Psychological Effects Of Patient Surge In: Fill & Download for Free

GET FORM

Download the form

The Guide of finalizing Psychological Effects Of Patient Surge In Online

If you are looking about Tailorize and create a Psychological Effects Of Patient Surge In, here are the simple ways you need to follow:

  • Hit the "Get Form" Button on this page.
  • Wait in a petient way for the upload of your Psychological Effects Of Patient Surge In.
  • You can erase, text, sign or highlight through your choice.
  • Click "Download" to preserver the documents.
Get Form

Download the form

A Revolutionary Tool to Edit and Create Psychological Effects Of Patient Surge In

Edit or Convert Your Psychological Effects Of Patient Surge In in Minutes

Get Form

Download the form

How to Easily Edit Psychological Effects Of Patient Surge In Online

CocoDoc has made it easier for people to Fill their important documents via the online platform. They can easily Tailorize through their choices. To know the process of editing PDF document or application across the online platform, you need to follow these simple ways:

  • Open CocoDoc's website on their device's browser.
  • Hit "Edit PDF Online" button and Import the PDF file from the device without even logging in through an account.
  • Edit the PDF online by using this toolbar.
  • Once done, they can save the document from the platform.
  • Once the document is edited using online browser, you can download or share the file as you need. CocoDoc promises friendly environment for implementing the PDF documents.

How to Edit and Download Psychological Effects Of Patient Surge In on Windows

Windows users are very common throughout the world. They have met lots of applications that have offered them services in modifying PDF documents. However, they have always missed an important feature within these applications. CocoDoc aims at provide Windows users the ultimate experience of editing their documents across their online interface.

The steps of modifying a PDF document with CocoDoc is simple. You need to follow these steps.

  • Pick and Install CocoDoc from your Windows Store.
  • Open the software to Select the PDF file from your Windows device and go ahead editing the document.
  • Fill the PDF file with the appropriate toolkit presented at CocoDoc.
  • Over completion, Hit "Download" to conserve the changes.

A Guide of Editing Psychological Effects Of Patient Surge In on Mac

CocoDoc has brought an impressive solution for people who own a Mac. It has allowed them to have their documents edited quickly. Mac users can make a PDF fillable with the help of the online platform provided by CocoDoc.

To understand the process of editing a form with CocoDoc, you should look across the steps presented as follows:

  • Install CocoDoc on you Mac in the beginning.
  • Once the tool is opened, the user can upload their PDF file from the Mac hasslefree.
  • Drag and Drop the file, or choose file by mouse-clicking "Choose File" button and start editing.
  • save the file on your device.

Mac users can export their resulting files in various ways. They can download it across devices, add it to cloud storage and even share it with others via email. They are provided with the opportunity of editting file through various methods without downloading any tool within their device.

A Guide of Editing Psychological Effects Of Patient Surge In on G Suite

Google Workplace is a powerful platform that has connected officials of a single workplace in a unique manner. If users want to share file across the platform, they are interconnected in covering all major tasks that can be carried out within a physical workplace.

follow the steps to eidt Psychological Effects Of Patient Surge In on G Suite

  • move toward Google Workspace Marketplace and Install CocoDoc add-on.
  • Attach the file and Press "Open with" in Google Drive.
  • Moving forward to edit the document with the CocoDoc present in the PDF editing window.
  • When the file is edited ultimately, download it through the platform.

PDF Editor FAQ

What are the psychological consequences of not having children?

