Chromosome-level genome provides insights into environmental adaptability and innate immunity in the common dolphin (delphinus delphis).

The common dolphin (Delphinus delphis) is widely distributed worldwide and well adapted to various habitats. Animal genomes store clues about their pasts, and can reveal the genes underlying their evolutionary success. Here, we report the first high-quality chromosome-level genome of D. delphis. The assembled genome size was 2.56 Gb with a contig N50 of 63.85 Mb. Phylogenetically, D. delphis was close to Tursiops truncatus and T. aduncus. The genome of D. delphis exhibited 428 expanded and 1,885 contracted gene families, and 120 genes were identified as positively selected. The expansion of the HSP70 gene family suggested that D. delphis has a powerful system for buffering stress, which might be associated with its broad adaptability, longevity, and detoxification capacity. The expanded IFN-α and IFN-ω gene families, as well as the positively selected genes encoding tripartite motif-containing protein 25, peptidyl-prolyl cis-trans isomerase NIMA-interacting 1, and p38 MAP kinase, were all involved in pathways for antiviral, anti-inflammatory, and antineoplastic mechanisms. The genome data also revealed dramatic fluctuations in the effective population size during the Pleistocene. Overall, the high-quality genome assembly and annotation represent significant molecular resources for ecological and evolutionary studies of Delphinus and help support their sustainable treatment and conservation.

Quantitative assessment of the erosion and deposition effects of landslide-dam outburst flood, Eastern Himalaya.

Both regular flow and infrequent outburst floods shape the mountain landscape, but their relative contributions have been widely debated, in part due to the paucity of quantitative data on historical outburst floods. In June 2000, an outburst flood was triggered by a landslide-dam failure in a rapidly exhumed region of the Eastern Himalaya. To investigate the role of this kind outburst flood on landscape evolution, we employ topographic differencing, satellite imagery, and 2D hydraulic simulations to quantify the equivalent erosion and deposition within ~ 80 km flood route downstream of the breach. The flood lasted for ~ 10 h, with a peak discharge of 105 m3/s, leading to average erosion of 10 m, and contributed ~ 1-2 × 103 times more sediment than over long-term mean fluvial processes. The flood produced extensive lateral erosion, which triggered a threefold widening of the valley floor and abundant subsequent landslides. The ubiquitous boulder bars deposited in the channel inhibited incision, and facilitated lateral erosion after the flood. The resulting channel configuration and extensive bank erosion continue to affect fluvial dynamics until the next catastrophic flood that remobilizes the boulders. Our quantitative findings highlight the profound importance of recurrent outburst floods for gorge development and landscape evolution in Eastern Himalaya.

Microplastics Prevalence in Different Cetaceans Stranded along the Western Taiwan Strait.

Microplastics (MPs) pollution is of global concern, which poses serious threats to various marine organisms, including many threatened apex predators. In this study, MPs were investigated from nine cetaceans of four different species, comprising one common dolphin (Delphinus delphis), two pygmy sperm whales (Kogia breviceps), one ginkgo-toothed beaked whale (Mesoplodon ginkgodens), and five Indo-Pacific humpback dolphins (Sousa chinensis) stranded along the western coast of the Taiwan Strait from the East China Sea based on Fourier transform infrared (FTIR) spectroscopy analysis. Mean abundances of 778 identified MPs items were 86.44 ± 12.22 items individual-1 and 0.43 ± 0.19 items g-1 wet weight of intestine contents, which were found predominantly to be transparent, fiber-shaped polyethylene terephthalate (PET) items usually between 0.5 and 5 mm. The abundance of MPs was found at a slightly higher level and significantly correlated with intestine contents mass (p = 0.0004*). The MPs source was mainly likely from synthetic fibers-laden sewage discharged from intense textile industries. Our report represents the first study of MPs in pelagic and deep-diving cetaceans in China, which not only adds baseline data on MPs for cetaceans in Asian waters but also highlights the further risk assessment of MPs consumption in these threatened species.

NO enhances the adaptability to high-salt environments by regulating osmotic balance, antioxidant defense, and ion homeostasis in eelgrass based on transcriptome and metabolome analysis.

