From Fuzzy Expert System to Artificial Neural Network: Application to Assisted Speech Therapy

This chapter addresses the following question: What are the advantages of extending a fuzzy expert system (FES) to an artificial neural network (ANN), within a computer‐based speech therapy system (CBST)? We briefly describe the key concepts underlying the principles behind the FES and ANN and their applications in assisted speech therapy. We explain the importance of an intelligent system in order to design an appropriate model for real‐life situations. We present data from 1‐year application of these concepts in the field of assisted speech therapy. Using an artificial intelligent system for improving speech would allow designing a training program for pronunciation, which can be individualized based on specialty needs, previous experiences, and the child\u27s prior therapeutical progress. Neural networks add a great plus value when dealing with data that do not normally match our previous designed pattern. Using an integrated approach that combines FES and ANN allows our system to accomplish three main objectives: (1) develop a personalized therapy program; (2) gradually replace some human expert duties; (3) use “self‐learning” capabilities, a component traditionally reserved for humans. The results demonstrate the viability of the hybrid approach in the context of speech therapy that can be extended when designing similar applications

Increased Oral Detection, but Decreased Intestinal Signaling for Fats in Mice Lacking Gut Microbiota

Germ-free (GF) mice lacking intestinal microbiota are significantly leaner than normal (NORM) control mice despite consuming more calories. The contribution of microbiota on the recognition and intake of fats is not known. Thus, we investigated the preference for, and acceptance of, fat emulsions in GF and NORM mice, and associated changes in lingual and intestinal fatty acid receptors, intestinal peptide content, and plasma levels of gut peptides. GF and NORM C57Bl/6J mice were given 48-h two-bottle access to water and increasing concentrations of intralipid emulsions. Gene expression of the lingual fatty acid translocase CD36 and protein expression of intestinal satiety peptides and fatty-acid receptors from isolated intestinal epithelial cells were determined. Differences in intestinal enteroendocrine cells along the length of the GI tract were quantified. Circulating plasma satiety peptides reflecting adiposity and biochemical parameters of fat metabolism were also examined. GF mice had an increased preference and intake of intralipid relative to NORM mice. This was associated with increased lingual CD36 (P<0.05) and decreased intestinal expression of fatty acid receptors GPR40 (P<0.0001), GPR41 (P<0.0001), GPR43 (P<0.05), and GPR120 (P<0.0001) and satiety peptides CCK (P<0.0001), PYY (P<0.001), and GLP-1 (P<0.001). GF mice had fewer enteroendocrine cells in the ileum (P<0.05), and more in the colon (P<0.05), relative to NORM controls. Finally, GF mice had lower levels of circulating leptin and ghrelin (P<0.001), and altered plasma lipid metabolic markers indicative of energy deficits. Increased preference and caloric intake from fats in GF mice are associated with increased oral receptors for fats coupled with broad and marked decreases in expression of intestinal satiety peptides and fatty-acid receptors

Why Can't Rodents Vomit? A Comparative Behavioral, Anatomical, and Physiological Study

The vomiting (emetic) reflex is documented in numerous mammalian species, including primates and carnivores, yet laboratory rats and mice appear to lack this response. It is unclear whether these rodents do not vomit because of anatomical constraints (e.g., a relatively long abdominal esophagus) or lack of key neural circuits. Moreover, it is unknown whether laboratory rodents are representative of Rodentia with regards to this reflex. Here we conducted behavioral testing of members of all three major groups of Rodentia; mouse-related (rat, mouse, vole, beaver), Ctenohystrica (guinea pig, nutria), and squirrel-related (mountain beaver) species. Prototypical emetic agents, apomorphine (sc), veratrine (sc), and copper sulfate (ig), failed to produce either retching or vomiting in these species (although other behavioral effects, e.g., locomotion, were noted). These rodents also had anatomical constraints, which could limit the efficiency of vomiting should it be attempted, including reduced muscularity of the diaphragm and stomach geometry that is not well structured for moving contents towards the esophagus compared to species that can vomit (cat, ferret, and musk shrew). Lastly, an in situ brainstem preparation was used to make sensitive measures of mouth, esophagus, and shoulder muscular movements, and phrenic nerve activity-key features of emetic episodes. Laboratory mice and rats failed to display any of the common coordinated actions of these indices after typical emetic stimulation (resiniferatoxin and vagal afferent stimulation) compared to musk shrews. Overall the results suggest that the inability to vomit is a general property of Rodentia and that an absent brainstem neurological component is the most likely cause. The implications of these findings for the utility of rodents as models in the area of emesis research are discussed. © 2013 Horn et al

