Protein Response Research Articles

Small heat shock proteins as relevant biomarkers for anthropogenic stressors in earthworms

Anthropogenic stressors in terrestrial ecosystems require focused research on adaptive responses in soil organisms such as Eisenia fetida, a model earthworm species. We analyzed the gene expression of five small heat shock proteins (sHSPs) in response to various stressors: heat stress (31 and 35 °C), desiccation (10 % and 20 % humidity), and chemical exposure (bisphenol A and endosulfan) under standard and elevated temperatures. Under moderate heat (31 °C), early upregulation of sHSP transcripts upregulation suggests their involvement in initial stress responses, possibly mitigating protein aggregation. At the higher temperature (35 °C), three sHSPs served as a defense against severe protein aggregation, a significant finding as previous studies identified only one activated heat shock protein (HSP70) in E. fetida under similar conditions. Desiccation stress at 10 % humidity activated more sHSPs than at 20 % humidity, and the expression profile at 10 % humidity closely resembled that observed under heat stress, suggesting overlapping adaptation pathways. Heat combined with chemical stress, particularly endosulfan, elevated sHSP transcription and underscored the potential of these proteins as biomarkers in multi-stressor environments. Monomeric sHSPs from E. fetida, which share homology with human sHSPs, showed the highest activity across all stressors, suggesting their key role in earthworm adaptation.

Protective effects of dietary protein against nitrite stress in grass carp (Ctenopharyngodon idella): A new perspective

Protein constitutes the predominant essential nutrient in fish feed. Despite extensive research efforts on the dietary protein of fish, limited attention has focused on its potential antistress properties. Therefore, this study sought to examine the impact of dietary protein on the liver structure of grass carp (Ctenopharyngodon idella) and its underlying molecular mechanism after nitrite stress, with the objective of elucidating the role of dietary protein in the stress response of fish. Specifically, various levels of dietary protein (16 %, 19 %, 22 %, 25 %, 28 % and 31 %) were investigated for their effects on liver tissue damage, oxidative stress, endoplasmic reticulum (ER) stress, autophagy and apoptosis in grass carp after exposure to a nitrite solution at a concentration of 10 mg/L for a duration of 96 h.Our study revealed that exposure to nitrite solution resulted in liver structural damage in grass carp. However, 22–25 % dietary protein levels might attenuate the impact of nitrite stress by decreasing liver contents of nitric oxide (NO), peroxynitrite anion (ONOO-), reactive oxygen species (ROS), protein carbonyl (PC), and malondialdehyde (MDA), which is reflected in serum activities of glutamic oxalacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT). Histological analysis further supported the protective role of appropriate protein levels (22–28 %) in alleviating nitrite-induced liver tissue damage. Subsequent investigations demonstrated that optimal dietary protein levels decreased ER stress and autophagy in fish by modulating the expression of gene and protein involved in 78 kDa glucose regulated protein (GRP78) pathway and autophagosome formation process, respectively. Meanwhile, appropriate dietary protein levels decreased the activities of caspase-3, caspase-8 and caspase-9 by inhibiting both death receptor pathway and mitochondrial pathway associated with apoptosis. Finally, based on regression analysis of liver ONOO− content, the dietary protein requirement for grass carp (721–1381 g) under nitrite stress was determined to be 25.07 %. Overall, this study provides novel evidence that optimal protein levels can enhance the resistance of grass carp to nitrite stress and mitigate liver tissue damage by reducing oxidative stress cascade damage.

Genotype-by-Environment Effects of Cis-Variations in the Atgl Promoter Mediate the Divergent Pattern of Phenotypic Plasticity for Temperature Adaptation in Two Congeneric Oyster Species.