Introduction: Eelgrass is a typical marine angiosperm that exhibits strong adaptability to high-salt environments. Previous studies have shown that various growth and physiological indicators were significantly affected after the nitrate reductase (NR) pathway for nitric oxide (NO) synthesis in eelgrass was blocked. Methods: To analyze the molecular mechanism of NO on the adaptability to high-salt environment in eelgrass, we treated eelgrass with artificial seawater (control group) and artificial seawater with 1 mM/L Na2WO4 (experimental group). Based on transcriptomics and metabolomics, we explored the molecular mechanism of NO affecting the salt tolerance of eelgrass. Results: We obtained 326, 368, and 859 differentially expressed genes (DEGs) by transcriptome sequencing in eelgrass roots, stems, and leaves, respectively. Meanwhile, we obtained 63, 52, and 36 differentially accumulated metabolites (DAMs) by metabolomics in roots, stems, and leaves, respectively. Finally, through the combined analysis of transcriptome and metabolome, we found that the NO regulatory mechanism of roots and leaves of eelgrass is similar to that of terrestrial plants, while the regulatory mechanism of stems has similar and unique features. Discussion: NO in eelgrass roots regulates osmotic balance and antioxidant defense by affecting genes in transmembrane transport and jasmonic acid-related pathways to improve the adaptability of eelgrass to high-salt environments. NO in eelgrass leaves regulates the downstream antioxidant defense system by affecting the signal transduction of plant hormones. NO in the stems of eelgrass regulates ion homeostasis by affecting genes related to ion homeostasis to enhance the adaptability of eelgrass to high-salt environments. Differently, after the NO synthesis was inhibited, the glyoxylate and dicarboxylate metabolism, as well as the tricarboxylic acid (TCA) cycle, was regulated by glucose metabolism as a complementary effect to cope with the high-salt environment in the stems of eelgrass. These are studies on the regulatory mechanism of NO in eelgrass, providing a theoretical basis for the study of the salt tolerance mechanism of marine plants and the improvement of terrestrial crop traits. The key genes discovered in this study can be applied to increase salt tolerance in terrestrial crops through cloning and molecular breeding methods in the future.

Annexin A7 and Its Related Protein Suppressor of Death Domains Regulates Migration and Proliferation of Hca-P Cells.

OBJECTIVE: This study was to investigate whether annexin A7 (AnnexinA7, ANXA7) and its co-related protein tumor cell death domain silencer [suppressor of death domains (SODD)] regulates the migratory phenotype of liver cancer cells. MATERIALS AND METHODS: In this experimental study, expression of ANXA7 in Hca-P cells, PANXA7 downregulated cells and PANXA7 unrelated sequence cells was detected by real-time quantitative polymerase chain reaction (PCR) at mRNA level and western blotting at protein level. Transwell migration and invasion assays were performed to determine the migratory phenotype. RESULTS: After inhibition of ANXA7 expression, expression of SODD protein was also significantly decreased (P<0.05). Transwell cell transfer experiments showed that number of tumor cells that penetrated into the cell membrane was significantly reduced after ANXA7 silencing (P<0.05). Transwell cell invasion assay showed that number of tumor cells penetrating into Matrigel was significantly reduced after ANXA7 down-regulation (P<0.05). The CCK8 assay was measured at 0, 24 and 48 hours, and proliferation rate of PANXA7 lower weir cells was slower than that of Hca-P cells and PANXA7 non-related sequence cells (P<0.05). CONCLUSION: SODD expression was decreased with the down-regulation of ANXA7. Down-regulating ANXA7 in Hca-P cells decreased proliferation, migration and invasion of tumor cells.

Subchronic exposure to di-(2-ethylhexyl) phthalate (DEHP) elicits blood-brain barrier dysfunction and neuroinflammation in male C57BL/6J mice.

