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Pulse rate and blood oxygen levels are crucial physiological parameters that reflect physiological and pathological information within the human body. The system designs a wireless pulse wave monitoring system utilizing a flexible reflective probe and the AFE4490, which is capable of monitoring pulse wave and blood oxygen levels on the human forehead. The system is predominantly based on a reflective flexible probe, the AFE4490, a power supply module, a control microcontroller unit (MCU), and a Wi-Fi module. Post-processing by a slave computer, the collected pulse wave data is wirelessly transmitted to a smartphone. The real-time pulse waveform, pulse rate, and blood oxygen levels are displayed on an application. Following relevant tests and verifications, the system can accurately detect pulse wave signals, meet the requirements for wearable technology, and possesses significant market application potential.
Subject(s)
Wireless Technology , Monitoring, Physiologic/instrumentation , Humans , Pulse Wave Analysis/instrumentation , Smartphone , Heart Rate , Oxygen , Signal Processing, Computer-Assisted , Wearable Electronic DevicesABSTRACT
Background: The incidence of deep vein thrombosis (DVT) in the lower extremities is increasing in the younger population. However, there are fewer reported comparisons in the literature for lower extremity DVT. Methods: Patients aged <40 years admitted with lower-extremity DVT between January 2018 and December 2023 were retrospectively analyzed and followed up for 1 year. Results: A total of 61 patients were included in the study and divided into two groups: 33 patients over 30 years of age (middle-aged group) and 28 patients under 30 years of age (young group). A significant gender difference was observed, with a higher proportion of males in the young group compared to the middle-aged group (P < 0.001). Five patients in the young group were treated with anticoagulation alone, whereas all patients in the middle-aged group underwent endovascular therapy. A higher prevalence of inferior vena cava thrombosis in the young group compared to the middle-aged group (60.71% vs. 33.3%, P = 0.032). The proportion of iliac vein stenosis was significantly higher in the middle-aged groups than in the young group (P = 0.002). There was no statistically significant difference in venous function scores (Villalta and rVCSS) between the two groups during both the preoperative period and the postoperative follow-up (P > 0.05). The incidence of lower-extremity DVT post-thrombotic syndrome and thrombus recurrence was higher in the young group than in the middle-aged group at 1 year postoperatively (PTS: 78.57% vs. 33.3%, P < 0.001, and thrombus recurrence: 28.57% vs. 9.09%, P < 0.05). Univariate and multivariate analyses revealed that inferior vena cava thrombosis was an independent risk factor for severe DVT post-thrombotic syndrome and recurrent DVT (P < 0.05), whereas gender was an independent risk factor for recurrent DVT (P < 0.05). Conclusions: This study suggests differences in the clinical characteristics and prognosis of lower-extremity DVT.
ABSTRACT
Pyoderma gangrenosum (PG) is a rare autoinflammatory neutrophilic dermatosis clinically characterized by painful nodules, red papules or plaques that rapidly erode into ulcers. We report a 53-year-old febrile male patient with acute peripheral arterial disease who underwent transtibial amputation after failed thrombolysis. Five days after amputation, an ulcer developed around the cannulation site of the right internal jugular vein that was indicative of pathergy. The patient's fever did not improve after surgery, and purpuric discoloration and punctate ulcers of the skin near the amputation site became apparent, leading to re-debridement. Finally, consultation with a dermatologist raised the possibility of postoperative PG, and additional laboratory tests revealed positive anticardiolipin autoantibodies consistent with antiphospholipid syndrome. The patient was treated with intravenous glucocorticosteroids and antibiotics, and the amputation wound and cannulation site ulcer were found to have healed at the 2-month follow-up. The current report raises the need for vascular surgeons to be aware of this uncommon etiology of arterial thrombosis, and the postoperative appearance of dermatosis and pathergy should alert for PG.