I’m 54 and have no children. I never felt a great pull to have them—except in my late 30s when I was shot through with baby-fever for a couple of years, but the feeling disappeared as suddenly as it arrived.After spending most of my life neutral about kids, I’m suddenly kid-crazy. Maybe now that there is no risk of my getting pregnant, my biology has given my psyche a green light to enjoy children like never before.And, lucky me, my husband and I moved to China only a few years after the end of the One Child policy, meaning there are babies everywhere. It’s so fun to fawn over all the cuties. The language barrier becomes a non-issue; everyone loves it when you love on their kids.My maternal instincts are also blooming because of my relationship with our teaching assistant. She was assigned to help us with everything from buying needed items to figuring out how to get around the city. We’ve spent hours with her, constantly amazed at her ability to translate, solve problems, and remain upbeat. Soon we were attending her dance performances and helping her with her homework.A strong feeling coursed through me as she danced on stage or practiced a speech in front us. I realized the feeling was this: I adored her and was proud of her. The feelings seemed a little out of proportion, since we’d known each other only a few months, but they surged every time I saw her.Once she saw me across campus and came running up and threw herself into my arms, and I felt what I can only describe as motherly.After her bike was stolen, we bought her one for her birthday and took her out to lunch. At the restaurant, she launched into what seemed to be a prepared speech about how much we mean to her.She had barely begun when tears started streaming down my face. She thanked us for being friendly and patient. She recounted fun experiences we’ve had and said, “You have taught me things about life.” She recalled when we went to the bank one day and it was so crowded that we decided to leave and come back another time. You said when things are ‘chaos’”—she remembered learning that word from my husband—“that it’s better to go away and do something else.”She also said she has learned from us how to appreciate small things in life. She was especially touched when one day I told someone she was like our daughter in China.Now I understand how parents feel when their kids come home for the holidays. I’m always happy to see her and spend time with her. During the semester break, we are going to travel together.Just when I thought these feelings might be an anomaly, my 17-year-old nephew sent me the manuscript of a novel he wrote. I was only a few pages in, reading it aloud to my husband, when I burst out in tears.His writing is good. Really good. And the narrator is a loving, observant, smart young man whose philosophy of life deeply resonates with me. For instance, after one dicey adventure in the book, the narrator says, “No longer did I fear death; I feared that I wouldn’t truly live.”We’ve messaged back and forth about the book. As a writer, writing coach and aunt, I am thrilled to be having these conversations with him. I still remember once when he was little he’d said to me, “You know what I love? Big fat books.” And now he’s doing what he loves. He’s become the other writer in the family.When people called me “childless,” I used to say, no, I was “child-free.” But now, I’m not so sure. Children, from babies to young adults, are touching my life. And I’m touching theirs.I know it’s not the same as having raised a child, but these kinds of connections are somehow creating a legacy. So perhaps we don't have to worry about negative psychological consequences of not having children when there are children everywhere ready to be part of our lives.

Why do so many doctors ignore the impact of nutrition on chronic illnesses, and even cancer, when there is so much evidence to prove that diet has a direct effect on health and curing disease?

We simply don't have enough time to do our job and teach nutrition; we can't cover every single aspect of the patient's wellbeing on our own.Allow me to clarify:Teaching nutrition isn't a five-minute thing, and even five minutes is about half the time an average doctor is able to spend on a patient on a busy day.Teaching good habits to somebody who has bad habits is even more demanding.Doctors can't cover every aspect of one's wellbeing: Other factors, like one's financial situation or their psychological wellbeing also contribute to their disease status, as much as we'd like to tackle these as well, we can't do everything on our own. Therefore:A modern doctor will need to be more of a manager of your healthcare and refer you to the appropriate specialists that will treat problems secondary to the main issue he'll treat you for. Just like an electrician won't come to your place and unexpectedly spend a bunch of hours soldering that cable box you just surged while other people are waiting further up his journey.The good news:Depending on specialty, most doctors do keep track of nutrition and will refer to nutrition specialists and to a certain extent they will certainly give advice themselves, but nutrition is a day-to-day habit you need to discuss in a certain amount of detail to reach any real result.It's not a black or white thing you can just ask and run through in your ten minute consultation with a chronic patient.A bad habit like smoking or how many drinks one has in a week is something you can tackle instantly with a straightforward address: "You need to stop smoking. You failed? Here's a good counselor." or "Try to drink less. Keep drinking too much? We need to do something about that, here's a book/support group that might help."Bad diet, in contrast, is not something you cannot simply address with a short "eat healty!"Where I work, we have a weight center and a large group of well-qualified dietary consultants that speak to a large amount of patients that will all benefit from this.As we start to realize the benefits of preventive medicine, I trust this aspect will get more and more of the well-deserved attention it needs in a sadly increasingly unhealthy eating society.

What is the role of bacteria in the gut?

