Mitochondrial genome in Hypsizygus marmoreus and its evolution in Dikarya

Background Hypsizygus marmoreus, a high value commercialized edible mushroom is widely cultivated in East Asia, and has become one of the most popular edible mushrooms because of its rich nutritional and medicinal value. Mitochondria are vital organelles, and play various essential roles in eukaryotic cells. Results In this study, we provide the Hypsizygus marmoreus mitochondrial (mt) genome assembly: the circular sequence is 102,752 bp in size and contains 15 putative protein-coding genes, 2 ribosomal RNAs subunits and 28 tRNAs. We compared the mt genomes of the 27 fungal species in the Pezizomycotina and Basidiomycotina subphyla, with the results revealing that H. marmoreus is a sister to Tricholoma matsutake and the phylogenetic distribution of this fungus based on the mt genome. Phylogenetic analysis shows that Ascomycetes mitochondria started to diverge earlier than that of Basidiomycetes and supported the robustness of the hyper metric tree. The fungal sequences are highly polymorphic and gene order varies significantly in the dikarya data set, suggesting a correlation between the gene order and divergence time in the fungi mt genome. To detect the mt genome variations in H. marmoreus, we analyzed the mtDNA sequences of 48 strains. The phylogeny and variation sited type statistics of H. marmoreus provide clear-cut evidence for the existence of four well-defined cultivations isolated lineages, suggesting female ancestor origin of H. marmoreus. Furthermore, variations on two loci were further identified to be molecular markers for distinguishing the subgroup containing 32 strains of other strains. Fifteen conserved protein-coding genes of mtDNAs were analyzed, with fourteen revealed to be under purifying selection in the examined fungal species, suggesting the rapid evolution was caused by positive selection of this gene. Conclusions Our studies have provided new reference mt genomes and comparisons between species and intraspecies with other strains, and provided future perspectives for assessing diversity and origin of H. marmoreus.Ope

A likelihood-based approach to estimating sensitivity and specificity with binocular diagnostic data-application in ophthalmology

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Effects of Different Postharvest Precooling Treatments on Cold-Storage Quality of Yellow Peach (Amygdalus persica)

The rapid precooling of yellow peaches after harvest can minimize the tissue damage and quality deterioration of yellow peaches during postharvest storage. Refrigerator precooling (RPC), cold-water precooling (CWPC), strong-wind precooling (SWPC), fluidized-ice precooling (FIPC), and vacuum precooling (VPC) were used to precool the fresh yellow peaches. The yellow peaches after different precooling treatments were stored at 4 °C for 15 days. CWPC and RPC can effectively retard the respiration and ethylene peak production, reduce the quality loss of yellow peaches during postharvest storage, maintain the color and fruit hardness of yellow peaches, inhibit browning, maintain the contents of soluble solids, titratable acids, and ascorbic acid, increase the activity contents of superoxide dismutase (SOD) and peroxidase (POD), inhibit the decrease in the phenylalanine ammonia-lyase (PAL) activity, and delay the increase in the polyphenol oxidase (PPO) activity. The shelf life of yellow peaches with cold-water precooling and refrigerator precooling reached 15 days, which was 6 days longer than those of the VPC- and FIPC-treated samples, and 3 days longer than that of the SWPC-treated samples. Therefore, CWPC and RPC were effective methods to prolong the storage period and maintain the quality of yellow peaches during postharvest storage

Apoptotic Changes, Oxidative Stress and Immunomodulatory Effects in the Liver of Japanese Seabass (<i>Lateolabrax japonicus</i>) Induced by Ammonia-Nitrogen Stress during Keep-Live Transport

This study investigated the effects of NH3-N on antioxidant responses, histoarchitecture, and immunity of Japanese seabass (Lateolabrax japonicus) during keep-live transport. The findings suggest that NH3-N stress transport alters the transcription of P53, Caspase 9, Bcl2, Caspase 3 and Bax genes, demonstrating that NH3-N stress can trigger the apoptotic pathway of P53-Bax-Bcl2 and Caspase and induce apoptosis. NH3-N stress transport also evoked transcriptional upregulation of inflammatory cytokines (tumor necrosis factor α (TNF-α), Toll-like receptor 3 (TLR-3), nuclear factor kappa β (NF-κB), interleukin 6 (IL-6) and interleukin 1β (IL-1β)) and increased complement C3, C4, lysozyme (LZM) and immunoglobulin (IgM) levels, activating the innate immunological system during keep-live transport. In addition, NH3-N stress transport altered changes in the levels of superoxide dismutase (SOD), catalase (CAT), glutathione-related enzymes, and heat shock proteins 70 and 90 in the liver, indicating that the antioxidant system and Hsp protected the cells from NH3-N-induced oxidative stress. When excess ROS were not removed, they caused the body to respond with immunological and inflammatory responses, as well as apoptosis and tissue damage. This helps towards understanding the effect of NH3-N levels on sea bass during keep-live transport

