Hypoxia tolerance in fish depends on catabolic preference between lipids and carbohydrates

Hypoxia is a common environmental stress factor in aquatic organisms,which varies among fish species.However,the mechanisms underlying the ability of fish species to tolerate hypoxia are not well known.Here,we showed that hypoxia response in different fish species was affected by lipid catabolism and preference for lipid or carbohydrate energy sources.Activation of biochemical lipid catabolism through peroxisome proliferator-activated receptor alpha(Pparα)or increasing mitochondrial fat oxidation in tilapia decreased tolerance to acute hypoxia by increasing oxygen consumption and oxidative damage and reducing carbohydrate catabolism as an energy source.Conversely,lipid catabolism inhibition by suppressing entry of lipids into mitochondria in tilapia or individually knocking out three key genes of lipid catabolism in zebrafish increased tolerance to acute hypoxia by decreasing oxygen consumption and oxidative damage and promoting carbohydrate catabolism.However,anaerobic glycolysis suppression eliminated lipid catabolism inhibition-promoted hypoxia tolerance in adipose triglyceride lipase(atgl)mutant zebrafish.Using 14 fish species with different trophic levels and taxonomic status,the fish preferentially using lipids for energy were more intolerant to acute hypoxia than those preferentially using carbohydrates.Our study shows that hypoxia tolerance in fish depends on catabolic preference for lipids or carbohydrates,which can be modified by regulating lipid catabolism.

Catabolic Response Profiles, Catabolic Uniformity and Richness as Microbiological Indicators in a Soil of Pergamino, Buenos Aires Province, with and without Previous Application of Glyphosate

Incubation assay in trays was performed with two soils with different application histories of glyphosate: no application, and previous application. The soils used were Typic Argiudolls of Pergamino, province of Buenos Aires, and the treatments were: control (no application), and 20, 200 and 2000 mg of active ingredient per kg of soil. Sampling was performed at the beginning (T0) and 45 days after (T45). Catabolic response profiles (CRP), catabolic richness and catabolic uniformity were determined according to the methodology based on measuring the differences in respiration induced by substrate in a short time (4 hours). The substrates used in this study were 20, namely, two amines, 5 aminoacids, two carbohydrates, and 11 carboxylic acids. The objective of this work was to compare soils with different histories of application of glyphosate, measuring its effect on catabolic response profiles, catabolic uniformity and catabolic richness. In this study, no differences were observed between catabolic richness among the different sampling times and doses of glyphosate applied. Glyphosate application affected the structure of the soil microbial communities. At the end of the test, soils with all doses of previous herbicide application showed greater catabolic uniformity than soils without previous application.

OsABA8ox2, an ABA catabolic gene, suppresses root elongation of rice seedlings and contributes to drought response

In rice, OsABA8ox encodes abscisic acid(ABA) 8′-hydroxylase, which catalyzes the committed step of ABA catabolism. The contribution of ABA catabolism in root development remains unclear. We investigated the role of OsABA8ox2 in root growth and development and drought response. GUS staining results showed that OsABA8ox2 was expressed mainly in roots at seedling stage and was strongly expressed in the meristematic zone of the radicle. OsABA8ox2 expression in roots was markedly decreased after 0.5 h polyethylene glycol(PEG) treatment and increased after 0.5 h rehydration, implying that OsABA8ox2 is a drought-responsive gene.OsABA8ox2 knockout mediated by the CRISPR-Cas9 system increased drought-induced ABA and indole-3-acetic acid accumulation in roots, conferred increased ABA sensitivity, and promoted a more vertically oriented root system architecture(RSA) beneficial to drought tolerance.OsABA8ox2 overexpression suppressed root elongation and increased stomatal conductance and transpiration rate. Consequently, OsABA8ox2 knockout dramatically improved rice drought tolerance, whereas OsABA8ox2 overexpression seedlings were hypersensitive to drought stress,suggesting that OsABA8ox2 contributes to drought response in rice. Compared with wild type,functional leaves of OsABA8ox2 knockout seedlings showed higher ABA levels, whereas overexpression lines showed lower ABA levels, suggesting that OsABA8ox2, as an ABA catabolic gene, modulates ABA concentration through ABA catabolism. OsABA8ox2 and OsABA8ox3 were both localized in the endoplasmic reticulum. Together, these results indicate that OsABA8ox2 suppresses root elongation of rice seedlings, increases water transpiration, and contributes to drought response through ABA catabolism, and that OsABA8ox2 knockout dramatically improves rice drought tolerance. They highlight the key role of ABA catabolism mediated by OsABA8ox2 on root growth and development. OsABA8ox2, as a novel RSA gene, would be a potential genetic target for the improvement of rice drought tolerance.