Gut Microbiota Restores Central Neuropeptide Deficits in Germ-Free Mice

Recent work has demonstrated the ability of the gut microbiota (GM) to alter the expression and release of gut peptides that control appetite and regulate energy homeostasis. However, little is known about the neuronal response of these hormones in germ-free (GF) animals, especially leptin, which is strikingly low in these animals. Therefore, we aimed to determine the response to exogenous leptin in GF mice as compared to conventionally raised (CONV-R) mice. Specifically, we injected and measured serum leptin in both GF and CONV-R mice and measured expression of orexigenic and anorexigenic peptides NPY, AgRP, POMC, and CART in the hypothalamus and hindbrain to examine whether the GM has an impact on central nervous system regulation of energy homeostasis. We found that GF mice had a significant increase in hypothalamic NPY and AgRP mRNA expression and a decrease in hindbrain NPY and AgRP mRNA, while mRNA expression of POMC and CART remained unchanged. Administration of leptin normalized circulating levels of leptin, GLP-1, PYY, and ghrelin, all of which were significantly decreased in GF mice. Finally, brief conventionalization of GF mice for 10 days restored the deficits in hypothalamic and hindbrain neuropeptides present in GF animals. Taken together, these results show that the GM regulates hypothalamic and hindbrain orexigenic/anorexigenic neuropeptide expression. This is in line with the role of gut microbiota in lipid metabolism and fat deposition that may contribute to excess fat in conventionalized animals under high feeding condition

Emerging roles of lactic acid bacteria in protection against colorectal cancer

Colorectal cancer (CRC) is the third leading cause of cancer deaths worldwide and the fourth most common cancer diagnosed among men and women in the United States. Considering the risk factors of CRC, dietary therapy has become one of the most effective approaches in reducing CRC morbidity and mortality. The use of probiotics is increasing in popularity for both the prevention and treatment of a variety of diseases. As the most common types of microbes used as probiotics, lactic acid bacteria (LAB) are comprised of an ecologically diverse group of microorganisms united by formation of lactic acid as the primary metabolite of sugar metabolism. Lhave been successfully used in managing diarrhea, food allergies, and inflammatory bowel disease. Lalso demonstrated a host of properties in preventing colorectal cancer development by inhibiting initiation or progression through multiple pathways. In this review, we discuss recent insights into cellular and molecular mechanisms of Lin CRC prevention including apoptosis, antioxidant DNA damages, immune responses, and epigenetics. The emerging experimental findings from clinical trials as well as the proposed mechanisms of gut microbiota in carcinogenesis will also be briefly discussed

Facteurs oraux et post-oraux contrôlant l'équilibre énergétique chez les rongeurs sans germes

The present studies examine intestinal, metabolic, and behavioral alterations in germ-free (GF) animals. The first set of experiments examine preference and acceptance for sweet solutions, sucrose and saccharin, in GF C57Bl/6J mice with associated changes in expression of lingual and intestinal nutrient-sensing sweet taste receptors, T1R2 and T1R3, and the glucose transporter, SGLT1. It demonstrates that GF mice consumed more of the highest concentration of sucrose relative to NORM controls, with an increased expression of intestinal T1R3 and SGLT1. The second set of studies examine if findings of increased sucrose intake extend to fat, and whether the GF mice display alterations in lingual and intestinal fat sensors as well as intestinal satiety peptides. We found that GF mice display increased intake and preference of fat at high and low concentrations, respectively. Additionally GF mice display decreased fatty-acid GPRs and satiety peptides in the intestine, decreased circulating gut peptide levels, increased lingual fat detecting receptors, and increased markers of fatty-acid metabolism, all of which are adaptive effects to the chronically depleted energy state of the GF mice. The final succession of experiments was to determine if the GF state, with its associated decreases in adiposity and chronic fasting state in mice, is present in the GF rat model. Interestingly, we found that GF rats display similar or increased levels of body adiposity, with decreased markers of liver lipogenesis, yet increased lipogenesis in adipose tissue associated with adipocyte hypertrophy. Overall, these data demonstrate that absence of gut microbiota in mice leads to increased energy consumption of sugars and fats associated with alterations in oral and intestinal nutrient sensors while the gut microbiota in the F344 does not play a pivotal role in adiposityMes études ont pour but d'examiner les altérations métaboliques et comportementales dans des modèles de souris axéniques. Nous avons démontré que les souris axéniques présentent une augmentation de préférence et d'acceptation des solutions sucrées. Cette augmentation est corrélée à des changements des niveaux d'expression des récepteurs du goût sucré au niveau de l'épithélium lingual et la muqueuse intestinale; T1R2, T1R3, et le transporteur de glucose SGLT-1. De plus, elles ont une préférence pour des fortes concentrations de saccharose comparées aux souris normales. Cet effet est associé à une augmentation des niveaux d'expression de T1R3 et SGLT-1 dans l'intestin. Nous avons étudié si cette augmentation de consommation de sucre était similaire à celle de acide gras, étayé les effets d'une consommation des lipides sur les niveaux d'expression des récepteurs des acides gras "CD36" au niveau de l'épithélium lingual et la muqueuse intestinale ainsi que les niveaux d'expression et de sécrétion des peptides intestinales à vocation satiétogène chez les souris axéniques comparées aux souris normales. En effet, nous avons démontré que les souris axéniques affichent une consommation accrue et une préférence pour les acides gras à des fortes et faibles concentrations respectivement. Ces changements étaient associés à une diminution des niveaux d'expression des détecteurs gustatifs de gras (GPRs), des faibles taux d'expression et de sécrétion des peptides intestinales, une augmentation d'expression du récepteur des acides gras au niveau de l'épithélium lingual et une augmentation des taux circulants des acides gras. Ces modifications peuvent constituer des mécanismes d'adaptation à l'état énergétique appauvri des souris axéniques. Nous avons essayé de savoir si ces altérations étaient présentes chez le rat dépourvu axénique. En effet, nous avons constaté que les rats axéniques présentent un niveau similaire ou élevé de la masse grasse, avec une diminution de la lipogenèse et une augmentation de l'adipogenèse expliquant l'hyperphagie du tissu adipeux. En résumé, nous avons démontré que l'absence du microbiote intestinal chez la souris conduit à une augmentation de l'apport énergétique en augmentant la consommation de sucres et de gras. Ces effets sont associés à des altérations orales et post-orales des niveaux d'expressions des détecteurs gustatifs tandis que le microbiote intestinal du rat F344 ne joue pas un rôle central dans l'adipositéPARIS-BIUSJ-Biologie recherche (751052107) / SudocSudocFranceF