Genomic Characteristics and Phylogenetic Analyses of a Multiple Drug-Resistant Klebsiella pneumoniae Harboring Plasmid-Mediated MCR-1 Isolated from Tai&rsquo;an City, China

Klebsiella pneumoniae is a clinically common opportunistic pathogen that causes pneumonia and upper respiratory tract infection in humans as well as community-and hospital-acquired infections, posing significant threats to public health. Moreover, the insertion of a plasmid carrying the mobile colistin resistance (MCR) genes brings obstacles to the clinical treatment of K. pneumoniae infection. In this study, a strain of colistin-resistant K. pneumoniae (CRKP) was isolated from sputum samples of a patient who was admitted to a tertiary hospital in Tai&rsquo;an city, China, and tested for drug sensitivity. The results showed that KPTA-2108 was multidrug-resistant (MDR), being resistant to 21 of 26 selected antibiotics, such as cefazolin, amikacin, tigecycline and colistin but sensitive to carbapenems via antibiotic resistance assays. The chromosome and plasmid sequences of the isolated strain KPTA-2108 were obtained using whole-genome sequencing technology and then were analyzed deeply using bioinformatics methods. The whole-genome sequencing analysis showed that the length of KPTA-2108 was 5,306,347 bp and carried four plasmids, pMJ4-1, pMJ4-2, pMJ4-3, and pMJ4-4-MCR. The plasmid pMJ4-4-MCR contained 30,124 bp and was found to be an IncX4 type. It was the smallest plasmid in the KPTA-2108 strain and carried only one resistance gene MCR-1. Successful conjugation tests demonstrated that pMJ4-4-MCR carrying MCR-1 could be horizontally transmitted through conjugation between bacteria. In conclusion, the acquisition and genome-wide characterization of a clinical MDR strain of CRKP may provide a scientific basis for the treatment of K. pneumoniae infection and epidemiological data for the surveillance of CRKP

Analysis of Acute Nitrite Exposure on Physiological Stress Response, Oxidative Stress, Gill Tissue Morphology and Immune Response of Large Yellow Croaker (Larimichthys crocea)

Nitrite is a common pollutant in aquaculture water, and nitrite toxicity that negatively affects aquatic species is common in aquaculture systems when the water quality is low. Therefore, the present research aimed to evaluate the effect of acute nitrite exposure on the hematological parameters, antioxidant enzymes, immune response, and gill morphology of large yellow croaker (Larimichthys crocea). The fish were randomly separated and exposed to four (i.e., 0, 29.36, 58.73, and 88.09 mg/L) nitrite concentrations for 48 h. The fish blood and gills were collected at 0, 12, 24, 36, and 48 h of nitrite exposure for further analysis. In hematological parameters, the results showed that the levels of hemoglobin, triglyceride, and total cholesterol in blood significantly decreased (p &lt; 0.05) in all nitrite-treated samples after 12 h, while the contents of methemoglobin in blood significantly increased (p &lt; 0.05) in these treatments. After 48 h of nitrite exposure, the levels of cortisol in serum showed a 94.5%, 132.1%, and 165.6% increase in fish exposed to 29.36, 58.73, and 88.09 mg/L nitrite, respectively. The nitrite (i.e., 29.36, 58.73, and 88.09 mg/L) exposure significantly increased (p &lt; 0.05) the levels of antioxidant enzymes (i.e., catalase and glutathione) in the gill and serum after 12 h of exposure compared with the control. The lysozyme levels in serum decreased in the nitrite (i.e., 29.36, 58.73, and 88.09 mg/L) exposure samples. It was found that immunoglobulin levels in the 29.36, 58.73, and 88.09 mg/L nitrite-treated samples (i.e., 1.86, 1.58, and 0.74 &mu;g/mL, respectively) were lower than that of the control (2.56 &mu;g/mL). In addition, the surface of the gill lamellae displayed deformation and contraction after 48 h of nitrite, especially in the fish exposed to 88.09 mg/L nitrite. These results indicate that the nitrite exposure induced the oxidative stress, affected the immune response, and changed the gill morphology, leading to nitrite poisoning in large yellow croaker

Yi Shen Juan Bi Pill Ameliorates Bone Loss and Destruction Induced by Arthritis Through Modulating the Balance of Cytokines Released by Different Subpopulations of T Cells

