Journal articles on the topic 'GI function'
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1
Shklennik, Maria A., and Alexander N. Moiseev. "Method of Markovian summation for study the repeated flow in queueing tandem M|GI|∞ → GI|∞." Izvestiya of Saratov University. New Series. Series: Mathematics. Mechanics. Informatics 21, no. 1 (February 24, 2021): 125–37. http://dx.doi.org/10.18500/1816-9791-2021-21-1-125-137.
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The paper presents a mathematical model of queueing tandem M|GI|∞ → GI|∞ with feedback. The service times at the first stage are independent and identically distributed (i.i.d.) with an arbitrary distribution function B1(x). Service times at the second stage are i.i.d. with an arbitrary distribution function B2(x). The problem is to determine the probability distribution of the number of repeated customers (r-flow) during fixed time period. To solve this problem, the Markov summation method was used, which is based on the consideration of Markov processes and the solution of the Kolmogorov equation. In the course of the solution, the so-called local r-flow was studied — the number of r-flow calls generated by one incoming customer received by the system. As a result, an expression is obtained for the characteristic probability distribution function of the number of calls in the local r-flow, which can be used to study queuing systems with a similar service discipline and non-Markov incoming flows. As a result of the study, an expression is obtained for the characteristic probability distribution function of the number of repeated calls to the system at a given time interval during non-stationary regime, which allows one to obtain the probability distribution of the number of calls in the flow under study, as well as its main probability characteristics.
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Cooper, Simon B., Stephan Bandelow, Maria L. Nute, John G. Morris, and Mary E. Nevill. "Breakfast glycaemic index and cognitive function in adolescent school children." British Journal of Nutrition 107, no. 12 (September 29, 2011): 1823–32. http://dx.doi.org/10.1017/s0007114511005022.
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It has been suggested that a low-glycaemic index (GI) breakfast may be beneficial for some elements of cognitive function (e.g. memory and attention), but the effects are not clear, especially in adolescents. Thus, the aim of the present study was to examine the effects of a low-GI breakfast, a high-GI breakfast and breakfast omission on cognitive function in adolescents. A total of fifty-two adolescents aged 12–14 years were recruited to participate in the study. Participants consumed a low-GI breakfast, a high-GI breakfast or omitted breakfast. A battery of cognitive function tests was completed 30 and 120 min following breakfast consumption and capillary blood samples were taken during the 120 min postprandial period. The findings show that there was a greater improvement in response times following a low-GI breakfast, compared with breakfast omission on the Stroop (P = 0·009) and Flanker (P = 0·041) tasks, and compared with a high-GI breakfast on the Sternberg paradigm (P = 0·013). Furthermore, accuracy on all three tests was better maintained on the low-GI trial compared with the high-GI (Stroop:P = 0·039; Sternberg:P = 0·018; Flanker:P = 0·014) and breakfast omission (Stroop:P < 0·001; Sternberg:P = 0·050; Flanker:P = 0·014) trials. Following the low-GI breakfast, participants displayed a lower glycaemic response (P < 0·001) than following the high-GI breakfast, but there was no difference in the insulinaemic response (P = 0·063) between the high- and low-GI breakfasts. Therefore, we conclude that a low-GI breakfast is most beneficial for adolescents' cognitive function, compared with a high-GI breakfast or breakfast omission.
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Brandoli, Claudio, Cesar Petri, Marcos Egea-Cortines, and Julia Weiss. "Gigantea: Uncovering New Functions in Flower Development." Genes 11, no. 10 (September 28, 2020): 1142. http://dx.doi.org/10.3390/genes11101142.
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GIGANTEA (GI) is a gene involved in multiple biological functions, which have been analysed and are partially conserved in a series of mono- and dicotyledonous plant species. The identified biological functions include control over the circadian rhythm, light signalling, cold tolerance, hormone signalling and photoperiodic flowering. The latter function is a central role of GI, as it involves a multitude of pathways, both dependent and independent of the gene CONSTANS(CO), as well as on the basis of interaction with miRNA. The complexity of the gene function of GI increases due to the existence of paralogs showing changes in genome structure as well as incidences of sub- and neofunctionalization. We present an updated report of the biological function of GI, integrating late insights into its role in floral initiation, flower development and volatile flower production.
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Greenwood-Van Meerveld, B. "Abnormalites in GI function associated with inflammation." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 124 (August 1999): S15. http://dx.doi.org/10.1016/s1095-6433(99)90059-4.
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He, Hongzhi, and Joomyeong Kim. "Regulation and Function of the Peg3 Imprinted Domain." Genomics & Informatics 12, no. 3 (2014): 105. http://dx.doi.org/10.5808/gi.2014.12.3.105.
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Mahdaleny and Febriana Catur Iswanti. "Gut microbiome diversity as adjuvant marker for immune function." Acta Biochimica Indonesiana 5, no. 1 (June 21, 2022): 80. http://dx.doi.org/10.32889/actabioina.80.
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The gastrointestinal (GI) tract represents our most intimate contact with the external environment. The GI tract responsible for extracting the appropriate nutrients we need to thrive, maintaining an appropriate balance of helpful and harmful microbes, and acting as a conduit for waste removal. In essence, the extracellular matrix of gut mucosal biofilm is a complex network of microbes and their secretions, as well as the host's secretions and signals (mainly mucus/mucin). Mucin, bacterial polysaccharides, and protein combine to form a unique mucosal biofilm that serves as a home for a variety of commensal and pathogenic organisms in the host. Maintaining proper mucosal barrier function is vital for both GI and systemic health. The lumen of the gut contains numerous entities that should never reach the bloodstream or lymphatic system. The mucosal barrier's integrity is maintained by a single layer of tightly fitted columnar epithelial, and more than 70% of the immune system components are closely associated with the GI tract.
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Gaesser, Rodriguez, Patrie, Whisner, and Angadi. "Effects of Glycemic Index and Cereal Fiber on Postprandial Endothelial Function, Glycemia, and Insulinemia in Healthy Adults." Nutrients 11, no. 10 (October 6, 2019): 2387. http://dx.doi.org/10.3390/nu11102387.
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Both glycemic index and dietary fiber are associated with cardiovascular disease risk, which may be related in part to postprandial vascular effects. We examined the effects of both glycemic index (GI) and dietary (mainly cereal) fiber on postprandial endothelial function. Eleven adults (5 men; 6 women; age = 42.4 ± 16.1 years; weight = 70.5 ± 10.7 kg; height = 173.7 ± 8.7 cm) consumed four different breakfast meals on separate, randomized occasions: High-Fiber, Low-GI (HF-LGI: Fiber = 20.4 g; GI = 44); Low-Fiber, Low-GI (LF-LGI: Fiber = 4.3 g; GI = 43); Low-Fiber, High-GI (LF-HGI: Fiber = 3.6 g; GI = 70); High-Fiber, High-GI (HF-HGI: Fiber = 20.3 g; GI = 71). Meals were equal in total kcal (~600) and macronutrient composition (~90 g digestible carbohydrate; ~21 g protein; ~15 g fat). The HF-LGI meal resulted in a significant increase in flow-mediated dilation (FMD) 4 hours after meal ingestion (7.8% ± 5.9% to 13.2% ± 5.5%; p = 0.02). FMD was not changed after the other meals. Regardless of fiber content, low-GI meals resulted in ~9% lower 4-hour glucose area under curve (AUC) (p < 0.05). The HF-LGI meal produced the lowest 4-hour insulin AUC, which was ~43% lower than LF-HGI and HF-HGI (p < 0.001), and 28% lower than LF-LGI (p = 0.02). We conclude that in healthy adults, a meal with low GI and high in cereal fiber enhances postprandial endothelial function. Although the effect of a low-GI meal on reducing postprandial glucose AUC was independent of fiber, the effect of a low-GI meal on reducing postprandial insulin AUC was augmented by cereal fiber.
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Martínez-Herrero, Sonia, and Alfredo Martínez. "Adrenomedullin: Not Just Another Gastrointestinal Peptide." Biomolecules 12, no. 2 (January 18, 2022): 156. http://dx.doi.org/10.3390/biom12020156.