AtzABC Catabolic Gene Probe from Novel Atrazine-Degrading Rhodococcus Strain Isolated from a Nigerian Agricultural Soil

A batch enrichment technique was used to isolate atrazine-degrading Rhodococcus sp strain from an agricultural land with history of atrazine application in Bauchi state, Northeastern Nigeria. The strain was identified on the basis of physiological, biochemical and 16S r RNA gene sequencing. Growth studies and HPLC analysis showed that the strain has potential of atrazine degradation. An investigation into the catabolic genes Atz ABC, which transform atrazine to cyanuric acid, confirms the chromosomal DNA of strain to harbor BC genes, as compared with the positive control, Rhodococcus jostii RHA1. The strain does not possess the Atz A in all catabolic gene probe carried out. The isolation and characterization of the Rhodococcus sp strain showed that catabolic genes may have evolved from a single origin with widespread global distribution, with possible potential in atrazine bioremediation.

Mediated Electrochemical Measurements of Intracellular Catabolic Activities of Yeast Cells

Coupling with the dual mediator system menadione/ferricyanide, microelectrode voltammetric measurements were undertaken to detect the ferrocyanide accumulations arising from the mediated reduction of ferricyanide by yeast cells. The results indicate that the dual mediator system menadione/ferricyanide could be used as a probe to detect cellular catabolic activities in yeast cells and the electrochemical response has a positive relationship with the specific growth rate of yeast cells.

Bioremediation of Textile Azo Dyes Amido Black 10B, Reactive Black 5, Reactive Blue 160 by Lentinus squarrosulus AF5 and Assessment of Toxicity of the Degraded Metabolites

Bioremediation is an eco-compatible and economical approach to counter textile dye menace. The isolated Lentinus squarrosulus AF5 was assessed for decolourization of textile azo dyes, and had shown ~93%, 88% and 70% decolorization of Reactive blue 160 (RB160), Reactive black 5 (RB5) and Amido black 10B (AB10B) respectively. Further analysis using UV-vis, HPLC, and FTIR, 1H NMR had shown the degradation of the dyes. Toxicity analysis of the metabolites was performed using seed germination and plant growth on two agriculturally important plants Guar (Cyamopsis tetragonoloba) and wheat (Triticum aestivum) as well as cytotoxicity analysis using the human keratinocyte cell line (HaCaT). The dye mix appeared inhibitory for seed germination (20% - 40%), whereas metabolites were non-inhibitory for germination. Treatment of HaCaT cells with of dye mix and metabolites led into 45% and ~100% of cell viability of HaCaT cells respectively. Therefore, metabolites following degradation of the dye mix were observed to be non-toxic.

Comparative genomic analysis of Lactobacillus crispatus strains Lc31 and Lc83 with anti-cervical cancer potential by complete genome sequencing

