PMID: 

PLoS One. 2014 ;9(4):e95503. Epub 2014 Apr 17. PMID: 24743689

Abstract Title: 

Reduction of phosphorylated synapsin I (ser-553) leads to spatial memory impairment by attenuating GABA release after microwave exposure in Wistar rats.

Abstract: 

BACKGROUND: Abnormal release of neurotransmitters after microwave exposure can cause learning and memory deficits. This study investigated the mechanism of this effect by exploring the potential role of phosphorylated synapsin I (p-Syn I).METHODS: Wistar rats, rat hippocampal synaptosomes, and differentiated (neuronal) PC12 cells were exposed to microwave radiation for 5 min at a mean power density of 30 mW/cm2. Sham group rats, synaptosomes, and cells were otherwise identically treated and acted as controls for all of the following post-exposure analyses. Spatial learning and memory in rats was assessed using the Morris Water Maze (MWM) navigation task. The protein expression and presynaptic distribution of p-Syn I and neurotransmitter transporters were examined via western blotting and immunoelectron microscopy, respectively. Levels amino acid neurotransmitter release from rat hippocampal synaptosomes and PC12 cells were measured using high performance liquid chromatograph (HPLC) at 6 hours after exposure, with or without synapsin I silencing via shRNA transfection.RESULTS: In the rat experiments, there was a decrease in spatial memory performance after microwave exposure. The expression of p-Syn I (ser-553) was decreased at 3 days post-exposure and elevated at later time points. Vesicular GABA transporter (VGAT) was significantly elevated after exposure. The GABA release from synaptosomes was attenuated and p-Syn I (ser-553) and VGAT were both enriched in small clear synaptic vesicles, which abnormally assembled in the presynaptic terminal after exposure. In the PC12 cell experiments, the expression of p-Syn I (ser-553) and GABA release were both attenuated at 6 hours after exposure. Both microwave exposure and p-Syn I silencing reduced GABA release and maximal reduction was found for the combination of the two, indicating a synergetic effect.CONCLUSION: p-Syn I (ser-553) was found to play a key role in the impaired GABA release and cognitive dysfunction that was induced by microwave exposure.

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PMID: 

Phys Med Biol. 2017 04 7 ;62(7):2741-2761. Epub 2017 Mar 7. PMID: 28267685

Abstract Title: 

Mobile phone types and SAR characteristics of the human brain.

Abstract: 

Mobile phones differ in terms of their operating frequency, outer shape, and form and location of the antennae, all of which affect the spatial distributions of their electromagnetic field and the level of electromagnetic absorption in the human head or brain. For this paper, the specific absorption rate (SAR) was calculated for four anatomical head models at different ages using 11 numerical phone models of different shapes and antenna configurations. The 11 models represent phone types accounting for around 86% of the approximately 1400 commercial phone models released into the Korean market since 2002. Seven of the phone models selected have an internal dual-band antenna, and the remaining four possess an external antenna. Each model was intended to generate an average absorption level equivalent to that of the same type of commercial phone model operating at the maximum available output power. The 1 g peak spatial SAR and ipsilateral and contralateral brain-averaged SARs were reported for all 11 phone models. The effects of the phone type, phone position, operating frequency, and age of head models on the brain SAR were comprehensively determined.

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PMID: 

Int J Radiat Biol. 2013 Dec ;89(12):1100-7. Epub 2013 Jul 24. PMID: 23786183

Abstract Title: 

Impairment of long-term potentiation induction is essential for the disruption of spatial memory after microwave exposure.

Abstract: 