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Adrenomedullin (AM) and proadrenomedullin N-terminal 20 peptide (PAMP) are two bioactive peptides derived from the same precursor with several biological functions including vasodilation, angiogenesis, or anti-inflammation, among others. AM and PAMP are widely expressed throughout the gastrointestinal (GI) tract where they behave as GI hormones, regulating numerous physiological processes such as gastric emptying, gastric acid release, insulin secretion, bowel movements, or intestinal barrier function. Furthermore, it has been recently demonstrated that AM/PAMP have an impact on gut microbiome composition, inhibiting the growth of bacteria related with disease and increasing the number of beneficial bacteria such as Lactobacillus or Bifidobacterium. Due to their wide functions in the GI tract, AM and PAMP are involved in several digestive pathologies such as peptic ulcer, diabetes, colon cancer, or inflammatory bowel disease (IBD). AM is a key protective factor in IBD onset and development, as it regulates cytokine production in the intestinal mucosa, improves vascular and lymphatic regeneration and function and mucosal epithelial repair, and promotes a beneficial gut microbiome composition. AM and PAMP are relevant GI hormones that can be targeted to develop novel therapeutic agents for IBD, other GI disorders, or microbiome-related pathologies.
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NELSON, ROXANNE. "Novel Agent Improves GI Function in Pain Patients." Clinical Psychiatry News 34, no. 10 (October 2006): 58. http://dx.doi.org/10.1016/s0270-6644(06)71839-2.
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Moss, Gerald. "QS70. Automatically Titrating Feeding to Match GI Function." Journal of Surgical Research 144, no. 2 (February 2008): 296–97. http://dx.doi.org/10.1016/j.jss.2007.12.309.
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Yu, Dong Su, and Byung Kwon Kim. "SFannotation: A Simple and Fast Protein Function Annotation System." Genomics & Informatics 12, no. 2 (2014): 76. http://dx.doi.org/10.5808/gi.2014.12.2.76.
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Joshi, Vikram, Peter R. Strege, Gianrico Farrugia, and Arthur Beyder. "Mechanotransduction in gastrointestinal smooth muscle cells: role of mechanosensitive ion channels." American Journal of Physiology-Gastrointestinal and Liver Physiology 320, no. 5 (May 1, 2021): G897—G906. http://dx.doi.org/10.1152/ajpgi.00481.2020.
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Mechanosensation, the ability to properly sense mechanical stimuli and transduce them into physiologic responses, is an essential determinant of gastrointestinal (GI) function. Abnormalities in this process result in highly prevalent GI functional and motility disorders. In the GI tract, several cell types sense mechanical forces and transduce them into electrical signals, which elicit specific cellular responses. Some mechanosensitive cells like sensory neurons act as specialized mechanosensitive cells that detect forces and transduce signals into tissue-level physiological reactions. Nonspecialized mechanosensitive cells like smooth muscle cells (SMCs) adjust their function in response to forces. Mechanosensitive cells use various mechanoreceptors and mechanotransducers. Mechanoreceptors detect and convert force into electrical and biochemical signals, and mechanotransducers amplify and direct mechanoreceptor responses. Mechanoreceptors and mechanotransducers include ion channels, specialized cytoskeletal proteins, cell junction molecules, and G protein-coupled receptors. SMCs are particularly important due to their role as final effectors for motor function. Myogenic reflex—the ability of smooth muscle to contract in response to stretch rapidly—is a critical smooth muscle function. Such rapid mechanotransduction responses rely on mechano-gated and mechanosensitive ion channels, which alter their ion pores’ opening in response to force, allowing fast electrical and Ca2+ responses. Although GI SMCs express a variety of such ion channels, their identities remain unknown. Recent advancements in electrophysiological, genetic, in vivo imaging, and multi-omic technologies broaden our understanding of how SMC mechano-gated and mechanosensitive ion channels regulate GI functions. This review discusses GI SMC mechanosensitivity's current developments with a particular emphasis on mechano-gated and mechanosensitive ion channels.
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Chen, Li-Han, Ming-Fu Wang, Chun-Chao Chang, Shih-Yi Huang, Chun-Hsu Pan, Yao-Tsung Yeh, Cheng-Hsieh Huang, Ching-Hung Chan, and Hui-Yu Huang. "Lacticaseibacillus paracasei PS23 Effectively Modulates Gut Microbiota Composition and Improves Gastrointestinal Function in Aged SAMP8 Mice." Nutrients 13, no. 4 (March 29, 2021): 1116. http://dx.doi.org/10.3390/nu13041116.
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Probiotics are reported to improve gastrointestinal (GI) function via regulating gut microbiota (GM). However, exactly how probiotics influence GM and GI function in elders is poorly characterized. Therefore, in this study, we assessed the effect of the probiotic Lacticaseibacillus paracasei PS23 (LPPS23) on the GM and GI function of aged mice. There were four groups of senescence-accelerated mouse prone-8 (SAMP8) mice (n = 4): a non-treated control group, a saline control group, a low dose LPPS23 group (1 × 108 colony-forming unit (CFU)/mouse/day), and a high dose LPPS23 group (1 × 109 CFU/mouse/day). Non-treated mice were euthanized at 16 weeks old, and others were euthanized at 28 weeks old. The next-generation sequencing results revealed that LPPS23 enriched Lactobacillus and Candidatus_Saccharimonas, while the abundance of Lachnospiraceae_UCG_001 decreased in aged mice given LPPS23. The abundance of Lactobacillus negatively correlated with the abundance of Erysipelotrichaceae. Moreover, LPPS23 improved the GI function of aged mice due to the longer intestine length, lower intestinal permeability, and higher phagocytosis in LPPS23-treated mice. The ELISA results showed that LPPS23 attenuated the alterations of pro-inflammatory factors and immunoglobulins. The abundance of LPPS23-enriched Lactobacillus was positively correlated with healthy GI function, while Lachnospiraceae_UCG_001, which was repressed by LPPS23, was negatively correlated with a healthy GI function in the aged mice according to Spearman’s correlation analysis. Taken together, LPPS23 can effectively modulate GM composition and improve GI function in aged SAMP8 mice.
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Bayer, Tomáš. "Efficient plotting the functions with discontinuities based on combined sampling." Geoinformatics FCE CTU 17, no. 2 (August 23, 2018): 9–30. http://dx.doi.org/10.14311/gi.17.2.2.
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This article presents a new algorithm for interval plotting of the function y = f(x) based on combined sampling. The proposed method synthesizes the uniform and adaptive sampling approaches and provides a more compact and efficient function representation. During the combined sampling, the polygonal approximation with a given threshold α between the adjacent segments is constructed. The automated detection and treatment of the discontinuities based on the LR criterion are involved. Two implementations, the recursive-based and stack-based, are introduced. Finally, several tests of the proposed algorithms for the different functions involving the discontinuities and several map projection graticules are presented. The proposed method may be used for more efficient sampling the curves (map projection graticules, contour lines, or buffers) in geoinformatics.
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Sanders, Kenton M., Yoshihiko Kito, Sung Jin Hwang, and Sean M. Ward. "Regulation of Gastrointestinal Smooth Muscle Function by Interstitial Cells." Physiology 31, no. 5 (September 2016): 316–26. http://dx.doi.org/10.1152/physiol.00006.2016.
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Interstitial cells of mesenchymal origin form gap junctions with smooth muscle cells in visceral smooth muscles and provide important regulatory functions. In gastrointestinal (GI) muscles, there are two distinct classes of interstitial cells, c-Kit+interstitial cells of Cajal and PDGFRα+cells, that regulate motility patterns. Loss of these cells may contribute to symptoms in GI motility disorders.
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Potkin, Ralph, Victor Cheng, and Robert Siegel. "Effects of glossopharyngeal insufflation on cardiac function: an echocardiographic study in elite breath-hold divers." Journal of Applied Physiology 103, no. 3 (September 2007): 823–27. http://dx.doi.org/10.1152/japplphysiol.00125.2007.
