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Regarding the limited information on species protein differences between sheep, goat, and cow milk, we analyzed the differentially expressed proteins in sheep, goat, and cow milk and their functional differences using label-free proteomics technology to identify potential biomarkers. In all, 770 proteins and 2,914 peptide segments were identified. Statistical analysis showed significant differences in the relative abundances of the 74 proteins among sheep, goat, and cow milk. CSN3 and LALBA can be used as potential biomarkers for goat milk, XDH can be used as a potential biomarker for cow milk, and CTSB and BPIFB1 can be used as potential biomarkers for sheep milk. Functional analysis using Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes showed that these significantly different proteins were enriched by different pathways, including thyroid hormone synthesis and glycerol phospholipid metabolism. The data revealed differences in the amounts and physiological functions of the milk proteins of different species, which may provide an important basis for research on the nutritional composition of dairy products and adulteration identification technology. The list of standard abbreviations for JDS is available at adsa.org/jds-abbreviations-24. Nonstandard abbreviations are available in the Notes. [ABSTRACT FROM AUTHOR]

• Different levels of drought stress result in changes in gene expression and reduce plant growth and development. • The proper concentration of nutrients can increase plant efficiency under stress and normal conditions. • Molybdenum can lead to dryness adjustment through different pathways, including the accumulation of osmolytes, increasing the activity of enzymes and reducing the content of oxidative markers. Drought stress is a multidimensional abiotic stress that negatively affects plant growth and yield. Therefore, identifying useful, low-cost, and low-risk solutions to deal with drought along with identifying tolerant plants is crucial for sustainable agriculture and crop production worldwide. In some cases, due to a lack of nutrients, even if there is enough moisture, the plants are still unable to absorb water. Increasing essential macro- and micronutrients may reduce the harmful effects of abiotic stresses, among which drought, while increasing yield. The essential element molybdenum (Mo) has a role in many processes such as photosynthesis, nitrogen (N) metabolism, hormone signaling and tolerance of abiotic stresses. Plants absorb Mo as molybdate anion (MoO 4 2−), which is the main common soluble form of Mo present in neutral to alkaline soils. Mo has a unique effect on the synthesis of hormones and enzymes, and thus affecting plant water relationships and response to environmental stresses. On the other hand, limited water resources and lack of access to adequate water for agricultural production in terms of quantity and quality risk compromising the uptake of Mo which is already critical in soils acidic and/or poor in this essential micronutrient. This study systematically investigated the response to Mo stress and provided valuable evidence for the efficacy of Mo as a candidate to temper the adverse effects of drought stress on crops. Further, this review article also explains the mechanistic actions exerted by Mo in alleviating the drastic effects of drought on crops. [ABSTRACT FROM AUTHOR]

Introduction: Body color is a prominent phenotypic trait and a significant economic characteristic in fish. While current research mainly examines the effects of genetic factors, less emphasis has been placed on the role of endogenous hormones in fish body color. Methods: In this study, we investigated the changes in phenotype and pigment content in juvenile Sinibrama taeniatus after a 30-day treatment with gradient concentrations of L-thyroxine. To further understanding of the regulatory roles of thyroid hormone on pigment synthesis, we investigated the expression changes in genes involved in melanin-based and non-melanin-based pigmentation under the different hormonal regimes. Results: Compared to the control group, the body color of the low-concentration L-thyroxine treatment group (20 nM) was lighter, while that of the highconcentration group (40 nM and 80 nM) was darker. Thyroid hormone treatment simultaneously affected melanophores, xanthophores, and iridophores in different ways, leading to an increase ofmelanin and guanine, and a reduction of pteridine and β-carotene. These findings suggest that thyroid hormone regulates fish body color pigment synthesis through both melanin-based and non-melanin-based mechanisms. Additionally, expression of genes involved in melanin-based (e.g. ctnnb1, wnt10b, and adcy3) and non-melanin-based pigmentation (e.g. xdh, ltk, pnp4a, and mpv17) weremodified by thyroid hormone treatment. Discussion: Our results enhanced the understanding of the role of thyroid hormone in fish pigmentation and provide useful information for cultivating fish with desirable body colors in aquaculture. [ABSTRACT FROM AUTHOR]

Leaf heading is an important agronomic trait of Chinese cabbage, which directly affects its yield. Leaf heading formation in Chinese cabbage is controlled by its internal genotype and external environmental factors, the underlying mechanism of which remains poorly understood. To discover the leaf heading formation mechanism more deeply, this study analyzed the correlation between proteomic and transcriptomic data in the leaf heading formation mutant fg-1 generated by EMS. iTRAQ-based quantitative proteomics techniques were performed to identify the protein expression profiles during the key periods of the early heading stage in the section of the soft leaf apical region (section a) and the whole leaf basal region (section d). We first identified 1,246 differentially expressed proteins (DEPs) in section a and 1,055 DEPs in section d. Notably, transcriptome–proteome integrated analysis revealed that 207 and 278 genes showed consistent trends at the genes’ and proteins’ expression levels in section a and section d, respectively. KEGG analyses showed that the phenylpropanoid biosynthesis pathway was enriched in both sections a and d. Furthermore, 86 TFs exhibited co-upregulation or co-downregulation, and seven out of 86 were involved in plant hormone synthesis and signal transduction pathways. This indicates that they are potentially related to the leaf heading formation in Chinese cabbage. Taken together, we have identified several key earlyheading-formation-related factors via integration analysis of the transcriptomics and proteomics data. This provides sufficient gene resources to discover the molecular mechanism of leaf heading formation. [ABSTRACT FROM AUTHOR]

Introduction: Citrus reticulata cv. ‘Chunhongtangju’ was mutated from Mandarin ‘Shatangju’, which has been identified as a new citrus variety. Mandarin ‘Chunhongtangju’ fruits were late-ripening for about two months than Mandarin ‘Shatangju’. Methods: To understand the pericarp differential development mechanism in Mandarin ‘Shatangju’ (CK) and ‘Chunhongtangju’ (LM), hormones and transcriptome profiles of pericarps were performed in different development stages: Young fruit stage (CK1/LM1), Expansion and Turning color stage (CK2), Expansion stage (LM2), Turning color stage (LM3), and Maturity stage (CK3/LM4). Results: In this study, the development of LM was significantly slower, and the maturity was significantly delayed. At the same stage, most hormones in Mandarin ‘Chunhongtangju’ pericarps were higher than that in ‘Shatangju’ such as gibberellin A24, cis(+)-12-oxophytodienoic acid, and L-phenylalanine. The deficiency of hormones in late-maturing pericarps was mainly manifested in ABA, 12-OHJA, MeSAG, and ABA-GE. Differences in transcriptome profiles between the two citrus varieties are primarily observed in energy metabolism, signal transduction such as MAPK signaling pathway and plant hormone signaling, and biosynthesis of secondary metabolites. After analyzing the hormones and transcriptome data, we found that the top genes and hormones, such as Cs_ont_5g020040 (transcription elongation factor, TFIIS), Cs_ont_7g021670 (BAG family molecular chaperone regulator 5, BAG5), Cs_ont_2g025760 (40S ribosomal protein S27, Rps27), 5-deoxystrigol, salicylic acid 2-O-βglucosid, and gibberellin A24, contributed significantly to gene transcription and hormone synthesis. Discussion: This study suggests that the variances of pericarp development between the two varieties are linked to variations in the transcription levels of genes associated with energy and secondary metabolism, signal transduction related genes. These findings expand our understanding of the complex transcriptional and hormonal regulatory hierarchy during pericarp development. [ABSTRACT FROM AUTHOR]

Plant somatic embryogenesis (SE) is an efficient regeneration system for propagation. It involves the regulation of a complex molecular regulatory network encompassing endogenous hormone synthesis, metabolism, and signal transduction processes, induced through exogenous plant growth regulators. Previous studies have focused primarily on traditional propagation methods for Tectona grandis, but there is limited knowledge on SE and its hormonal regulatory mechanisms. In our study, different SE stages, including the nonembryogenic callus (NEC), embryogenic callus (EC), and globular and heartshaped embryo (E-SEs) stages, were induced in teak cotyledons incubated on MS medium supplemented with 0.1 mg/L thidiazuron (TDZ). Morphological and histological observations indicated that EC primarily originates from the development of embryogenic cell clusters. During SE induction, the levels of six classes of endogenous hormones, IAA, CTK, ETH, ABA, SA, and JA, changed significantly. Transcriptome analysis revealed that endogenous hormones participate in SE induction in teak through various biological processes, such as biosynthesis, metabolism, and signal transduction pathways. We found that IAA biosynthesis primarily occurs through the IAM pathway during these three stages. The ETH receptor kinase gene SERF1 exhibited the highest expression levels in E-SEs. The ABA-, SA-, and JA-related signal transduction genes ABI3, NPR1, and JAZ exhibited no differential expression during different stages. Moreover, key encoding genes of SE regulators, including WUS, WOX and SERK, were differentially expressed during SE. In conclusion, this study offers insights into the roles of endogenous hormones and their interactions during SE induction. [ABSTRACT FROM AUTHOR]