Impact of Nutrition, Microbiota Transplant and Weight Loss Surgery on Dopaminergic Alterations in Parkinson&rsquo;s Disease and Obesity

Parkinson&rsquo;s disease (PD), the second most common neurodegenerative disorder worldwide, is characterized by dopaminergic neuron degeneration and &alpha;-synuclein aggregation in the substantia nigra pars compacta of the midbrain. Emerging evidence has shown that dietary intake affects the microbial composition in the gut, which in turn contributes to, or protects against, the degeneration of dopaminergic neurons in affected regions of the brain. More specifically, the Mediterranean diet and Western diet, composed of varying amounts of proteins, carbohydrates, and fats, exert contrasting effects on PD pathophysiology via alterations in the gut microbiota and dopamine levels. Interestingly, the negative changes in the gut microbiota of patients with PD parallel changes that are seen in individuals that consume a Western diet, and are opposite to those that adhere to a Mediterranean diet. In this review, we first examine the role of prominent food groups on dopamine bioavailability, how they modulate the composition and function of the gut microbiota and the subsequent effects on PD and obesity pathophysiology. We then highlight evidence on how microbiota transplant and weight loss surgery can be used as therapeutic tools to restore dopaminergic deficits through optimizing gut microbial composition. In the process, we revisit dietary metabolites and their role in therapeutic approaches involving dopaminergic pathways. Overall, understanding the role of nutrition on dopamine bioavailability and gut microbiota in dopamine-related pathologies such as PD will help develop more precise therapeutic targets to rescue dopaminergic deficits in neurologic and metabolic disorders

Probiotics: How Effective Are They in the Fight against Obesity?

Obesity has been associated with structural and functional changes in the gut microbiota. The abundance in, and diversity of, certain bacteria may favor energy harvest and metabolic pathways leading to obesity. Therefore, gut microbiota has become a potential target that can be manipulated to obtain optimal health. Probiotics have been shown to influence the composition of the gut microbiota, improve gut integrity, and restore the microbial shifts characteristic of obesity. Based on physical and biochemical parameters, metabolic and inflammatory markers, and alterations in gut microbe diversity, animal studies revealed beneficial results in obese models whereas the results in humans are sparse and inconsistent. Thus, the purpose of this review is to present evidence from animal studies and human clinical trials demonstrating the effects of various probiotic strains and their potential efficacy in improving obesity and associated metabolic dysfunctions. Furthermore, the review discusses current gaps in our understanding of how probiotics modulate gut microflora to protect against obesity. Finally, we propose future studies and methodological approaches that may shed light on the challenges facing the scientific community in deciphering the host&#8315;bacteria interaction in obesity

A Conservative Replacement in the Transmembrane Domain of SARS-CoV-2 ORF7a as a Putative Risk Factor in COVID-19

The ongoing COVID-19 pandemic follows an unpredictable evolution, driven by both host-related factors such as mobility, vaccination status, and comorbidities and by pathogen-related ones. The pathogenicity of its causative agent, SARS-CoV-2 virus, relates to the functions of the proteins synthesized intracellularly, as guided by viral RNA. These functions are constantly altered through mutations resulting in increased virulence, infectivity, and antibody-evasion abilities. Well-characterized mutations in the spike protein, such as D614G, N439K, Δ69–70, E484K, or N501Y, are currently defining specific variants; however, some less studied mutations outside the spike region, such as p. 3691 in NSP6, p. 9659 in ORF-10, 8782C > T in ORF-1ab, or 28144T > C in ORF-8, have been proposed for altering SARS-CoV-2 virulence and pathogenicity. Therefore, in this study, we focused on A105V mutation of SARS-CoV-2 ORF7a accessory protein, which has been associated with severe COVID-19 clinical manifestation. Molecular dynamics and computational structural analyses revealed that this mutation differentially alters ORF7a dynamics, suggesting a gain-of-function role that may explain its role in the severe form of COVID-19 disease