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Glossopharyngeal insufflation (GI), a technique used by breath-hold divers to increase lung volume and augment diving depth and duration, is associated with untoward hemodynamic consequences. To study the cardiac effects of GI, we performed transthoracic echocardiography, using the subcostal window, in five elite breath-hold divers at rest and during GI. During GI, heart rate increased in all divers (mean of 53 beats/min to a mean of 100 beats/min), and blood pressure fell dramatically (mean systolic, 112 to 52 mmHg; mean diastolic, 75 mmHg to nondetectable). GI induced a 46% decrease in mean left ventricular end-diastolic area, 70% decrease in left ventricular end-diastolic volume, 49% increase in mean right ventricular end-diastolic area, and 160% increase in mean right ventricular end-diastolic volume. GI also induced biventricular systolic dysfunction; left ventricular ejection fraction decreased from 0.60 to a mean of 0.30 ( P = 0.012); right ventricular ejection fraction, from 0.75 to a mean of 0.39 ( P < 0.001). Wall motion of both ventricles became significantly abnormal during GI; the most prominent left ventricular abnormalities involved hypokinesis or dyskinesis of the interventricular septum, while right ventricular wall motion abnormalities involved all visible segments. In two divers, the inferior vena cava dilated with the appearance of spontaneous contrast during GI, signaling increased right atrial pressure and central venous stasis. Hypotension during GI is associated with acute biventricular systolic dysfunction. The echocardiographic pattern of right ventricular systolic dysfunction is consistent with acute pressure overload, whereas concurrent left ventricular systolic dysfunction is likely due to ventricular interdependence.
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Zaretsky, Arielle Glatman, Seong-Ji Han, Denise Morais da Fonseca, Timothy Hand, and Yasmine Belkaid. "Long Term Impact of Acute Infection on Lymphatic Function." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 123.18. http://dx.doi.org/10.4049/jimmunol.198.supp.123.18.
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Abstract The lymphatic system facilitates critical processes for immunity, including immune cell trafficking, lipid transport, and the maintenance of tissue homeostasis. In the mesentery, these lymphatic vessels (LVs) allow drainage and cell trafficking from the gastrointestinal (GI) tract through the mesenteric adipose tissue (mAT) to the mesenteric lymph nodes (mLNs). During GI infection, this vasculature is altered by inflammation, which can induce lymphatic leakage. Repair of LVs after infection is resolved is necessary to restore lymphatic function. Although preliminary studies have found acute lymphatic leakage is conserved between GI pathogens, in an acute Yersinia pseudotuberculosis infection, mice control bacterial growth, but develop a chronic mesenteric lymphadenopathy and the increased permeability of LVs does not resolve after the infection is cleared. Consequently, the migratory CD103+CD11b+dendritic cells (DP DCs) cannot reach the mLN and instead pass through the dysregulated LVs into the mAT. The absence of DP DCs in the mLN is associated with impaired development of Th17 adaptive immunity to oral vaccination. Little is known about the mechanisms that regulate lymphatic integrity, however these studies reveal a remodeling of the adipose tissue after infection, and are ongoing to understand the long-term increased permeability of LVs and the potential to restore function. Our results support the idea that acute GI infections are associated with permanent changes in DC traffic, which interfere with the activation of immune responses and can have severe implications for GI tract integrity and predisposition to inflammatory diseases and suggest that dysregulation of the mAT may contribute to the prolonged disruption.
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Karpiesiuk, Aleksandra, and Katarzyna Palus. "Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) in Physiological and Pathological Processes within the Gastrointestinal Tract: A Review." International Journal of Molecular Sciences 22, no. 16 (August 12, 2021): 8682. http://dx.doi.org/10.3390/ijms22168682.
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Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide widely distributed in the central nervous system (CNS) and many peripheral organs, such as the digestive tract, endocrine, reproductive and respiratory systems, where it plays different regulatory functions and exerts a cytoprotective effect. The multifarious physiological effects of PACAP are mediated through binding to different G protein-coupled receptors, including PAC1 (PAC1-R), VPAC1 (VPAC1-R) and VPAC2 (VPAC2-R) receptors. In the gastrointestinal (GI) tract, PACAP plays an important regulatory function. PACAP stimulates the secretion of digestive juices and hormone release, regulates smooth muscle contraction, local blood flow, cell migration and proliferation. Additionally, there are many reports confirming the involvement of PACAP in pathological processes within the GI tract, including inflammatory states, neuronal injury, diabetes, intoxication and neoplastic processes. The purpose of this review is to summarize the distribution and pleiotropic action of PACAP in the control of GI tract function and its cytoprotective effect in the course of GI tract disorders.
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Álvarez-Bueno, Celia, Vicente Martínez-Vizcaíno, Estela Jiménez López, María Eugenia Visier-Alfonso, Andrés Redondo-Tébar, and Iván Cavero-Redondo. "Comparative Effect of Low-Glycemic Index versus High-Glycemic Index Breakfasts on Cognitive Function: A Systematic Review and Meta-Analysis." Nutrients 11, no. 8 (July 24, 2019): 1706. http://dx.doi.org/10.3390/nu11081706.
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This systematic review and meta-analysis aims to compare the effect of High-Glycemic Index (GI) versus Low-GI breakfasts on cognitive functions, including memory and attention, of children and adolescents. We systematically searched the MEDLINE (via PubMed), EMBASE, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews, and Web of Science databases, from their inception until June 2019. Articles comparing the effect of Low-GI versus High-GI breakfasts on the cognitive function (i.e., immediate memory, delayed memory, and attention) of children and adolescents were included. The DerSimonian and Laird method was used to compute the pooled effect sizes (ESs) and their respective 95% confidence intervals (CIs). The pooled ESs were 0.13 (95% CI: −0.11, 0.37) for immediate memory and 0.07 (95% CI: −0.15, 0.28) for delayed memory. For attention, the pooled ES was −0.01 (95% CI: −0.27, 0.26). In summary, GI breakfasts do not affect cognitive domains in children and adolescents.
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Waly, Mostafa I., Mady Hornig, Malav Trivedi, Nathaniel Hodgson, Radhika Kini, Akio Ohta, and Richard Deth. "Prenatal and Postnatal Epigenetic Programming: Implications for GI, Immune, and Neuronal Function in Autism." Autism Research and Treatment 2012 (2012): 1–13. http://dx.doi.org/10.1155/2012/190930.
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Although autism is first and foremost a disorder of the central nervous system, comorbid dysfunction of the gastrointestinal (GI) and immune systems is common, suggesting that all three systems may be affected by common molecular mechanisms. Substantial systemic deficits in the antioxidant glutathione and its precursor, cysteine, have been documented in autism in association with oxidative stress and impaired methylation. DNA and histone methylation provide epigenetic regulation of gene expression during prenatal and postnatal development. Prenatal epigenetic programming (PrEP) can be affected by the maternal metabolic and nutritional environment, whereas postnatal epigenetic programming (PEP) importantly depends upon nutritional support provided through the GI tract. Cysteine absorption from the GI tract is a crucial determinant of antioxidant capacity, and systemic deficits of glutathione and cysteine in autism are likely to reflect impaired cysteine absorption. Excitatory amino acid transporter 3 (EAAT3) provides cysteine uptake for GI epithelial, neuronal, and immune cells, and its activity is decreased during oxidative stress. Based upon these observations, we propose that neurodevelopmental, GI, and immune aspects of autism each reflect manifestations of inadequate antioxidant capacity, secondary to impaired cysteine uptake by the GI tract. Genetic and environmental factors that adversely affect antioxidant capacity can disrupt PrEP and/or PEP, increasing vulnerability to autism.
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Micha, Renata, Peter J. Rogers, and Michael Nelson. "Glycaemic index and glycaemic load of breakfast predict cognitive function and mood in school children: a randomised controlled trial." British Journal of Nutrition 106, no. 10 (June 8, 2011): 1552–61. http://dx.doi.org/10.1017/s0007114511002303.
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The macronutrient composition of a breakfast that could facilitate performance after an overnight fast remains unclear. As glucose is the brain's major energy source, the interest is in investigating meals differing in their blood glucose-raising potential. Findings vary due to unaccounted differences in glucoregulation, arousal and cortisol secretion. We investigated the effects of meals differing in glycaemic index (GI) and glycaemic load (GL) on cognition and mood in school children. A total of seventy-four school children were matched and randomly allocated either to the high-GL or low-GL group. Within each GL group, children received high-GI and low-GI breakfasts. Cognitive function (CF) and mood were measured 95–140 min after breakfast. Blood glucose and salivary cortisol were measured at baseline, before and after the CF tests. Repeated-measures ANOVA was used to identify differences in CF, mood, glucose and cortisol levels between the breakfasts. Low-GI meals predicted feeling more alert and happy, and less nervous and thirsty (P < 0·05 for each); high-GL meals predicted feeling more confident, and less sluggish, hungry and thirsty (P < 0·05 for each). High-GL (P < 0·001) and high-GI (P = 0·05) meals increased glucose levels 90 min after breakfast, and high-GI meals increased cortisol levels (P < 0·01). When baseline mood, glucose and cortisol levels were considered, low-GI meals predicted better declarative-verbal memory (P = 0·03), and high-GI meals better vigilance (P < 0·03); observed GI effects were valid across GL groups. GI effects on cognition appear to be domain specific. On balance, it would appear that the low-GI high-GL breakfast may help to improve learning, and of potential value in informing government education policies relating to dietary recommendations and implementation concerning breakfast.