Simpler question is what isn't. Gut bacteria influence our entire physiology from the basic such as what and how much we eat to the synthesis of essential vitamins, from our immune function and metabolism to even our mood. The study of microbiota, much of it mouse model data, has exploded over the past decade. Instead, I specifically highlight human data from peer-reviewed scientific studies.Antibiotic usage, diet, hygiene and lifestyle shape our microbiota, particularly gut microbiota. In turn, they shape our immune and metabolic function.From 1Let's start from first principles. Food. How do microbes control our eating behavior?From 2. I highlight human data in purple.They influence our reward pathway. After all, our enteric (gut-associated) nervous system is the major source of dopamine and serotonin (3, 4).They modulate our taste perception (5).They play on our vagus nerve as a musician plays his instrument (6, 7). What's the importance of the vagus nerve? It's the main nerve communication between our gut and brain.Our gut microbiota is exquisitely adapted to our diet.a) One of the most compelling examples is of a gut bacterium found in the Japanese. Bacteroides plebeius has a horizontally transferred gene from the marine bacterium Zobellia galactanivorans that gives it the capacity to digest seaweed polysaccharides (8). In fact, human-associated bacteria have a 25-fold higher rate of gene transfer compared to bacteria in other environments (9), implying host-microbe association imposes stringent selection pressures on our microbiota.b) Obese have altered gut microbiota with reduced diversity and greater variability (10, 11, 12, 13).c) US population microbiome appears adapted for a high-fat, high-protein diet while that of people living in rural Malawi and the Amazonas in Venezuela for breaking down complex carbohydrates (14).Gut microbes influence every aspect of our physiologyWhat about the rest of our body functions? Even surprising ones such as metabolism and behavior are profoundly influenced by our microbiota.From 15Our metabolome refers to the variety of metabolites present in our blood circulation. About a third of our metabolome is estimated to be of microbial origin. Using our circulation system as their communication network, animal model studies show that our microbial products can reach every part of our body (16, 17, 18), and influence the metabolism and physiology of distant organs and each other. For example, people with symptomatic atherosclerosis have altered gut microbiota (19). A potential mechanism by which our gut microbes could jeopardize cardiovascular health is through conversion of dietary phosphatidylcholine into the proatherosclerotic metabolite, trimethylamine (20), a result that needs to be independently verified.Possible Gut-Brain communication mechanismsFrom 21Short-chain fatty acids (SCFA). Colonic gut microbes digest dietary carbohydrates to generate SCFA such as acetate, butyrate and propionate (22). Signaling through G protein coupled receptors such as (GPRs), GPR41 and GPR43, SCFA induce colonic motility, regulate appetite (23) and even suppress colon cancer (24) in human colon cancer cell lines. While colon cells (colonocytes) use butyrate as an energy source, acetate and propionate enter the blood stream and thence to other organs (25, 26). These SCFAs can stimulate the sympathetic nervous system (27).Gut microbiota can also modulate neurotransmitters within the gut. This includes acetylcholine, gamma-aminobutyric acid, histamines, melatonin and serotonin. Gut microbes can express and secrete neuropeptide-like molecules that could influence behavior and emotion (28, 29).Tryptophan is an essential amino acid we only get from our diet (30), and is the precursor of serotonin (31), most of it synthesized by our gut enterochromaffin cells and enteric nerves (32, 33, 34).Gut microbes synthesize vitamins essential for nervous system function. For example, Lactobacillus reuteri is a major source of Vitamin B12 or cobalamin (35), a vitamin important for the development of the nervous system (36).GI diseases and psychiatric comorbiditiesCause and effect or correlation?While that's still debatable, up to 80% of patients with GI diseases (IBS, Irritable Bowel Syndrome; IBD, Inflammatory Bowel Disease) also have psychiatric illnesses such as depression and anxiety (37, 38, 39). Changes in psychological