The Yi Shen Juan Bi Pill (YSJB), a traditional Chinese compound herbal drug, has been used as an anti-rheumatic drug in clinical practice. Cartilage and bone destruction of inflamed joints is the hallmark of rheumatoid arthritis (RA). Our previous study suggested that YSJB had a protective effect on joint damage in collagen-induced (CIA) rats. However, the role and the mechanism of YSJB in inflammation-induced bone loss are unavailable. The current study aimed to further evaluate the effect of YSJB on the joint destruction and the systemic bone loss, and to clarify the potential mechanism. CIA model was generated by using collagen II and incomplete Freund's adjuvant in Sprague-Dawley rats. After 4 weeks treatment, arthritic index, tissue pathology, micro-computed tomography scanning (μ-CT), and bone mineral density (BMD) analysis were performed. YSJB decreased arthritic scores and bone destruction; improved the BMD of lumbar vertebrae and bone volume fraction of inflamed joints. Moreover, YSJB significantly decreased the production of serum bone resorption markers, including Tartrate-Resistant Acid Phosphatase (TRACP), N-terminal telopeptide of type I collagen and C-terminal telopeptide of type I collagen. Meanwhile, it increased the level of serum bone formation marker type I collagen N-terminal propeptide. These results revealed that YSJB ameliorated bone destruction and reduced bone loss induced by arthritis. We have previously showed that Tregs inhibited osteoclast differentiation and bone resorption in vitro. Furthermore, others suggested that abnormality of Th1, Th17 may contribute to bone destruction. Here, we showed YSJB significantly up-regulated the percentage of Tregs, while also down-regulated the percentage of Th1 and Th17 cells. Our findings provide the evidence that YSJB ameliorates the severity of disease and joint degradation, and reduces systemic bone loss induced by arthritis. We propose YSJB modulates the balance of T cell phenotype, which affects the activation and differentiation of osteoclasts

Mesenchymal stem cells attenuate blood-brain barrier leakage after cerebral ischemia in mice

Abstract Background Ischemic stroke induced matrixmetallo-proteinase-9 (MMP-9) upregulation, which increased blood-brain barrier permeability. Studies demonstrated that mesenchymal stem cell therapy protected blood-brain barrier disruption from several cerebrovascular diseases. However, the underlying mechanism was largely unknown. We therefore hypothesized that mesenchymal stem cells reduced blood-brain barrier destruction by inhibiting matrixmetallo-proteinase-9 and it was related to intercellular adhesion molecule-1 (ICAM-1). Methods Adult ICR male mice (n = 118) underwent 90-min middle cerebral artery occlusion and received 2 × 105 mesenchymal stem cell transplantation. Neurobehavioral outcome, infarct volume, and blood-brain barrier permeability were measured after ischemia. The relationship between myeloperoxidase (MPO) activity and ICAM-1 release was further determined. Results We found that intracranial injection of mesenchymal stem cells reduced infarct volume and improved behavioral function in experimental stroke models (p < 0.05). IgG leakage, tight junction protein loss, and inflammatory cytokines IL-1β, IL-6, and TNF-α reduced in mesenchymal stem cell-treated mice compared to the control group following ischemia (p < 0.05). After transplantation, MMP-9 was decreased in protein and activity levels as compared with controls (p < 0.05). Furthermore, myeloperoxidase-positive cells and myeloperoxidase activity were decreased in mesenchymal stem cell-treated mice (p < 0.05). Conclusion The results showed that mesenchymal stem cell therapy attenuated blood-brain barrier disruption in mice after ischemia. Mesenchymal stem cells attenuated the upward trend of MMP-9 and potentially via downregulating ICAM-1 in endothelial cells. Adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) pathway may influence MMP-9 expression of neutrophils and resident cells, and ICAM-1 acted as a key factor in the paracrine actions of mesenchymal stem cell

Endothelial progenitor cells transplantation attenuated blood-brain barrier damage after ischemia in diabetic mice via HIF-1α

Abstract Background Blood-brain barrier impairment is a major indicator of endothelial dysfunction in diabetes. Studies showed that endothelial progenitor cell (EPC) transplantation promoted angiogenesis and improved function recovery after hind limb ischemia in diabetic mice. The effect of EPC transplantation on blood-brain barrier integrity after cerebral ischemia in diabetic animals is unknown. The aim of this study is to explore the effect of EPC transplantation on the integrity of the blood-brain barrier after cerebral ischemia in diabetic mice. Methods EPCs were isolated by density gradient centrifugation and characterized by flow cytometry and immunostaining. Diabetes was induced in adult male C57BL/6 mice by a single injection of streptozotocin at 4 weeks before surgery. Diabetic mice underwent 90-minute transient middle cerebral artery occlusion surgery and received 1 × 106 EPCs transplantation immediately after reperfusion. Brain infarct volume, blood-brain barrier permeability, tight junction protein expression, and hypoxia inducible factor-1α (HIF-1α) mRNA level were examined after treatment. Results We demonstrated that neurological deficits were attenuated and brain infarct volume was reduced in EPC-transplanted diabetic mice after transient cerebral ischemia compared to the controls (p < 0.05). Blood-brain barrier leakage and tight junction protein degradation were reduced in EPC-transplanted mice (p <0.05). EPCs upregulated HIF-1α expression while HIF-1α inhibitor PX-478 abolished the beneficial effect of EPCs. Conclusions We conclude that EPCs protected blood-brain barrier integrity after focal ischemia in diabetic mice through upregulation of HIF-1α signaling