Phenotypic plasticity plays an essential role in adaptive evolution. However, the molecular mechanisms of how genotype-by-environment interaction (G × E) effects shape phenotypic plasticity in marine organisms remain poorly understood. The crucial temperature-responsive trait triacylglycerol (TAG) content and its major gene adipose triglyceride lipase (Atgl) expression have divergent plastic patterns in two congeneric oyster species (Crassostrea gigas and Crassostrea angulata) to adapt to relative-cold/northern and relative-warm/southern habitats, respectively. In this study, eight putative loci were identified in the Atgl promoter region (cis-variations) between wild C. gigas and C. angulata that exhibited differential environmental responsiveness (G × E). The G and G × E effects of each locus were further dissected by measuring the Atgl gene expression of different genotypes in response to temperature changes at the cellular and organismal levels. Two transcription factors, non-environmentally responsive non-POU domain-containing octamer-binding protein (Nono) and environmentally responsive heterogeneous nuclear ribonucleoprotein K (Hnrnpk), were screened for binding to g.-1804 (G locus) and g.-1919 (G + G × E locus), respectively. The specificity of Nono binding to the C. angulata allele mediated the G effects of g.-1804, and the lower environmental sensitivity of Hnrnpk in C. angulata mediated the G × E effects of g.-1919, jointly regulating the trade-offs between higher constitutive and lower plastic expression of Atgl gene expression in C. angulata. This study served as an experimental case to reveal how the genetic variations with G and (or) G × E effects propagate into the divergent pattern of plasticity in environmental adaptive traits, which provides new insights into predicting the adaptability of marine organisms to future climate changes.

Abstract TP347: Sex differences of immunosuppression and phagocytosis after stroke as a correlative measure for post-stroke functional recovery

Background: Stroke remains a leading cause of death globally, with significant sex differences in post-stroke outcomes. Additionally, post-stroke infections and sepsis are linked to differences in innate immune responses. The glycosidase, Chitotriosidase 1 (CHIT1), has emerged as an important regulator of innate immunity and lower levels of CHIT1 and chitinases-like proteins are associated with disease severity and progression including multiple sclerosis. However, whether CHIT1 plays a role in the response to acute ischemic stroke is unknown. Hypothesis: We hypothesized that sex-specific alterations in pro-inflammatory factors, including CHIT1, contribute to differential patterns of phagocytosis and post-stroke outcomes. Methods: We examined the effects of acute ischemic stroke (AIS) in older men and women, specifically circulatory cytokine production, circulatory phagocytosis assessment utilizing fluorescent bead engulfment assay, and if these correlated with post-stroke complications in peripheral blood mononuclear cells (PBMCs). We examined relationships with stroke severity, as measured by the NIH Stroke Scale (NIHSS) in patients with a NIHSS>6. Results: Our findings reveal that older women exhibit lower levels of CHIT1 activity correlating with poorer survival outcomes in AIS (p<0.05, n=7-11/grp) compared to men (ns, n=21-22/grp). Female presented a robust phagocytic capability and CHIT1 depression on peripheral monocytes (p<0.05, n=7-11/grp). This effect is not observed in men, who exhibit greater phagocytic capacity after 1 day after stroke (p<0.01, n=21-22/grp) measured by bead uptake assay using flow cytometry. Variations in CHIT1 levels in PBMCs correlated with stroke severity and infection risk, underscoring its potential role in sex-dependent outcomes. Conclusion: Our data suggests that peripheral reduction of CHIT1 levels impairs phagocytosis and increases susceptibility to infections as a risk factor for poorer stroke outcomes. CHIT1 appears to be a novel mediator of sex differences in post-stroke immune suppression. Targeting the anti-fungal response protein CHIT1 could help normalize phagocytic responses in older women, potentially reducing infection rates and improving post-stroke outcomes. Further research into CHIT1's interaction with pathogen-associated molecular patterns could provide new therapeutic strategies for stroke management.

The impact of chronic intermittent hypoxia on enzymatic activity in memory-associated brain regions of male and female rats