Lactobacillus crispatus is a commonly found species in the urogenital tract(UGT)of healthy females and can also colonize other niches,such as the gastrointestinal tract(GIT).Although its potential protective role in cervical cancer has been reported,the anticancer mechanisms involved are still unclear.In this study,we sequenced and characterized the complete genomes of two L.crispatus strains(Lc31 and Lc83)isolated from the UGT of healthy women of reproductive age.Phylogenetic and phylogenomic analyses of these two strains and 15 other L.crispatus strains with complete genome sequences revealed that strains from the UGT and GIT clustered separately.UGT strains had a larger genome size,higher GC contents,and more protein-coding sequences and insertion sequence(Is)elements,indicating the likelihood of active horizontal gene transfer in this niche.We found a universal presence of genes encoding bacteriocins and the absence of virulence factors and antibiotic resistance genes in UGT strains,suggesting the potential of L.crispatus as a urogenital probiotic.Comparative genomic analysis identified an ula gene cluster responsible for L-ascorbate catabolism exclusively in UGT strains,and carbohydrate fermentation experiments confirmed that this substrate supported the growth of L.crispatus Lc31 and Lc83.Our findings improve the understanding of how the genome determines niche adaptation by L.crispatus,providing a foundation for investigating the mechanisms by which urogenital-derived L.crispatus promotes female health.

Late immune consequences of combat trauma: A review of trauma-related immune dysfunction and potential therapies

With improvements in personnel and vehicular body armor,robust casualty evacuation capabilities,and damage control resuscitation strategies,more combat casualties are surviving to reach higher levels of care throughout the casualty evacuation system.As such,medical centers are becoming more accustomed to managing the deleterious late consequences of combat trauma related to the dysregulation of the immune system.In this review,we aim to highlight these late consequences and identify areas for future research and therapeutic strategies.Trauma leads to the dysregulation of both the innate and adaptive immune responses,which places the injured at risk for several late consequences,including delayed wound healing,late onset sepsis and infection,multi-organ dysfunction syndrome,and acute respiratory distress syndrome,which are significant for their association with the increased morbidity and mortality of wounded personnel.The mechanisms by which these consequences develop are complex but include an imbalance of the immune system leading to robust inflammatory responses,triggered by the presence of damage associated molecules and other immune-modifying agents following trauma.Treatment strategies to improve outcomes have been difficult to develop as the immunophenotype of injured personnel following trauma is variable,fluid and difficult to determine.As more information regarding the triggers that lead to immune dysfunction following trauma is elucidated,it may be possible to identify the immunophenotype of injured personnel and provide targeted treatments to reduce the late consequences of trauma,which are known to lead to significant morbidity and mortality.

The Effects of Glucose Load on Catabolism during Remifentanil-Based Anesthesia in Patients with Diabetes Mellitus: A Prospective Randomized Trial

Background: General anesthesia using remifentanil may suppress the unwanted metabolic changes caused by surgical stress including hyperglycemia and ketogenesis. Surgery-related changes in catabolism can be attenuated with low-dose glucose load, without causing hyperglycemia. However, the impact of glucose load in diabetic patients during surgery is unknown. In this study, we investigated the effect of glucose load on catabolism during remifentanil-based anesthesia in patients with diabetes mellitus. Methods: Twenty-nine patients with diabetes mellitus undergoing elective surgery were randomly assigned to receive a glucose load (1.5 mg/kg/min) or not. Plasma levels of glucose, insulin, cortisol, dopamine, adrenaline, noradrenaline, acetoacetic acid, free fatty acid, ketone bodies, 3-hydroxybutyric acid, and 3-methylhistidine/creatinine, a marker of protein catabolism were measured at the start of surgery and 3 h after the start of surgery. Results: Glucose and insulin levels were significantly higher in patients who received a glucose load than in those who did not. Cortisol levels decreased at 3 h after the start of surgery in both groups whereas the levels of catecholamines were unchanged. Acetoacetic acid and total ketone body levels were significantly lower in patients given a glucose load than in those who were not 3 h after the start of surgery. The difference in the 3 methylhistidine/creatinine ratio between the two groups was not significant. Conclusions: The infusion of glucose suppressed lipid catabolism in diabetic patients under remifentanil-based anesthesia during surgery. Our study also suggests that in patients with diabetes mellitus, protein sparing is inhibited by remifentanil-based anesthesia, regardless of the glucose load. Trial registration: the University Hospital Medical Information Network identifier: UMIN000010914.