There is growing concern that sprayed neonicotinoid pesticides (neonics) persist in mixed forms in the environmental soil and water systems, and these concerns stem from reports of increase in both the detection frequency and concentration of these pollutants. To confirm the toxic effects of neonics,we conducted toxicity tests on two neonics, clothianidin (CLO) and imidacloprid (IMD), in embryos of zebrafish. Toxicity tests were performed with two different types of mixtures: potential mixture compounds and realistic mixture compounds. Potential mixtures of CLO and IMD exhibited synergistic effects, in a dose-dependent manner, in zebrafish embryonic toxicity. Realistic mixture toxicity tests that are reflecting the toxic effects of mixture in the aquatic environment were conducted with zebrafish embryos. The toxicity of the CLO and IMD mixture at environmentally-relevant concentrations was confirmed by the alteration of the transcriptional levels of target genes, such as cell damage linked to oxidative stress response and thyroid hormone synthesis related to zebrafish embryonic development. Consequently, the findings of this study can be considered a strategy for examining mixture toxicity in the range of detected environmental concentrations. In particular, our results will be useful in explaining the mode of toxic action of chemical mixtures following short-term exposure. Finally, the toxicity information of CLO and IMD mixtures will be applied for the agricultural environment, as a part of chemical regulation guideline for the use and production of pesticides. [ABSTRACT FROM AUTHOR]

Copyright of Food & Fermentation Industries is the property of Food & Fermentation Industries and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background & Objective: Graves' disease (GD) is an autoimmune condition that targets the thyroid gland, resulting in excessive stimulation and synthesis of thyroid hormones. Excessive synthesis of these hormones can lead to symptoms such as loss of body weight, accelerated heart rate, irritability, reduced tolerance to heat, and excessive perspiration. Alpha-Klotho (KL), a protein crucial for physiological processes, is also involved in GD. The defective immunological condition of GD patients may increase Klotho expression, and the enhanced expression of fibroblast growth factor-23 (FGF23) in GD may be linked to the disease pathophysiology. We investigated serum levels of KL and FGF23 in Iraqi patients with Graves' disease, analyzing correlations with clinical status and evaluating their potential as biomarkers for disease activity. Methodology: We conducted this cross-sectional study at The National Diabetes Center, Mustansiriyah University, between December 2022 and April 2023. The study involved 103 patients diagnosed with GD, and 103 patients, aged 21-70 y, as a control group. Patients with multinodular goiter, single thyroid nodules, thyroiditis, pregnant women, and those on medications or oral contraceptives, were excluded. Result: clinical significance of FGF23 and Klotho (KL) levels in patients with Graves' disease (GD) compared to a control group. Results indicate that the median of KL levels are significantly higher in GD patients (KL = 6.31) compared to the control group (KL = 2.40), with a highly significant difference (P < 0.001). In contrast, differences in median of FGF23 levels between GD patients (149) and controls (86.05) were not statistically significant (P = 0.07). Furthermore, KL levels were significantly higher in hyperthyroid patients compared to other thyroid statuses (P = 0.023), while FGF23 levels did not significantly differ across thyroid statuses (P = 0.255). Additionally, the study found a strong correlation between TRAb levels and both KL (r = 0.291, P < 0.001) and FGF23 (r = 0.211, P = 0.003), and between KL and FGF23 directly (r = 0.412, P < 0.001). These findings suggest that while KL may be a significant biomarker in GD, FGF23 relevance appears limited in this context. Conclusion: In Graves' Disease patients have significantly higher levels of KL and FGF23 compared to controls, suggesting a distinct pathophysiological role for these biomarkers in mineral homeostasis and thyroid hormone regulation. [ABSTRACT FROM AUTHOR]

Carotenoid cleavage oxygenases (CCOs) cleave carotenoid molecules to produce bioactive products that influence the synthesis of hormones such as abscisic acid (ABA) and strigolactones (SL), which regulate plant growth, development, and stress adaptation. Here, to explore the molecular characteristics of all members of the OsCCO family in rice, fourteen OsCCO family genes were identified in the genome-wide study. The results revealed that the OsCCO family included one OsNCED and four OsCCD subfamilies. The OsCCO family was phylogenetically close to members of the maize ZmCCO family and the Sorghum SbCCO family. A collinearity relationship was observed between OsNCED3 and OsNCED5 in rice, as well as OsCCD7 and OsNCED5 between rice and Arabidopsis, Sorghum, and maize. OsCCD4a and OsCCD7 were the key members in the protein interaction network of the OsCCO family, which was involved in the catabolic processes of carotenoids and terpenoid compounds. miRNAs targeting OsCCO family members were mostly involved in the abiotic stress response, and RNA-seq data further confirmed the molecular properties of OsCCO family genes in response to abiotic stress and hormone induction. qRT-PCR analysis showed the differential expression patterns of OsCCO members across various rice organs. Notably, OsCCD1 showed relatively high expression levels in all organs except for ripening seeds and endosperm. OsNCED2a, OsNCED3, OsCCD1, OsCCD4a, OsCCD7, OsCCD8a, and OsCCD8e were potentially involved in plant growth and differentiation. Meanwhile, OsNCED2a, OsNCED2b, OsNCED5, OsCCD8b, and OsCCD8d were associated with reproductive organ development, flowering, and seed formation. OsNCED3, OsCCD4b, OsCCD4c, OsCCD8b, and OsCCD8c were related to assimilate transport and seed maturation. These findings provide a theoretical basis for further functional analysis of the OsCCO family. [ABSTRACT FROM AUTHOR]

The membrane‐integrated NADPH oxidases DUOX1 and DUOX2 are recruited to the apical plasma membrane in epithelial cells to release hydrogen peroxide, thereby playing crucial roles in various functions such as thyroid hormone synthesis and host defense. However, it has remained unknown about the molecular mechanism for apical sorting of DUOX1 and DUOX2. Here we show that DUOX1 and DUOX2 are correctly sorted to the apical membrane via the membrane‐spanning DUOX maturation proteins DUOXA1 and DUOXA2, respectively, when co‐expressed in MDCK epithelial cells. Impairment of N‐glycosylation of DUOXA1 results in mistargeting of DUOX1 to the basolateral membrane. Similar to DUOX1 complexed with the glycosylation‐defective DUOXA1, the naturally non‐glycosylated oxidase NOX5, which forms a homo‐oligomer, is targeted basolaterally. On the other hand, a mutant DUOXA2 deficient in N‐glycosylation is less stable than the wild‐type protein but still capable of recruiting DUOX2 to the apical membrane, whereas DUOX2 is missorted to the basolateral membrane when paired with DUOXA1. These findings indicate that DUOXA2 is crucial but its N‐glycosylation is dispensable for DUOX2 apical recruitment; instead, its C‐terminal region seems to be involved. Thus, apical sorting of DUOX1 and DUOX2 is likely regulated in a distinct manner by their respective partners DUOXA1 and DUOXA2. [ABSTRACT FROM AUTHOR]

Seasonal reproduction is an adaptive strategy that benefits the survival and growth of offspring. However, the regulatory mechanisms affecting spermatogenesis in male seasonal breeders are not well understood. We examined the actions of testosterone on seasonal spermatogenesis of Plateau Pika (Ochotona curzoniae), a typical long-day breeder living on the Qinghai–Tibetan Plateau. The annual dynamics of germ cell development and steroid hormone synthesis were confirmed and were consistent with testicular morphology. Furthermore, a testosterone regulation experiment showed that elevated testosterone stimulated proliferation of spermatogonia and regeneration of advanced spermatogenic cells in reproductively dormant pika, while testosterone suppression induced cell apoptosis both in reproductively active and dormant pikas. Transcriptomic analyses indicated that testosterone-regulated genes related to spermatogonial fate determination by binding to androgen receptors and inducing the production of retinoic acid, which was responsible for the initiation of spermatogonial differentiation. We show that testosterone orchestrates downstream signaling pathways to balance spermatogonial self-renewal and development. These findings provide a new perspective on seasonal regulation of mammalian spermatogenesis. [ABSTRACT FROM AUTHOR]