BACKGROUND: Exposure to di-(2-ethylhexyl) phthalate (DEHP) can cause neurotoxicity but the mechanism is not clear. Blood brain barrier (BBB) is one of the most important tissues to protect the brain. However, whether DEHP can disrupt the BBB or not remains unclear. The objective of this study is to investigate the potential effects of subchronic DEHP exposure on BBB integrity and discuss the role of BBB in DEHP inducible neurotoxicity with an emphasis on neuroinflammatory responses. Male adult C57BL/6J mice were orally administered with vehicle or 200 or 750 mg/kg/day DEHP for 90 days. Subchronic exposure to high-dose DEHP increased water intake but decreased body weight and brain weight. The concentrations of DEHP metabolites increased in serum from all DEHP-exposed groups while increased in brain only from the high-dose group. DEHP induced neurobehavioural alterations and damaged hippocampal neurons. DEHP increased BBB permeability by Evans blue (EB) extravasation and decreased tight junction proteins (ZO-1, occludin, and claudin-5) while presenting a neuroinflammatory feature characterized by the upregulated inflammatory mediators TNF-α and the NLRP3/caspase-1/IL-1ß inflammasome pathway. Our data provide new insights into neurotoxicity caused by subchronic DEHP exposure, which is probably involved in BBB dysfunction and neuroinflammatory responses.

Denoising odontocete echolocation clicks using a hybrid model with convolutional neural network and long short-term memory network.

Ocean noise negatively influences the recording of odontocete echolocation clicks. In this study, a hybrid model based on the convolutional neural network (CNN) and long short-term memory (LSTM) network-called a hybrid CNN-LSTM model-was proposed to denoise echolocation clicks. To learn the model parameters, the echolocation clicks were partially corrupted by adding ocean noise, and the model was trained to recover the original echolocation clicks. It can be difficult to collect large numbers of echolocation clicks free of ambient sea noise for training networks. Data augmentation and transfer learning were employed to address this problem. Based on Gabor functions, simulated echolocation clicks were generated to pre-train the network models, and the parameters of the networks were then fine-tuned using odontocete echolocation clicks. Finally, the performance of the proposed model was evaluated using synthetic data. The experimental results demonstrated the effectiveness of the proposed model for denoising two typical echolocation clicks-namely, narrowband high-frequency and broadband echolocation clicks. The denoising performance of hybrid models with the different number of convolution and LSTM layers was evaluated. Consequently, hybrid models with one convolutional layer and multiple LSTM layers are recommended, which can be adopted for denoising both types of echolocation clicks.

Identification and prediction model of placenta-brain axis genes associated with neurodevelopmental delay in moderate and late preterm children.

BACKGROUND: Moderate and late preterm (MLPT) birth accounts for the vast majority of preterm births, which is a global public health problem. The association between MLPT and neurobehavioral developmental delays in children and the underlying biological mechanisms need to be further revealed. The "placenta-brain axis" (PBA) provides a new perspective for gene regulation and risk prediction of neurodevelopmental delays in MLPT children. METHODS: The authors performed multivariate logistic regression models between MLPT and children's neurodevelopmental outcomes, using data from 129 MLPT infants and 3136 full-term controls from the Ma'anshan Birth Cohort (MABC). Furthermore, the authors identified the abnormally regulated PBA-related genes in MLPT placenta by bioinformatics analysis of RNA-seq data and RT-qPCR verification on independent samples. Finally, the authors established the prediction model of neurodevelopmental delay in children with MLPT using multiple machine learning models. RESULTS: The authors found an increased risk of neurodevelopmental delay in children with MLPT at 6 months, 18 months, and 48 months, especially in boys. Further verification showed that APOE and CST3 genes were significantly correlated with the developmental levels of gross-motor domain, fine-motor domain, and personal social domain in 6-month-old male MLPT children. CONCLUSIONS: These findings suggested that there was a sex-specific association between MLPT and neurodevelopmental delays. Moreover, APOE and CST3 were identified as placental biomarkers. The results provided guidance for the etiology investigation, risk prediction, and early intervention of neurodevelopmental delays in children with MLPT.

Identification of novel cell-free RNAs in maternal plasma as preterm biomarkers in combination with placental RNA profiles.

