Editor\u27s Notes, Chiba Medical Journal 90-1

Multiple sequence alignment of deduced amino acid sequences of 25 wheat annexin genes with rice annexin OsAnn2 (Os05g31760) obtained by ClustalW. (PDF 212 kb

Upregulation of Formaldehyde in Parkinson’s Disease Found by a Near-Infrared Lysosome-Targeted Fluorescent Probe

Parkinson’s disease (PD) is one of the major neurodegenerative diseases caused by complex pathological processes. As a signal molecule, formaldehyde is closely linked to nervous systems, but the relationship between PD and formaldehyde levels remains largely unclear. We speculated that formaldehyde might be a potential biomarker for PD. To prove it, we constructed the first near-infrared (NIR) lysosome-targeted formaldehyde fluorescent probe (named NIR-Lyso-FA) to explore the relationship between formaldehyde and PD. The novel fluorescent probe achieves formaldehyde detection in vitro and in vivo, thanks to its excellent properties such as NIR emission, large Stokes shift, and fast response to formaldehyde. Crucially, utilizing the novel probe NIR-Lyso-FA, formaldehyde overexpression was discovered for the first time in cellular, zebrafish, and mouse PD models, supporting our guess that formaldehyde can function as a possible biomarker for PD. We anticipate that this finding will offer insightful information for PD pathophysiology, diagnosis, medication development, and treatment

Upregulation of Formaldehyde in Parkinson’s Disease Found by a Near-Infrared Lysosome-Targeted Fluorescent Probe

Parkinson’s disease (PD) is one of the major neurodegenerative diseases caused by complex pathological processes. As a signal molecule, formaldehyde is closely linked to nervous systems, but the relationship between PD and formaldehyde levels remains largely unclear. We speculated that formaldehyde might be a potential biomarker for PD. To prove it, we constructed the first near-infrared (NIR) lysosome-targeted formaldehyde fluorescent probe (named NIR-Lyso-FA) to explore the relationship between formaldehyde and PD. The novel fluorescent probe achieves formaldehyde detection in vitro and in vivo, thanks to its excellent properties such as NIR emission, large Stokes shift, and fast response to formaldehyde. Crucially, utilizing the novel probe NIR-Lyso-FA, formaldehyde overexpression was discovered for the first time in cellular, zebrafish, and mouse PD models, supporting our guess that formaldehyde can function as a possible biomarker for PD. We anticipate that this finding will offer insightful information for PD pathophysiology, diagnosis, medication development, and treatment

Effect of Dietary Exposure to Acrylamide on Diabetes-Associated Cognitive Dysfunction from the Perspectives of Oxidative Damage, Neuroinflammation, and Metabolic Disorders

Acrylamide is a toxic compound that is produced widely during food processing, but whether the daily dietary consumption of acrylamide can impair the cognitive dysfunction in diabetic individuals and the potential underlying mechanisms are unknown. The aim of the present study was to observe the changes in cognitive and memory performance caused by chronic acrylamide exposure and to evaluate its influence on the brain morphology, oxidative damage, neuroinflammation, and brain metabolic disturbance. Goto-Kakizaki (GK) rats, a rat model of diabetes, were orally administered acrylamide at 1 mg/kg body weight for 8 weeks. The results of the novel object recognition and Y-maze tests showed that the consumption of acrylamide significantly aggravated diabetes-associated cognitive dysfunction in GK rats. Acrylamide increased reactive oxygen species and malondialdehyde formation and reduced glutathione levels, catalase, and total antioxidant capacity activity, which caused a succession of events associated with oxidative damage, including glial cell activation. After the activation of astrocytes and microglia, related cytokines, including interleukin-1β, interleukin-6, tumor necrosis factor-α, and lipopolysaccharide, were released, amyloid β-protein was accumulated, brain-derived neurotrophic factor was decreased, and the expression of caspase-3 and caspase-9 was increased, which aggravated neuroinflammation. Furthermore, there was perturbation of some important metabolites, including glutamic acid, citric acid, pyruvic acid, lactate, and sphinganine, and their related glucose, amino acid, and energy metabolism pathways in the brain. This work helps to demonstrate the effect of consumption of acrylamide in the daily diet on diabetes-associated cognitive dysfunction and its underlying mechanisms

Data_Sheet_1_The Simultaneous Formation of Acrylamide, β-carbolines, and Advanced Glycation End Products in a Chemical Model System: Effect of Multiple Precursor Amino Acids.docx