Receptor-like cytoplasmic kinases (RLCKs) have become major players in plant immunity regardless of the pathways involved. RLCKs form regulatory nodes that link receptors to downstream regulators that modulate plant hormones, Ca2+ signaling, reactive oxygen species (ROS) accumulation as well as activation of mitogen-activated protein kinases (MAPKs), transcription regulators, and immune gene expression. Phosphorylation, ubiquitination, and other post-translational modifications by effectors regulate RLCKs, enabling functional versatility and homeostasis. As major integrators of signals from receptors, RLCKs are potential targets for biotechnological applications. RLCKs play pivotal roles in plant immunity by contributing to both PTI and ETI. Due to their critical functions, these kinases are targets for manipulation by pathogen effectors to attenuate PTI. RLCKs also directly or indirectly recognize effectors and activate ETI. The function of RLCKs in crop plant immunity is emerging. The receptor-like kinase (RLK) family of receptors and the associated receptor-like cytoplasmic kinases (RLCKs) have expanded in plants because of selective pressure from environmental stress and evolving pathogens. RLCKs link pathogen perception to activation of coping mechanisms. RLK–RLCK modules regulate hormone synthesis and responses, reactive oxygen species (ROS) production, Ca2+ signaling, activation of mitogen-activated protein kinase (MAPK), and immune gene expression, all of which contribute to immunity. Some RLCKs integrate responses from multiple receptors recognizing distinct ligands. RLKs/RLCKs and nucleotide-binding domain, leucine-rich repeats (NLRs) were found to synergize, demonstrating the intertwined genetic network in plant immunity. Studies in arabidopsis (Arabidopsis thaliana) have provided paradigms about RLCK functions, but a lack of understanding of crop RLCKs undermines their application. In this review, we summarize current understanding of the diverse functions of RLCKs, based on model systems and observations in crop species, and the emerging role of RLCKs in pathogen and abiotic stress response signaling. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Agricultural Science & Technology (1008-0864) is the property of Journal of Agricultural Science & Technology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Sinopodophyllum hexandrum (Royle) Ying, an endangered perennial medicinal herb, exhibits morpho-physiological dormancy in its seeds, requiring cold stratification for germination. However, the precise molecular mechanisms underlying this transition from dormancy to germination remain unclear. This study integrates transcriptome and plant hormone-targeted metabolomics techniques to unravel these intricate molecular regulatory mechanisms during cold stratification in S. hexandrum seeds. Significant alterations in the physicochemical properties (starch, soluble sugars, soluble proteins) and enzyme activities (PK, SDH, G-6-PDH) within the seeds occur during stratification. To characterize and monitor the formation and transformation of plant hormones throughout this process, extracts from S. hexandrum seeds at five stratification stages of 0 days (S0), 30 days (S1), 60 days (S2), 90 days (S3), and 120 days (S4) were analyzed using UPLC-MS/MS, revealing a total of 37 differential metabolites belonging to seven major classes of plant hormones. To investigate the biosynthetic and conversion processes of plant hormones related to seed dormancy and germination, the transcriptome of S. hexandrum seeds was monitored via RNA-seq, revealing 65,372 differentially expressed genes associated with plant hormone synthesis and signaling. Notably, cytokinins (CKs) and gibberellins (GAs) exhibited synergistic effects, while abscisic acid (ABA) displayed antagonistic effects. Furthermore, key hub genes were identified through integrated network analysis. In this rigorous scientific study, we systematically elucidate the intricate dynamic molecular regulatory mechanisms that govern the transition from dormancy to germination in S. hexandrum seeds during stratification. By meticulously examining these mechanisms, we establish a solid foundation of knowledge that serves as a scientific basis for facilitating large-scale breeding programs and advancing the artificial cultivation of this highly valued medicinal plant. [ABSTRACT FROM AUTHOR]

Thiourea, a widely used agrochemical, is known to inhibit the activity of thyroid peroxidase, a key enzyme in the biosynthetic pathway of thyroid hormones. Thyroid insufficiency compromises the basal metabolic rate in warm‐blooded organisms and embryonic development in vertebrates. In this study, we looked for developmental defects by exposing the zebrafish embryos to an environmentally relevant dose of thiourea (3 mg/mL). Liquid chromatography–tandem mass spectrometry (LC‐MS/MS) was performed to validate thiourea's presence in the treated zebrafish embryos. Structural anomalies like bent tail and pericardial edema were noticed in 96‐h post‐fertilization (hpf) larvae. On histological examination, underdeveloped swim bladder was noticed in 96 hpf larvae exposed to 3 mg/mL thiourea. The treated larvae also failed to follow the characteristic swimming behavior in response to stimuli due to defective swim bladder. Swim bladder being homologous to the lung of tetrapod, the role of Bmp4, a major regulator of lung development, was studied along with the associated regulatory genes. Gene expression analysis revealed that thiourea administration led to the downregulation of bmp4, shh, pcna, anxa5, acta2, and the downstream effector snail3 but the upregulation of caspase3. The protein expression showed a similar trend, wherein Bmp4, Shh, and Pcna were downregulated, but Cleaved Caspase3 showed an increased expression in the treated group. Therefore, it is prudent to presume that exposure to thiourea significantly reduces the expression of Bmp4 and other key regulators; hence, the larvae fail to develop a swim bladder, a vital organ that regulates buoyancy. Thiourea, an agrochemical, inhibits thyroid peroxidase activity, which is crucial for thyroid hormone synthesis. Exposure to thiourea disrupted swim bladder development in zebrafish embryos. Histological examination revealed disorganized tissue layers of swim bladder, indicating its detrimental effect on swim bladder morphogenesis. Thiourea downregulated genes involved in swim bladder development, notably bmp4, acta2, anxa5, and shh. This study highlights the potential developmental toxicity of thiourea and emphasizes the importance of understanding its impact on aquatic organisms. [ABSTRACT FROM AUTHOR]

Objectives: To examine the putative functions and mechanisms of lysine crotonylation (Kcr) during the development and progression of papillary thyroid cancer (PTC). Methods: Samples of thyroid cancer tissues were collected and subjected to liquid chromatography–tandem mass spectrometry. Crotonylated differentially expressed proteins (DEPs) and differentially expressed Kcr sites (DEKSs) were analyzed by Motif, dynamic expression model analysis (Mfuzz), subcellular localization, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway annotation, Go Ontology (GO) annotation, and protein–protein interaction analysis (PPI). Validation was performed by immunohistochemistry (IHC). Results: A total of 262 crotonylated DEPs and 702 DEKSs were quantitated. First, for the tumor/normal comparison, a dynamic expression model analysis (Mfuzz) of the DEKSs revealed that clusters 1, 3, and 4 increased with the progression of thyroid cancer; however, cluster 6 showed a dramatic increase during the transition from N0-tumor to N1-tumor. Furthermore, based on GO annotation, KEGG, and PPI, the crotonylated DEPs were primarily enriched in the PI3K-Akt signaling pathway, Cell cycle, and Hippo signaling pathway. Of note, crosstalk between the proteome and Kcr proteome suggested a differential changing trend, which was enriched in Thyroid hormone synthesis, Pyruvate metabolism, TCA cycle, Cell cycle, and Apoptosis pathways. Similarly, for the LNM comparison group, the DEKSs and related DEPs were primarily enriched in Hydrogen peroxide catabolic process and Tight junction pathway. Finally, according to The Cancer Genome Atlas Program (TCGA) database, the differential expression of Kcr DEPs were associated with the prognosis of thyroid cancer, indicating the prognostic significance of these proteins. Moreover, based on the clinical validation of 47 additional samples, Kcr was highly expressed in thyroid tumor tissues compared with normal tissue (t = 9.792, P < 0.001). In addition, a positive correlation was observed between Kcr and N-cadherin (r = 0.5710, P = 0.0015). Moreover, N-cadherin expression was higher in the relatively high Kcr expression group (χ2 = 18.966, P < 0.001). Conclusions: Higher Kcr expression was correlated with thyroid tumorigenesis and lymphatic metastasis, which may regulate thyroid cancer progression by Pyruvate metabolism, TCA cycle, Cell cycle, and other pathways. [ABSTRACT FROM AUTHOR]

Background: Ovarian granulosa cells (GCs) play crucial roles in follicular growth and development. Their normal function is influenced by various factors, including oxidative stress, which is a significant factor. Afamin protein is a vitamin E-specific binding protein that acts as a vitamin E carrier in follicular fluid. Although the mechanism of the protective effect of afamin on human ovarian GCs is still unclear, there is evidence it has an antioxidant effect in neuronal cells. Methods: In this study, we investigated the protective effects of afamin proteins on testosterone propionate (TP)-induced ovarian GCs using a human ovarian tumor granulosa cell line (KGN). Results: The results showed that afamin reduced TP-induced oxidative stress in KGN cells by decreasing the levels of oxidative damage markers, enhancing the activity of antioxidant enzymes, and exerting a protective effect on GCs. Supplementation with afamin repaired mitochondrial dysfunction by improving mitochondrial membrane potential damage and ATP levels. It counteracted TP-induced apoptosis by decreasing the activity of Caspase-3 and upregulating the expression of the anti-apoptotic gene (BCL-2) while downregulating the expression of the pro-apoptotic gene BCL-2-associated X protein (BAX). In addition, afamin regulated the expression of genes related to ovarian steroid hormone synthesis, ameliorating the endocrine dysfunction observed in TP-induced KGN cells. Conclusion: Therefore, Afamin proteins may serve as important complementary factors that protect GCs from other types of damage, such as oxidative stress, and may help improve ovarian follicle quality and female reproductive function. [ABSTRACT FROM AUTHOR]