BackgroundObstructive sleep apnea (OSA) is an intermittent hypoxia disorder associated with cognitive dysfunction, including learning and memory impairments. There is evidence that alterations in protease activity and neuronal activation are associated with cognitive dysfunction, are dependent on sex, and may be brain region-specific. However, the mechanisms mediating OSA-induced cognitive impairments are unclear. Therefore, we used a rat model of OSA, chronic intermittent hypoxia (CIH) to investigate protease activity (e.g., calpain and caspase-3) on spectrin, a cytoskeletal protein associated with neurotransmitter release, and neuronal activation (early growth response protein 1, EGR-1) in brain regions associated with learning and memory.MethodsMale and female Sprague Dawley rats were exposed to CIH or room air (normoxic) for 14 days. We quantified protease activity and cleaved spectrin products, along with EGR-1 protein expression in hippocampal subregions (CA1, CA3), cortical regions [entorhinal cortex (ETC), retrosplenial cortex (RSC), cerebellar cortex (CC)], and subcortical regions [raphe nucleus (RN), locus coeruleus (LC)] associated with learning and memory. Within each group, Pearson correlations of calpain activity, caspase-3 activity, and EGR-1 expression were performed between brain regions. Sex differences within normoxic and CIH correlations were examined.ResultsCIH dysregulated calpain activity in male ETC, and female CA1 and RSC. CIH dysregulated caspase-3 activity in male RN, and female CA1 and RSC. CIH decreased calpain and caspase-3 cleavage products in male ETC. CIH decreased calpain-cleaved spectrin in male RSC but increased these products in female RSC. EGR-1 expression was decreased in male and female RN. Correlational analysis revealed CIH increased excitatory connections in males and increased inhibitory connections in females. EGR-1 expression in males shifted from negative to positive correlations.ConclusionsOverall, these data indicate CIH dysregulates protease activity and impairs neuronal function in a brain region- and sex-dependent manner. This indicates that males and females exhibit sex-specific vulnerabilities to mild OSA. These findings concur with our previous behavioral studies that demonstrated memory impairment in CIH-exposed rats.

Back2Basics: study on stress–responsive protein expression during seed development in the recalcitrant Artocarpus hirsutus Lam.

Back2Basics: study on stress–responsive protein expression during seed development in the recalcitrant Artocarpus hirsutus Lam.

The Causal Relationships and Therapeutic Targets of Plasma Proteins in Ankylosing Spondylitis

Objective: The purpose of this study was to assess the causal effects of circulating plasma proteins on ankylosing spondylitis (AS) and to explore potential therapeutic targets. Methods: The study used protein quantitative trait loci (pQTLs) for thousands of plasma proteins from nine genome-wide association studies (GWAS) as instrumental variables. The relationship between genetically predicted plasma proteins and AS was assessed through Mendelian randomization (MR) analysis. Further analyses, including colocalization analysis, Steiger filtering analysis, protein-altering variant assessment, protein–protein interaction (PPI), and pathway enrichment analysis, were conducted to validate the robustness and causal direction of the results, as well as to investigate the protein functions and potential drug targets. Results: Nine unique proteins were found to have strong causal associations with AS. Steiger filtering analysis confirmed that all associations identified by MR analysis have a direct causal link from the proteins to AS. Colocalization analysis identified four unique proteins—Interleukin-6 receptor alpha (IL-6Rα), Interleukin-23 receptor (IL-23R), Thrombospondin-2 (THBS2), and Interleukin-1 receptor type 2 (IL-1R2)—that share the same causal variants with AS. PPI and pathway enrichment analysis revealed the potential roles of these proteins in inflammatory responses and immune regulation. Moreover, these proteins were valuable drug targets or considered druggable. Conclusions: This study has identified multiple plasma proteins associated with AS, revealing the important roles of these proteins in the pathogenesis of AS and providing potential therapeutic targets for AS.

Synergistic antitumor effect of MK-1775 and CUDC-907 against prostate cancer.

Due to the emergence of drug resistance, androgen receptor (AR)-targeted drugs still pose great challenges in the treatment of prostate cancer, and it is urgent to explore an innovative therapeutic strategy. MK-1775, a highly selective WEE1 inhibitor, is shown to have favorable therapeutic benefits in several solid tumor models. Recent evidence suggests that the combination of MK-1775 with DNA-damaging agents could lead to enhanced antitumor efficacy. Here, our results demonstrate that MK-1775 alone could indeed inhibit proliferation and induce apoptosis in prostate cancer. Moreover, the combination of MK-1775 and a dual PI3K and HDAC inhibitor, CUDC-907, can synergistically inhibit cell proliferation and dramatically induces apoptosis in prostate cancer cells. This effect is partially mediated by DNA damage, resulting from the downregulation of DNA damage response (DDR) proteins such as CDK, CHK, and RRM1/2. Notably, the combination of MK-1775 and CUDC-907 leads to significant antitumor effects in vivo. Our findings provide a strong basis for a promising combination strategy against prostate cancer.

