters it generates, until new mutation-deriving biological activities maintain homeostasis in offspring. In summary, evolution depends on feedforward and feedback loops between genome and phenotype, as the internal physicochemical conditions that a genome generates ─ through its derived phenotype in response to environmental fluctuations ─ in turn either guarantee its stability or direct its variation. Evolution may not be explained by the Darwinism-derived, unidirectional principle (random mutations-phenotypes-natural selection) but rather by the bidirectional relationship between genome and phenotype, in which the phenotype in interaction with the environment directs the evolution of the genome it derives from.The condition 17a-Hydroxylase/17,20-lyase deficiency (17-OHD) is a rare kind of congenital adrenal hyperplasia (CAH) characterized by failure to synthetize cortisol, adrenal androgens and gonadal steroids. Partial deficiency is much rarer, presenting with subtler symptoms. In this study, we summarized the clinical characteristics and identified the underlying gene mutation in four Chinese 46,XX patients with partial 17-OHD. Mutational analysis of the CYP17A1 gene was performed by polymerase chain reaction (PCR) and Sanger sequencing. Clinical and hormonal findings in these patients were consistent with typical manifestations of partial 17-OHD. All patients were found to have a compound heterozygous mutation of the CYP17A1 gene, with five mutations identified. Among them, c.887 T > C(p. I296T), c.1019G > A(p. R340H) and c.1346G > A(p. R449H) were novel missense mutations. In conclusion, we identified three novel missense mutations of the CYP17A1 gene from four patients with partial 17-OHD deficiency. Genotype-phenotype correlation analysis revealed that these novel mutations can lead to partial 17-OHD. Our findings thus provide novel insight into the clinical evaluations and molecular basis of 17-OHD.Clonal transgenic silkworms are useful for the functional analysis of insect genes and for the production of recombinant proteins. Such silkworms have previously been created using an existing ameiotic parthenogenetic strain. However, the process was labor intensive, and the efficiency of producing transgenic silkworms was very low. To overcome this issue, we developed a more convenient and efficient method by breeding non-diapausing parthenogenetic strains. The strains produced non-diapausing eggs only when the embryogenesis of the parent eggs was performed at low temperatures, which could then be used for injecting vector plasmids. This demonstrated that transgenic silkworms could be produced with greater ease and efficiency. To breed the strains, we crossed the existing parthenogenetic strains with bivoltine strains and made F1 and F2 from each cross. Then we selected the silkworms whose eggs have a high ability of parthenogenesis and became non-diapausing. We also demonstrated that the germplasm could be cryopreserved in liquid nitrogen. Thus, this method increases the efficiency and ease of using genetically engineered silkworms to analyze gene function and produce recombinant proteins, potentially impacting various industries.The number of US adults identifying as lesbian, gay, bisexual, transgender, or a different sexual identity has doubled since 2008, and about 40 % of the sexual and gender minority population identify as people of color. Minority stress theory posits that sexual and gender minorities are at particular risk for stress via stigma and discrimination at the structural, interpersonal, and individual levels. This stress, in turn, elevates the risk of adverse health outcomes across several domains. However, there remains a conspicuously limited amount of research on the psychoneuroimmunology of stress among sexual and gender minorities. We developed the Biopsychosocial Minority Stress Framework which posits that sexual minority status leads to unique experiences of minority stress which results in adverse health behavioral factors, elevated psychological distress and sleep disturbance, and immune dysregulation. Moderators in the model include both individual differences and intersectional identities. selleck compound There is a crucial need to understand the biological-psychological axis of stress among the increasingly visible sexual and gender minority population to increase their health, longevity, and quality of life.Transcription and epigenetic changes are integral components of the neuronal response to stimulation and have been postulated to be drivers or substrates for enduring changes in animal behavior, including learning and memory. Memories are thought to be deposited in neuronal assemblies called engrams, i.e., groups of cells that undergo persistent physical or chemical changes during learning and are selectively reactivated to retrieve the memory. Despite the research progress made in recent years, the identity of specific epigenetic changes, if any, that occur in these cells and subsequently contribute to the persistence of memory traces remains unknown. The analysis of these changes is challenging due to the difficulty of exploring molecular alterations that only occur in a relatively small percentage of cells embedded in a complex tissue. In this review, we discuss the recent advances in this field and the promise of next-generation sequencing (NGS) and epigenome editing methods for overcoming these challenges and address long-standing questions concerning the role of epigenetic mechanisms in memory encoding, maintenance and expression.
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