Summary Kernel row number (KRN) is a major yield related trait for maize (Zea mays L.) and is also a major goal of breeders, as it can increase the number of kernels per plant. Thus, identifying new genetic factors involving in KRN formation may accelerate improving yield‐related traits genetically. We herein describe a new kernel number‐related gene (KRN5b) identified from KRN QTL qKRN5b and encoding an inositol polyphosphate 5‐phosphatase (5PTase). KRN5b has phosphatase activity towards PI(4,5)P2, PI(3,4,5)P3, and Ins(1,4,5)P3 in vitro. Knocking out KRN5b caused accumulation of PI(4,5)P2 and Ins(1,4,5)P3, resulting in disordered kernel rows and a decrease in the number of kernels and tassel branches. The introgression of the allele with higher expression abundance into different inbred lines could increase the ear weight of the inbred lines and the corresponding hybrids by 10.1%–12.2% via increasing KRN, with no adverse effects on other agronomic traits. Further analyses showed that KRN5b regulates inflorescence development through affecting the synthesis and distribution of hormones. Together, KRN5b contributes to spikelet pair meristem development through inositol phosphate and phosphatidylinositols, making it a selecting target for yield improvement. [ABSTRACT FROM AUTHOR]

Nature offers a variety of structurally unique, sulfated endobiotics including sulfated glycosaminoglycans, sulfated tyrosine peptides, sulfated steroids/bile acids/catecholamines. Sulfated molecules display a large number of biological activities including antithrombotic, antimicrobial, anticancer, anti‐inflammatory, and others, which arise from modulation of intracellular signaling and enhanced in vivo retention of certain hormones. These characteristics position sulfated molecules very favorably as drug‐like agents. However, few have reached the clinic. Major hurdles exist in realizing sulfated molecules as drugs. This state‐of‐the‐art has been transformed through recent works on the development of sulfate masking technologies for both alkyl (sulfated carbohydrates, sulfated steroids) and aryl (sTyr‐bearing peptides/proteins, sulfated flavonoids) sulfates. This review compiles the literature on different strategies implemented for different types of sulfate groups. Starting from early efforts in protection of sulfate groups to the design of newer SuFEx, trichloroethyl, and gem‐dimethyl‐based protection technologies, this review presents the evolution and application of concepts in realizing highly diverse, sulfated molecules as candidate drugs and/or prodrugs. Overall, the newer strategies for sulfate masking and demasking are likely to greatly enhance the design and development of sulfated molecules as non‐toxic drugs of the future. [ABSTRACT FROM AUTHOR]

Background: Risperidone is one of the most reliable and effective antipsychotics for schizophrenia treatment. However, the mechanism of action of risperidone is not yet fully understood. Traf2 and Nck-interacting protein kinase (TNIK), a schizophrenia susceptibility gene, is associated with risperidone treatment response. Our previous in vitro experiments confirmed that downregulated TNIK affected the effect of risperidone on downstream targets. However, the effect of downregulated TNIK on risperidone-induced molecular expression remains to be further explored. Methods: Transcriptome analysis was performed on U251 cells subjected to risperidone, TNIK siRNA, and no treatment, respectively. Compared to the notreatment group, two groups of DEGs were screened out and then intersected with the schizophrenia-related genes to screen the cross-talk genes. Those DEGs were analyzed using GO and KEGG. STRING and Cytoscape were used to construct a protein-protein interaction (PPI) network for the cross-talk gene. Results: The results showed that the parathyroid hormone synthesis, secretion, and action were significantly enriched after risperidone treatment. Downregulated TNIK could have an impact on the collagen-containing extracellular matrix, signaling receptor activator activity, and PI3K-Akt signaling pathway. Interestingly, bone mineralization function and calcium signaling pathway were enriched in the cross-talk genes. Additionally, FGFR2, FGF1, and FGFR might be the potential targets for TNIK affecting the effects of risperidone. Conclusion: The study indicated that risperidone primarily influences functions and/or pathways associated with bone metabolism, potentially contributing to the adverse effect of osteoporosis. Our study may offer a novel perspective on investigating the mechanisms underlying the adverse effects of risperidone. [ABSTRACT FROM AUTHOR]

Background: Suicide is a significant public health problem influenced by various risk factors, including dysregulation of the hypothalamus-pituitary-adrenal (HPA) axis. Zinc (Zn), essential for pituitary function in hormone synthesis and release, has been linked to suicide, with studies noting reduced serum levels and altered brain transport mechanisms. Despite Zn's crucial role in pituitary function and its involvement in suicidal behavior, information on pituitary Zn in suicide is scarce. Tumor cells modify Zn dynamics in tissues, and a previous report suggests microadenomas in the anterior pituitary as a risk factor for suicide. Methods: Histopathological analysis with hematoxylin-eosin stain and histochemical techniques to assess Zn homeostasis were carried out on anterior pituitary postmortem samples from 14 suicide completers and 9 nonsuicidal cases. Results: Pituitary microadenomas were identified in 35% of suicide cases and none in the non-suicidal cases. Furthermore, compartmentalized Zn (detected via dithizone reactivity), but not free Zn levels (detected via zinquin reactivity), was lower in the suicide cases compared to the non-suicidal group. Conclusion: This is the first report of a potential association between disrupted Zn homeostasis and microadenomas in the anterior pituitary as a feature in suicide and provides critical insights for future neuroendocrine Znrelated research. [ABSTRACT FROM AUTHOR]

Background: Testicular macrophages (TM) have long been recognized for their role in immune response within the testicular environment. However, their involvement in steroid hormone synthesis, particularly testosterone, has not been fully elucidated. This study aims to explore the capability of TM to synthesize and secrete testosterone de novo and to investigate the regulatory mechanisms involved. Results: Transcriptomic analysis revealed significant expression of Cyp11a1, Cyp17a1, Hsd3b1, and Hsd17b3 in TM, which are key enzymes in the testosterone synthesis pathway. qPCR analysis and immunofluorescence validation confirmed the autonomous capability of TM to synthesize testosterone. Ablation of TM in mice resulted in decreased physiological testosterone levels, underscoring the significance of TM in maintaining testicular testosterone levels. Additionally, the study also demonstrated that Cebpb regulates the expression of these crucial genes, thereby modulating testosterone synthesis. Conclusions: This research establishes that TM possess the autonomous capacity to synthesize and secrete testosterone, contributing significantly to testicular testosterone levels. The transcription factor Cebpb plays a crucial role in this process by regulating the expression of key genes involved in testosterone synthesis. [ABSTRACT FROM AUTHOR]

Introduction: Excessive synthesis of thyroid hormone in hyperthyroidism is related to the imbalance of oxidative status in living organisms. Melatonin mediates its effects either directly through scavenging free radicals or indirectly through the activation of melatonin receptors (MT1 and MT2). The present study investigated the involvement of melatonin receptors in the melatonin-mediated attenuation of hyperthyroidism-induced oxidative stress in the spleen of laboratory mice. Methods: The hyperthyroidism was induced by L-thyroxine (0.6μg/g B. wt.) supplementation. The experimental mice were supplemented with melatonin (25 μg/100g B. wt.) subcutaneously. Oxidative stress, melatonin receptor expression in the spleen tissues, and circulatory levels of thyroid hormone were determined. Results: L-thyroxine treatment caused a significant increase in serum T3 and T4 levels. Melatonin supplementation caused a significant decrease in serum T3 and T4 levels in L-thyroxine-treated mice. L-thyroxine treatment increased MDA levels and suppressed catalase and SOD enzyme activities. Melatonin treatment caused suppression of MDA levels and an increase in SOD and catalase activities. L-thyroxine treatment caused significant suppression in MT1 receptor expression and a significant increase in MT2 receptor expression. Melatonin supplementation significantly induced the MT2 receptor protein expression in the spleen tissues of experimental mice. Conclusion: This study suggests that alterations in MT2 melatonin receptor expression may be associated with melatonin-mediated attenuation of oxidative stress in the spleen tissues of hyperthyroid mice. [ABSTRACT FROM AUTHOR]