Effects of Glucose Load on Catabolism during Propofol-Based Anesthesia with Remifentanil in Patients with Diabetes Mellitus: A Prospective Randomized Trial

Background: Perioperative exacerbation of hyperglycemia and insulin resistance is associated with increased complications in patients with diabetes mellitus. We recently reported that glucose load during anesthesia with sevoflurane suppressed lipid catabolism in diabetic patients. In contrast to inhaled anesthetics, propofol solution contains triglycerides, which can be an energy source during surgery. However, the clinical relevance of glucose load under propofol-based anesthesia in diabetic patients is unknown. Therefore, we investigated the effect of intraoperative glucose load on catabolism during propofol-based anesthesia in patients with diabetes mellitus. Methods: Twenty-three patients with diabetes mellitus undergoing elective surgery with propofol-remifentanil-based anesthesia were randomly assigned to receive a glucose load (1.5 mg/kg/ min) or not. Plasma levels of glucose, insulin, cortisol, catecholamines, acetoacetic acid, free fatty acids, ketone bodies, 3-hydroxybutyric acid, and 3-methylhistidine/creatinine, used as a marker for protein catabolism, were measured at the start of surgery and 3 h later. Results: Glucose and insulin levels were significantly higher in patients who received a glucose load than in those who did not. Nonetheless, the levels of cortisol and catecholamines were unchanged during surgery. Similarly, the difference in the levels of markers for lipid as well as protein catabolism was not significant between the groups at 3 h after the start of surgery. Conclusions: Changes in lipid as well as protein catabolism were not altered by glucose load in diabetic patients under propofol-based anesthesia with remifentanil. Our study suggested that continuous infusion of propofol at a clinical dose is sufficient to reduce the requirement for glucose infusion during surgery in patients with diabetes.

Dietary methionine deficiency stunts growth and increases fat deposition via suppression of fatty acids transportation and hepatic catabolism in Pekin ducks

Background:Although methionine(Met),the first-limiting dietary amino acid,has crucial roles in growth and regulation of lipid metabolism in ducks,mechanisms underlying are not well understood.Therefore,the objective was to use dietary Met deficiency to investigate the involvement of Met in lipid metabolism and fat accumulation of Pekin ducks.Methods:A total of 150 male Pekin ducks(15-d-old,558.5±4.4 g)were allocated into 5 groups(6 replicates with 5 birds each)and fed corn and soybean meal-based diets containing 0.28%,0.35%,0.43%,0.50%,and 0.58%Met,respectively,for 4 weeks.Met-deficient(Met-D,0.28%Met)and Met-adequate(Met-A,0.43%Met)groups were selected for subsequent molecular studies.Serum,liver,and abdominal fat samples were collected to assess the genes and proteins involved in lipid metabolism of Pekin ducks and hepatocytes were cultured in vivo for verification.Results:Dietary Met deficiency caused growth depression and excess fat deposition that were ameliorated by feeding diets with adequate Met.Serum triglyceride and non-esterified fatty acid concentrations increased(P<0.05),whereas serum concentrations of total cholesterol,low density lipoprotein cholesterol,total protein,and albumin decreased(P<0.05)in Met-D ducks compared to those in Met-A ducks.Based on hepatic proteomics analyses,dietary Met deficiency suppressed expression of key proteins related to fatty acid transport,fatty acid oxidation,tricarboxylic acid cycle,glycolysis/gluconeogenesis,ketogenesis,and electron transport chain;selected key proteins had similar expression patterns verified by qRT-PCR and Western blotting,which indicated these processes were likely impaired.In vitro verification with hepatocyte models confirmed albumin expression was diminished by Met deficiency.Additionally,in abdominal fat,dietary Met deficiency increased adipocyte diameter and area(P<0.05),and down-regulated(P<0.05)of lipolytic genes and proteins,suggesting Met deficiency may suppress lipolysis in adipocyte.Conclusion:Taken together,these data demonstrated that dietary Met deficiency in Pekin ducks resulted in stunted growth and excess fat deposition,which may be related to suppression of fatty acids transportation and hepatic catabolism.