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BACKGROUND: High blood pressure has been suggested to accelerate vascular injury-induced neointimal formation and progression. However, little is known about the intricate relationships between vascular injury and hypertension in the context of arterial remodeling. METHODS: Single-cell RNA-sequencing analysis was used to depict the cell atlas of carotid arteries of Wistar Kyoto rats and spontaneously hypertensive rats with or without balloon injury. RESULTS: We found that hypertension significantly aggravated balloon injury-induced arterial stenosis. A total of 36â 202 cells from carotid arteries with or without balloon injury were included in single-cell RNA-sequencing analysis. Cell composition analysis showed that vascular injury and hypertension independently induced distinct aortic cell phenotypic alterations including immune cells, endothelial cells (ECs), and smooth muscle cells. Specifically, our data showed that injury and hypertension-induced specific EC phenotypic alterations, and revealed a transition from functional ECs to hypermetabolic, and eventually dysfunctional ECs in hypertensive rats upon balloon injury. Importantly, our data also showed that vascular injury and hypertension-induced different smooth muscle cell phenotypic alterations, characterized by deferential expression of synthetic signatures. Interestingly, pathway analysis showed that dysregulated metabolic pathways were a common feature in monocytes/macrophages, ECs, and smooth muscle cells in response to injury and hypertension. Functionally, we demonstrate that inhibition of mitochondrial respiration significantly ameliorated injury-induced neointimal formation in spontaneously hypertensive rats. CONCLUSIONS: This study provides the cell landscape changes of the main aortic cell phenotypic alterations in response to injury and hypertension. Our findings suggest that targeting cellular mitochondrial respiration could be a novel therapeutic for patients with hypertension undergoing vascular angioplasty.
Subject(s)
Carotid Artery Injuries , Hypertension , Vascular System Injuries , Humans , Rats , Animals , Rats, Inbred SHR , Endothelial Cells/metabolism , Carotid Artery Injuries/metabolism , Carotid Artery Injuries/pathology , Carotid Artery Injuries/therapy , Neointima/pathology , Rats, Inbred WKY , RNAABSTRACT
INTRODUCTION: The objective of this study is to evaluate and compare the effectiveness of endovenous microwave ablation (EMA) and high ligation and strippingn (HLS) of the great saphenous vein (GSV) in the treatment of varicose veins. METHODS: We included 182 patients in each EMA and HLS groups. Follow-up outcomes included AVVQ, VCSS, chronic venous insufficiency questionnaire-14 (CIVIQ14) score, clinical recurrence rate of varicose vein treatment, and patient satisfaction during the 1-year follow-up period. RESULTS: At the 1-year follow-up, no significant difference was found in the clinical recurrence rate of varicose veins between the EMA and HLS groups (p = .75). The duration of the operation and the length of hospital stay for patients in the EMA group was shorter than that for the HLS group (p < .01). The Aberdeen Varicose Vein Questionnaire (AVVQ), Venous Clinical Severity Score (VCSS) score, and ecchymosis were lower for patients who underwent EMA surgery (p < .01). CONCLUSION: Our research results confirm that EMA improves patients' quality of life with lower limb varicose veins, with EMA showing higher patient satisfaction.
Subject(s)
Laser Therapy , Varicose Veins , Venous Insufficiency , Humans , Saphenous Vein/surgery , Quality of Life , Microwaves/therapeutic use , Treatment Outcome , Varicose Veins/surgery , Ligation , Venous Insufficiency/surgery , Laser Therapy/methodsABSTRACT
Isthmin is a polypeptide secreted by adipocytes that was first detected in Xenopus gastrula embryos. Recent studies have focused on the biological functions of isthmin in growth and development, angiogenesis, and metabolism. Distinct spatiotemporal expression of isthmin-1 (ISM-1) was observed during growth and development. ISM-1 plays an important role in the occurrence and development of cancer by regulating cell proliferation, migration, angiogenesis, and immune microenvironments. Moreover, ISM-1, as a newly identified insulin-like adipokine, increases adipocyte glucose uptake and inhibits hepatic lipid synthesis. However, the biological function of ISM-1 remains largely unknown. In this review, we highlight the structure and physiological functions of isthmin and explore its application potential, contributing to a better understanding of its function and providing prevention and treatment strategies for various diseases.