Background: Fibroblast growth factor 19 (FGF19) is an enterohepatic hormone the synthesis of which is stimulated by bile acid activation of the nuclear farnesoid X receptor (FXR) in ileal enterocytes. Increased production of FGF19 downregulates hepatocyte bile acid synthesis and gluconeogenesis, while concurrently upregulating hepatocyte glycogenesis and gallbladder (GB) filling. The physiologic impact of this regulatory cycle is illustrated in cholecystectomized humans, in whom the disturbed meal‐related flux of GB bile decreases serum FGF19 concentrations. Objective: Determine if serum FGF19 concentrations are lower in dogs with clinical GB mucoceles (GBMs) than in control dogs. Animals: Seven dogs with GBM diagnosed using abdominal ultrasonography, biochemical markers, and GB histopathology. Forty‐two control dogs without gastrointestinal or hepatobiliary disorders also were evaluated. Health status of controls was assessed by physical examination and diagnostic hematologic and biochemical test results. Methods: Prospective cross‐sectional study to compare fasting plasma or serum FGF19 concentrations between groups. Concentrations of FGF19 were quantified by a commercially available FGF19 ELISA. Results: Concentrations of FGF19 were significantly lower in dogs with clinical GBM (median, 14.0 pg/mL; range, 12.8‐67.2) than in control dogs (median, 145.3 pg/mL; range, 36.5‐285.1). Conclusions and Clinical Importance: In dogs, GBM is associated with significantly decreased serum FGF19 concentrations. We speculate that this finding reflects compromised GB contraction and decreased enterohepatic circulation of bile flow. Subnormal FGF19 concentrations may influence bile acid synthesis and hepatic metabolism. [ABSTRACT FROM AUTHOR]

The KCNE2 protein is encoded by the kcne2 gene and is a member of the KCNE protein family, also known as the MinK-related protein 1 (MiRP1). It is mostly present in the epicardium of the heart and gastric mucosa, and it is also found in the thyroid, pancreatic islets, liver and lung, among other locations, to a lesser extent. It is involved in numerous physiological processes because of its ubiquitous expression and partnering promiscuity, including the modulation of voltage-dependent potassium and calcium channels involved in cardiac action potential repolarization, and regulation of secretory processes in multiple epithelia, such as gastric acid secretion, thyroid hormone synthesis, generation and secretion of cerebrospinal fluid. Mutations in the KCNE2 gene or aberrant expression of the protein may play a critical role in cardiovascular, neurological, metabolic and multisystem disorders. This article provides an overview of the advancements made in understanding the physiological functions in organismal homeostasis and the pathophysiological consequences of KCNE2 in multisystem diseases. [ABSTRACT FROM AUTHOR]

As an important part of heat shock response module, heat shock proteins (HSP) play an important role in plant defense response against heat stress; however, the involvement of the majority of the HSP family members against other abiotic stresses remains poorly understood. In the present study, LrHSP17.2 was identified and its function against abiotic stress was analyzed. The expression level of LrHSP17.2 was significantly induced by heat. Heterologous transgenes of LrHSP17.2 showed that LrHSP17.2 can increase the activity of catalase, peroxidase, superoxide dismutase to removes excess reactive oxygen species (ROS), maintain the stability of the membrane structure, and regulate genes related to antioxidant enzymes and defense under abiotic stress. In addition, LrHSP17.2 could be regulated by exogenous abscisic acid and melatonin, and the related hormone synthesis genes of transgenic plants were significantly up-regulated under heat stress. Taken together, our results revealed that LrHSP17.2 is involved in regulating abiotic stress responses by regulating ROS scavenging and stress-related genes in Lilium regale. [ABSTRACT FROM AUTHOR]

In this study, we aimed to develop a novel directional electromagnetic field (EMF) application method for promoting plant growth using a solenoid coil-based cultivation system. The emergence of plant shoots from seeds, shoot elongation, root proliferation, and plant growth hormones were monitored in the presence of a directional EMF using our solenoid coil system. To observe the effect of the directional EMF on seed germination, radish and sugarcane seedlings were cultivated in the system. At the seed germination stage, the EMF applied had no significant effect on germination or growth. However, after germination, shoot growth was sensitive to a directional EMF, as it was promoted by different conditions in a plant-species-dependent manner. The maximum growth promotion rates were 25.65% ± 4.21% and 38.57% ± 12.81% for radish and sugarcane, respectively. Similarly, plant root proliferation and indole-3-acetic acid (IAA) analyses indicated that directional EMF application was associated with root proliferation and hormone synthesis. Plant growth in the experimental system proved controllable; either growth stimulation or reduction were possible as the system operating conditions were made to vary. Our findings indicate that the application of a specific directional EMF could serve as an electrical plant stimulant (or electrical fertilizer). [ABSTRACT FROM AUTHOR]

Salinity stress is the most pernicious abiotic stress negatively affecting crop productivity around the globe. Soil salinity is significantly decreasing the agricultural lands every year which is posing serious food security threats. The global population is rapidly increasing and it demands the use of every soil for crop production. Salt stress negatively affects plant growth and development by inducing ionic, osmotic, and oxidative stress and it also negatively affects soil biological properties and microbial activities. Using microbial-based techniques is considered an effective, and environmentally friendly way to mitigate stress effects and improve crop production. The application of plant growth-promoting rhizobacteria (PGPR) is an imperious way to improve plant productivity and reclaim salt-affected soils. The use of PGPR can reduce the production of reactive oxygen species (ROS), facilitate nutrient uptake, and regulate gene expression, osmolyte, and hormone synthesis which helps mitigate deleterious impacts of salinity. Besides this, PGPR also improves antioxidant activities, and they produce organic acids, and siderophores which help to counter ROS production. Thus, in the present review, we discussed the different mechanisms of PGPR in modulating plant growth under saline conditions. We also identified different research gaps that must be abridged in future studies. This review will provide better insights into the present knowledge and will help to improve crop production in saline soils using PGRP. [ABSTRACT FROM AUTHOR]

Simple Summary: At present, studies have shown that organic trace minerals have a positive impact on animal health compared with inorganic trace minerals. However, the effect of organic trace minerals on the intestinal health of adult cats has not been extensively explored. In our study, we investigated the effects of different trace mineral sources on the gut microbiota and digestive health in British Shorthair cats and dietary organic trace minerals on the intestinal barrier, immune function, anti-inflammatory ability, gut microbiota, and metabolites in adult British Shorthair cats. Our results suggest that compared to inorganic trace minerals, dietary organic trace minerals could enhance immune function, improve inflammatory state, and regulate the gut microbiota structure in cats. Trace minerals are essential for biological processes, including enzyme function, immune response, and hormone synthesis. The study assessed the effects of different dietary trace minerals on the gut health, microbiota composition, and immune function of cats. Eighteen adult British Shorthair cats were divided into three groups receiving inorganic trace minerals (ITM), a 50/50 mix of inorganic and organic trace minerals (ITM + OTM), or organic trace minerals (OTM) for 28 days. The OTM showed enhanced immune capacities, reduced intestinal barrier function, and lower inflammation condition. The OTM altered gut microbiota diversity, with a lower Simpson index and higher Shannon index (p < 0.05). Specifically, the abundance of Bacteroidota, Lachnospiraceae, and Prevotella in the OTM group were higher than the ITM group (p < 0.05). Metabolomic analysis identified 504 differential metabolites between the OTM and ITM groups (p < 0.05, VIP-pred-OPLS-DA > 1), affecting pathways related to steroid hormone biosynthesis and glycerophospholipid metabolism (p < 0.05, VIP-pred-OPLS-DA > 2). Additionally, there was a significant correlation between intestinal microbiota and differential metabolites. To conclude, dietary OTM can modulate the gut metabolite and microbiota composition, enhance immune and intestinal barrier function, and mitigate inflammation in cats, highlighting the benefit of using OTM in feline diet to promote the intestinal and overall health. [ABSTRACT FROM AUTHOR]

Context Thyroglobulin (Tg), encoded by TG , is essential for thyroid hormone synthesis. TG defects result in congenital hypothyroidism (CH). Most reported patients were born before the introduction of newborn screening (NBS). Objective We aimed to clarify the phenotypic features of patients with TG defects diagnosed and treated since the neonatal period. Methods We screened 1061 patients with CH for 13 CH-related genes and identified 30 patients with TG defects. One patient was diagnosed due to hypothyroidism-related symptoms and the rest were diagnosed via NBS. Patients were divided into 2 groups according to their genotypes, and clinical characteristics were compared. We evaluated the functionality of the 7 missense variants using HEK293 cells. Results Twenty-seven rare TG variants were detected, including 15 nonsense, 3 frameshift, 2 splice-site, and 7 missense variants. Patients were divided into 2 groups: 13 patients with biallelic truncating variants and 17 patients with monoallelic/biallelic missense variants. Patients with missense variants were more likely to develop thyroid enlargement with thyrotropin stimulation than patients with biallelic truncating variants. Patients with biallelic truncating variants invariably required full hormone replacement, whereas patients with missense variants required variable doses of levothyroxine. Loss of function of the 7 missense variants was confirmed in vitro. Conclusion To our knowledge, this is the largest investigation on the clinical presentation of TG defects diagnosed in the neonatal period. Patients with missense variants showed relatively mild hypothyroidism with compensative goiter. Patients with only truncating variants showed minimal or no compensative goiter and required full hormone replacement. [ABSTRACT FROM AUTHOR]