PURPOSE: To assess the impact of microwave exposure on learning and memory and to explore the underlying mechanisms.MATERIALS AND METHODS: 100 Wistar rats were exposed to a 2.856 GHz pulsed microwave field at average power densities of 0 mW/cm(2), 5 mW/cm(2), 10 mW/cm(2) and 50 mW/cm(2) for 6 min. The spatial memory was assessed by the Morris Water Maze (MWM) task. An in vivo study was conducted soon after microwave exposure to evaluate the changes of population spike (PS) amplitudes of long-term potentiation (LTP) in the medial perforant path (MPP)-dentate gyrus (DG) pathway. The structure of the hippocampus was observed by the light microscopy and the transmission electron microscopy (TEM) at 7 d after microwave exposure.RESULTS: Our results showed that the rats exposed in 10 mW/cm(2) and 50 mW/cm(2) microwave displayed significant deficits in spatial learning and memory at 6 h, 1 d and 3 d after exposure. Decreased PS amplitudes were also found after 10 mW/cm(2) and 50 mW/cm(2) microwave exposure. In addition, varying degrees of degeneration of hippocampal neurons, decreased synaptic vesicles and blurred synaptic clefts were observed in the rats exposed in 10 mW/cm(2) and 50 mW/cm(2) microwave. Compared with the sham group, the rats exposed in 5 mW/cm(2) microwave showed no difference in the above experiments.CONCLUSIONS: This study suggested that impairment of LTP induction and the damages of hippocampal structure, especially changes of synapses, might contribute to cognitive impairment after microwave exposure.

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PMID: 

Nutrition. 2019 Jun ;62:162-168. Epub 2019 Jan 2. PMID: 30921552

Abstract Title: 

Effects of probiotic yogurt on glycemic indexes and endothelial dysfunction markers in patients with metabolic syndrome.

Abstract: 

OBJECTIVES: The relationship between gut microflora and metabolic syndrome components such as obesity, low-grade chronic systemic inflammation, dyslipidemia, and altered glucose metabolism is now acknowledged. The aim of this study was to assess the effects of probiotic yogurt on glycemic indexes and endothelial dysfunction markers in patients with metabolic syndrome.METHODS: This was a randomized, double-blind, placebo-controlled clinical trial of 44 patients with metabolic syndrome (22 men and 22 women), who were 20 to 65 y of age. The patients were assigned to either a treatment or control group and consumed 300g/d of probiotic yogurt containing Lactobacillus acidophilus La5 and Bifidobacterium lactis Bb12 or a regular yogurt for 2 mo, respectively. Each group contained 22 participants. Fasting blood glucose and serum insulin was performed to derive homeostasis model assessment of insulin resistance (HOMA-IR), insulin sensitivity (Quicki), and HOMA ofβ-cell function (HOMA- β). In addition, markers of vascular cell adhesion molecule cell (VCAM)-1, intercellular adhesion molecule cell (ICAM)-1, and plasminogen activator inhibitor (PAI)-1 were measured to evaluate endothelial function at the beginning and at the end of the study.RESULTS: Consumption of probiotic yogurt resulted in a significant reduction in the level of blood glucose and VCAM-1. Significant changes in PAI-1, VCAM-1, insulin, HOMA-IR, and Quicki were observed in the probiotic yogurt group after intervention compared with baseline.CONCLUSION: Consumption of probiotic yogurt improved fasting blood glucose and partly modified serum endothelial function markers. These results suggest that regular intake of probiotic yogurt may exert positive effects on the treatment of metabolic syndrome.

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PMID: 

J Dent Sci. 2019 Jun ;14(2):198-205. Epub 2019 Mar 30. PMID: 31205608

Abstract Title: 

Inhibition ofby a commercial yogurt drink.

Abstract: 

Background/Purpose: Studies have been focused on using probiotics to prevent caries. The lactobacillus probiotic bacteria in Yakult(LcY) has been shown to inhibit the growth or biofilm formation of. However, sucrose in Yakultraised concerns. The purpose of this study was to determine effects of Yakulton the growth and adhesion of.Materials and methods: was grown in serial diluted Yakult, filtered Yakultor 20% heated Yakult.was co-cultured with LcY in media with or without diluted filtered Yakult, or in LcY grown in media with or without sugars. Colony forming units and pH values of bacterial cultures were determined. SYTO 9-stained adhered bacteria were observed.Results: Yakultinhibited the growth of. Filtering or heating Yakultreduced its inhibitory ability against. The inhibitory effect of LcY againstwas enhanced when cultured in the presence of 20% filtered Yakult. LcY cultured in sucrose media for 24 h inhibited the growth of, but this effect was less evident when LcY was grown for 48 h. LcY grown in glucose or lactose media similarly reducedgrowth. Culturingwith LcY grown in sucrose or glucose media reduced bacterial adhesion. However, co-culturingwith LcY grown in the lactose media did not decrease bacterial adhesion.Conclusion: Yakultand its probiotic content may inhibitgrowth and the effect may be moderated by the type of sugar added for LcY cultivation.