Subject(s)
Thrombospondins , Cell Proliferation , Glucose , Insulin , Liver/metabolism , Humans , Animals , Thrombospondins/physiologyABSTRACT
Background: Ischemiaâreperfusion (IR) is a pathological process that causes secondary damage to blood vessels. However, whether IR can further worsen neointima formation after balloon injury and the detailed mechanism are unclear. Methods: An in vivo model of balloon injury to the rat carotid artery was established to study the effect of IR following balloon injury on neointima formation. Smooth muscle cells (SMCs) were isolated from rat aortas and exposed to hypoxia-reoxygenation to mimic the IR process in vitro. The in vitro cell model was used to investigate the mechanism of IR-mediated neointima formation after balloon injury, which was further confirmed in an in vivo rat model. Results: IR aggravated neointima formation in the rat carotid artery 2 weeks after balloon injury compared with that observed in the absence of balloon injury (P < 0.001). Compared with that of normal SMCs in the rat carotid artery, the expression of IL-1ß, a key proinflammatory cytokine associated with pyroptosis, was increased more than 3-fold in the IR-induced neointima (P < 0.0001) and contributed to the proliferation and migration of rat primary aortic SMCs (P < 0.0001). This process was alleviated by the antioxidant acetylcysteine (NAC), suggesting its partial dependence on intracellular ROS. In the rat model of IR following balloon injury in the carotid artery, the carotid artery that was locally transfected with AAV carrying sh-IL-1ß or sh-caspase-1, which alleviated neointima formation, as indicated by a reduction in intima-media thickness in the rat carotid artery (P < 0.0001). Conclusion: Our results suggested that IR could promote IL-1ß production in SMCs in the carotid artery after balloon injury and aggravate neointimal hyperplasia, which was alleviated by silencing caspase-1/IL-1ß signaling in SMCs in the carotid artery. These results suggest that IL-1ß may be an effective target to combat IR-related neointima formation.
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BACKGROUND: Although the candy-plug technique has been reported to be useful for the treatment of post-dissection aortic aneurysm, the stent graft needs be to customized to accommodate the size of vascular occluders. CASE PRESENTATION: We present a case of a persistent false lumen successfully treated with endovascular stent-graft and atrial septal defect occluder in a patient with Stanford Type B dissection. A covered stent graft was implanted into the false cavity through a distal rupture, and an atrial septal defect occluder was inserted into the covered stent to seal of the false cavity. Decreased aneurysmal diameter and false lumen thrombosis were noted by CT scan at 6-month follow-up. CONCLUSIONS: Our case showed that combined use of a stent graft and atrial septal defect occluder is safe, technically feasible and effective in sealing of the false lumen in post-dissection aortic aneurysm patients with previously failed false lumen thrombosis.
ABSTRACT
BACKGROUND: Tunneled-cuffed catheter (TCC) reaching the mid-atrium has been demonstrated to be associated with improved catheter survival. However, whether similar conclusions can be made for femoral TCC reaching the inferior vena cava (IVC) remains unknown. METHODS: Data from 47 patients with end-stage renal disease receiving right femoral TCC were retrospectively collected and analyzed. The primary patency, catheter dysfunction, and TCC-associated infection rate were compared between patients with TCC tip at the IVC and those with TCC tip at non-IVC. RESULTS: TCC tips were located at the IVC in 26 patients and non-IVC in 21 patients. The technical success rates for both groups were 100%. The primary patency of the former group were significantly higher than those of the latter group at 3 months (92.3% vs 61.9%, p = 0.011), 6 months (80.8% vs 52.4%, p = 0.017), and 12 months (50.0% vs 28.5%, p = 0.024) follow-up, respectively. Kaplan-Meier curve analysis demonstrated significantly different catheter dysfunction-free survival between the two groups (log-rank p = 0.017). The overall TCC-associated infection rate was similar between the two groups (7.7% vs 9.5%, p = 0.82). CONCLUSION: Femoral TCC with tips at IVC was associated with higher primary patency, lower catheter dysfunction but similar TCC-associated infection rate as compared with those at non-IVC.
ABSTRACT
For mechanical equipment, the wear particle in the lubrication system during equipment operation can reflect the lubrication condition, wear mechanism, and severity of wear between equipment friction pairs. To solve the problems of false detection and missed detection of small, dense, and overlapping wear particles in the current ferrography wear particle detection model in a complex oil background environment, a new ferrography wear particle detection network, EYBNet, is proposed. Firstly, the MSRCR algorithm is used to enhance the contrast of wear particle images and reduce the interference of complex lubricant backgrounds. Secondly, under the framework of YOLOv5s, the accuracy of network detection is improved by introducing DWConv and the accuracy of the entire network is improved by optimizing the loss function of the detection network. Then, by adding an ECAM to the backbone network of YOLOv5s, the saliency of wear particles in the images is enhanced, and the feature expression ability of wear particles in the detection network is enhanced. Finally, the path aggregation network structure in YOLOv5s is replaced with a weighted BiFPN structure to achieve efficient bidirectional cross-scale connections and weighted feature fusion. The experimental results show that the average accuracy is increased by 4.46%, up to 91.3%, compared with YOLOv5s, and the detection speed is 50.5FPS.