activities are seen both before and after diagnosis of IBD.Serum cortisol, a marker of elevated anxiety, was reduced in patients who consumed probiotics, Lactobacillus helveticus and Bifidobacterium longum (40) while healthy subjects showed significantly less psychological distress compared to the placebo group in a double- blind, placebo-controlled, randomized parallel group clinical trial with the same probiotic mixture for 30 days (41).Treatment with a probiotic- containing milk drink resulted in improved mood and cognition in healthy subjects when compared to the placebo group (42).There are signs of cognitive impairment in IBS patients (43).After 4 weeks of treatment with a fermented milk product with probiotics, healthy women volunteers performed a specific cognition test faster (44). Analysis of their brain function indicated specific uptick in activity in regions innervated by serotonergic nerves.Neuroimaging studies suggest abnormal brain function in GI disorders. This includes thinning of the anterior cingulate and insular cortex, and increased activation of the thalamus, anterior cingulate and prefrontal cortex of IBS patients (45, 46).Lactobacillus and Clostridium species are reduced in stool samples from IBS patients (47, 48).Deconstructing our Gut microbe-Brain connectionHow to infer a connection between our gut microbiota and brain? We could if specifically targeting microbes affected our brain and/or behavior. Antibiotics directly and specifically target microbes. If antibiotic therapy also resulted in any change in brain function and/or behavior, it could be inferred as evidence of microbe-brain connection. As a direct effect, gut microbes synthesize vitamins essential for brain function.Hepatic EncephalopathyIn the first stages of liver disease, cirrhosis, the liver compensates to perform its functions. In later stages, it can no longer compensate. At this stage, there is attendant encephalopathy (degeneration of brain function). Several lines of evidence suggest a link between gut microbiota disturbance (dysbiosis), liver disease and brain function.Oral antibiotics can reverse encephalopathy in decompensated liver disease patients (49, 50, 51)Compared to healthy controls, encephalopathic cirrhosis patients have altered gut microflora (52, 53).In particular, reduced Alcaligenaceae and Porphyromonadaceae and increased Enterococcus, Megasphaera and Burkholderia correlate with poor cognition and increased inflammation in encephalopathic patients with cirrhosis and cognitive dysfunction (54, 55).AutismMost children with Autism often experience a range of GI problems (56).Disease onset usually follows antimicrobial use in a high percentage of late-onset Autism (18–24 mo of age) children having a history of extensive antibiotic use. One study observed a 10-fold increase in certain clusters of Clostridium spp in stool samples from Autistic children compared with healthy controls. The authors speculated that exposure to trimethoprim/ sulfamethoxazole rather than exposure to other antibiotics could be linked to the diagnosis of late-onset Autism since the former are not effective against Clostridium spp, while oral vancomycin specifically targets Gram positive organisms which include Clostridium spp (57). Increased clostridial species in stool samples of Autistic patients was confirmed by another study (58). Indeed, oral vancomycin treatment showed a decrease in Autistic symptoms, while relapse occurred following cessation of treatment (59).Clostridia spores are also implicated in the high rates of Autism seen among siblings (60).Real time qPCR (61) and culture-based microbiota (57) profiling techniques suggest that alteration in microbiota may contribute to disease phenotype.Intestinal biopsy of late-onset Autism spectrum disorder (ASD) patients revealed reductions in Bifidobacterium spp. and the mucolytic bacterium Akkermansia mucini­phila (62).Late-onset Autism patients have marked reduction in Bacteroides and Prevotella species and increase in Sutterella species compared to controls (63, 64, 65, 66).At least one study refutes differences in gut microbiota between Autistic patients and controls (67). Possible reasons for the different result could be they used a different approach for taking samples and used a different technique for microbiome analysis.Altered expression in the ileum of carbohydrate transporters