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PMID: 

Nutrients. 2019 Jun 28 ;11(7). Epub 2019 Jun 28. PMID: 31261830

Abstract Title: 

Probiotic Ingestion, Obesity, and Metabolic-Related Disorders: Results from NHANES, 1999-2014.

Abstract: 

Gut microbiota dysbiosis has been recognized as having key importance in obesity- and metabolic-related diseases. Although there is increasing evidence of the potential benefits induced by probiotics in metabolic disturbances, there is a lack of large cross-sectional studies to assess population-based prevalence of probiotic intake and metabolic diseases. Our aim was to evaluate the association of probiotic ingestion with obesity, type 2 diabetes, hypertension, and dyslipidemia. A cross-sectional study was designed using data from the National Health and Nutrition Examination Survey (NHANES), 1999-2014. Probiotic ingestion was considered when a subject reported consumption of yogurt or a probiotic supplement during the 24-hour dietary recall or during the Dietary Supplement Use 30-Day questionnaire. We included 38,802 adults and 13.1% reported probiotic ingestion. The prevalence of obesity and hypertension was lower in the probiotic group (obesity-adjusted Odds Ratio (OR): 0.84, 95% CI 0.76-0.92,

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PMID: 

Diabetologia. 2019 Sep ;62(9):1689-1700. Epub 2019 May 28. PMID: 31139852

Abstract Title: 

Targeting gut microbiota and barrier function with prebiotics to alleviate autoimmune manifestations in NOD mice.

Abstract: 

AIMS/HYPOTHESIS: Adopting a diet containing indigestible fibre compounds such as prebiotics to fuel advantageous bacteria has proven beneficial for alleviating inflammation. The effect of the microbial changes on autoimmunity, however, remains unknown. We studied the effects of prebiotic xylooligosaccharides (XOS) on pancreatic islet and salivary gland inflammation in NOD mice and tested whether these were mediated by the gut microbiota.METHODS: Mother and offspring mice were fed an XOS-supplemented diet until diabetes onset or weaning and were compared with a control-fed group. Diabetes incidence was monitored, insulitis and sialadenitis were scored in histological sections from adult mice, and several metabolic and immune variables were analysed in mice before the development of diabetes. Gut barrier function was assessed using an in vivo FITC-dextran permeability test. The importance of XOS-mediated gut microbial changes were evaluated in antibiotic-treated mice fed either XOS or control diet or given a faecal microbiota transplant from test animals.RESULTS: Diabetes onset was delayed in the XOS-fed mice, which also had fewer cellular infiltrations in their pancreatic islets and salivary glands. Interestingly, insulitis was most reduced in the XOS-fed groups when the mice were also treated with an antibiotic cocktail. There was no difference in sialadenitis between the dietary groups treated with antibiotics; the mice were protected by microbiota depletion regardless of diet. Faecal microbiota transplantation was not able to transfer protection. No major differences in glucose-insulin regulation, glucagon-like peptide-1, or short-chain fatty acid production were related to the XOS diet. The XOS diet did, however, reduce gut permeability markers in the small and large intestine. This was accompanied by a more anti-inflammatory environment locally and systemically, dominated by a shift from M1 to M2 macrophages, a higher abundance of activated regulatory T cells, and lower levels of induction of natural killer T cells and cytotoxic T cells.CONCLUSIONS/INTERPRETATION: Prebiotic XOS have microbiota-dependent effects on salivary gland inflammation and microbiota-independent effects on pancreatic islet pathology that are accompanied by an improved gut barrier that seems able to heighten control of intestinal diabetogenic antigens that have the potential to penetrate the mucosa to activate autoreactive immune responses.

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PMID: 

Chin Med J (Engl). 2019 Jul 1. Epub 2019 Jul 1. PMID: 31268903

Abstract Title: 

Effects of probiotics and prebiotics on intestinal microbiota in mice with acute colitis based on 16S rRNA gene sequencing.