Frequent outbreaks of infectious diseases in aquaculture have led to significant economic losses. The leopard coral grouper (Plectropomus leopardus) often suffers from vibriosis. Improving host immunity presents a superior strategy for disease control, with minimal side effects compared to the use of antibiotics, highlighting the necessity of exploring the mechanisms underlying the fish's response to pathogen infections. Here, we conducted a comparative metabolomic analysis on the livers of the P. leopardus infected with Vibrio harveyi. A total of 1124 differential metabolites (DMs) were identified, with 190, 218, 359, and 353 DMs being identified at 6, 12, 24, and 48 h post‐infection (hpi), respectively. Then, based on the time series analysis, we found that the lipid metabolism pathways were modulated in response to the Vibrio infection, with an increase in the quantity of eicosanoids and gycerophospholipids (GPLs), as well as a decrease in the quantity of bile acids (BAs), vitamin D, and sex hormones. Furthermore, 13 enriched pathways involving 31 DMs were identified through KEGG (Kyoto Encyclopedia of Genes and Genomes) enrichment analyses. We identified histamine, 15(S)‐HpETE, and anandamide in the transient receptor potential (TRP) channels pathway, as well as (7S,8S)‐DiHODE, 5S,8R‐DiHODE, and 13(S)‐HpODE in the linoleic acid (LA) metabolism pathway. The DM levels increased, which may be attributed to inflammation. The DMs in the thyroid hormone synthesis pathway were identified, and the contents of nicotinamide adenine dinucleotide phosphate (NADPH) and glutathione (GSH) decreased, which may be crucial in antioxidants. Our findings highlighted the dynamic adjustments in lipid metabolism and the response to inflammation and oxidative stress during the infection of V. harveyi in P. leopardus. This study not only deepens our understanding of the metabolic underpinnings of fish immune responses but also lays the groundwork for research into functional metabolomics and mechanisms of disease resistance. [ABSTRACT FROM AUTHOR]

High temperature stress is one of the most severe forms of abiotic stress in alfalfa. With the intensification of climate change, the frequency of high temperature stress will further increase in the future, which will bring challenges to the growth and development of alfalfa. Therefore, untargeted metabolomic and RNA-Seq profiling were implemented to unravel the possible alteration in alfalfa seedlings subjected to different temperature stress (25 ℃, 30 ℃, 35 ℃, 40 ℃) in this study. Results revealed that High temperature stress significantly altered some pivotal transcripts and metabolites. The number of differentially expressed genes (DEGs) markedly up and down-regulated was 1876 and 1524 in T30_vs_CK, 2, 815 and 2667 in T35_vs_CK, and 2115 and 2, 226 in T40_vs_CK, respectively. The number for significantly up-regulated and down-regulated differential metabolites was 173 and 73 in T30_vs_CK, 188 and 57 in T35_vs_CK, and 220 and 66 in T40_vs_CK, respectively. It is worth noting that metabolomics and transcriptomics co-analysis characterized enriched in plant hormone signal transduction (ko04705), glyoxylate and dicarboxylate metabolism (ko00630), from which some differentially expressed genes and differential metabolites participated. In particular, the content of hormone changed significantly under T40 stress, suggesting that maintaining normal hormone synthesis and metabolism may be an important way to improve the HTS tolerance of alfalfa. The qRT-PCR further showed that the expression pattern was similar to the expression abundance in the transcriptome. This study provides a practical and in-depth perspective from transcriptomics and metabolomics in investigating the effects conferred by temperature on plant growth and development, which provided the theoretical basis for breeding heat-resistant alfalfa. [ABSTRACT FROM AUTHOR]

The R2R3-MYB gene family represents a widely distributed class of plant transcription factors. This gene family plays an important role in many aspects of plant growth and development. However, the characterization of R2R3-MYB genes present in the genome of Coptis teeta has not been reported. Here, we describe the bioinformatic identification and characterization of 88 R2R3-MYB genes in this species, and the identification of members of the R2R3-MYB gene family in species within the order Ranales most closely related to Coptis teeta. The CteR2R3-MYB genes were shown to exhibit a higher degree of conservation compared to those of A. thaliana, as evidenced by phylogeny, conserved motifs, gene structure, and replication event analyses. Cis-acting element analysis confirmed the involvement of CteR2R3-MYB genes in a variety of developmental processes, including growth, cell differentiation, and reproduction mediated by hormone synthesis. In addition, through homology comparisons with the equivalent gene family in A. thaliana, protein regulatory network prediction and transcriptome data analysis of floral organs across three time periods of flower development, 17 candidate genes were shown to exhibit biased expression in two floral phenotypes of C. teeta. This suggests their potential involvement in floral development (anther development) in this species. [ABSTRACT FROM AUTHOR]

Pheochromocytomas (PC) and paragangliomas (PG) are rare neuroendocrine tumors with varied genetic makeup and are associated with high cardiovascular morbidity and a variable risk of malignancy. The source of the transcriptional heterogeneity of the disease and the underlying biological processes that determine the outcome of PCPG remain largely unclear. We focused on PCPG tumors with germline SDHB and RET mutations, which represent distinct prognostic groups with worse or better prognoses, respectively. We applied single-nuclei RNA sequencing (snRNA-seq) to tissue samples from 11 patients and found high patient-to-patient transcriptome heterogeneity in neuroendocrine tumor cells. The tumor microenvironment also showed heterogeneous profiles, mainly contributed bymacrophages of the immune cell clusters and Schwann cells of the stroma. By performing non-negative matrix factorization, we identified common transcriptional programs active in RET and SDHB, as well as distinct modules, including neuronal development, hormone synthesis and secretion, and DNA replication. Similarities between the transcriptomes of the tumor cells and those of the chromaffin- and precursor cell types suggests different developmental stages at which PC and PG tumors appear to be arrested. [ABSTRACT FROM AUTHOR]

Many persistent organic pollutants (POPs) are suspected endocrine disruptors and it is important to investigate their effects at low concentrations relevant to human exposure. Here, the OECD test guideline #456 steroidogenesis assay was downscaled to a 96-well microplate format to screen 24 POPs for their effects on viability, and testosterone and estradiol synthesis using the human adrenocortical cell line H295R. The compounds (six polyfluoroalkyl substances, five organochlorine pesticides, ten polychlorinated biphenyls and three polybrominated diphenyl ethers) were tested at human-relevant levels (1 nM to 10 µM). Increased estradiol synthesis, above the OECD guideline threshold of 1.5-fold solvent control, was shown after exposure to 10 µM PCB-156 (153%) and PCB-180 (196%). Interestingly, the base hormone synthesis varied depending on the cell batch. An alternative data analysis using a linear mixed-effects model that include multiple independent experiments and considers batch-dependent variation was therefore applied. This approach revealed small but statistically significant effects on estradiol or testosterone synthesis for 17 compounds. Increased testosterone levels were demonstrated even at 1 nM for PCB-74 (18%), PCB-99 (29%), PCB-118 (16%), PCB-138 (19%), PCB-180 (22%), and PBDE-153 (21%). The MTT assay revealed significant effects on cell viability after exposure to 1 nM of perfluoroundecanoic acid (12%), 3 nM PBDE-153 (9%), and 10 µM of PCB-156 (6%). This shows that some POPs can interfere with endocrine signaling at concentrations found in human blood, highlighting the need for further investigation into the toxicological mechanisms of POPs and their mixtures at low concentrations relevant to human exposure. [ABSTRACT FROM AUTHOR]