ABSTRACT
BACKGROUND: Our previous works demonstrated that ß2-microglobulin (ß2m), a systemic pro-aging factor, induce depressive-like behaviors. Hydrogen sulfide (H2S) is identified as a potential target for treatment of depression. The aim of the present work is to explore whether H2S antagonizes ß2m-induced depressive-like behaviors and the underlying mechanisms. METHODS: The depressive-like behaviors were detected using the novelty suppressed feeding test (NSFT), tail suspension test (TST), forced swimming test (FST) and open field test (OFT). The expressions of Warburg-related proteins, including hexokinase II (HK II), pyruvate kinase M2 (PKM2), Lactate dehydrogenase A (LDHA), pyruvate dehydrogenase (PDH) and pyruvate dehydrogenase kinase 1(PDK1), and synaptic plasticity-related proteins, including postsynaptic density protein 95 (PSD95) and synaptophysin1 (SYN1), were determined by western blotting. RESULT: we found that NaHS (the donor of H2S) attenuated the depressive-like behaviors in the ß2m-exposed rats, as judged by NSFT, TST, FST, and OFT. We also demonstrated that NaHS enhanced the synaptic plasticity, as evidenced by the upregulations of PSD95 and SYN1 expressions in the hippocampus of ß2m-exposed rats. Furthermore, NaHS improved the Warburg effect in the hippocampus of ß2m-exposed rats, as evidenced by the upregulations of HK II, PKM2, LDHA and PDK1 expressions, and the downregulation of PDH expression. CONCLUSION: H2S prevents ß2m-induced depressive-like behaviors, which is involved in improvement of hippocampal synaptic plasticity as a result of enhancement of hippocampal Warburg effect.
Subject(s)
Abnormalities, Multiple , Cataract/congenital , Cornea/abnormalities , Depression , Hippocampus/drug effects , Hypogonadism , Intellectual Disability , Microcephaly , Neuronal Plasticity/drug effects , Optic Atrophy , Sulfides/pharmacology , beta 2-Microglobulin/adverse effects , Animals , Depression/chemically induced , Depression/drug therapy , Male , Rats , Rats, Sprague-DawleyABSTRACT
Formaldehyde (FA) causes neurotoxicity and contributes to the occurrence of neurodegenerative diseases. However, the mechanism of FA-induced neurotoxicity has not been fully elucidated. Ferritinophagy, an autophagy process of ferritin mediated by the nuclear receptor coactivator 4 (NCOA4), is a potential mechanism of neurotoxicity. In this study, we explored whether ferritinophagy is associated with the neurotoxicity of FA. Our results showed that FA (50, 100, 200 µM; 24 h) exposure upregulated ferritinophagy in the mouse hippocampal neuronal HT22 cells, which was evidenced by the upregulated autophagic flux, the increased colocalizations of NCOA4 with ferritin heavy chain (FTH1) and NCOA4 with microtubule-associated protein 1 light chain-3B (LC3B), the augmented expression of NCOA4, and the reduced content of FTH1. We also found that FA (0.1, 1, and 10 µmol, i.c.v., 7d) administration boosted ferritinophagy in the hippocampus of Sprague-Dawley (SD) rats, which was demonstrated by the accumulated autophagosomes, the increased expressions of LC3II/I and NCOA4, and the decreased contents of p62 and FTH1 in the hippocampus. Further, we confirmed that inhibition of ferritinophagy by silencing the expression of NCOA4 decreased FA-induced toxic damage in HT22 cells. These results indicated that FA induces neurotoxicity by promoting ferritinophagy. Our findings suggest a potential mechanism insight into the FA-induced neurotoxicity, which in turn provides a new thought for the treatment of FA-related neurodegenerative diseases.