Abstract: 

BACKGROUND: Imbalance of intestinal microbiota was closely related to colitis. Under these circumstances, regulation of enteric flora may be beneficial to the repair of inflammation. We aimed to investigate the effects of probiotics (Bifidobacterium and Lactobacillus), prebiotics and their combination on inflammation, and microflora in mice of acute colitis.METHODS: C57BL/6J mice were divided into six groups randomly (blank control group, model control group, probiotics group, synbiotics group, lactitol group and probiotics + lactitol group). Each group was given 2.5% dextran sulfate sodium drinking water for 5 days other than the blank control group. Except for the model control group, the other four groups were intervened with probiotics, synbiotics (probiotics and inulin), lactitol, and probiotics + lactitol. Mice were sacrificed after 1 week of gavage, and pathologic scores were calculated. The feces of different periods and intestinal mucosa samples were collected to analyze the differences of intestinal microbiota by 16S rRNA sequencing. Differences of two groups or multiple groups were statistically examined through unpaired Student t test and analysis of variance (ANOVA), respectively. ANOVA, Tukey, Anosim, and metastats analysis were used to compare differences of microbiota among different groups.RESULTS: After gavage for 1 week, the pathologic scores of groups with the intervention were significantly lower than those in the model control group, and the difference was statistically significant (P 

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PMID: 

World J Hepatol. 2019 Jun 27 ;11(6):489-512. PMID: 31293718

Abstract Title: 

Dietary approach and gut microbiota modulation for chronic hepatic encephalopathy in cirrhosis.

Abstract: 

Hepatic encephalopathy (HE) is a common and serious neuropsychiatric complication of cirrhosis, acute liver failure, and porto-systemic shunting. HE largely contributes to the morbidity of patients with liver disease, severely affecting the quality of life of both patients and their relatives and being associated with poor prognosis. Its presentation is largely variable, manifesting with a broad spectrum of cognitive abnormalities ranging from subtle cognitive impairment to coma. The pathogenesis of HE is complex and has historically been linked with hyperammonemia. However, in the last years, it has become evident that the interplay of multiple actors, such as intestinal dysbiosis, gut hyperpermeability, and neuroinflammation, is of crucial importance in its genesis. Therefore, HE can be considered a result of a dysregulated gut-liver-brain axis function, where cognitive impairment can be reversed or prevented by the beneficial effects induced by"gut-centric"therapies, such as non-absorbable disaccharides, non-absorbable antibiotics, probiotics, prebiotics, and fecal microbiota transplantation. In this context dietary modifications, by modulating the intestinal milieu, can also provide significant benefit to cirrhotic patients with HE. This review will provide a comprehensive insight into the mechanisms responsible for gut-liver-brain axis dysregulation leading to HE in cirrhosis. Furthermore, it will explore the currently available therapies and the most promising future treatments for the management of patients with HE, with a special focus on the dietary approach.

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PMID: 

Clin Rev Allergy Immunol. 2019 Jul 15. Epub 2019 Jul 15. PMID: 31309394

Abstract Title: 

Supporting a Healthy Microbiome for the Primary Prevention of Eczema.

Abstract: 

Eczema is increasing worldwide with associated increases in health costs and decreases in quality of life. There are many factors that are speculated to interact in the development of eczema including genetics and environmental exposures. Prevention of the development of eczema may prevent the further development of food allergies and asthma. This concept has prompted a variety of research into the area of primary prevention of eczema in infants. This exploration includes a growing body of research examining infants supplemented with probiotics, prebiotics, or both (synbiotics) often compared with their breastfed counterparts. The goal of this paper is to examine the evidence for manipulating the microbiome in the prevention of eczema. Several strains of probiotics, compositions of prebiotics, and varied combinations of both are commercially available. Evidence supports altering the microbiome in infants at high risk of atopy who are not able to breastfeed with Lactobacillus strains when given both prenatally followed by prolonged use (greater than 6 months) postnatally for the primary prevention of eczema. Prebiotics have also been shown beneficial for primary prevention of eczema in formula-fed infants with prolonged use greater than 6 months. These findings are in keeping with the World Allergy Organization (WAO) recommendations that support interventions to manipulate the microbiome with both probiotics and prebiotics.

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