The fodder soybean (Glycine max) is an excellent leguminous forage with a high protein content and hay yield, cultivated comprehensively in alpine regions, but seasonal drought in northern regions severely impacts the growth of seedlings. Melatonin (MT) and strigolactone (SL) are critical in relieving the restraint of plant growth in water-deficient environments, but the mechanisms of MT- and SL-mediated drought resistance in fodder soybean needs to be explored. This study mainly investigated the potential morphophysiological mechanism of MT and SL treatments in protecting fodder soybean from drought stress. The fodder soybean 'Gongnong 535' was treated with 100 µM MT or 1 µM SL under normal, moderate, and severe water deficit conditions. The results showed that MT and SL treatments enhanced the plant growth parameters and stomatal aperture under drought stress. Moreover, the observed reductions in superoxide ion (O2.-), malondialdehyde (MDA), and relative electrical conductivity (REC), along with enhancements in the activities of superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT), as well as higher levels of ascorbate (AsA), glutathione (GSH), soluble sugar (SS), soluble protein (SP), and free proline (Pro), indicated that MT and SL application effectively alleviated the oxidative damage and prevented the cell membrane disruption caused by drought stress. Additionally, MT and SL treatments improved photosynthesis and growth in fodder soybean seedlings under water stress by adjusting chlorophyll pigments, gas exchange indexes, and chlorophyll fluorescence parameters, as well as endogenous hormone levels. Simultaneously, MT and SL influenced the expression of genes associated with photosynthesis and antioxidant defenses, as well as phytohormone concentrations. Notably, the protective effect of the SL treatment was superior to that of MT in water-deficient conditions. This study contributes to further understanding the defensive mechanism of MT and SL against drought stress. [ABSTRACT FROM AUTHOR]

Background: The thyroid gland is susceptible to abnormal epithelial cell growth, often resulting in thyroid dysfunction. The serine–threonine protein kinase mechanistic target of rapamycin (mTOR) regulates cellular metabolism, proliferation, and growth through two different protein complexes, mTORC1 and mTORC2. The PI3K-Akt-mTORC1 pathway's overactivity is well associated with heightened aggressiveness in thyroid cancer, but recent studies indicate the involvement of mTORC2 as well. Methods: To elucidate mTORC1's role in thyrocytes, we developed a novel mouse model with mTORC1 gain of function in thyrocytes by deleting tuberous sclerosis complex 2 (TSC2), an intracellular inhibitor of mTORC1. Results: The resulting TPO-TSC2KO mice exhibited a 70–80% reduction in TSC2 levels, leading to a sixfold increase in mTORC1 activity. Thyroid glands of both male and female TPO-TSC2KO mice displayed rapid enlargement and continued growth throughout life, with larger follicles and increased colloid and epithelium areas. We observed elevated thyrocyte proliferation as indicated by Ki67 staining and elevated cyclin D3 expression in the TPO-TSC2KO mice. mTORC1 activation resulted in a progressive downregulation of key genes involved in thyroid hormone biosynthesis, including thyroglobulin (Tg), thyroid peroxidase (Tpo), and sodium–iodide symporter (Nis), while Tff1, Pax8, and Mct8 mRNA levels remained unaffected. NIS protein expression was also diminished in TPO-TSC2KO mice. Treatment with the mTORC1 inhibitor rapamycin prevented thyroid mass expansion and restored the gene expression alterations in TPO-TSC2KO mice. Although total thyroxine (T4), total triiodothyronine (T3), and TSH plasma levels were normal at 2 months of age, a slight decrease in T4 and an increase in TSH levels were observed at 6 and 12 months of age while T3 remained similar in TPO-TSC2KO compared with littermate control mice. Conclusions: Our thyrocyte-specific mouse model reveals that mTORC1 activation inhibits thyroid hormone (TH) biosynthesis, suppresses thyrocyte gene expression, and promotes growth and proliferation. [ABSTRACT FROM AUTHOR]

SUMMARY: Plants possess an outstanding capacity to regenerate enabling them to repair damages caused by suboptimal environmental conditions, biotic attacks, or mechanical damages impacting the survival of these sessile organisms. Although the extent of regeneration varies greatly between localized cell damage and whole organ recovery, the process of regeneration can be subdivided into a similar sequence of interlinked regulatory processes. That is, competence to regenerate, cell fate reprogramming, and the repatterning of the tissue. Here, using root tip regeneration as a paradigm system to study plant regeneration, we provide a synthesis of the molecular responses that underlie both regeneration competence and the repatterning of the root stump. Regarding regeneration competence, we discuss the role of wound signaling, hormone responses and synthesis, and rapid changes in gene expression observed in the cells close to the cut. Then, we consider how this rapid response is followed by the tissue repatterning phase, where cells experience cell fate changes in a spatial and temporal order to recreate the lost stem cell niche and columella. Lastly, we argue that a multi‐scale modeling approach is fundamental to uncovering the mechanisms underlying root regeneration, as it allows to integrate knowledge of cell‐level gene expression, cell‐to‐cell transport of hormones and transcription factors, and tissue‐level growth dynamics to reveal how the bi‐directional feedbacks between these processes enable self‐organized repatterning of the root apex. [ABSTRACT FROM AUTHOR]

To explore the regulatory mechanism of endogenous hormones in the synthesis of anthocyanins in Anoectochilus roxburghii (Wall.) Lindl (A. roxburghii) under different light intensities, this study used metabolomics and transcriptomics techniques to identify the key genes and transcription factors involved in anthocyanin biosynthesis. We also analyzed the changes in and correlations between plant endogenous hormones and anthocyanin metabolites under different light intensities. The results indicate that light intensity significantly affects the levels of anthocyanin glycosides and endogenous hormones in leaves. A total of 38 anthocyanin-related differential metabolites were identified. Under 75% light transmittance (T3 treatment), the leaves exhibited the highest anthocyanin content and differentially expressed genes such as chalcone synthase (CHS), flavonol synthase (FLS), and flavonoid 3′-monooxygenase (F3′H) exhibited the highest expression levels. Additionally, 13 transcription factors were found to have regulatory relationships with 7 enzyme genes, with 11 possessing cis-elements responsive to plant hormones. The expression of six genes and two transcription factors was validated using qRT-PCR, with the results agreeing with those obtained using RNA sequencing. This study revealed that by modulating endogenous hormones and transcription factors, light intensity plays a pivotal role in regulating anthocyanin glycoside synthesis in A. roxburghii leaves. These findings provide insights into the molecular mechanisms underlying light-induced changes in leaf coloration and contribute to our knowledge of plant secondary metabolite regulation caused by environmental factors. [ABSTRACT FROM AUTHOR]

Background: Ulcerative colitis (UC) is a common chronic disease associated with inflammation and oxidative stress. This study aimed to construct a long noncoding RNA (lncRNA)-microRNA (miRNA)-messenger RNA (mRNA) network based on bioinformatics analysis and to explore oxidative stress-related genes underlying the pathogenesis of UC. Methods: The GSE75214 , GSE48959 , and GSE114603 datasets were downloaded from the Gene Expression Omnibus database. Following differentially expressed (DE) analysis, the regulatory relationships among these DERNAs were identified through miRDB, miRTarBase, and TargetScan; then, the lncRNA-miRNA-mRNA network was established. The Molecular Signatures Database (MSigDB) was used to search oxidative stress-related genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed for functional annotation and enrichment analyses. Based on the drug gene interaction database DGIdb, drugs that interact with oxidative stress-associated genes were explored. A dextran sulfate sodium (DSS)-induced UC mouse model was used for experimental validation. Results: A total of 30 DE-lncRNAs, 3 DE-miRNAs, and 19 DE-mRNAs were used to construct a lncRNA-miRNA-mRNA network. By comparing these 19 DE-mRNAs with oxidative stress-related genes in MSigDB, three oxidative stress-related genes (CAV1, SLC7A11, and SLC7A5) were found in the 19 DEM sets, which were all negatively associated with miR-194. GO and KEGG analyses showed that CAV1, SLC7A11, and SLC7A5 were associated with immune inflammation and steroid hormone synthesis. In animal experiments, the results showed that dexamethasone, a well-known glucocorticoid drug, could significantly decrease the expression of CAV1, SLC7A11, and SLC7A5 as well as improve UC histology, restore antioxidant activities, inhibit inflammation, and decrease myeloperoxidase activity. Conclusion: SLC7A5 was identified as a representative gene associated with glucocorticoid therapy resistance and thus may be a new therapeutic target for the treatment of UC in the clinic. [ABSTRACT FROM AUTHOR]

