Species distribution modeling combined with environmental DNA analysis to explore distribution of invasive alien mosquitofish (Gambusia affinis) in China.

China has become one of the most serious countries suffering from biological invasions in the world. In the context of global climate change, invasive alien species (IAS) are likely to invade a wider area, posing greater ecological and economic threats in China. Western mosquitofish (Gambusia affinis), which is known as one of the 100 most invasive alien species, has distributed widely in southern China and is gradually spreading to the north, causing serious ecological damage and economic losses. However, its distribution in China is still unclear. Hence, there is an urgent need for a more convenient way to detect and monitor the distribution of G. affinis to put forward specific management. Therefore, we detected the distribution of G. affinis in China under current and future climate change by combing Maxent modeling prediction and eDNA verification, which is a more time-saving and reliable method to estimate the distribution of species. The Maxent modeling showed that G. affinis has a broad habitat suitability in China (especially in southern China) and would continue to spread in the future with ongoing climate change. However, eDNA monitoring showed that occurrences can already be detected in regions that Maxent still categorized as unsuitable. Besides temperature, precipitation and human influence were the most important environmental factors affecting the distribution of G. affinis in China. In addition, by environmental DNA analysis, we verified the presence of G. affinis predicted by Maxent in the Qinling Mountains where the presence of G. affinis had not been previously recorded.

Single-cell transcriptome profiling implicates the psychological stress-induced disruption of spermatogenesis.

Male infertility has emerged as a global issue, partly attributed to psychological stress. However, the cellular and molecular mechanisms underlying the adverse effects of psychological stress on male reproductive function remain elusive. We created a psychologically stressed model using terrified-sound and profiled the testes from stressed and control rats using single-cell RNA sequencing. Comparative and comprehensive transcriptome analyses of 11,744 testicular cells depicted the cellular landscape of spermatogenesis and revealed significant molecular alterations of spermatogenesis suffering from psychological stress. At the cellular level, stressed rats exhibited delayed spermatogenesis at the spermatogonia and pachytene phases, resulting in reduced sperm production. Additionally, psychological stress rewired cellular interactions among germ cells, negatively impacting reproductive development. Molecularly, we observed the down-regulation of anti-oxidation-related genes and up-regulation of genes promoting reactive oxygen species (ROS) generation in the stress group. These alterations led to elevated ROS levels in testes, affecting the expression of key regulators such as ATF2 and STAR, which caused reproductive damage through apoptosis or inhibition of testosterone synthesis. Overall, our study aimed to uncover the cellular and molecular mechanisms by which psychological stress disrupts spermatogenesis, offering insights into the mechanisms of psychological stress-induced male infertility in other species and promises in potential therapeutic targets.

Head and Neck Cancer Segmentation in FDG PET Images: Performance Comparison of Convolutional Neural Networks and Vision Transformers.

Convolutional neural networks (CNNs) have a proven track record in medical image segmentation. Recently, Vision Transformers were introduced and are gaining popularity for many computer vision applications, including object detection, classification, and segmentation. Machine learning algorithms such as CNNs or Transformers are subject to an inductive bias, which can have a significant impact on the performance of machine learning models. This is especially relevant for medical image segmentation applications where limited training data are available, and a model's inductive bias should help it to generalize well. In this work, we quantitatively assess the performance of two CNN-based networks (U-Net and U-Net-CBAM) and three popular Transformer-based segmentation network architectures (UNETR, TransBTS, and VT-UNet) in the context of HNC lesion segmentation in volumetric [F-18] fluorodeoxyglucose (FDG) PET scans. For performance assessment, 272 FDG PET-CT scans of a clinical trial (ACRIN 6685) were utilized, which includes a total of 650 lesions (primary: 272 and secondary: 378). The image data used are highly diverse and representative for clinical use. For performance analysis, several error metrics were utilized. The achieved Dice coefficient ranged from 0.833 to 0.809 with the best performance being achieved by CNN-based approaches. U-Net-CBAM, which utilizes spatial and channel attention, showed several advantages for smaller lesions compared to the standard U-Net. Furthermore, our results provide some insight regarding the image features relevant for this specific segmentation application. In addition, results highlight the need to utilize primary as well as secondary lesions to derive clinically relevant segmentation performance estimates avoiding biases.