Subject(s)
Autophagy/drug effects , Ferritins/metabolism , Formaldehyde/toxicity , Hippocampus/drug effects , Neurons/drug effects , Animals , Male , Mice , Nuclear Receptor Coactivators , Rats , Rats, Sprague-Dawley , Up-RegulationABSTRACT
The hair follicle dermal papilla is critical for hair generation and de novo regeneration. When cultured in vitro, dermal papilla cells from different species demonstrate two distinguishable growth patterns under the conventional culture condition: a self-aggregative three dimensional spheroidal (3D) cell pattern and a two dimensional (2D) monolayer cell pattern, correlating with different hair inducing properties. Whether the loss of self-aggregative behavior relates to species-specific differences or the improper culture condition remains unclear. Can the fixed 2D patterned dermal papilla cells recover the self-aggregative behavior and 3D pattern also remains undetected. Here, we successfully constructed the two growth patterns using sika deer (Cervus nippon) dermal papilla cells and proved it was the culture condition that determined the dermal papilla growth pattern. The two growth patterns could transit mutually as the culture condition was exchanged. The fixed 2D patterned sika deer dermal papilla cells could recover the self-aggregative behavior and transit back to 3D pattern, accompanied by the restoration of hair inducing capability when the culture condition was changed. In addition, the global gene expressions during the transition from 2D pattern to 3D pattern were compared to detect the potential regulating genes and pathways involved in the recovery of 3D pattern and hair inducing capability.
Subject(s)
Deer/anatomy & histology , Hair Follicle/cytology , AC133 Antigen/biosynthesis , AC133 Antigen/genetics , Alkaline Phosphatase/biosynthesis , Alkaline Phosphatase/genetics , Animals , Biomarkers , Cell Aggregation , Cell Culture Techniques , Cell Division , Cells, Cultured , Deer/genetics , Gene Expression Regulation , Gene Ontology , Hair , Hair Follicle/growth & development , Hair Follicle/metabolism , Mesoderm/cytology , SOXB1 Transcription Factors/biosynthesis , SOXB1 Transcription Factors/genetics , Species Specificity , Spheroids, Cellular/cytology , Spheroids, Cellular/metabolism , Transcriptome , Versicans/biosynthesis , Versicans/geneticsABSTRACT
Diabetes-associated cognitive dysfunction (DACD) characterized by hippocampal injury increases the risk of major cerebrovascular events and death. Endoplasmic reticulum (ER) stress and synaptic dysfunction play vital roles in the pathological process. At present, no specific treatment exists for the prevention and/or the therapy of DACD. We have recently reported that hydrogen sulfide (H2S) exhibits therapeutic potential for DACD, but the underlying mechanism has not been fully elucidated. Silent information regulator 1 (SIRT1) has been shown to play a role in regulating the progression of diabetes and is also indispensable for memory formation and cognitive performance. Hence, the present study was performed to explore whether SIRT1 mediates the protective effect of H2S on streptozotocin (STZ)-induced cognitive deficits, an in vivo rat model of DACD, via inhibiting hippocampal ER stress and synaptic dysfunction. The results showed that administration of NaHS (an exogenous H2S donor) increased the expression of SIRT1 in the hippocampus of STZ-induced diabetic rats. Then, results proved that sirtinol, a special blocker of SIRT1, abrogated the inhibition of NaHS on STZ-induced cognitive deficits, as appraised by Morris water maze test, Y-maze test, and Novel object recognition behavioral test. In addition, administration of NaHS eliminated STZ-induced ER stress as evidenced by the decreases in the expressions of ER stress-related proteins including glucose-regulated protein 78, C/EBP homologous protein, and cleaved caspase-12 in the hippocampus, while these effects of NaHS were also reverted by sirtinol. Furthermore, the NaHS-induced up-regulation of hippocampal synapse-related protein (synapsin-1, SYN1) expression in STZ-induced diabetic rats was also abolished by sirtinol. Taken together, these results demonstrated that SIRT1 mediates the protection of H2S against cognitive dysfunction in STZ-diabetic rats partly via inhibiting hippocampal ER stress and synaptic dysfunction.