GW842166X Alleviates Osteoarthritis by Repressing LPS-mediated Chondrocyte Catabolism in Mice

Objective To explore the role and underlying mechanism of GW842166X on osteoarthritis and osteoarthritis-associated abnormal catabolism.Methods The extracted mouse chondrocytes were treated with GW842166X followed by lipopolysaccharide(LPS).The chondrocytes were divided into the control group,LPS group,LPS+50 nmol/L GW842166X group,and LPS+100 nmol/L GW842166X group.The cytotoxicity of GW842166X was tested using the CCK-8 assay.Western blot,RT-qPCR,and ELISA were applied to evaluate the expression of the inflammatory biomarkers in mouse chondrocytes.The expression of extracellular matrix molecules was detected by the Western blot,RT-qPCR,and immunofluorescence.Additionally,the activity of NF-κB was checked by the Western blot and immunofluorescence.The mouse Hulth models were generated to examine the in vivo effects of GW842166X on osteoarthritis.Hematoxylin and eosin staining,safranin O/fast green staining,and immunohistochemistry were applied to detect the histological changes.Results GW842166X below 200µmol/L had no cytotoxicity on the mouse chondrocytes.LPS-induced high expression of TGF-β1,IL-10,TNF-α,and IL-6 was significantly reduced by GW842166X.In addition,GW842166X upregulated the expression of aggrecan and collagen type III,which was downregulated after the LPS stimulation.The upregulated expression of ADAMTS-5 and MMP-13 by LPS stimulation was dropped in response to the GW842166X treatment.Furthermore,LPS decreased the IκBαexpression in the cytoplasm and increased the nuclear p65 expression.However,these changes were reversed by the GW842166X pretreatment.Moreover,the damages in the knees caused by the Hulth surgery in mice were restored by GW842166X.Conclusion GW842166X impeded the LPS-mediated catabolism in mouse chondrocytes,thereby inhibiting the progression of osteoarthritis.

Giving maize an excited start-Effects of dopamine on maize germination

Dopamine(DA)is a neurotransmitter which takes charge of brain activities about memory and self-stimulation behavior in animals.Interestingly,our results suggest that DA could also give maize an“excited state”.The results showed that 1 mmol L–1 DA promoted maize germination by 23.2%significantly,and accelerated the growth rate of roots and shoots by 21.4 and 24.7%,respectively.As we all known,abscisic acid(ABA)is the key hormone involved in seed dormancy.In our research,ABA levels in roots and shoots dramatically decreased by 16.45 and 57.57%,respectively.To further investigate how DA reduces the ABA level in budding seed,we studied ABA synthesis and catabolism pathway.Specific expression of key ABA-synthesis genes,such as ZmNCED1,ZmNCED3 and ZmZEP were down-regulated by DA.Simultaneously,the expression levels of ABA8OX1a and ABA8OX1b which are major transcripts of ABA 8´-hydroxylase in ABA catabolism were up-regulated at least 1.5-and 4.6-fold,respectively.Our results enriched the functions of animal hormones in plants.

Dynamic study of TNF effects on skeletal muscle proteolysis in early stage of severe scalding in rats

The protein catabolic rate and tumor necrosis factor (TNF) content of the soleus muscle of the scalded region and remote region were dynamically determined in the first week after the rats were inflicted with 37% TBSA full thickness scading. It was found

The Sucrose Starvation Signal Mediates Induction of Autophagy- and Amino Acid Catabolism-Related Genes in Cowpea Seedling