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Marchand, Olivia M., Fiona E. Kendall, Charlene M. Rapsey, Jillian J. Haszard, and Bernard J. Venn. "The effect of postprandial glycaemia on cognitive function: a randomised crossover trial." British Journal of Nutrition 123, no. 12 (February 12, 2020): 1357–64. http://dx.doi.org/10.1017/s0007114520000458.
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AbstractThe effect on cognitive test scores of generating differences in postprandial glycaemia using test foods or beverages has been inconsistent. Methodological issues may account for some of the variable results requiring further investigation using strong study designs into the relationship between glycaemia and cognitive functioning. The objective of this study was to determine the effects of postprandial glycaemia on cognitive function by examining cognition after consumption of foods that differ only by the rate of digestion of available carbohydrate in a population of young adults. In a double-blind, randomised, crossover trial, sixty-five participants received trifle sweetened either with a higher-glycaemic index (GI) sugar (sucrose; GI 65) or a lower-GI sugar (isomaltulose; GI 34). Cognitive tests were completed prior to trifle consumption, and 60 and 120 min after. There was no between-trifle difference at 60 min in performance on free word recall (0·0 (95 % CI –0·6, 0·5)), short delay word recall (0·0 (95 % CI –0·5, 0·5)), long delay word recall (0·0 (95 % CI –0·6, 0·6)), letter–number sequence recall (0·3 (95 % CI − 0·2, 0·7)) and visuo-spatial recall (–0·2 (95 % CI –0·6, 0·2)) tests. At 120 min, no difference was detected in any of these tests. The participants performed 7·7 (95 % CI 0·5,14·9) s faster in Reitan’s trail-making test B 60 min after the higher-GI trifle than the lower-GI trifle (P = 0·037). Our findings of a null effect on memory are generally consistent with other works in which blinding and robust control for confounding have been used.
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Sipe, Alexander T., Marian L. Neuhouser, Kara L. Breymeyer, and Kristina M. Utzschneider. "Effect of Dietary Glycemic Index on β-Cell Function in Prediabetes: A Randomized Controlled Feeding Study." Nutrients 14, no. 4 (February 19, 2022): 887. http://dx.doi.org/10.3390/nu14040887.
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The glycemic index (GI) reflects the relative ability of carbohydrates to raise blood glucose. We utilized a controlled feeding study to assess the impact of the dietary GI on β-cell function in adults with prediabetes (17F/18M, mean ± SEM: BMI 32.44 ± 0.94 kg/m2, age 54.2 ± 1.57 years). Following a 2 week Control diet (GI = 55–58), participants were randomized to either a 4 week low GI (LGI: GI < 35, n = 17) or high GI (HGI: GI > 70, n = 18) diet (55% of energy from carbohydrate/30% fat/15% protein). The data from 4 h meal tolerance tests (MTTs) underwent mathematical modeling to assess insulin sensitivity, insulin secretion and β-cell function. Glucose concentrations during the MTT decreased on the LGI diet (p < 0.001) and trended to increase on the HGI diet (p = 0.14; LGI vs. HGI p < 0.001), with parallel changes in insulin and C-peptide concentrations. Total insulin secretion, adjusted for glucose and insulin sensitivity, increased on the LGI diet (p = 0.002), and trended lower on the HGI diet (p = 0.10; LGI vs. HGI p = 0.001). There was no significant diet effect on insulin sensitivity or other measures of β-cell function. Total insulin clearance increased on the LGI diet (p = 0.01; LGI vs. HGI p < 0.001). We conclude that short-term consumption of an LGI diet reduced glucose exposure and insulin secretion but had no impact on measures of β-cell function.
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Taché, Yvette, Vicente Martinez, Mulugeta Million, and Lixin Wang. "III. Stress-related alterations of gut motor function: role of brain corticotropin-releasing factor receptors." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 2 (February 1, 2001): G173—G177. http://dx.doi.org/10.1152/ajpgi.2001.280.2.g173.
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Alterations of gastrointestinal (GI) motor function are part of the visceral responses to stress. Inhibition of gastric emptying and stimulation of colonic motor function are the commonly encountered patterns induced by various stressors. Activation of brain corticotropin-releasing factor (CRF) receptors mediates stress-related inhibition of upper GI and stimulation of lower GI motor function through interaction with different CRF receptor subtypes. CRF subtype 1 receptors are involved in the colonic and anxiogenic responses to stress and may have clinical relevance in the comorbidity of anxiety/depression and irritable bowel syndrome.
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Kirkham, D. M., G. J. Murphy, and P. Young. "Demonstration of inhibitory guanine nucleotide regulatory protein (Gi) function in liver and hepatocyte membranes from streptozotocin-treated rats." Biochemical Journal 284, no. 2 (June 1, 1992): 301–4. http://dx.doi.org/10.1042/bj2840301.
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By using a defined plasma-membrane preparation, functional inhibition of adenylate cyclase activity by the inhibitory G-protein (Gi) was observed in liver and hepatocyte membranes from rats made diabetic by streptozotocin. These observations contrast with previous reports which have shown a defect in Gi in this diabetic animal model. These results suggest that Gi function is not impaired in the livers of streptozotocin-treated rats and that plasma-membrane preparation procedures should be clearly defined before ascribing Gi defects to a pathological state such as diabetes.
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HEITKEMPER, MARGARET, MONICA JARRETT, ELEANOR F. BOND, and PAMELA TURNER. "GI Symptoms, Function, and Psychophysiological Arousal In Dysmenorrheic Women." Nursing Research 40, no. 1 (January 1991): 20???27. http://dx.doi.org/10.1097/00006199-199101000-00005.
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Tsukamoto, Hayato, Aya Ishibashi, Christopher J. Marley, Yasushi Shinohara, Soichi Ando, Damian M. Bailey, Takeshi Hashimoto, Ogoh Shigehiko, and Shigehiko Ogoh. "Plasma brain-derived neurotrophic factor and dynamic cerebral autoregulation in acute response to glycemic control following breakfast in young men." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 320, no. 1 (January 1, 2021): R69—R79. http://dx.doi.org/10.1152/ajpregu.00059.2020.
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We examined the acute impact of both low- and high-glycemic index (GI) breakfasts on plasma brain-derived neurotrophic factor (BDNF) and dynamic cerebral autoregulation (dCA) compared with breakfast omission. Ten healthy men (age 24 ± 1 yr) performed three trials in a randomized crossover order; omission and Low-GI (GI = 40) and High-GI (GI = 71) breakfast conditions. Middle cerebral artery velocity (transcranial Doppler ultrasonography) and arterial pressure (finger photoplethysmography) were continuously measured for 5 min before and 120 min following breakfast consumption to determine dCA using transfer function analysis. After these measurements of dCA, venous blood samples for the assessment of plasma BDNF were obtained. Moreover, blood glucose was measured before breakfast and every 30 min thereafter. The area under the curve of 2 h postprandial blood glucose in the High-GI trial was higher than the Low-GI trial ( P < 0.01). The GI of the breakfast did not affect BDNF. In addition, both very-low (VLF) and low-frequency (LF) transfer function phase or gains were not changed during the omission trial. In contrast, LF gain (High-GI P < 0.05) and normalized gain (Low-GI P < 0.05) were decreased by both GI trials, while a decrease in VLF phase was observed in only the High-GI trial ( P < 0.05). These findings indicate that breakfast consumption augmented dCA in the LF range but High-GI breakfast attenuated cerebral blood flow regulation against slow change (i.e., the VLF range) in arterial pressure. Thus we propose that breakfast and glycemic control may be an important strategy to optimize cerebrovascular health.