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Copyright of Journal of Northwest A & F University - Natural Science Edition is the property of Editorial Department of Journal of Northwest A&F University (Natural Science Edition) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Salinity is a crucial environmental factor influencing the survival, growth, development, and reproduction of aquatic animals. However, the underlying molecular mechanisms of the shrimp's response to salinity stress are not yet fully understood. Therefore, we used the Illumina NovaSeq 6000 platform to perform transcriptome sequencing of the hepatopancreas of Litopenaeus vannamei under high-salinity (30 PSU), medium-salinity (10 PSU), and low-salinity (0.5 PSU) conditions. We obtained 63.23 Gb of high-quality data and identified 3589 differentially expressed genes (DEGs), including 1638 upregulated and 1951 downregulated genes. Notably, a comparison between the control group (30 PSU) and the low-salinity group (0.5 PSU) revealed that the BBOX1 and CHE1 genes were significantly upregulated, while the ACOX1, MPV, CYP2L1, GCH, MVK, TREt1, and XDH genes were significantly downregulated. These genes are primarily involved in key metabolic pathways, such as fatty acid oxidation, cholesterol metabolism, and hormone synthesis and metabolism. The key genes involved in fatty acid β-oxidation, such as ACOX1, ACAD, HADH, HSD17B4, PECR, CROT, PIPOX, and CG5009, all showed a downward trend, suggesting that L. vannamei may respond to salt stress by regulating fatty acid oxidative metabolism, optimizing energy utilization, and maintaining cell homeostasis under low-salinity conditions. Functional annotation of gene ontology (GO) and KEGG pathway enrichment analysis highlighted the roles of these significant DEGs in the adaptation of L. vannamei to environments of varying salinity, underscoring the importance of metabolic pathways in their adaptive physiological responses. This study provides a crucial molecular biological basis for understanding the molecular mechanisms and physiological protection strategies of L. vannamei under salinity stress. [ABSTRACT FROM AUTHOR]

Introduction: Defects in any thyroid hormone synthesis steps cause thyroid dyshormonogenesis (THD). THD due to thyroglobulin (TG) gene variants is a cause of congenital hypothyroidism (CH) with a wide clinical spectrum, ranging from mild to severe permanent hypothyroidism. We present high-throughput sequencing results of patients with TG variants. Methods: A CH high-throughput sequencing-panel of the main genes involved in the regulation of thyroid hormonogenesis was performed to identify those TG variants that may be related to patient THD phenotype. Results: We identified 21 TG gene variants in 19 patients (11.8%) which could explain their phenotype. Ten of those (47.6%) were not previously described. CH was biochemically severe in these 19 patients. Eight of them were reevaluated after one month of discontinuing LT4 treatment and all had severe permanent hypothyroidism. We also identified another 16 patients who presented heterozygous TG variants, of whom, at reevaluation, five had mild permanent and only one had severe permanent hypothyroidisms. Discussions: In this study, 10 novel and 11 previously reported variants in the TG gene have been identified that could explain the phenotype of 19 patients from non-consanguineous families from a large THD cohort. Although not all these TG gene variants can explain all the patients' THD phenotypes, some of them had severe or mild permanent hypothyroidism at reevaluation. [ABSTRACT FROM AUTHOR]

To analyze the differential expression genes of polycystic ovary syndrome (PCOS), clarify their functions and pathways, as well as the protein–protein interaction network, identify HUB genes, and explore the pathological mechanism. PCOS microarray datasets were screened from the GEO database. Common differentially expressed genes (co-DEGs) were obtained using GEO2R and Venn analysis. Enrichment and pathway analyses were conducted using the DAVID online tool, with results presented in bubble charts. Protein–protein interaction analysis was performed using the STRING tool. HUB genes were identified using Cytoscape software and further interpreted with the assistance of the GeneCards database. A total of two sets of co-DEGs (108 and 102), key proteins (15 and 55), and hub genes (10 and 10) were obtained. The co-DEGs: (1) regulated inflammatory responses and extracellular matrix, TNF, and IL-17 signaling pathways; (2) regulated ribosomes and protein translation, ribosome and immune pathways. The key proteins: (1) regulated inflammation, immunity, transcription, matrix metabolism, proliferation/differentiation, energy, and repair; (2) regulated ubiquitination, enzymes, companion proteins, respiratory chain components, and fusion proteins. The Hub genes: (1) encoded transcription factors and cytokines, playing vital roles in development and proliferation; (2) encoded ribosomes and protein synthesis, influencing hormone and protein synthesis, associated with development and infertility. The dysregulated expression of inflammation and protein synthesis genes in PCOS may be the key mechanism underlying its onset and progression. [ABSTRACT FROM AUTHOR]

Grafting as a crucial horticultural technique has been widely used in the cultivation of Carya cathayensis (Chinese hickory), which is a unique and important economic tree in the northeast of Zhejiang Province and the south of Anhui Province. However, the existing literature lacks research on the potential impact of various rootstocks on the thermal tolerance of Chinese hickory. The objectives of this study were to evaluate heat tolerance in four distinct groups of Chinese hickory, including C. cathayensis grafted onto Carya hunanensis and Carya illinoinensis, one self-grafted group (C. cathayensis grafted onto C. cathayensis), and one non-grafted group (C. cathayensis). We examined photosynthesis parameters, phytohormones, and differentially expressed genes in the four various hickory groups subjected to 25 °C, 35 °C, and 40 °C heat stress (HS). The results demonstrated that grafting onto C. hunanensis and C. illinoinensis exhibited a higher net photosynthetic rate and stomatal conductance, lower intercellular CO2 concentration, and smaller changes in plant hormone content compared to self-grafted and non-grafted group under HS. The transcriptome results revealed that the majority of differentially expressed genes (DEGs) associated with photosynthetic pathways exhibited downregulation under HS, while the degree of variation in grafted groups using C. hunanensis and C. illinoinensis as rootstocks was comparatively lower than that observed in self-grafted and non-grafted groups. The alteration in the expression patterns of DEGs involved in plant hormone synthesis and metabolism under HS corresponded to changes in plant hormone contents. Overall, Chinese hickory grafted onto C. hunanensis and C. illinoinensis exhibited enhanced resistance to high-temperature stress at the juvenile stage. [ABSTRACT FROM AUTHOR]

The review discusses how microbial metabolism in stingless bees contributes to their survival. Eight specific functions that support the survival of stingless bees were identified: (1) nutrient assimilation in larvae; (2) assimilation of nutrients in imagoes; (3) hormone synthesis; (4) food production; (5) food preservation; (6) resistance and resilience to pollution; (7) resistance to detriment of floral diversity; and (8) protection against pathogens. These specific functions are grouped within two general processes: (a) bee development and nutrition, and (b) colony protection. Elucidating the functions of the microbiota in stingless bees can optimize strategies to enhance their resilience against climate change, global warming, and ecosystem degradation. However, it is important to point out that in general the microbiota associated with stingless bees has been scarcely explored as a genetic reservoir of microorganisms with biotechnological potential. [ABSTRACT FROM AUTHOR]

Vitamin D has a crucial role in maintaining thyroid and immune function. In hypothyroidism, the gland is underactive and Vitamin D impacts this condition. Vitamin D regulates gene expression in thyroid hormone synthesis and influences the immune system, affecting overall thyroid health. From the literatures, it is evident that hypothyroidism is correlated with hypovitaminosis D. The immune-mediated properties of Vitamin D reduce the symptoms of hypothyroidism caused by autoimmune conditions. Understanding the correlation of Vitamin D with hypothyroidism is crucial as it holds potential therapeutic implications. Maintaining adequate Vitamin D improves gland function and prevents disease-related complications. [ABSTRACT FROM AUTHOR]

Per- and polyfluoroalkyl substances (PFAS) are a group of synthetic chemicals that are resistant to biodegradation and are environmentally persistent. PFAS are found in many consumer products and are a major source of water and soil contamination. This study investigated the effects of an environmentally relevant PFAS mixture (perfluorooctanoic acid [PFOA], perfluorooctanesulfonic acid [PFOS], perfluorohexanesulfonic acid [PFHxS]) on the transcriptome and function of human granulosa cells (hGCs). Primary hGCs were harvested from follicular aspirates of healthy, reproductive-age women who were undergoing oocyte retrieval for in vitro fertilization. Liquid Chromatography with tandem mass spectrometry (LC/MS-MS) was performed to identify PFAS compounds in pure follicular fluid. Cells were cultured with vehicle control or a PFAS mixture (2 nM PFHxS, 7 nM PFOA, 10 nM PFOS) for 96 h. Analyses of cell proliferation/apoptosis, steroidogenesis, and gene expression were measured via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays/immunofluorescence, ELISA/western blotting, and RNA sequencing/bioinformatics, respectively. PFOA, PFOS, and PFHxS were detected in 100% of follicle fluid samples. Increased cell proliferation was observed in hGCs treated with the PFAS mixture with no impacts on cellular apoptosis. The PFAS mixture also altered steroid hormone synthesis, increasing both follicle-stimulating hormone-stimulated and basal progesterone secretion and concomitant upregulation of STAR protein. RNA sequencing revealed inherent differences in transcriptomic profiles in hGCs after PFAS exposure. This study demonstrates functional and transcriptomic changes in hGCs after exposure to a PFAS mixture, improving our knowledge about the impacts of PFAS exposures and female reproductive health. These findings suggest that PFAS compounds can disrupt normal granulosa cell function with possible long-term consequences on overall reproductive health. [ABSTRACT FROM AUTHOR]