Cell apoptosis in the testis of male rats is elevated by intervention with ß-endorphin and the mu opioid receptor.

ß-endorphin (ß-EP) is involved in the regulation of male germ cells; however, little is known about the effect of ß-EP on primary germ cells via opioid receptors. In this study, we first revealed significant cell apoptosis in the testis of male rats after ß-EP intervention. Subsequently, the expression of the mu opioid receptor (MOR) was detected in both Leydig cells (LCs) and spermatogonia (SGs) by fluorescence colocalization; overlapping signals were also detected in apoptotic cells. In addition, LCs and SGs were separated from the testis of male rats and primary cells were treated with ß-EP; this increased the mRNA levels of MOR and was accompanied by acute cell apoptosis. Our findings provide a foundation for the further study of apoptosis in reproductive cells regulated by ß-EP and the MOR receptor.

Identification of USP29 as a key regulator of nucleotide biosynthesis in neuroblastoma through integrative analysis of multi-omics data.

Cancer cells show enhanced nucleotide biosynthesis, which is essential for their unlimited proliferation, but the underlying mechanisms are not entirely clear. Ubiquitin specific peptidase 29 (USP29) was reported to sustain neuroblastoma progression by promoting glycolysis and glutamine catabolism; however, its potential role in regulating nucleotide biosynthesis in tumor cells remains unknown. In this study, we depleted endogenous USP29 in MYCN-amplified neuroblastoma SK-N-BE2 cells by sgRNAs and conducted metabolomic analysis in cells with or without USP29 depletion, we found that USP29 deficiency caused a disorder of intermediates involved in glycolysis and nucleotide biosynthesis. De novo nucleotide biosynthesis was analyzed using 13C6 glucose as a tracer under normoxia and hypoxia. The results indicated that USP29-depleted cells showed inhibition of nucleotide anabolic intermediates derived from glucose, and this inhibition was more significant under hypoxic conditions. Analysis of RNA sequencing data in SK-N-BE2 cells demonstrated that USP29 promoted the gene expression of metabolic enzymes involved in nucleotide anabolism, probably by regulating MYC and E2F downstream pathways. These findings indicated that USP29 is a key regulator of nucleotide biosynthesis in tumor cells.

A terrified-sound stress causes cognitive impairment in female mice by impairing neuronal plasticity.

Stress is an important environmental factor affecting mental health that cannot be ignored. Moreover, due to the great physiological differences between males and females, the effects of stress may vary by sex. Previous studies have shown that terrified-sound stress, meaning exposed mice to the recorded vocalizations in response to the electric shock by their kind to induce psychological stress, can cause cognitive impairment in male. In the study, we investigated the effects of the terrified-sound stress on adult female mice. METHODS: 32 adults female C57BL/6 mice were randomly divided into control (n = 16) and stress group (n = 16). Sucrose preference test (SPT)was carried out to evaluate the depressive-like behavior. Using Open field test (OFT) to evaluate locomotor and exploratory alterations in mice. Spatial learning and memory ability were measured in Morris Water maze test (MWM), Golgi staining and western blotting showed dendritic remodeling after stress. In addition, serum hormone quantifications were performed by ELISA. RESULTS: we found the sucrose preference of stress group was significantly decreased (p < 0.05) compared with control group; the escape latency of the stress group was significantly prolonged (p < 0.05), the total swimming distance and the number of target crossings(p < 0.05) were significantly increased (p < 0.05) in MWM; Endocrine hormone, Testosterone (T) (p < 0.05), GnRH (p < 0.05), FSH and LH levels was decreased; Golgi staining and western blotting showed a significant decrease in dendritic arborization, spine density and synaptic plasticity related proteins PSD95 and BDNF in the stress group. CONCLUSION: Terrified-sound stress induced depressive-like behaviors, locomotor and exploratory alterations. And impaired cognitive by altering dendritic remodeling and the expression of synaptic plasticity-related proteins. However, females are resilient to terrified-sound stress from a hormonal point of view.