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Philippou, Elena, Gerda K. Pot, Alexandros Heraclides, Marcus Richards, and Rebecca Bendayan. "Dietary glycaemic index and cognitive function: prospective associations in adults of the 1946 British birth cohort." Public Health Nutrition 22, no. 8 (December 26, 2018): 1415–24. http://dx.doi.org/10.1017/s136898001800352x.
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AbstractObjectiveEvidence suggests that the rate of glucose release following consumption of carbohydrate-containing foods, defined as the glycaemic index (GI), is inversely associated with cognitive function. To date, most of the evidence stems from either single-meal studies or highly heterogeneous cohort studies. We aimed to study the prospective associations of diet GI at age 53 years with outcomes of verbal memory and letter search tests at age 69 years and rate of decline between 53 and 69 years.DesignLongitudinal population-based birth cohort study.SettingMRC National Survey for Health and Development.ParticipantsCohort members (n 1252).ResultsUsing multivariable linear and logistic regression, adjusted for potential confounders, associations of higher-GI diet with lower verbal memory, lower letter search speed and lower number of hits in a letter search test were attenuated after adjustments for cognitive ability at age 15 years, educational attainment, further training and occupational social class. No association was observed between diet GI at 53 years and letter search accuracy or speed–accuracy trade-off at 69 years, or between diet GI at 53 years and rate of decline between 53 and 69 years in any cognitive measure.ConclusionsDiet GI does not appear to predict cognitive function or decline, which was mainly explained by childhood cognitive ability, education and occupational social class. Our findings confirm the need for further research on the association between diet and cognition from a life-course perspective.
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Polcicova, Katarina, Kim Goldsmith, Barb L. Rainish, Todd W. Wisner, and David C. Johnson. "The Extracellular Domain of Herpes Simplex Virus gE Is Indispensable for Efficient Cell-to-Cell Spread: Evidence for gE/gI Receptors." Journal of Virology 79, no. 18 (September 15, 2005): 11990–2001. http://dx.doi.org/10.1128/jvi.79.18.11990-12001.2005.
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ABSTRACT Herpes simplex virus (HSV) spreads rapidly and efficiently within epithelial and neuronal tissues. The HSV glycoprotein heterodimer gE/gI plays a critical role in promoting cell-to-cell spread but does not obviously function during entry of extracellular virus into cells. Thus, gE/gI is an important molecular handle on the poorly understood process of cell-to-cell spread. There was previous evidence that the large extracellular (ET) domains of gE/gI might be important in cell-to-cell spread. First, gE/gI extensively accumulates at cell junctions, consistent with being tethered there. Second, expression of gE/gI in trans interfered with HSV spread between epithelial cells. To directly test whether the gE ET domain was necessary for gE/gI to promote virus spread, a panel of gE mutants with small insertions in the ET domain was constructed. Cell-to-cell spread was reduced when insertions were made within either of two regions, residues 256 to 291 or 348 to 380. There was a strong correlation between loss of cell-to-cell spread function and binding of immunoglobulin. gE ET domain mutants 277, 291, and 348 bound gI, produced mature forms of gE that reached the cell surface, and were incorporated into virions yet produced plaques similar to gE null mutants. Moreover, all three mutants were highly restricted in spread within the corneal epithelium, in the case of mutant 277 to only 4 to 6% of the number of cells compared with wild-type HSV. Therefore, the ET domain of gE is indispensable for efficient cell-to-cell spread. These observations are consistent with our working hypothesis that gE/gI can bind extracellular ligands, so-called gE/gI receptors that are concentrated at epithelial cell junctions. This fits with similarities in structure and function of gE/gI and gD, which is a receptor binding protein.
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Chen, Danyu, Henley Cheung, Harry Cheuk-Hay Lau, Jun Yu, and Chi Chun Wong. "N6-Methyladenosine RNA-Binding Protein YTHDF1 in Gastrointestinal Cancers: Function, Molecular Mechanism and Clinical Implication." Cancers 14, no. 14 (July 18, 2022): 3489. http://dx.doi.org/10.3390/cancers14143489.
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N6-methyladenosine (m6A) is the most abundant internal modification in eukaryotic cell mRNA, and this modification plays a key role in regulating mRNA translation, splicing, and stability. Emerging evidence implicates aberrant m6A as a crucial player in the occurrence and development of diseases, especially GI cancers. Among m6A regulators, YTHDF1 is the most abundant m6A reader that functionally connects m6A-modified mRNA to its eventual fate, mostly notably protein translation. Here, we summarized the function, molecular mechanisms, and clinical implications of YTHDF1 in GI cancers. YTHDF1 is largely upregulated in multiple GI cancer and its high expression predicts poor patient survival. In vitro and in vivo experimental evidence largely supports the role of YTDHF1 in promoting cancer initiation, progression, and metastasis, which suggests the oncogenic function of YTHDF1 in GI cancers. Besides, YTHDF1 overexpression is associated with changes in the tumor microenvironment that are favorable to tumorigenesis. Mechanistically, YTHDF1 regulates the expression of target genes by promoting translation, thereby participating in cancer-related signaling pathways. Targeting YTHDF1 holds therapeutic potential, as the overexpression of YTHDF1 is associated with tumor resistance to chemotherapy and immunotherapy. In summary, YTHDF1-mediated regulation of m6A modified mRNA is an actionable target and a prognostic factor for GI cancers.
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Mari, Amir. "Diagnostics of Gastrointestinal Motility and Function: Update for Clinicians." Diagnostics 12, no. 11 (November 4, 2022): 2698. http://dx.doi.org/10.3390/diagnostics12112698.
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Swiderski, Kristy, Suzannah J. Read, Audrey S. Chan, Jin D. Chung, Jennifer Trieu, Timur Naim, René Koopman, and Gordon S. Lynch. "Investigating the Potential for Sulforaphane to Attenuate Gastrointestinal Dysfunction in mdx Dystrophic Mice." Nutrients 13, no. 12 (December 20, 2021): 4559. http://dx.doi.org/10.3390/nu13124559.
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Gastrointestinal (GI) dysfunction is an important, yet understudied condition associated with Duchenne muscular dystrophy (DMD), with patients reporting bloating, diarrhea, and general discomfort, contributing to a reduced quality of life. In the mdx mouse, the most commonly used mouse model of DMD, studies have confirmed GI dysfunction (reported as altered contractility and GI transit through the small and large intestine), associated with increased local and systemic inflammation. Sulforaphane (SFN) is a natural isothiocyanate with anti-inflammatory and anti-oxidative properties via its activation of Nrf2 signalling that has been shown to improve aspects of the skeletal muscle pathology in dystrophic mice. Whether SFN can similarly improve GI function in muscular dystrophy was unknown. Video imaging and spatiotemporal mapping to assess gastrointestinal contractions in isolated colon preparations from mdx and C57BL/10 mice revealed that SFN reduced contraction frequency when administered ex vivo, demonstrating its therapeutic potential to improve GI function in DMD. To confirm this in vivo, four-week-old male C57BL/10 and mdx mice received vehicle (2% DMSO/corn oil) or SFN (2 mg/kg in 2% DMSO/corn oil) via daily oral gavage five days/week for 4 weeks. SFN administration reduced fibrosis in the diaphragm of mdx mice but did not affect other pathological markers. Gene and protein analysis revealed no change in Nrf2 protein expression or activation of Nrf2 signalling after SFN administration and oral SFN supplementation did not improve GI function in mdx mice. Although ex vivo studies demonstrate SFN’s therapeutic potential for reducing colon contractions, in vivo studies should investigate higher doses and/or alternate routes of administration to confirm SFN’s potential to improve GI function in DMD.
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Whiteley, Paul. "Food and the gut: relevance to some of the autisms." Proceedings of the Nutrition Society 76, no. 4 (September 26, 2017): 478–83. http://dx.doi.org/10.1017/s0029665117002798.