Subject(s)
Cognitive Dysfunction/drug therapy , Endoplasmic Reticulum Stress/drug effects , Hippocampus/drug effects , Hydrogen Sulfide/therapeutic use , Neuroprotective Agents/therapeutic use , Sirtuin 1/metabolism , Animals , Cognitive Dysfunction/etiology , Diabetes Mellitus, Experimental/complications , Diabetes Mellitus, Experimental/metabolism , Male , Morris Water Maze Test/drug effects , Open Field Test/drug effects , Rats, Sprague-Dawley , Sulfides/therapeutic use , Up-Regulation/drug effectsABSTRACT
Hydrogen sulfide (H2 S) plays antidepressant-like roles in diabetic rats. However, the underlying mechanisms remain unclear. Brain-derived neurotropic factor (BDNF), a neurotrophic factor, plays important regulatory roles in depression by its high-affinity tropomysin-related kinase B (TrkB) receptor. Autophagy also is implicated in modulation of depression. Previous work confirmed the modulatory roles of H2 S in BDNF protein expression and autophagy. Thus, in this study, we explored whether the BDNF-TrkB pathway mediates the antidepressant-like effects of H2 S in diabetic rats and whether this process is achieved via promoting hippocampal autophagy. We demonstrated that H2 S upregulated the expressions of BDNF and p-TrkB proteins in the hippocampus of streptozotocin (STZ)-induced diabetic rats. K252a (an inhibitor of BDNF-TrkB pathway) reversed the antidepressant-like roles of H2 S, as evidenced by the tail suspension, forced swimming, novelty suppressed feeding, and elevated plus-maze tests. Furthermore, K252a abolished H2 S-promoted hippocampal autophagy in diabetic rats, as evidenced by a decrease in the number of autolysosome, downregulation of Beclin-1 (a regulator of autophagy in the early stage of the formation of autophagosomal membranes and its level is positively correlated with autophagic activity) expression, and upregulation of P62 (a substrate of autophagic degradation and its level is inversely correlated with autophagic activity) expression, in the hippocampus of rats co-treated with NaHS and STZ. Taken together, these data indicated that the BDNF-TrkB pathway mediates the antidepressant-like roles of H2 S in diabetic rats by enhancing hippocampal autophagy.
Subject(s)
Antidepressive Agents/therapeutic use , Brain-Derived Neurotrophic Factor/metabolism , Diabetes Mellitus, Experimental/metabolism , Hippocampus/metabolism , Hydrogen Sulfide/therapeutic use , Receptor, trkB/metabolism , Animals , Antidepressive Agents/pharmacology , Autophagy/drug effects , Autophagy/physiology , Depression/drug therapy , Depression/metabolism , Diabetes Mellitus, Experimental/drug therapy , Diabetes Mellitus, Experimental/pathology , Hippocampus/drug effects , Hippocampus/pathology , Hydrogen Sulfide/pharmacology , Male , Rats , Rats, Sprague-Dawley , Signal Transduction/drug effects , Signal Transduction/physiologyABSTRACT
The reindeer is an Arctic species that exhibits distinctive biological characteristics, for which the underlying genetic basis remains largely unknown. We compared the genomes of reindeer against those of other ruminants and nonruminant mammals to reveal the genetic basis of light arrhythmicity, high vitamin D metabolic efficiency, the antler growth trait of females, and docility. We validate that two reindeer vitamin D metabolic genes (CYP27B1 and POR) show signs of positive selection and exhibit higher catalytic activity than those of other ruminants. A mutation upstream of the reindeer CCND1 gene endows an extra functional binding motif of the androgen receptor and thereby may result in female antlers. Furthermore, a mutation (proline-1172âthreonine) in reindeer PER2 results in loss of binding ability with CRY1, which may explain circadian arrhythmicity in reindeer.
Subject(s)
Adaptation, Biological , Antlers/growth & development , Circadian Rhythm/physiology , Reindeer/genetics , Reindeer/physiology , Amino Acid Motifs/genetics , Amino Acid Substitution , Animals , Arctic Regions , Binding Sites/genetics , Circadian Rhythm/genetics , Cyclin D1/genetics , Female , Period Circadian Proteins/genetics , Proline/genetics , Reindeer/metabolism , Threonine/genetics , Vitamin D/metabolismABSTRACT
Cutis laxa represents a heterogeneous group of rare, inherited, or acquired connective tissue disorders with the common feature of loose and redundant skin with decreased elasticity. The skin of affected deer showed abnormal collagen fiber morphology. To identify the differentially expressed genes of the unusual localized skin laxity in sika deer, we performed transcriptome analysis in the affected and control sika deer. The transcriptome analysis showed 700 genes with significant differential expression in the affected skin as compared with normal skin. Pathway analysis revealed an enrichment of genes involved in tumor necrosis factor signaling, the extracellular matrix-receptor interaction, platelet activation, and Huntington's disease. A gene network was constructed, and the hub nodes such as PTGS2, THBS1, COL1A1, FOS, and NOS3 were found through PPI network analysis, which may contributed to the unusual localized skin laxity in sika deer. Abnormal expression patterns of genes during the development of the affected sika deer were successfully uncovered in the present study, which provides a reference for revealing the related mechanism underlying cutis laxa in sika deer and human beings.