In higher plants, autophagy is bulk degradation process in vacuole necessary for survival under nutrient-limited conditions and plays important roles in senescence, development and pathogenic response, etc. Cowpea is one of the most important legume crops in semi-aride region, which is highly tolerant to drought stress. Changes of photoassimilate status by drought stress and/or sink-source balance appeared to affect autophagy and senescence of leaf in cowpea. Accordingly, we focused on roles of sucrose signal in autophagy and amino acid recycling in cowpea. Effects of starvation stress on the expression of autophagy-related genes (ATGs) and amino acid catabolism-related genes in cowpea [Vigna unguiculata (L.) Walp] were examined by Reverse transcription-polymerase chain reaction (RT-PCR) and anti-ATG8i specific antibody. Sucrose starvation stress enhanced the expression levels of VuATG8i, VuATG8c and VuATG4 incowpea seedlings. The expressions of amino acid catabolism related genes, such as asparagine synthase (VuASN1), proline dehydrogenase1 (VuProDH) and branched chain amino acid transaminase (VuBCAT2), are also up-regulated under the sucrose starvation. In contrast, high sucrose condition suppressed autophagy and the expressions of ATGs. These results indicate that sucrose starvation stress stimulates both autophagy and amino acid catabolism by regulation of ATGs and VuBCAT2. It is conceivable that sucrose starvation stress enhances autophagy in cowpea, possibly via branched chain amino acid level regulated by the starvation-induced BCAT.

Comparison of Substrate Specificity of <em>Escherichia Coli</em>p-Aminobenzoyl-Glutamate Hy-drolase with <em>Pseudomonas</em>Carboxypeptidase G

Reduced folic acid derivatives support biosynthesis of DNA, RNA and amino acids in bacteria as well as in eukaryotes, including humans. While the genes and steps for bacterial folic acid synthesis are known, those associated with folic acid catabolism are not well understood. A folate catabolite found in both humans and bacteria is p-aminobenzoyl-glutamate (PABA-GLU). The enzyme p-aminobenzoyl-glutamate hydrolase (PGH) breaks down PABA-GLU and is part of an apparent operon, the abg region, in E. coli. The subunits of PGH possess sequence and catalytic similarities to carboxypeptidase enzymes from Pseudomonas species. A comparison of the subunit sequences and activity of PGH, relative to carboxypeptidase enzymes, may lead to a better understanding of bacterial physiology and pathway evolution. We first compared the amino acid sequences of AbgA, AbgB and carboxypeptidase G2 from Pseudomonas sp. RS-16, which has been crystallized. Then we compared the enzyme activities of E. coli PGH and commercially available Pseudomonas carboxypeptidase G using spectrophotometric assays measuring cleavage of PABA-GLU, folate, aminopterin, methotrexate, 5-formyltetrahydrofolate, and 5-methyltetrahydrofolate. The Km and Vmax values for the folate and anti-folate substrates of PGH could not be determined, because the instrument reached its limit before the enzyme was saturated. Therefore, activity of PGH was compared to the activity of CPG, or normalized to PABA-GLU (nmole/min/μg). Relative to its activity with 10 μM PABA-GLU (100%), PGH cleaved glutamate from methotrexate (48%), aminopterin (45%) and folate (9%). Reduced folates leucovorin (5-formyltetrahydrofolate) and 5-methyltetrahydrofolate were not cleaved by PGH. Our data suggest that E. coli PGH is specific for PABA-GLU as its activity with natural folates (folate, 5-methyltetrahydrofolate, and leucovorin) was very poor. It does, however, have some ability to cleave anti-folates which may have clinical applications in treatment of chemotherapy overdose.