SERPINA5 promotes tumour cell proliferation by modulating the PI3K/AKT/mTOR signalling pathway in gastric cancer.

SERPINA5 belongs to the serine protease inhibitor superfamily and has been reported to be lowly expressed in a variety of malignancies. However, few report of SERPINA5 in gastric cancer has been found. The purpose of this study was to determine the role of SERPINA5 in GC and to investigate potential tumorigenic mechanisms. We performed qPCR to determine the level of SERPINA5 expression in GC. We used public databases to evaluate whether SERPINA5 could be utilized to predict overall survival and disease-free survival in GC patients. We also knocked down the expression of SERPINA5 and evaluated its effect on cell proliferation and migration. Furthermore, we explored the signal pathways and regulatory mechanisms related to SERPINA5 functions. According to our findings, SERPINA5 was shown to exhibit high expression in GC. Notably, SERPINA5 was prognostic in GC with high expression being unfavourable. SERPINA5 was further observed to promote GC tumorigenesis by modulating GC cell proliferation ability. Mechanically, SERPINA5 could inhibit CBL to regulate the PI3K/AKT/mTOR signalling pathway, thereby promoting GC carcinogenesis progression. These results highlight the important role of SERPINA5 in GC cell proliferation and suggest that SERPINA5 could be a novel target for GC treatment and a predictor for GC prognosis.

Pt3R5G inhibits colon cancer cell proliferation through inducing ferroptosis by down-regulating SLC7A11.

AIMS: Colon cancer (CC) is a prevalent malignancy worldwide and is one of the most easily altered cancers by dietary regulation. Petunidin 3-O-[rhamnopyranosyl-(trans-p-coumaroyl)]-5-O-(ß-D-glucopyranoside) (Pt3R5G) isolated and purified from Lycium ruthenicum Murray, which exhibits highly efficient antioxidant activity and specific anticancer effects, is the flavonoids compound. We aimed to study the effect of Pt3R5G on CC cells and elucidate the potential underlying mechanisms. MAIN METHODS: Cell proliferation was measured by the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) and colony formation assays. Cell cycle, cell apoptosis and reactive oxygen species (ROS) analysis were performed by flow cytometry. RNA-sequencing was performed to elucidate the potential underlying mechanisms. The lipid peroxidation level of cells was detected by malondialdehyde (MDA) assay. The mitochondrial morphology of cells was inspected using a transmission electron microscope. Additionally, we overexpressed SLC7A11 to perform rescue experiments. In vivo, xenograft mice assay was performed to verify the effect of Pt3R5G on the growth of colon cancer. KEY FINDINGS: Pt3R5G reduced the cell activity by blocking the cell cycle in G0/G1 phase, inducing the apoptosis and ferroptosis in RKO cells. The overexpressed of SLC7A11, a significantly down-regulated expression gene caused by Pt3R5G, rescued the cell proliferation inhibition and ferroptosis process. Furthermore, Pt3R5G inhibited tumor growth in nude mice. Our study suggests that Pt3R5G inhibits RKO cell proliferation through mainly reducing ferroptosis by down-regulated SLC7A11. SIGNIFICANCE: As a potential therapeutic drug, Pt3R5G showed efficient anticancer activity through a variety of pathways.

Toxic Effect of Combined Exposure of Microplastics and Copper on Goldfish (Carassius auratus): Insight from Oxidative Stress, Inflammation, Apoptosis and Autophagy in Hepatopancreas and Intestine.