Potential roles of mitochondrial carrier proteins in plant responses to abiotic stress.

The transport of metabolites across the inner mitochondrial membrane (IMM) is crucial for maintaining energy balance and efficient distribution of metabolic intermediates between cellular compartments. Under abiotic stress, mitochondrial function becomes particularly critical, activating complex signaling pathways essential for plant stress responses. These pathways modulate stress-responsive gene expression, influencing key physiological processes such as cell respiration and senescence, helping plants adapt to stress. Recent studies have emphasized the importance of finely tuned regulation of mitochondrial metabolite transport through the IMM, particularly under stress conditions, to optimize plant survival and resilience. This review summarizes the current knowledge on the possible roles of mitochondrial transport proteins and their contributions to plant adaptation under abiotic stress.

CaXML: Chemistry-informed machine learning explains mutual changes between protein conformations and calcium ions in calcium-binding proteins using structural and topological features.

Proteins' flexibility is a feature in communicating changes in cell signaling instigated by binding with secondary messengers, such as calcium ions, associated with the coordination of muscle contraction, neurotransmitter release, and gene expression. When binding with the disordered parts of a protein, calcium ions must balance their charge states with the shape of calcium-binding proteins and their versatile pool of partners depending on the circumstances they transmit. Accurately determining the ionic charges of those ions is essential for understanding their role in such processes. However, it is unclear whether the limited experimental data available can be effectively used to train models to accurately predict the charges of calcium-binding protein variants. Here, we developed a chemistry-informed, machine-learning algorithm that implements a game theoretic approach to explain the output of a machine-learning model without the prerequisite of an excessively large database for high-performance prediction of atomic charges. We used the ab initio electronic structure data representing calcium ions and the structures of the disordered segments of calcium-binding peptides with surrounding water molecules to train several explainable models. Network theory was used to extract the topological features of atomic interactions in the structurally complex data dictated by the coordination chemistry of a calcium ion, a potent indicator of its charge state in protein. Our design created a computational tool of CaXML, which provided a framework of explainable machine learning model to annotate ionic charges of calcium ions in calcium-binding proteins in response to the chemical changes in an environment. Our framework will provide new insights into protein design for engineering functionality based on the limited size of scientific data in a genome space.

TFII-I/GTF2I regulates globin gene expression and stress response in erythroid cells.

Transcription factor TFII-I/GTF2I is ubiquitously expressed and has been shown to play a role in the differentiation of hematopoietic cells and in the response to various cellular stressors. We previously demonstrated that TFII-I acts as a repressor of adult β-globin gene transcription and positively regulates expression of stress response proteins, including ATF3. Here we analyzed the function of TFII-I in TF-1 cells during erythroid differentiation and in response to cellular stress, including unfolded protein response, hypoxia, and oxidative stress. Ablation of TFII-I leads to mild changes in cell cycle and proliferation of TF-1 cells. Importantly, TFII-I deficiency increased expression of the adult β-globin gene with concomitant reduction in the expression of the fetal γ-globin genes during erythropoietin mediated erythroid differentiation of TF-1 cells. Furthermore, TFII-I regulates genes involved in stress response, including CHOP, Elongin A, ATF3, ATF4, and Grp78, and participates in the apoptotic response to stressors. In summary, the data provide further support for a role of TFII-I in stress response and in the regulation of globin genes.

Genome-Wide Identification and Characterization of the Pirin Gene Family in Nicotiana benthamiana