such as hexoses and for enzymes such as disaccharidases suggest a role for carbohydrate malabsorption in Autism (68).Urine and fecal sample metabolites are different in Autism patients (69, 70, 71, 72).Casein- and gluten-free diets are reported to improve behavior of patients with Autism (73, 74, 75).Problems with many Autism-GI disorder association studiesThey study different types of populations (possibly different diseases).Population sizes differ considerably between studies.Different studies use different controls.Do not control for the unique diets of the patients. Diet itself could be a reason for different gut microbe distribution in patients compared to controls.A better controlled and more comprehensive US study (76) examined 589 patients with a history of familial ASD and their unaffected sibling controls. Separating 'Full' from 'Spectrum', they reported constipation (20%) and chronic diarrhea (19%) as the most common symptoms among those with 'Full' Autism. Another study of >140000 ASD patients showed higher prevalence of IBD (0.83% vs 0.54%) and other bowel disorders (11.74% vs 4.5%) compared to hospitalized controls (77).This comprehensive table summarizes findings from various Autism-GI disorder association studiesFrom 78Antibiotic associated behavior changesSometimes antibiotics are associated with behavioral changes spanning insomnia, mood alteration (79, 80), to mania, particularly in elderly patients, ('antibomania') (81).BibliographySommer, Felix, and Fredrik Bäckhed. "The gut microbiota—masters of host development and physiology." Nature Reviews Microbiology 11.4 (2013): 227-238. Page on hmphanmi.com.cnAlcock, Joe, Carlo C. Maley, and C. Aktipis. "Is eating behavior manipulated by the gastrointestinal microbiota? Evolutionary pressures and potential mechanisms." Bioessays 36.10 (2014): 940-949. Is eating behavior manipulated by the gastrointestinal microbiota? Evolutionary pressures and potential mechanismsEisenhofer G, Aneman A, Friberg P, Hooper D, et al. 1997. Substantial production of dopamine in the human gastrointestinal tract. J Clin Endocrinol Metab 82: 3864–71.Kim DY, Camilleri M. 2000. Serotonin: a mediator of the brain-gut connection. Am J Gastroenterol 95: 2698–709.Miras AD, le Roux CW. 2013. Mechanisms underlying weight loss after bariatric surgery. Nat Rev Gastroenterol Hepatol 10: 575–84.Camilleri M, Toouli J, Herrera MF, Kulseng B, et al. 2008. Intra- abdominal vagal blocking (VBLOC therapy): clinical results with a new implantable medical device. Surgery 143: 723–31. Page on vblocmaestro.comSarr MG, Billington CJ, Brancatisano R, Brancatisano A, et al. 2012. The EMPOWER study: randomized, prospective, double-blind, multi- center trial of vagal blockade to induce weight loss in morbid obesity. Obes Surg 22: 1771–82.Hehemann JH, et al. (2010) Transfer of carbohydrate-active enzymes from marine bacteria to Japanese gut microbiota. Nature 464(7290):908–912.Smillie CS, et al. (2011) Ecology drives a global network of gene exchange connecting the human microbiome. Nature 480(7376): 241–244. Page on unal.edu.coLey, R. E. et al. Obesity alters gut microbial ecology. Proc. Natl Acad. Sci. USA 102, 11070–11075 (2005). Obesity alters gut microbial ecologyTurnbaugh, P. J. et al. A core gut microbiome in obese and lean twins. Nature 457, 480–484 (2009). A core gut microbiome in obese and lean twinsLey, R. E., Turnbaugh, P. J., Klein, S. & Gordon, J. I. Microbial ecology: human gut microbes associated with obesity. Nature 444, 1022–1023 (2006)).Holmes, Ian, Keith Harris, and Christopher Quince. "Dirichlet multinomial mixtures: generative models for microbial metagenomics." PLoS One 7.2 (2012): e30126 Dirichlet Multinomial Mixtures: Generative Models for Microbial MetagenomicsYatsunenko T, et al. (2012) Human gut microbiome viewed across age and geography. Nature 486(7402):222–227. Human gut microbiome viewed across age and geographyMcFall-Ngai, Margaret, et al. "Animals in a bacterial world, a new imperative for the life sciences." Proceedings of the National Academy of Sciences 110.9 (2013): 3229-3236. Animals in a bacterial world, a new imperative for the life sciencesNicholson JK, et al. (2012) Host-gut microbiota metabolic interactions. Science 336(6086):1262–1267. Page on uncg.eduSwann JR, et al. (2011) Systemic gut microbial modulation of bile acid metabolism in host tissue compartments. Proc Natl Acad Sci USA 108(Suppl 1):4523–4530. Systemic gut microbial modulation of bile acid metabolism in host tissue compartmentsWikoff WR, et al. (2009) Metabolomics analysis reveals large effects of gut microflora on mammalian blood metabolites. Proc Natl Acad Sci USA 106(10):3698–3703. Metabolomics analysis reveals large effects of gut microflora on mammalian blood metabolitesKarlsson, F. H. et al. Symptomatic atherosclerosis is associated with an altered gut metagenome. Nature Commun. 