BACKGROUND: Preterm birth (PTB) is the main driver of newborn deaths. The identification of pregnancies at risk of PTB remains challenging, as the incomplete understanding of molecular mechanisms associated with PTB. Although several transcriptome studies have been done on the placenta and plasma from PTB women, a comprehensive description of the RNA profiles from plasma and placenta associated with PTB remains lacking. METHODS: Candidate markers with consistent trends in the placenta and plasma were identified by implementing differential expression analysis using placental tissue and maternal plasma RNA-seq datasets, and then validated by RT-qPCR in an independent cohort. In combination with bioinformatics analysis tools, we set up two protein-protein interaction networks of the significant PTB-related modules. The support vector machine (SVM) model was used to verify the prediction potential of cell free RNAs (cfRNAs) in plasma for PTB and late PTB. RESULTS: We identified 15 genes with consistent regulatory trends in placenta and plasma of PTB while the full term birth (FTB) acts as a control. Subsequently, we verified seven cfRNAs in an independent cohort by RT-qPCR in maternal plasma. The cfRNA ARHGEF28 showed consistence in the experimental validation and performed excellently in prediction of PTB in the model. The AUC achieved 0.990 for whole PTB and 0.986 for late PTB. CONCLUSIONS: In a comparison of PTB versus FTB, the combined investigation of placental and plasma RNA profiles has shown a further understanding of the mechanism of PTB. Then, the cfRNA identified has the capacity of predicting whole PTB and late PTB.

FGFR2-CCDC6 fusion gene promotes the proliferation of Hucct-1 cells.

To investigate the effect of the FGFR2-CCDC6 fusion gene on cell proliferation and its mechanism of action, pCDNA3.1- FGFR2bWT, pCDNA3.1- FGFR2-CCDC6 expression plasmids were transiently transfected into Hucct-1 cells using Lipo-2000 liposomes. The effect of the fusion gene on cell proliferation was examined by MTT and the expression of FGFR2/AKT/signaling pathway proteins was detected by Western blot. Results showed that Hucct-1 cells transfected with the FGFR2-CCDC6 fusion gene showed increased FGFR2 protein expression (P<0.001) and significantly higher cell proliferation capacity (P<0.001) compared to normal controls. It was concluded that The FGFR2-CCDC6 fusion gene excessively activates the AKT, and ERK signaling pathway downstream of FGFR2 and plays a role in promoting cell proliferation.

miR-22 Suppresses EMT by Mediating Metabolic Reprogramming in Colorectal Cancer through Targeting MYC-Associated Factor X.

Colorectal cancer (CRC) is one of the most frequent gastrointestinal cancers. MicroRNAs (miRNAs) have been proved to be unusually expressed in CRC progression and thus alter multiple pathological processes in CRC cells. However, the specific roles and mechanisms of miR-22 in CRC have not been clearly reported. MicroRNA-22 (miR-22) and MYC-associated factor X (MAX) expressions were determined by RT-qPCR in CRC tissues and cells. The targeted regulatory effects of miR-22 and MAX were confirmed by luciferase reporter and coimmunoprecipitation assays. Also, gain- and loss-of-function and rescue experiments were used to elucidate the function and mechanism of miR-22 and MAX in CRC cells and the mouse xenograft model. We discovered that miR-22 was hypermethylated and downregulated, while MAX was upregulated in CRC. miR-22 markedly inhibited migration, invasion, glycolysis, and cancer stem cell transcription factors in CRC cells. In addition, it was found that miR-22 can directly target MAX. Additional functional experiments confirmed that MAX overexpression can rescue the effects of miR-22 on the behavior of CRC cells. This study suggested that miR-22, as a cancer suppressor, participates in CRC progression by targeting MAX, which might provide basic information for therapeutic targets for CRC.

Relationship and effect of miR-1-3p expression and BDNF level in patients with primary hypertension complicated with depression.

This experiment was designed to explore the relationship and effect of miR-1-3p expression and BDNF level in patients with primary hypertension complicated with depression. The subjects of the study were 145 patients with hypertension with a small fluctuation range of blood pressure in recent three months. Within 48 hours after admission, patients were evaluated with the Hospital Anxiety and Depression Scale (HADS) and Hamilton Depression Rating Scale (HAMD). After fasting for 12 hours, enrolled subjects were subject to blood collection (5 ml) in the morning for detecting blood lipid levels, miR-1-3p expression and BDNF by using an automatic biochemical analyzer, real-time fluorescence quantitative PCR (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Results showed that compared with the normal control group, while miR-1-3p expression increased obviously in patients with hypertension, while the level of BDNF decreased significantly; and compared with patients with simple hypertension, the expression of miR-1-3p in hypertension patients with depression was significantly increased, while BDNF level was decreased evidently (All P < 0.05). miR-1-3p expression in patients with hypertension complicated with depression was negatively correlated with serum BDNF level (r=-0.302, P < 0.05). In relative to the normal control population, the area under the curve (AUC) of ROC produced by serum miR-1-3p and BDNF in patients with primary hypertension complicated with depression was 0.971 (95% CI = 0.945-0.998, P < 0.0001) and 0.875 (95% CI = 0.808-0.942, P < 0.0001); and in relative to primary hypertension patients without depression, the AUC of ROC produced by serum miR-1-3p and BDNF in patients with primary hypertension with depression was 0.957 (95% CI = 0.925-0.989, P < 0.0001) and 0.883 (95% CI = 0.821-0.944, P < 0.0001), respectively. HADS-D score, HAMD score, course of the disease, miR-1-3p expression and BDNF level showed statistical differences in primary hypertension patients with and without depression (All P < 0.05). It was concluded that there are high miR-1-3p expression and low serum BDNF levels in patients with primary hypertension complicated with depression. miR-1-3p has a negative correlation with BDNF, and it may play a role by negatively regulating the expression of BDNF. Detecting miR-1-3p and BDNF in patients with primary hypertension can indicate the occurrence of depression to some extent.