The enhancement of the toxic effect of microplastics (MPs) on heavy metals and its mechanism needs more in-depth and systematic research. In this study, the copper (Cu) accumulation, histological injury, and expression of genes involved in oxidative stress, inflammation, apoptosis, and autophagy of goldfish after single or combined exposure of MPs (1 mg/L) and Cu2+ (0.1 mg/L) for 7 days were determined. The results demonstrated that MPs enhanced the Cu accumulation in hepatopancreas and intestine of goldfish and induced more severe oxidative stress in the hepatopancreas and intestine of goldfish. Additionally, combined exposure of MPs and Cu induced inflammation, excessive apoptosis and insufficient autophagy in the hepatopancreas. Contrary, the inflammation and apoptosis were depressed in the intestine after combined exposure of MPs and Cu, which still requires further exploration. Hence, these findings provide further evidence for the threat of MPs and its adsorbed heavy metals.

LGR6 Acts as an Oncogene and Induces Proliferation and Migration of Gastric Cancer Cells.

Leucine rich repeat containing G protein-coupled receptor 6 (LGR6) belongs to the G protein-coupled receptor family, and it exhibits up-regulated expression in various types of human cancer. However, there are few reports of LGR6 contributing to gastric cancer (GC). Herein, we investigated the function of LGR6 and associated tumorigenic mechanisms in GC. LGR6 expression in GC was analyzed in the cancer genome atlas (TCGA) dataset and further confirmed in GC cell lines and fifteen paired tissue samples via quantitative real-time polymerase chain reaction (qRT-PCR). LGR6 expression was knocked down via small interfering RNA (siRNA), after which the impacts of silencing LGR6 on cell function were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT), cell colony formation, wound-healing, and cell cycle assays. Western blot was performed to explore signaling pathways and regulatory mechanisms associated with LGR6 function. In this study, we showed that LGR6 was at higher levels in GC cell lines and gastric adenocarcinoma tissues. We found that silencing LGR6 in MKN-45 and BGC-823 cells inhibited cell proliferation and migration ability, which accompanied with an obvious regulation of MMP-9, ß-catenin, CCNA2, CDK-2, and ERK1/2. In conclusion, this study demonstrated that LGR6 could act as an oncogene and may be a therapeutic target in GC.

Mitochondrial changes in fish cells in vitro in response to serum deprivation.

Mitochondria are critical to cellular activity that implicated in expansive networks to maintain organismal homeostasis under external stimuli of nutrient variability, a common and severe stress to fish performance during the intensive culture conditions. In the present study, zebrafish embryonic fibroblast cells were used to investigate the fish mitochondrial changes upon serum deprivation. Results showed that mitochondrial content and membrane potential were significantly reduced with increased intracellular ROS level in the serum deprivation treated fish cells. And the impaired mitochondria were characterized by rough and fracted outer membrane, and more fused mitochondria were frequently observed with the upregulated mRNA expressions of mitochondrial fusion genes (mfn1b, mfn2, and opa1). Besides, the mitochondrial DNA (mtDNA) copy numbers of mtatp6, mtcox1, mtcytb, mtnd4, and mtnd6 were overall showing the highly significant reduction, together with the mRNA expressions of these genes significantly increased, exhibiting the compensatory effects in mitochondria. Furthermore, the methyl-cytosine of whole mtDNA was compared and the methyl-reads numbers were distinctly increased in the treatment group, reflecting the instability of fish mtDNA with mitochondrial dysfunction under nutrient fluctuations. Collectively, current findings could facilitate the integrated research between fish mitochondrial response and external variables that indicates the potentially profound and durative deficits in fish health during the aquaculture processes.

c-MYC-USP49-BAG2 axis promotes proliferation and chemoresistance of colorectal cancer cells in vitro.