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Complex, diverse and rarely appearing without comorbidity, the autism spectrum disorders continue to be a source of research interest. With core symptoms variably impacting on social communication skills, the traditional focus of many research efforts has centred on the brain and how genetic and environmental processes impact on brain structure, function and/or connectivity to account for various behavioural presentations. Alongside emerging ideas on autistic traits being present in various clinical states, the autisms, and the overrepresentation of several comorbid conditions impacting on quality of life, other research avenues have opened up. The central role of the brain in relation to autism may be at least partially influenced by the functions of other organs. The gastrointestinal (GI) tract represents an important biological system pertinent to at least some autism. The notion of a gut–brain–behaviour axis has garnered support from various findings: an overrepresentation of functional and pathological bowel states, bowel and behavioural findings showing bidirectional associations, a possible relationship between diet, GI function and autism and recently, greater focus on aspects of the GI tract such as the collected gut microbiota in relation to autism. Gaps remain in our knowledge of the functions of the GI tract linked to autism, specifically regarding mechanisms of action onward to behavioural presentation. Set however within the context of diversity in the presentation of autism, science appears to be moving towards defining important GI-related autism phenotypes with the possibility of promising dietary and other related intervention options onward to improving quality of life.
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Gugusheff, J., P. Sim, A. Kheng, S. Gentili, M. Al-Nussairawi, J. Brand-Miller, and B. Muhlhausler. "The effect of maternal and post-weaning low and high glycaemic index diets on glucose tolerance, fat deposition and hepatic function in rat offspring." Journal of Developmental Origins of Health and Disease 7, no. 3 (December 10, 2015): 320–29. http://dx.doi.org/10.1017/s2040174415007965.
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Clinical studies have reported beneficial effects of a maternal low glycaemic index (GI) diet on pregnancy and neonatal outcomes, but the impact of the diet on the offspring in later life, and the mechanisms underlying these effects, remain unclear. In this study, Albino Wistar rats were fed either a low GI (n=14) or high GI (n=14) diet during pregnancy and lactation and their offspring weaned onto either the low or high GI diet. Low GI dams had better glucose tolerance (AUC[glucose], 1322±55 v. 1523±72 mmol min/l, P<0.05) and a lower proportion of visceral fat (19.0±2.9 v. 21.7±3.8% of total body fat, P<0.05) compared to high GI dams. Female offspring of low GI dams had lower visceral adiposity (0.45±0.03 v. 0.53±0.03% body weight, P<0.05) and higher glucose tolerance (AUC[glucose], 1243±29 v. 1351±39 mmol min/l, P<0.05) at weaning, as well as lower hepatic PI3K-p85 mRNA at 12 weeks of age. No differences in glucose tolerance or hepatic gene expression were observed in male offspring, but the male low GI offspring did have reduced hepatic lipid content at weaning. These findings suggest that consuming a low GI diet during pregnancy and lactation can improve glucose tolerance and reduce visceral adiposity in the female offspring at weaning, and may potentially produce long-term reductions in the hepatic lipogenic capacity of these offspring.
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Ye, Diya, Yuting Hu, Ning Zhu, Weizhong Gu, Gao Long, Enfu Tao, Marong Fang, and Mizu Jiang. "Exploratory Investigation of Intestinal Structure and Function after Stroke in Mice." Mediators of Inflammation 2021 (February 15, 2021): 1–12. http://dx.doi.org/10.1155/2021/1315797.
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Stroke is the second leading cause of death worldwide. Patients who have a stroke are susceptible to many gastrointestinal (GI) complications, such as dysphagia, GI bleeding, and fecal incontinence. However, there are few studies focusing on the GI tract after stroke. The current study is to investigate the changes of intestinal structure and function in mice after ischemic stroke. Ischemic stroke was made as a disease model in mice, in which brain and ileal tissues were collected for experiments on the 1st and 7th day after stroke. Intestinal motility of mice was inhibited, and intestinal permeability was increased after stroke. Hematoxylin-eosin (HE) staining showed the accumulation of leucocytes in the intestinal mucosa. Myeloperoxidase (MPO) activity and inflammatory proteins (nuclear factor kappa-B (NF-κB), inducible nitric oxide synthase (iNOS)) in the small intestine were significantly increased in mice after stroke. The expression of tight junction (TJ) proteins (zonula occludens-1 (ZO-1), occludin, and claudin-1) was downregulated, and transmission electron microscopy (TEM) showed broken TJ of the intestinal mucosa after stroke. Glial fibrillary acidic protein (GFAP) and the apoptosis-associated proteins (tumor necrosis factor (TNF-α), caspase-3, and cleaved caspase-3) were notably upregulated as well. Ischemic stroke led to negative changes on intestinal structure and function. Inflammatory mediators and TNF-α-induced death receptor signaling pathways may be involved and disrupt the small intestinal barrier function. These results suggest that stroke patients should pay attention to GI protection.
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Shao, Huamei, and Gunwoo Kim. "A Comprehensive Review of Different Types of Green Infrastructure to Mitigate Urban Heat Islands: Progress, Functions, and Benefits." Land 11, no. 10 (October 14, 2022): 1792. http://dx.doi.org/10.3390/land11101792.
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Climate change and rapid urbanization increase/amplify urban heat islands (UHIs). Green infrastructure (GI) is an effective and popularly strategy used to moderate UHIs. This paper aims to better understand the progress of different GI types (urban parks, urban forests, street trees, green roofs, green walls) in mitigating UHIs, and what benefits they provide. Firstly, this paper used CiteSpace to analyze 1243 publications on the Web of Science from 1990 to 2021, then analyzed the function/regulation of ecosystem services/benefits and values of GI types in reducing UHIs. The historical review results show that research on all GI types showed rapid growth since 2013, and their GR increased rapidly. The highest-ranking keywords were urban heat island/heat island, climate/climate change/microclimate, and temperature/land surface temperature/air temperature. “Design,” “vegetation,” “quality,” and “reduction” are the top four strongest keyword bursts. The most published countries are the People’s Republic of China, USA, Australia, Germany, and Italy, and the top three institutions are the Chinese Academy of Sciences, Arizona State University, and the National University of Singapore. Landscape and Urban Planning, Building and Environment, Energy and Building, and Urban Forestry and Urban Greening are the most published journals. In urban areas, different GI types as a form of ecosystem hardware provide multiple functions (reduced land surface temperatures, lower building energy usage, improved thermal comfort and enhanced human health, reduced morbidity and mortality, etc.). GI thus provides a regulated ecosystem service to ameliorate UHIs primarily through temperature regulation and shade. At the same time, GI provides benefits and values (ecological, economic, social, and cultural) to humans and urban sustainable development. GI types determine the functions they provide, afford corresponding regulated ecosystem services, and provide benefits and values in a logical/recycle system. Overall, this review highlights the development and importance of GI, as well as the relationship of GI types and functions of regulating the ecosystem service benefits and values to mitigate UHI, and advances the study of climate change adaptation in cities.
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López-Gómez, Laura, Agata Szymaszkiewicz, Marta Zielińska, and Raquel Abalo. "The Enteric Glia and Its Modulation by the Endocannabinoid System, a New Target for Cannabinoid-Based Nutraceuticals?" Molecules 27, no. 19 (October 10, 2022): 6773. http://dx.doi.org/10.3390/molecules27196773.
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The enteric nervous system (ENS) is a part of the autonomic nervous system that intrinsically innervates the gastrointestinal (GI) tract. Whereas enteric neurons have been deeply studied, the enteric glial cells (EGCs) have received less attention. However, these are immune-competent cells that contribute to the maintenance of the GI tract homeostasis through supporting epithelial integrity, providing neuroprotection, and influencing the GI motor function and sensation. The endogenous cannabinoid system (ECS) includes endogenous classical cannabinoids (anandamide, 2-arachidonoylglycerol), cannabinoid-like ligands (oleoylethanolamide (OEA) and palmitoylethanolamide (PEA)), enzymes involved in their metabolism (FAAH, MAGL, COX-2) and classical (CB1 and CB2) and non-classical (TRPV1, GPR55, PPAR) receptors. The ECS participates in many processes crucial for the proper functioning of the GI tract, in which the EGCs are involved. Thus, the modulation of the EGCs through the ECS might be beneficial to treat some dysfunctions of the GI tract. This review explores the role of EGCs and ECS on the GI tract functions and dysfunctions, and the current knowledge about how EGCs may be modulated by the ECS components, as possible new targets for cannabinoids and cannabinoid-like molecules, particularly those with potential nutraceutical use.
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Liu, Albert T., Shuai Chen, Prasant Kumar Jena, Lili Sheng, Ying Hu, and Yu-Jui Yvonne Wan. "Probiotics Improve Gastrointestinal Function and Life Quality in Pregnancy." Nutrients 13, no. 11 (November 3, 2021): 3931. http://dx.doi.org/10.3390/nu13113931.