Expression Characteristics of SODD and ALG-2 as Possible Biomarkers for Evaluating Lymphatic Metastasis Potential of Hepatocarcinoma in a Mouse Model.

Annexin A7 has been confirmed in our previous research to be an important factor in lymph node metastasis (LNM) of hepatocellular carcinoma (HCC). SODD and ALG-2 are the binding proteins of Annexin A7 and can work in protein complexes. The present study was carried out with the constructed cell lines in mouse model of metastasis for further elaboration of possible mechanisms and identification of associated genes in the LNM of HCC. This experiment used inbred Chinese 615 mice, as well as Hca-F and Hca-P cells. Quantification of the relative messenger RNA (mRNA) expression of SODD and ALG-2 was realized by using qRT-PCR. Quantification of the protein expressions of SODD and ALG-2 was achieved by using western blot. Experimental mice (n=160) (6-8weeks old, 18-22g, SCXK [LIAO] 2008-0002) were randomly classified into four groups equally, which were separately inoculated with Hca-F, Hca-P, FAnxa7-upregulated, and PAnxa7-upregulated cells. Serum levels of SODD and ALG-2 were measured by ELISA. Immunohistochemical analysis of SODD and ALG-2 was further conducted. Tumor LNM-related factors of SODD and ALG-2 showed the same tendency in their expression correspondingly with the up-regulated expression of Annexin A7. Our experiment further explored the roles of SODD and ALG-2 based on Annexin A7 up-regulation vectors construction and the establishment of corresponding controls in vivo. Furthermore, the mouse model of primary tumors was constructed by injecting Hca-F, FAnxa7-upregulated and Hca-P, PAnxa7-upregulated cells into the mouse footpad. Mice were sacrificed at the designated time points for detecting SODD and ALG-2 expression in tumor tissue and serum samples. Collectively, our work indicates SODD in tumors and in serum and ALG-2 in serum are valuable in evaluating LNM in mice with HCC.

High genetic differentiation of Indo-Pacific humpback dolphins (Sousa chinensis) along the Asian Coast of the Pacific Ocean.

The Indo-Pacific humpback dolphin (Sousa chinensis) is a vulnerable marine mammal species that inhabits shallow, coastal waters from Southeast China, southward throughout Southeast Asia, and westward around the Bay of Bengal to eastern India. Polymorphic microsatellites are useful for elucidating ecological and population genetics-related questions. Here, 18 new polymorphic microsatellites were developed from S. chinensis genomic DNA by Illumina MiSeq sequencing. Population genetic analyses were conducted on 42 S. chinensis individuals from three geographic locations, including the Xiamen Bay of China, the Western Gulf of Thailand, and Andaman Sea. Our microsatellite data revealed a strong and significant population structure among the three sampling regions (overall F ST = 0.371, p = .001). Pairwise mutual information index also demonstrated high levels of genetic differentiation between different region pairs (values range from 0.272 to 0.339, p < .001). Moreover, Structure analysis inferred three genetic clusters, with the high assignment probabilities of 95.92%, 99.47%, and 99.68%, respectively. Principal coordinate analysis plots of individuals divided entire genotypes into three clusters, indicating high level of genetic differentiation. Our results indicated the strong genetic structure in S. chinensis populations is a result of geographic distances. Other factors such as environmental variables, anthropogenic interference, and social behavior may also have contributed to population differentiation.