Background: Pirins are nuclear cupin proteins, one of several gene families within the plant cupin superfamily. However, the identification and functional analysis of Pirin proteins in Nicotiana benthamiana have not been explored. Methods: In this study, genome-wide analysis identifying NbPirin genes in N. benthamiana was conducted, as was phylogenetic analysis of Pirin genes in four Solanaceae species (including Capsicum annuum, Solanum lycopersicum, Solanum tuberosum, and N. benthamiana). In addition, we also evaluated the expression pattern of NbPirins under abiotic stress (temperature and phytohormones) and biotic stress (TMV, TuMV, and PVX). Results: A total of six Nbpirin genes were identified, which can be divided into three clades, and NbPirins also embraced a variety of abiotic or biotic cis-acting elements. The results showed that the expression of NbPirin1-6 was influenced by temperature variations, of which NbPirin6 was significantly upregulated at high temperatures (42 °C) but downregulated at low temperatures (4 °C). Notably, the expression of NbPirin6 exhibited a consistent decrease under ABA and MeJA treatments. Moreover, the expression of NbPirin1-6 was also affected by TMV, TuMV, and PVX infection. NbPirin1, NbPirin2, NbPirin3, and NbPirin5 showed higher expression levels under different viral infections compared to non-infection. Interestingly, NbPirin3 showed the highest expression level during TuMV infection (approximately a 20-fold increase compared to non-infection). Conclusions: Our study proposes the potential role of NbPirin6 in plant responses to abiotic stress, and the role of NbPirin3 in plant antiviral defense, and further lays the groundwork for future research on the functions of NbPirin proteins in responses to various stressors.

Rice Responses to Abiotic Stress: Key Proteins and Molecular Mechanisms

The intensification of global climate change and industrialization has exacerbated abiotic stresses on crops, particularly rice, posing significant threats to food security and human health. The mechanisms by which rice responds to these stresses are complex and interrelated. This review aims to provide a comprehensive understanding of the molecular mechanisms underlying rice’s response to various abiotic stresses, including drought, salinity, extreme temperatures, and heavy metal pollution. We emphasize the molecular mechanisms and structural roles of key proteins involved in these stress responses, such as the roles of SLAC1 and QUAC1 in stomatal regulation, HKT and SOS proteins in salinity stress, heat shock proteins (HSPs) and heat stress transcription factors (HSFs) in temperature stress, and Nramp and ZIP transport proteins in response to heavy metal stress. This review elucidates the complex response networks of rice to various abiotic stresses, highlighting the key proteins and their related molecular mechanisms, which may further help to improve the strategies of molecular breeding.

The SERPINB4 gene mutation identified in twin patients with Crohn’s disease impaires the intestinal epithelial cell functions

Crohn’s disease (CD) is a chronic inflammatory autoimmune disease of unknown etiology. To identify new targets related to the initiation of CD, we screened a pair of twins with CD, which is a rare phenomenon in the Chinese population, for genetic susceptibility factors. Whole-exome sequencing (WES) of these patients revealed a mutation in their SERPINB4 gene. Therefore, we studied a wider clinical cohort of patients with CD or ulcerous colitis (UC), healthy individuals, and those with a family history of CD for this mutation by Sanger sequencing. The single-nucleotide difference in the SERPINB4 gene, which was unique to the twin patients with CD, led to the substitution of lysine by a glutamic acid residue. Functional analysis indicated that this mutation of SERPINB4 inhibited the proliferation, colony formation, wound healing, and migration of intestinal epithelial cells (IECs). Furthermore, mutation of SERPINB4 induced apoptosis and activated apoptosis-related proteins in IECs, and a caspase inhibitor significantly reduced these effects. Transcriptome sequencing revealed that the expression of genes encoding proinflammatory proteins (IL1B, IL6, IL17, IL24, CCL2, and CXCR2) and key proteins in the immune response (S100A9, MMP3, and MYC) was significantly upregulated during SERPINB4 mutant-induced apoptosis. Thus, the heterozygous SERPINB4 gene mutation causes the dysfunction of IECs, which would disrupt the intestinal epithelial barrier and contribute to the development of intestinal inflammation. The activation of SERPINB4 might represent a novel therapeutic target for inflammatory bowel disease.

A central role of stimulator of interferon genes' adaptor protein in defensive immune response.