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We studied whether probiotics were beneficial for hormonal change-associated dysbiosis, which may influence the enteric nervous system and GI function during early pregnancy. The study was 16 days consisting of two cycles of six daily probiotics mainly Lactobacillus and 2 days without probiotics. Daily surveys were conducted to monitor GI function and life quality. A subset of the participants who contributed fecal specimens was used for microbiota metagenomic sequencing, metabolomics, and quantification of bacterial genes to understand potential underlying mechanisms. Statistical analyses were done by generalized linear mixed-effects models. Thirty-two obstetric patients and 535 daily observations were included. The data revealed that probiotic supplementation significantly reduced the severity of nausea, vomiting, constipation, and improved life quality. Moreover, a low copy number of fecal bsh (bile salt hydrolase), which generates free bile acids, was associated with high vomiting scores and probiotic intake increased fecal bsh. In exploratory analysis without adjusting for multiplicity, a low fecal α-tocopherol, as well as a high abundance of Akkemansia muciniphila, was associated with high vomiting scores and times, respectively. The potential implications of these biomarkers in pregnancy and GI function are discussed. Probiotics likely produce free bile acids to facilitate intestinal mobility and metabolism.
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Xie, Qiguang, Ping Lou, Victor Hermand, Rashid Aman, Hee Jin Park, Dae-Jin Yun, Woe Yeon Kim, et al. "Allelic polymorphism of GIGANTEA is responsible for naturally occurring variation in circadian period in Brassica rapa." Proceedings of the National Academy of Sciences 112, no. 12 (March 9, 2015): 3829–34. http://dx.doi.org/10.1073/pnas.1421803112.
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GIGANTEA (GI) was originally identified by a late-flowering mutant in Arabidopsis, but subsequently has been shown to act in circadian period determination, light inhibition of hypocotyl elongation, and responses to multiple abiotic stresses, including tolerance to high salt and cold (freezing) temperature. Genetic mapping and analysis of families of heterogeneous inbred lines showed that natural variation in GI is responsible for a major quantitative trait locus in circadian period in Brassica rapa. We confirmed this conclusion by transgenic rescue of an Arabidopsis gi-201 loss of function mutant. The two B. rapa GI alleles each fully rescued the delayed flowering of Arabidopsis gi-201 but showed differential rescue of perturbations in red light inhibition of hypocotyl elongation and altered cold and salt tolerance. The B. rapa R500 GI allele, which failed to rescue the hypocotyl and abiotic stress phenotypes, disrupted circadian period determination in Arabidopsis. Analysis of chimeric B. rapa GI alleles identified the causal nucleotide polymorphism, which results in an amino acid substitution (S264A) between the two GI proteins. This polymorphism underlies variation in circadian period, cold and salt tolerance, and red light inhibition of hypocotyl elongation. Loss-of-function mutations of B. rapa GI confer delayed flowering, perturbed circadian rhythms in leaf movement, and increased freezing and increased salt tolerance, consistent with effects of similar mutations in Arabidopsis. Collectively, these data suggest that allelic variation of GI—and possibly of clock genes in general—offers an attractive target for molecular breeding for enhanced stress tolerance and potentially for improved crop yield.
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Farré, Ricard, Marcello Fiorani, Saeed Abdu Rahiman, and Gianluca Matteoli. "Intestinal Permeability, Inflammation and the Role of Nutrients." Nutrients 12, no. 4 (April 23, 2020): 1185. http://dx.doi.org/10.3390/nu12041185.
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The interaction between host and external environment mainly occurs in the gastrointestinal tract, where the mucosal barrier has a critical role in many physiologic functions ranging from digestion, absorption, and metabolism. This barrier allows the passage and absorption of nutrients, but at the same time, it must regulate the contact between luminal antigens and the immune system, confining undesirable products to the lumen. Diet is an important regulator of the mucosal barrier, and the cross-talk among dietary factors, the immune system, and microbiota is crucial for the modulation of intestinal permeability and for the maintenance of gastrointestinal tract (GI) homeostasis. In the present review, we will discuss the role of a number of dietary nutrients that have been proposed as regulators of inflammation and epithelial barrier function. We will also consider the metabolic function of the microbiota, which is capable of elaborating the diverse nutrients and synthesizing products of great interest. Better knowledge of the influence of dietary nutrients on inflammation and barrier function can be important for the future development of new therapeutic approaches for patients with mucosal barrier dysfunction, a critical factor in the pathogenesis of many GI and non-GI diseases.
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Nétek, Rostislav. "Possibilities of contactless control of web map applications by sight." Geoinformatics FCE CTU 7 (December 29, 2011): 55–72. http://dx.doi.org/10.14311/gi.7.5.
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This paper assesses possibilities of a new approach of control map applications on the screen without locomotive system. There is a project about usability of Eye Tracking System in Geoinformatic and Cartographic fields at Department of Geoinformatics at Palacky University. The eye tracking system is a device for measuring eye/gaze positions and eye/gaze movement ("where we are looking"). There is a number of methods and outputs, but the most common are "heat-maps" of intensity and/or time. Just this method was used in the first part, where was analyzed the number of common web map portals, especially distribution of their tools and functions on the screen. The aim of research is to localize by heat-maps the best distribution of control tools for movement with map (function "pan"). It can analyze how sensitive are people on perception of control tools in different web pages and platforms. It is a great experience to compare accurate survey data with personal interpretation and knowledge. Based on these results is the next step – design of "control tools" which is command by eye-tracking device. There has been elected rectangle areas located on the edge of map (AOI – areas of interest), with special function which have defined some time delay. When user localizes one of these areas the map automatically moves to the way on which edge is localized on, and time delay prevents accidental movement. The technology for recording the eye movements on the screen offers this option because if you properly define the layout and function controls of the map, you need only connect these two systems. At this moment, there is a technical constrain. The solution of movement control is based on data transmission between eye-tracking-device-output and converter in real-time. Just real-time transfer is not supported in every case of SMI (SensoMotoric Instruments company) devices. More precisely it is the problem of money, because eye-tracking device and every upgrade is very expensive. This constrains and their solutions are also discussed in paper. Main aim of the project is to design (both economically and technologically), optimal way how to record and convert eye-movement in a program with sophisticated control of movements.
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Liu, Zijing, Yuehan Yang, Jingxuan Hou, and Haifeng Jia. "Decision-Making Framework for GI Layout Considering Site Suitability and Weighted Multi-Function Effectiveness: A Case Study in Beijing Sub-Center." Water 14, no. 11 (May 30, 2022): 1765. http://dx.doi.org/10.3390/w14111765.
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The effectiveness of runoff control infrastructure depends on infrastructure arrangement and the severity of the problem in the study area. Green infrastructure (GI) has been widely demonstrated as a practical approach to runoff reduction and ecological improvement. However, decision-makers usually consider the cost-efficacy of the GI layout scheme as a primary factor, leading to less consideration of GI’s environmental and ecological functions. Thus, a multifunctional decision-making framework for evaluating the suitability of GI infrastructure was established. First, the study area was described by regional pollution load intensity, slope, available space, and constructible area. Then, to assess the multifunctional performance of GI, a hierarchical evaluation framework comprising three objectives, seven indices, and sixteen sub-indices was established. Weights were assigned to different indices according to stakeholders’ preferences, including government managers, researchers, and residents. The proposed framework can be extended to other cities to detect GI preference.
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Pierre, Joseph F. "Gastrointestinal immune and microbiome changes during parenteral nutrition." American Journal of Physiology-Gastrointestinal and Liver Physiology 312, no. 3 (March 1, 2017): G246—G256. http://dx.doi.org/10.1152/ajpgi.00321.2016.
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Parenteral nutrition (PN) is a lifesaving therapy that provides intravenous nutrition support to patients who cannot, or should not, feed via the gastrointestinal (GI) tract. Unfortunately, PN also carries certain risks related to infection and metabolic complications compared with enteral nutrition. In this review, an overview of PN and GI immune and microbiome changes is provided. PN impacts the gut-associated lymphoid tissue functions, especially adaptive immune cells, changes the intestinal epithelium and chemical secretions, and significantly alters the intestinal microbiome. Collectively, these changes functionally result in increased susceptibility to infectious and injurious challenge. Since PN remains necessary in large numbers of patients, the search to improve outcomes by stimulating GI immune function during PN remains of interest. This review closes by describing recent advances in using enteric nervous system neuropeptides or microbially derived products during PN, which may improve GI parameters by maintaining immunity and physiology.