Deubiquitinases (DUBs) play critical roles in tumorigenesis and are emerging as potential therapeutic targets. However, it remains less clear which DUBs may play important roles and represent a realistic vulnerability for a particular type of tumor. Here we revealed that Ubiquitin Specific Peptidase 49 (USP49) is transcriptionally activated by c-MYC in colorectal cancer (CRC), and CRC patients with elevated USP49 levels exhibited significantly shorter survival. Knockdown of USP49 markedly inhibited CRC cell proliferation, colony formation, and chemotherapy resistance in vitro. Investigation of mechanisms unravels that USP49 deubiquitinates and stabilizes Bcl-2-Associated Athanogene 2 (BAG2), a well-known protein that antagonizes apoptosis and enables adaptive response of CRC cells. This study identified a novel mechanism by which USP49 promotes CRC cell survival by stabilizing BAG2 through the c-MYC-USP49-BAG2 axis, indicating that USP49 may become a potential therapeutic target for CRC.

TDG suppresses the migration and invasion of human colon cancer cells via the DNMT3A/TIMP2 axis.

Background: Colorectal cancer (CRC) is one of the most common malignant tumors with high rates of recurrence and mortality. Thymine DNA glycosylase (TDG) is a key molecule in the base excision repair pathway. Recently, increasing attention has been paid to the role of TDG in tumor development. However, the specific functions of TDG in CRC remain unclear. Methods: The biological functions of TDG and DNA methyltransferase 3 alpha (DNMT3A) in CRC were evaluated using migration and invasion assays, respectively. A tumor metastasis assay was performed in nude mice to determine the in vivo role of TDG. The interaction between TDG and DNMT3A was determined via co-immunoprecipitation (Co-IP). Chromatin immunoprecipitation analysis (ChIP) was used to predict the DNA-binding site of DNMT3A. We also performed methylation-specific PCR (MSP) to detect changes in TIMP2 methylation. Results: TDG inhibited the migration and invasion of human colon cancer cells both in vitro and in vivo. TDG promoted the ubiquitination and degradation of DNMT3A by binding to it. Its interference with siDNMT3A also inhibits the migration and invasion of human colon cancer cells. Furthermore, the ChIP, MSP, and rescue experiments results confirmed that TDG accelerated the degradation of DNMT3A and significantly regulated the transcription and expression of TIMP2, thereby affecting the migration and invasion of human colon cancer cells. Conclusion: Our findings reveal that TDG inhibits the migration and invasion of human colon cancer cells through the DNMT3A-TIMP2 axis, which may be a potential therapeutic strategy for the development and treatment of CRC.

The emerging role of deubiquitylating enzymes as therapeutic targets in cancer metabolism.

Cancer cells must rewire cellular metabolism to satisfy the unbridled proliferation, and metabolic reprogramming provides not only the advantage for cancer cell proliferation but also new targets for cancer treatment. However, the plasticity of the metabolic pathways makes them very difficult to target. Deubiquitylating enzymes (DUBs) are proteases that cleave ubiquitin from the substrate proteins and process ubiquitin precursors. While the molecular mechanisms are not fully understood, many DUBs have been shown to be involved in tumorigenesis and progression via controlling the dysregulated cancer metabolism, and consequently recognized as potential drug targets for cancer treatment. In this article, we summarized the significant progress in understanding the key roles of DUBs in cancer cell metabolic rewiring and the opportunities for the application of DUBs inhibitors in cancer treatment, intending to provide potential implications for both research purpose and clinical applications.

BPA disrupts the SC barrier integrity by activating the cytokines/JNK signaling pathway in rare minnow Gobiocypris rarus.