Cytotoxic DNAs, methylation, histones and histones binding proteins are speculated to induce DNA sensors. Under stressed condition, the antigenic patterns, PAMPs and DAMPs, trigger the hyperactive innate response through DNA, DNA-RNA hybrids, oligonucleotides, histones and mtDNA to initiate cGAMP-STING-IFN I cascade. HSV -1&2, HIV, Varicella- Zoster virus, Polyomavirus, Cytomegalovirus, and KSHV negatively regulate the STING-MAVS-TBK-1/1KKE pathway. Implications in STING-PKR-ER regulation often run into causing senescence and organ fibrosis. Post-translational modifications such as, phosphorylation, ubiquitination, SUMOylation, hydrolysis etc. downstream the processing of cGAS-STING that determine the fate of disease prognosis. Self-DNA under normal circumstances is removed through DNase III action; however, its deficiency is the great cause of RA diseases. Regular STING activation in chronic diseases could lead to exacerbate the neurodegenerative disorders due to constant mtDNA leakage. 2' 3' cGAMP or CDN or its associates are being explored as STING agonist therapeutics to treat solid/metastatic tumors to help infiltrate the immune cells, cytokines and chemokines to regulate the protective response. Liposomes, polymer nanoparticles, and cell-derived nanoparticles are also meant to increase the drug efficiency and stability for desired immune response to enhance the IFN I production. This review highlights the implications of cGAMP-STING- IFN I cascade and related pathways involved in the disease prognosis, therapeutics and considering the gaps on different aspects to utilize its greater potential in disease control.

Genome-Wide Identification and Characterization of the CDPK Family of Genes and Their Response to High-Calcium Stress in Yinshania henryi.

Background/Objectives: Calcium-dependent protein kinases (CDPKs) are a crucial class of calcium-signal-sensing and -response proteins that significantly regulate abiotic stress. Yinshania henryi is a member of the Brassicaceae family that primarily grows in the karst regions of southwestern China, with a notable tolerance to high-calcium soils. Currently, the function of the CDPK family of genes in Y. henryi has yet to be explored. Methods: This study employed a comprehensive approach starting with bioinformatic methods to analyze the whole-genome sequencing data of Y. henryi and identified YhCDPK genes by combining phylogenetic characteristics and protein domain analysis. Results: It then delved into the physicochemical properties, gene structure, chromosomal localization, phylogenetic tree, and promoter cis-acting elements of these YhCDPK genes. Subsequently, RNA-seq data and qRT-PCR analysis were utilized to understand the expression patterns of YhCDPK genes. Twenty-eight YhCDPK genes were found to be unevenly distributed across six chromosomes; these can be classified into four subfamilies, with many cis-acting elements in their promoter regions involved in plant growth and stress responses. Furthermore, the differential expression patterns of YhCDPK genes under different concentrations of calcium treatments were investigated using RNA-seq data and qRT-PCR analysis. Conclusions: These results are a critical first step in understanding the functions of YhCDPK genes, and they lay a foundation for further elucidating the adaptability and response mechanism of YhCDPK genes in Y. henryi to the karst environment.

Metabolomic and gene networks approaches reveal the role of mitochondrial membrane proteins in response of human melanoma cells to THz radiation.

Terahertz (THz) radiation has gained attention due to technological advancements, but its biological effects remain unclear. We investigated the impact of 2.3 THz radiation on SK-MEL-28 cells using metabolomic and gene network analysis. Forty metabolites, primarily related to purine, pyrimidine synthesis and breakdown pathways, were significantly altered post-irradiation. Lipids, such as ceramides and phosphatidylcholines, were also affected. Gene network reconstruction and analysis identified key regulators of the enzymes involved in biosynthesis and degradation of significantly altered metabolites. Mitochondrial membrane components, such as the respiratory chain complex, the proton-transporting ATP synthase complex, and components of lipid rafts, reacted to THz radiation. We propose that THz radiation induces reversible disruption of the lipid raft macromolecular structure, thereby altering mitochondrial molecule transport while maintaining protein integrity, which explains the high cell survival rate. Our findings enhance the understanding of THz biological effects and emphasize the role of membrane components in the cellular response to THz radiation.

Role of Thyroid Hormone in Neurodegenerative Disorders of Older People.