The prevalence and potential implications of microplastic contamination in marine fishes from Xiamen Bay, China.

The wide presence of microplastics (MPs) in the ocean leads their exposure on marine fish. MP contamination was reported for the gastrointestinal tracts and gills of 117 marine fishes attributed to nine species from Xiamen Bay, a special economic zone in China. Among species, MP abundance ranged from 1.07 items individual-1 to 8.00 items individual -1. Fibers dominated MP shapes, accounting for 59.03% of all MPs. Polymer composition was dominated by polyamide (26.97%) and rayon (17.56%). MPs were most commonly (55.22%) transparent, and most (77.61%) were < 1 mm in size. Our report represents the first of MP contamination in wild marine fish from Xiamen Bay, which we determine to be at an intermediate to slightly higher level compared with levels reported elsewhere, and provides further insights into potential risks of MPs pose to fish and human health.

Identification of mercury-containing nanoparticles in the liver and muscle of cetaceans.

Natural mercury-containing nanoparticles (Hg-NPs) have been found in the environment, but the information for Hg-NPs in organisms was still limited. Clarifying the unique roles of Hg-NPs in organisms is crucial to fully understand the health risks of Hg. Herein, liver and muscle tissues of cetaceans were collected to identify the presence and characteristics of Hg-NPs. We found that methylmercury (MeHg) was the dominant species of Hg in muscles, while inorganic Hg (IHg) accounted for 84.4-99.0% (average 94.0%) of Hg in livers. By using transmission electron microscopy (TEM), size exclusion chromatography coupled with inductively coupled plasma mass spectrometry (SEC-ICPMS) and single particle ICPMS (sp-ICPMS), large amounts (9-161 µg/g) of Hg-NPs in livers and small amounts (0.1-0.4 µg/g) in muscles were observed, indicating that Hg-NPs was an important form of Hg in livers. Both small sized (5-40 nm) and large sized (>100 nm) Hg-NPs were identified, which were mainly complexed with selenium (Se) and sulfur (S) as well as a few cadmium (Cd), lead (Pb) and silver (Ag). This study provided direct evidence of Hg-NPs in marine mammals as well as their chemical form and size distribution, which are helpful for further understanding the biogeochemical cycle and health risk of Hg.

Expression and significance of miR-34 with PI3K, AKT and mTOR proteins in colorectal adenocarcinoma tissues.

This research was carried out to investigate the expression of miR-34a, miR-34b and p-PI3K, p-AKT, and mTOR proteins in colorectal adenocarcinoma and corresponding distal cutaneous normal mucosal tissues and their relationship with the clinicopathological parameters of colorectal adenocarcinoma as well as the correlation between miR-34a, miR-34b and PI3K/AKT/mTOR signaling pathway. The expression of p-PI3K, p-AKT, and mTOR proteins in 67 colorectal adenocarcinomas and the corresponding distal cut-off normal mucosa were assayed by immunohistochemistry. Their relationship with clinicopathological parameters and the correlation of the three proteins were evaluated. The expression of miR-34a and miR-34b in colorectal adenocarcinoma and the corresponding distal cutaneous normal mucosa was detected by applying real-time quantitative PCR. The correlation between colorectal adenocarcinoma tissue miR-34a, miR-34b and p-PI3K, p-AKT, and mTOR proteins, respectively, was analyzed. Results showed that the expression of p-PI3K, p-AKT and mTOR proteins in colorectal adenocarcinoma tissues was higher than that in the corresponding distal cutaneous normal mucosa (P=0.000), and there was a positive correlation between the expression of the three proteins in colorectal adenocarcinoma tissues. The expression of p-PI3K and p-AKT protein in colorectal adenocarcinoma tissues were correlated with tumor size, differentiation degree, infiltration degree, lymph node metastasis and TNM stage (P<0.05). The expression of mTOR protein was related to tumor size and differentiation degree (P<0.05). The relative expression of miR-34a and miR-34b in colorectal adenocarcinoma tissues was less than that in the corresponding distal cutaneous normal mucosa (P<0.05), and the expression of miR-34a and miR-34b was positively correlated. The expression of miR-34a and miR-34b in colorectal adenocarcinoma tissues was negatively correlated with the expression of p-PI3K, p-AKT and mTOR proteins. In conclusion, the PI3K/AKT/mTOR signaling pathway may promote colorectal adenocarcinoma and differentially participate in differentiation, infiltration and lymph node metastasis. Also, miR-34a and miR-34b may inhibit colorectal adenocarcinoma. Importantly, miR-34a and miR-34b may affect the development and progression of colorectal adenocarcinoma by regulating PI3K/AKT/mTOR signaling pathway.