Bisphenol-A (BPA) has been reported to disrupt blood-testis barrier (BTB) integrity in mammals. However, its effects on fish testis sertoli cell (SC) barrier and the underlying mechanisms have been largely unknown to date. To study the SC barrier toxicity induced by BPA, male rare minnows (Gobiocypris rarus) were exposed to 15 µg L - 1 BPA for 7, 14 and 21 d. Meanwhile, a 25 ng L-1 17α-ethynyl estradiol (EE2) group was set up as the positive control. Results showed that BPA induced immune response in the testes and decreased offspring hatching rate. The biotin tracer assay showed that BPA exposure destroyed the integrity of the testis SC barrier. In addition, BPA exposure decreased the expressions of occludin, ZO-1, CX43 and N-cadherin proteins. The transcripts of CX43 and occludin were significantly decreased and SP1 recruitment in each gene promoter was repressed after BPA exposure. Moreover, the cytokines (TNFα and IL-1ß) were significantly increased while the JNK signal pathway was activated after BPA exposure. BPA also increased the matrix metalloproteinases 1 (MMP1) and MMP2 levels in the testes. In addition, estrogenic effect did not entirely explain the mechanism by which BPA disrupted the SC barrier in G. rarus testes. These results suggested that BPA disrupted the SC barrier integrity by inhibiting SP1 enrichments within CX43 and occludin 5' flanking regions through activated cytokines/JNK signaling pathway. MMPs were also involved in the disruption of SC barrier caused by BPA exposure.

Quantification of uptake in pelvis F-18 FLT PET-CT images using a 3D localization and segmentation CNN.

PURPOSE: The purpose of this work was to develop and validate a deep convolutional neural network (CNN) approach for the automated pelvis segmentation in computed tomography (CT) scans to enable the quantification of active pelvic bone marrow by means of Fluorothymidine F-18 (FLT) tracer uptake measurement in positron emission tomography (PET) scans. This quantification is a critical step in calculating bone marrow dose for radiopharmaceutical therapy clinical applications as well as external beam radiation doses. METHODS: An approach for the combined localization and segmentation of the pelvis in CT volumes of varying sizes, ranging from full-body to pelvis CT scans, was developed that utilizes a novel CNN architecture in combination with a random sampling strategy. The method was validated on 34 planning CT scans and 106 full-body FLT PET-CT scans using a cross-validation strategy. Specifically, two different training and CNN application options were studied, quantitatively assessed, and statistically compared. RESULTS: The proposed method was able to successfully locate and segment the pelvis in all test cases. On all data sets, an average Dice coefficient of 0.9396 ± $\pm$ 0.0182 or better was achieved. The relative tracer uptake measurement error ranged between 0.065% and 0.204%. The proposed approach is time-efficient and shows a reduction in runtime of up to 95% compared to a standard U-Net-based approach without a localization component. CONCLUSIONS: The proposed method enables the efficient calculation of FLT uptake in the pelvis. Thus, it represents a valuable tool to facilitate bone marrow preserving adaptive radiation therapy and radiopharmaceutical dose calculation. Furthermore, the method can be adapted to process other bone structures as well as organs.

Chronic stress inhibits testosterone synthesis in Leydig cells through mitochondrial damage via Atp5a1.

Stress is one of the leading causes of male infertility, but its exact function in testosterone synthesis has scarcely been reported. We found that adult male rats show a decrease in bodyweight, genital index and serum testosterone level after continual chronic stress for 21 days. Two-dimensional gel electrophoresis (2-DE) and MALDI-TOF-MS analysis identified 10 differentially expressed proteins in stressed rats compared with controls. A strong protein interaction network was found to be centred on Atp5a1 among these proteins. Atp5a1 expression significantly decreased in Leydig cells after chronic stress. Transfection of Atp5a1 siRNAs decreased StAR, CYP11A1, and 17ß-HSD expression by damaging the structure of mitochondria in TM3 cells. This study confirmed that chronic stress plays an important role in testosterone synthesis by regulating Atp5a1 expression in Leydig cells.

Benchmarking automated detection of the retinal external limiting membrane in a 3D spectral domain optical coherence tomography image dataset of full thickness macular holes.