The Cancer Patient Drowns in the Waves of Homeostatic Disorder

Neoplastic cells are formed as a result of reprogramming the gene expression. It is only when these cells are classified as non-local by the normal cells that confrontation occurs, and thus cancer begins as a disease. The tumorogenic degradation of the skeletal muscle plays a highly important role in the pathomechanism of the disease. It transforms a diminishing differentiation into an increasing homeostatic disorder, and is forced to provide energy to the malignant cells. This characterizes the completed form of the pathomechanism. Blocking the pathomechanism is the goal of a therapy that can be realized on two levels: At the level of reprogramming of the gene expression, which initiates the formation of neoplastic cells, a “reprogramming” of the reprogramming of gene expression could be achieved by altering the genomic flow of information. Increased anabolism (corresponding to the nutrient surplus) as well as increased catabolism (corresponding to nutrient) could lead to respective changes of the flows of genomic information. These opposing flows in a patient could be expected to result in interference or a shearing effect. Patients with acromegaly exhibit a 9.25% increased neoplasia prevalence, whilst patients with hyperthyroidism have 8.41% increased neoplasia prevalence. Patients with acromegaly and hyperthyroidism have a lower prevalence of neoplasia of 3.30%, i.e. the chance of these patients not contracting cancer is three times greater than patients with either only acromegaly or only hyperthyroidism. At the level of tumorogenic degradation of skeletal muscle, inhibition of muscle degradation by means of hypertriglyceridemia results in a significant prolongation of the life of carcinoma patients. This is based on the fact that inhibition of muscle degradation occurs after infusion of triglyceride emulsion. In the case of S. sanguinis bacteremia, there may be an interaction between enzymes from S. sanguinis, from the digestive tract and from the tumor. The source of infection determines the inactivation of the tumor enzyme and thus suppresses tumor development.

Methemoglobinemia—A biomarker and a link to ferric iron accumulation in Alzheimer’s disease

Understanding the mechanism of oxidative stress is likely to yield new insights regarding the pathogenesis of Alzheimer’s disease (AD). Our earlier work focused on the difference between hemoglobin and methemoglobin degradation, respectively leading to ferrous (Fe2+) iron, or ferric (Fe3+) iron. Methemoglobin has the role of carrier, the donor of cytotoxic and redox-active ferric (Fe3+) iron, which can directly accumulate and increase the rate of capillary endothelial cell apoptosis, and may cross into the brain parenchyma, to the astrocytes, glia, neurons, and other neuronal cells (neurovascular unit). This supposition helps us to understand the transport and neuronal accumulation process of ferric iron, and determine how iron is transported and accumulated intracellularly, identifiable as “Brain rust”. Earlier research found that the incidences of neonatal jaundice (p = 0.034), heart murmur (p = 0.011) and disorders such as dyslalia and learning/memory impairments (p = 0.002) were significantly higher in those children born from mothers with methemoglobinemia. Our hypothesis suggests that prenatal iron abnormalities could lead to greater neuronal death, the disease ageing process, and neurodegenerative disorders such as AD and other neurodegenerative diseases.

Dysfunction of branded-chain amino acids catabolism in rat cardiac allograft

Objective Allograft vasculopathy ( AV) ,feature of chronic rejection,is a major serious long - term post - operation complication in organ transplantation. The accurate mechanisms for AV have not been definitively established,but extensive basic and clinical studies dem-

Botrytis cinerea-induced F-box protein 1 enhances disease resistance by inhibiting JAO/JOX-mediated jasmonic acid catabolism in Arabidopsis

Jasmonic acid(JA)is a crucial phytohormone that regulates plant immunity.The endogenous JA level is determined by the rates of its biosynthesis and catabolism in plants.The activation of JA biosynthesis has been well documented;however,how plants repress JA catabolism upon pathogen infection remains elusive.In this study,we identified and characterized Botrytis cinerea-induced F-box protein 1(BFP1)in Arabidopsis.The expression of BFP1 was induced by B.cinerea in a JA signaling-dependent manner,and BFP1 protein was critical for plant defense against B.cinerea and plant response to JA.In addition,BFP1 overexpression increased plant defenses against broad-spectrum pathogens without fitness costs.Further experiments demonstrated that BFP1 interacts with and mediates the ubiquitination and degrada-tion of jasmonic acid oxidases(JAOs,also known as jasmonate-induced oxygenases,JoXs),the enzymes that hydroxylate JA to 12OH-JA.Consistent with this,BFP1 affects the accumulation of JA and 12OH-JA during B.cinerea infection.Moreover,mutation of JAo2 complemented the phenotypes of the bfp1 mutant.Collectively,our results unveil a new mechanism used by plants to activate immune responses upon path-ogeninfection:suppressing JA catabolism.