Comparative genomics provides insights into the aquatic adaptations of mammals.

The ancestors of marine mammals once roamed the land and independently committed to an aquatic lifestyle. These macroevolutionary transitions have intrigued scientists for centuries. Here, we generated high-quality genome assemblies of 17 marine mammals (11 cetaceans and six pinnipeds), including eight assemblies at the chromosome level. Incorporating previously published data, we reconstructed the marine mammal phylogeny and population histories and identified numerous idiosyncratic and convergent genomic variations that possibly contributed to the transition from land to water in marine mammal lineages. Genes associated with the formation of blubber (NFIA), vascular development (SEMA3E), and heat production by brown adipose tissue (UCP1) had unique changes that may contribute to marine mammal thermoregulation. We also observed many lineage-specific changes in the marine mammals, including genes associated with deep diving and navigation. Our study advances understanding of the timing, pattern, and molecular changes associated with the evolution of mammalian lineages adapting to aquatic life.

Transfer learning for denoising the echolocation clicks of finless porpoise (Neophocaena phocaenoides sunameri) using deep convolutional autoencoders.

Ocean noise has a negative impact on the acoustic recordings of odontocetes' echolocation clicks. In this study, deep convolutional autoencoders (DCAEs) are presented to denoise the echolocation clicks of the finless porpoise (Neophocaena phocaenoides sunameri). A DCAE consists of an encoder network and a decoder network. The encoder network is composed of convolutional layers and fully connected layers, whereas the decoder network consists of fully connected layers and transposed convolutional layers. The training scheme of the denoising autoencoder was applied to learn the DCAE parameters. In addition, transfer learning was employed to address the difficulty in collecting a large number of echolocation clicks that are free of ambient sea noise. Gabor functions were used to generate simulated clicks to pretrain the DCAEs; subsequently, the parameters of the DCAEs were fine-tuned using the echolocation clicks of the finless porpoise. The experimental results showed that a DCAE pretrained with simulated clicks achieved better denoising results than a DCAE trained only with echolocation clicks. Moreover, deep fully convolutional autoencoders, which are special DCAEs that do not contain fully connected layers, generally achieved better performance than the DCAEs that contain fully connected layers.

Mild Hypothermia Therapy Lowers the Inflammatory Level and Apoptosis Rate of Myocardial Cells of Rats with Myocardial Ischemia-Reperfusion Injury via the NLRP3 Inflammasome Pathway.

OBJECTIVE: To explore the protective effects and mechanism of mild hypothermia treatment in the treatment of myocardial ischemia-reperfusion injury. Material and Methods. A total of 20 Sprague-Dawley (SD) rats were assigned to 4 groups: the blank control group, sham operation group, ischemia reperfusion group, and mild hypothermia therapy group (each n = 5). Some indexes were detected. In addition, myocardial cell models of oxygen-glucose deprivation/reoxygenation injury (OGD) were established. The expression of mRNA IL-6 and TNF-α and the key enzyme levels of apoptosis (cleaved-Caspase-3) and the NLRP3 inflammasome/p53 signaling pathway in the models were determined. RESULTS: The expression of serum IL-6 and TNF-α in the mild hypothermia therapy group was significantly lower than that in the ischemia reperfusion group. The mild hypothermia therapy group also showed a significantly lower TUNEL cell count and NLRP3 and p53 phosphorylation levels than the ischemia reperfusion group (all p < 0.05). The in vitro mild hypothermia + OGD group also showed significantly lower mRNA expression of IL-6 and TNF-α and levels of cleaved Caspase-3, NLRP3, and phosphorylated p53 protein than the OGD group (all p < 0.05). CONCLUSION: In conclusion, mild hypothermia therapy can inhibit the apoptosis and myocardial inflammation of cells induced by MI/R injury in rats and inhibiting the activity of the NLRP3 inflammasome pathway and p53 signaling pathway may be the mechanism.