In this article, we present a new benchmark for the segmentation of the retinal external limiting membrane (ELM) using an image dataset of spectral domain optical coherence tomography (OCT) scans in a patient population with idiopathic full-thickness macular holes. Specifically, the dataset used contains OCT images from one eye of 107 patients with an idiopathic full-thickness macular hole. In total, the dataset contains 5243 individual 2-dimensional (2-D) OCT image slices, with each patient contributing 49 individual spectral-domain OCT tagged image slices. We display precise image-wise binary annotations to segment the ELM line. The OCT images present high variations in image contrast, motion, brightness, and speckle noise which can affect the robustness of applied algorithms, so we performed an extensive OCT imaging and annotation data quality analysis. Imaging data quality control included noise, blurriness and contrast scores, motion estimation, darkness and average pixel scores, and anomaly detection. Annotation quality was measured using gradient mapping of ELM line annotation confidence, and idiopathic full-thickness macular hole detection. Finally, we compared qualitative and quantitative results with seven state-of-the-art machine learning-based segmentation methods to identify the ELM line with an automated system.

Clinical Analysis and Proteomic Screening Biomarkers for Graft-Versus-Host Disease After Liver Transplant.

OBJECTIVES: Graft-versus-host disease is a serious, fatal complication following liver transplantation. The diagnosis is challenging, owing to nonspecific clinical features and invasive procedures. High-throughput proteomics could provide an effective approach to identifying potential serum biomarkers for graft-versus-host disease. MATERIALS AND METHODS: We retrospectively analyzed the clinical information of 3 patients with graft-versus-host disease treated at our center from 2016 to 2018. We compared serum samples from the 3 patients with the disease, patients with excellent posttransplant outcomes, and healthy controls using mass spectrometry-based proteomics in discovery study. Probable peptides were further identified by a tandem mass spectrometry system and verified by enzyme-linked immunosorbent assay. RESULTS: Of 343 patients, 3 patients (0.875%) had graft-versus-host disease. Two of these patients died of sepsis and multiorgan failure despite intensive therapy. We observed no correlation between severity of clinical manifestation and prognosis; however, the patients with graft-versus-host disease had early onset and infection and showed worse outcome. Serum peptidome profiling showed 65 differentially expressed peaks among the 3 groups; the 2 peptides with the most significant changes (m/z values of 1950.29 and 2088.16) were further sequenced and identified as ATP citrate lyase and fibrinogen alpha chain. Western blot and enzyme-linked immunosorbent assay showed that both peptides gradually decreased among all groups. CONCLUSIONS: Graft-versus-host disease is a complication of organ and tissue transplantation with a high mortality rate. Our identification of potential biomarkers for graft-versus-host disease associated with liver transplant may aid in diagnosis and help to reduce patient mortality in those cases.

Early maternal deprivation impairs learning and memory and alters hippocampal gene expression in adult male rats.

Maternal deprivation (MD) in early life severely disrupts hippocampal development, leading to persistent cognitive and behavior deficits. The current study uncovered that early MD (P1-P21) impaired spatial learning and memory capacity detected by Morris water maze (MWM) tests from juvenile (P31) to adult (P81) rats compared to age-matched controls. And the protein expression in hippocampus were detected by two-dimensional gel electrophoresis (2-DE) before MWM, respectively. Protein changes in hippocampal were examined to identify the molecular pathways underlying MD-induced hippocampal dysfunction. There were 11 differentially expressed proteins analyzed between adult MD and control male rats, while the 8 proteins were then identified by UPLC-ESI-Q-TOF-MS. Gene Ontology (GO) annotations of the identified proteins were related to neuronal and glial cytoskeletal dynamics, membrane signaling, stress responses, biosynthesis, and metabolism. The different expression proteins spectrin alpha chain, non-erythrocytic 1 (Sptan1), ATP-citrate synthase (Acly), and heat shock protein 90-alpha (Hsp90aa1) have been verified by western blot analysis, and their expression levels showed consistent with 2-DE analysis. In addition, glial fibrillary acidic protein (GFAP) was also found reduced in adult hippocampus of MD rats. This study identifies candidate proteins encompassing a range of functional categories that may contribute to persistent learning and memory deficits due to early life MD.