Subject(s)
Cutis Laxa/veterinary , Deer/genetics , Transcriptome , Animals , Collagen/genetics , Collagen/metabolism , Cutis Laxa/genetics , Cyclooxygenase 2/genetics , Cyclooxygenase 2/metabolism , Gene Regulatory Networks , Nitric Oxide Synthase Type III/genetics , Nitric Oxide Synthase Type III/metabolism , Proto-Oncogene Proteins c-fos/genetics , Proto-Oncogene Proteins c-fos/metabolism , Thrombospondin 1/genetics , Thrombospondin 1/metabolismABSTRACT
Embryo implantation in the mink follows the pattern of many carnivores, in that preimplantation embryo diapause occurs in every gestation. Details of the gene expression and regulatory networks that terminate embryo diapause remain poorly understood. Illumina RNA-Seq was used to analyze global gene expression changes in the mink uterus during embryo diapause and activation leading to implantation. More than 50 million high quality reads were generated, and assembled into 170,984 unigenes. A total of 1684 differential expressed genes (DEGs) in uteri with blastocysts in diapause were compared to the activated embryo group (p < 0.05). Among these transcripts, 1527 were annotated as known genes, including 963 up-regulated and 564 down-regulated genes. The gene ontology terms for the observed DEGs, included cellular communication, phosphatase activity, extracellular matrix and G-protein couple receptor activity. The KEGG pathways, including PI3K-Akt signaling pathway, focal adhesion and extracellular matrix (ECM)-receptor interactions were the most enriched. A protein-protein interaction (PPI) network was constructed, and hub nodes such as VEGFA, EGF, AKT, IGF1, PIK3C and CCND1 with high degrees of connectivity represent gene clusters expected to play an important role in embryo activation. These results provide novel information for understanding the molecular mechanisms of maternal regulation of embryo activation in mink.
Subject(s)
Blastocyst/metabolism , Uterus/metabolism , Animals , Blastocyst/physiology , Embryo Implantation/genetics , Embryo Implantation/physiology , Embryo, Mammalian/cytology , Embryo, Mammalian/metabolism , Female , Mink , Pregnancy , Transcriptome/genetics , Uterus/physiologyABSTRACT
The oocyte-specific protein JY-1 was reported as an important regulator of both function of ovarian granulosa cells and early embryogenesis in cattle. Here, we found that the transcripts of JY-1 were also present in sika deer granulosa cells (GCs) through in situ hybridization and qRT-PCR. The complete sika deer JY-1 coding sequence was identified, which had three exons separated by two introns. It was detected that JY-1 knockdown caused apoptosis and abnormal cell cycle progression in GCs of sika deer cultured in vitro. Taken together, these data suggest that JY-1 is involved in the regulation of proliferation in sika deer ovarian GCs.
Subject(s)
Egg Proteins/metabolism , Granulosa Cells/physiology , Oocytes/physiology , Animals , Apoptosis , Cells, Cultured , Deer , Egg Proteins/genetics , Female , Gene Knockdown Techniques , In Situ Hybridization , Real-Time Polymerase Chain ReactionABSTRACT
Deer is valuable all over the body,which is rich in nutritional value and medicinal value. Deer breeding and processing are very advanced in North America and New Zealand where many related standards have been published. The development of Chinese deer industry lack standard and normal management,neither standards' number nor coverage area formed complete frame structure. The international standards like Panax ginseng and P. notoginseng were more lacked. This paper makes a classification statistics on standardization organizations at home and abroad,foreign standards,Chinese national standards,industry standards,local standards and enterprise standards. The classes,contents,ages,implementation and promotion and demonstration area construction of standards were compared and analyzed. We found Chinese deer industry standards were deficient in coverage,uniformity,innovation,repeatability and support. And we give advises for the construction of industry quality standard system,organizational mobility and ideology of consumers,hoping to boost the standard construction and promote international competitiveness of Chinese deer industry.