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Singh, Rajan, Hannah Zogg, and Seungil Ro. "Role of microRNAs in Disorders of Gut–Brain Interactions: Clinical Insights and Therapeutic Alternatives." Journal of Personalized Medicine 11, no. 10 (October 12, 2021): 1021. http://dx.doi.org/10.3390/jpm11101021.
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Disorders of gut–brain interactions (DGBIs) are heterogeneous in nature and intertwine with diverse pathophysiological mechanisms. Regular functioning of the gut requires complex coordinated interplay between a variety of gastrointestinal (GI) cell types and their functions are regulated by multiple mechanisms at the transcriptional, post-transcriptional, translational, and post-translational levels. MicroRNAs (miRNAs) are small non-coding RNA molecules that post-transcriptionally regulate gene expression by binding to specific mRNA targets to repress their translation and/or promote the target mRNA degradation. Dysregulation of miRNAs might impair gut physiological functions leading to DGBIs and gut motility disorders. Studies have shown miRNAs regulate gut functions such as visceral sensation, gut immune response, GI barrier function, enteric neuronal development, and GI motility. These biological processes are highly relevant to the gut where neuroimmune interactions are key contributors in controlling gut homeostasis and functional defects lead to DGBIs. Although extensive research has explored the pathophysiology of DGBIs, further research is warranted to bolster the molecular mechanisms behind these disorders. The therapeutic targeting of miRNAs represents an attractive approach for the treatment of DGBIs because they offer new insights into disease mechanisms and have great potential to be used in the clinic as diagnostic markers and therapeutic targets. Here, we review recent advances regarding the regulation of miRNAs in GI pacemaking cells, immune cells, and enteric neurons modulating pathophysiological mechanisms of DGBIs. This review aims to assess the impacts of miRNAs on the pathophysiological mechanisms of DGBIs, including GI dysmotility, impaired intestinal barrier function, gut immune dysfunction, and visceral hypersensitivity. We also summarize the therapeutic alternatives for gut microbial dysbiosis in DGBIs, highlighting the clinical insights and areas for further exploration. We further discuss the challenges in miRNA therapeutics and promising emerging approaches.
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Takagi, Yasutaka, Haruaki Ninomiya, Tatsuya Sawamura, Soichi Miwa, Aiji Sakamoto, and Tomoh Masaki. "Structure-function relationship of endothelin receptors: coupling with Gs/Gi." Japanese Journal of Pharmacology 64 (1994): 306. http://dx.doi.org/10.1016/s0021-5198(19)50859-9.
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Shea-Donohue, Terez, Joseph F. Urban, Luigi Notari, and Aiping Zhao. "Immune regulation of epithelial cell function: Implications for GI pathologies." International Dairy Journal 20, no. 4 (April 2010): 248–52. http://dx.doi.org/10.1016/j.idairyj.2009.11.005.
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Bozomitu, Laura, Ingrith Miron, Anca Adam Raileanu, Ancuta Lupu, Gabriela Paduraru, Florin Mihai Marcu, Ana Maria Laura Buga, Daniela Carmen Rusu, Felicia Dragan, and Vasile Valeriu Lupu. "The Gut Microbiome and Its Implication in the Mucosal Digestive Disorders." Biomedicines 10, no. 12 (December 2, 2022): 3117. http://dx.doi.org/10.3390/biomedicines10123117.
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The gastrointestinal (GI) tract is one of the most studied compartments of the human body as it hosts the largest microbial community including trillions of germs. The relationship between the human and its associated flora is complex, as the microbiome plays an important role in nutrition, metabolism and immune function. With a dynamic composition, influenced by many intrinsic and extrinsic factors, there is an equilibrium maintained in the composition of GI microbiota, translated as “eubiosis”. Any disruption of the microbiota leads to the development of different local and systemic diseases. This article reviews the human GI microbiome’s composition and function in healthy individuals as well as its involvement in the pathogenesis of different digestive disorders. It also highlights the possibility to consider flora manipulation a therapeutic option when treating GI diseases.
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Lomax, Alan E., Sabindra Pradhananga, and Paul P. Bertrand. "Plasticity of neuroeffector transmission during bowel inflammation1." American Journal of Physiology-Gastrointestinal and Liver Physiology 312, no. 3 (March 1, 2017): G165—G170. http://dx.doi.org/10.1152/ajpgi.00365.2016.
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Altered gastrointestinal (GI) function contributes to the debilitating symptoms of inflammatory bowel diseases (IBD). Nerve circuits contained within the gut wall and outside of the gut play important roles in modulating motility, mucosal fluid transport, and blood flow. The structure and function of these neuronal populations change during IBD. Superimposed on this plasticity is a diminished responsiveness of effector cells — smooth muscle cells, enterocytes, and vascular endothelial cells — to neurotransmitters. The net result is a breakdown in the precisely orchestrated coordination of motility, fluid secretion, and GI blood flow required for health. In this review, we consider how inflammation-induced changes to the effector innervation of these tissues, and changes to the tissues themselves, contribute to defective GI function in models of IBD. We also explore the evidence that reversing neuronal plasticity is sufficient to normalize function during IBD.
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Auman, J. T., F. J. Seidler, and T. A. Slotkin. "β-Adrenoceptor control of G protein function in the neonate: determinant of desensitization or sensitization." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 5 (November 1, 2002): R1236—R1244. http://dx.doi.org/10.1152/ajpregu.00409.2002.
Full textAbstract:
Neonatal β-adrenoceptors (β-ARs) are resistant to agonist-induced desensitization. We examined the functioning of Gi and Gs after repeated administration of β-AR agonists to newborn rats. Isoproterenol (β1/β2 agonist) obtunded Gi function in the heart but not the liver; in contrast, terbutaline, a β2-selective agonist, enhanced Gi function. Isoproterenol, but not terbutaline, increased membrane-associated Gsα, which would enhance receptor function. In addition, isoproterenol increased and terbutaline maintained the proportion of the short-splice (S) variant of Gsα in the membrane fraction; GsαS is functionally more active than the long-splice variant. Either isoproterenol or terbutaline treatment increased Gsα in the cytosolic fraction, a characteristic usually associated with desensitization in the adult. Decreased Gi activity, coupled with increased membrane-associated Gsαconcentrations and maintenance or increases in membrane GsαS, provide strong evidence that unique effects on G protein function underlie the ability of the immature organism to sustain β-AR cell signaling in the face of excessive or prolonged stimulation; these mechanisms also contribute to tissue selectivity of the effects of β-agonists with divergent potencies toward different β-AR subtypes.
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Shi, B., J. E. Heavner, J. E. Spallholz, and L. M. Boylan. "Severe dietary magnesium deficiency does not alter levels and function of myocardial Gs alpha and Gi alpha." Journal of Applied Physiology 81, no. 1 (July 1, 1996): 335–40. http://dx.doi.org/10.1152/jappl.1996.81.1.335.
Full textAbstract:
Magnesium ions (Mg2+) play a crucial role in the activation and synthesis of guanine nucleotide-binding proteins (G proteins). However, there is no information about the influence of in vivo magnesium deficiency on the function and levels of G proteins. This study was done to investigate whether dietary magnesium deficiency alters function and levels of the two major myocardial G proteins, Gi alpha and Gs alpha. Severe hypomagnesemia and a significant reduction of myocardial magnesium occurred in rats fed a magnesium-deficient diet for 6 wk vs. rats fed a normal-magnesium diet (control). The magnesium-deficient rats developed focal myocardial lesions but their cardiac function was not impaired. Myocardial immunodetectable Gs alpha and Gi alpha levels of magnesium-deficient rats did not differ from control (Gs alpha: 2.39 +/- 0.52 vs. 2.76 +/- 0.72 arbitrary units/microgram protein, P > 0.05; Gi alpha: 1.60 +/- 0.52 vs. 1.89 +/- 0.30 arbitrary units/microgram protein, P > 0.05). Similarly, the function of Gs alpha and Gi alpha estimated by basal and ligand-stimulated adenylyl cyclase activity was not significantly different between the two groups of animals. The results show that dietary-derived magnesium deficiency sufficient to produce severe hypomagnesemia does not produce any significant change in levels or function of myocardial G proteins.