Thyroid dysfunction is associated with a number of neuropsychiatric manifestations. Cognitive decline is a common feature of hypothyroidism and clinical or subclinical hyperthyroidism. In addition, there is a significant association between thyroid hormone (TH) levels and the degree of cognitive impairment in Parkinson's disease (PD). The pathophysiology of TH-related neurodegeneration include changes in the blood-brain barrier, increased cellular stress, altered processing of β-amyloid precursor protein and the effect of TH on neuronal cell viability. The neurotoxicity of TH is partially mediated by the thyroid hormone responsive protein (THRP). This protein is 83% homologous to mouse c-Abl-interacting protein-2 (Abi2), a c-Abl-modulating protein with tumor suppressor activity. In cell cultures, increasing THRP expression either with TH treatment or exogenously through transfecting neuronal or PC 12 cells causes cell necrosis. The expression of exogenous THRP in other cells such as the colonic epithelial cell line Caco-2 and the glial cell line U251 has no effect on cell viability. The effect of THRP on cell viability is not modulated by c-Abl tyrosine kinase. The causal relationship between specific biochemical perturbations in cerebral tissue and thyroid dysfunction remains to be elucidated.

The Erythrocyte Sedimentation Rate (ESR) in Veterinary Medicine: A Focused Review in Dogs and Cats.

The erythrocyte sedimentation rate (ESR) measures the rate at which erythrocytes aggregate and sediment in a fixed time in an anticoagulated blood tube and is expressed as a speed (mm/h). The ESR is still widely used in human medicine mainly as a modified or alternate method to the original Westergren. In veterinary medicine, it was employed in the 1940s-1960s after which it was gradually abandoned or rarely employed. More papers using the Westergren method have been published in dogs rather than in cats. In recent years, the test has regained importance. This narrative review describes the principle of ESR, which is related to the increase in a few acute response proteins such as fibrinogen, immunoglobulin M, and α2-macroglobulin which act to aggregate RBCs. Reference intervals were established for dogs and cats for the original and modified Westergren method. The ESR is mainly used to detect inflammatory conditions derived from infection, urinary or orthopedic disorders, and also miscellaneous diseases. The application of the modified ESR is supported by appropriate reference intervals; however, further studies are needed to assess the influence of age, sex, and breed both for dogs and cats.

A comparative study of the genetically improved Abbassa Nile tilapia strain (GIANT-G9) and a commercial strain in Egypt: growth vs. stress response

Selective breeding is a potent method for developing strains with enhanced traits. This study compared the growth performance and stress responses of the genetically improved Abbassa Nile tilapia strain (G9; GIANT-G9) with a local commercial strain over 12 weeks, followed by exposure to stressors including high ammonia (10 mg TAN/L), elevated temperature (37 °C), and both for three days. The GIANT-G9 showed superior growth, including greater weight gain, final weight, length gain, specific growth rate, and protein efficiency ratio, as well as a lower feed conversion ratio and condition factor compared to the commercial strain. The expression of growth hormone in the brain of the GIANT‐G9 increased significantly after 6 weeks, although it slightly decreased after 12 weeks. Growth hormone receptor 1 expression also increased significantly after 6 weeks. Muscle insulin-like growth factors (igf1 and igf2) levels up-regulated significantly only after 12 weeks in the GIANT‐G9. Under stress, serum enzymes (alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase (ALP)) were significantly higher in the GIANT‐G9, while the commercial strain had lower levels. No significant changes were observed in liver ALP activity among stressed strains. Under stress, the GIANT‐G9 exhibited marked upregulation of splenic Toll-like receptors (tlr2, tlr9, tlr21), myeloid differentiation primary response protein 88 (myd88), nuclear factor kappa B (nf-κB), interleukin (il) 1β, and il6. Notably, il6 expression was higher than il1β in the spleen, with the opposite pattern in the head kidney. In response to immune stimulation, globulin levels significantly increased in the GIANT‐G9 but with similar values to the stressed commercial strain. Myostatin expression increased in the spleen of the stressed GIANT‐G9. The commercial strain exhibited the best liver catalase and superoxide dismutase activities under stress, while the GIANT‐G9 showed increased liver glutathione-S-transferase (GST) activity after exposure to ammonia and temperature stress. Serum lysozyme activity increased in the stressed commercial strain and under temperature stress in the GIANT‐G9 but decreased under other stress conditions. Overall, the stressed commercial strain demonstrated higher survivability than the stressed GIANT‐G9. The study revealed significant interactions between strains and stress factors. The GIANT‐G9 exhibited higher growth rates but lower antioxidant and immune capacities compared to the commercial strain at the juvenile stage of life and production cycle.