This study investigated the effect of multiple precursor amino acids on the simultaneous formation of acrylamide, β-carbolines (i. e., harmane and norharmane), and advanced glycation end products (AGEs) [i.e., Nε-(carboxymethyl)lysine and Nε-(carboxyethyl)lysine] via a chemical model system. This model system was established with single or multiple precursor amino acids, including lysine–glucose (Lys/Glu), asparagine–glucose (Asn/Glu), tryptophan–glucose (Trp/Glu), and a combination of these amino acids (Com/Glu). Kinetic parameters were calculated by multiresponse non-linear regression models. We found that the k values of the AGEs and of acrylamide decreased, while those of harmane increased in the Com/Glu model when heated to 170 and 200°C. Our results indicated that the precursor amino acid of acrylamide and AGEs compete for α-dicarbonyl compounds, leading to a decrease in the formation of AGEs and acrylamide. Moreover, compared with asparagine, the precursor amino acid of β-carbolines was more likely to react with acetaldehyde by Pictet–Spengler condensation, which increased the formation of harmane and decreased the formation of acrylamide via the acrolein pathway.</p

Additional file 1 of Increased circulating innate lymphoid cell (ILC)1 and decreased circulating ILC3 are involved in the pathogenesis of Henoch-Schonlein purpura

Additional file 1

Additional file 2 of Increased circulating innate lymphoid cell (ILC)1 and decreased circulating ILC3 are involved in the pathogenesis of Henoch-Schonlein purpura

Additional file 2

Data_Sheet_1_Low-protein diets supplemented with glycine improves pig growth performance and meat quality: An untargeted metabolomic analysis.doc

For the purpose to improve meat quality, pigs were fed a normal diet (ND), a low protein diet (LPD) and a LPD supplemented with glycine (LPDG). Chemical and metabolomic analyses showed that LPD increased IMF deposition and the activities of GPa and PK, but decreased glycogen content, the activities of CS and CcO, and the abundance of acetyl-CoA, tyrosine and its metabolites in muscle. LPDG promoted muscle fiber transition from type II to type I, increased the synthesis of multiple nonessential amino acids, and pantothenic acid in muscle, which should contributed to the improved meat quality and growth rate. This study provides some new insight into the mechanism of diet induced alteration of animal growth performance and meat quality. In addition, the study shows that dietary supplementation of glycine to LPD could be used to improved meat quality without impairment of animal growth.</p

Can habitual tea drinking be an effective approach against age-related neurodegenerative cognitive disorders: A systematic review and meta-analysis of epidemiological evidence

Our present knowledge about the efficacy of tea consumption in improving age-related cognitive disorders is incomplete since previous epidemiological studies provide inconsistent evidence. This unified systematic review and meta-analysis based on updated epidemiological cohort studies and randomized controlled trials (RCTs) evidence aimed to overcome the limitations of previous reviews by examining the efficacy of distinct types of tea consumption. PubMed, Embase, and MEDLINE were searched up to May 20, 2022, and 23 cohorts and 12 cross-sectional studies were included. Random-effects meta-analyses were conducted to obtain pooled RRs or mean differences with 95% CIs. The pooled RRs of the highest versus lowest tea consumption categories were 0.81 (95% CIs: 0.75–0.88) and 0.69 (95% CIs: 0.61–0.77), respectively. The pooled mean difference of four included RCTs revealed a beneficial effect of tea on cognitive dysfunction (MMSE ES: 1.03; 95% CI, 0.14–1.92). Subgroup analyses further demonstrated that green and black tea intake was associated with a lower risk of cognitive disorders in eastern countries, especially in women. The evidence quality was generally low to moderate. The present review provides insight into whether habitual tea consumption can be an effective approach against age-related neurodegenerative cognitive disorders and summarizes potential mechanisms based on currently published literature.</p

Theaflavins in Black Tea Mitigate Aging-Associated Cognitive Dysfunction via the Microbiota–Gut–Brain Axis

Aging-associated cognitive dysfunction has a great influence on the lifespan and healthspan of the elderly. Theaflavins (TFs), a mixture of ingredients formed from enzymatic oxidation of catechins during the manufacture of tea, have a positive contribution to the qualities and antiaging activities of black tea. However, the role of TFs in mitigating aging-induced cognitive dysfunction and the underlying mechanism remains largely unknown. Here, we find that TFs effectively improve behavioral impairment via the microbiota–gut–brain axis: TFs maintain gut homeostasis by improving antioxidant ability, strengthening the immune response, increasing the expression of tight junction proteins, restructuring the gut microbiota, and altering core microbiota metabolites, i.e., short-chain fatty acids and essential amino acids (SCFAs and AAs), and upregulating brain neurotrophic factors. Removing the gut microbiota with antibiotics partly abolishes the neuroprotective effects of TFs. Besides, correlation analysis indicates that the decrease in gut microbiota, such as Bacteroidetes and Lachnospiraceae, and the increase in microbiota metabolites’ levels are positively correlated with behavioral improvements. Taken together, our findings reveal a potential role of TFs in mitigating aging-driven cognitive dysfunction via the microbiota–gut–brain axis. The intake of TFs can be translated into a novel dietary intervention approach against aging-induced cognitive decline