3, 1245 (2012). Page on www.gu.seWang Z, et al. (2011) Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature 472(7341):57–63. Page on keckmedicineofusc.orgPetschow, Bryon, et al. "Probiotics, prebiotics, and the host microbiome: the science of translation." Annals of the New York Academy of Sciences 1306.1 (2013): 1-17. Page on www.ucl.beRoy CC, Kien CL, Bouthillier L, Levy E. Short-chain fatty acids: ready for prime time? Nutr Clin Pract 2006; 21:351-66; PMID:16870803; Page on doi.org 77/0115426506021004351.Sleeth ML, Thompson EL, Ford HE, Zac-Varghese SE, Frost G. Free fatty acid receptor 2 and nutrient sensing: a proposed role for fibre, fermentable carbohydrates and short-chain fatty acids in appetite regulation. Nutr Res Rev 2010; 23:135-45. Page on researchgate.netTang Y, Chen Y, Jiang H, Robbins GT, Nie D. G-protein-coupled receptor for short-chain fatty acids suppresses colon cancer. Int J Cancer 2011; 128:847- 56. G-protein-coupled receptor for short-chain fatty acids suppresses colon cancerWolever TMS, Spadafora P, Eshuis H. Interaction between colonic acetate and propionate in humans. Am J Clin Nutr 1991; 53:681-7. Page on nutrition.orgScheppach W. Effects of short chain fatty acids on gut morphology and function. Gut 1994; 35(Suppl):S35-8. Page on bmj.comKimura I, Inoue D, Maeda T, Hara T, Ichimura A, Miyauchi S, et al. Short-chain fatty acids and ketones directly regulate sympathetic nervous system via G protein-coupled receptor 41 (GPR41). Proc Natl Acad Sci USA 2011; 108:8030-5. Short-chain fatty acids and ketones directly regulate sympathetic nervous system via G protein-coupled receptor 41 (GPR41)Tsavkelova E, Klimova SY, Cherdyntseva T, Netrusov A. 2006. Hormones and hormone-like substances of microorganisms: a review. Appl Biochem Microbiol 42: 229–35. Page on bioon.com.cnFetissov SO, Déchelotte P. The new link between gut-brain axis and neuropsychiatric disorders. Curr Opin Clin Nutr Metab Care 2011; 14:477- 82.Le Floc’h N, Otten W, Merlot E. Tryptophan metabolism, from nutrition to potential therapeutic applications. Amino Acids 2011;41:1195–205.Ruddick JP, Evans AK, Nutt DJ, Lightman SL, Rook GA, Lowry CA. Tryptophan metabolism in the central nervous system: medical implications. Expert Rev Mol Med 2006;8:1–27.Mawe GM, Hoffman JM. Serotonin signalling in the gut–functions, dysfunctions and therapeutic targets. Nature Rev 2013;10:473–86. Serotonin Signaling in the Gastrointestinal Tract:Spiller R. Serotonin and GI clinical disorders. Neuropharmacology 2008;55:1072–80.Gershon MD. 5-Hydroxytryptamine (serotonin) in the gastrointestinal tract. Curr Opin Endocrinol Diabetes Obesity 2013;20:14–21. 5-Hydroxytryptamine (serotonin) in the gastrointestinal tractSantos F, Wegkamp A, de Vos WM, Smid EJ, Hugenholtz J. High-Level folate production in fermented foods by the B12 producer Lactobacillus reuteri JCM1112. Appl Environ Microbiol 2008; 74:3291- 4. High-Level Folate Production in Fermented Foods by the B12 Producer Lactobacillus reuteri JCM1112Dror DK, Allen LH. Effect of vitamin B12 deficiency on neurodevelopment in infants: current knowledge and possible mechanisms. Nutr Rev 2008; 66:250-5.Whitehead WE, Palsson O, Jones KR. Systematic review of the comorbidity of irritable bowel syndrome with other disorders: what are the causes and implications? Gastroenterology 2002; 122:1140- 56.Garakani A, Win T, Virk S, Gupta S, Kaplan D, Masand PS. Comorbidity of irritable bowel syndrome in psychiatric patients: a review. Am J Ther 2003; 10:61-7.Bonaz, B.L., Bernstein, C.N., 2013. Brain–gut interactions in inflammatory bowel disease. Gastroenterology 144, 36–49. Page on hal.inserm.frMessaoudi M, Lalonde R, Violle N, Javelot H, Desor D, Nejdi A, et al. Assessment of psychotropic-like properties of a probiotic formulation (Lactobacillus helveticus R0052 and Bifidobacterium longum R0175) in rats and human subjects. Br J Nutr 2011; 105:755- 64. Page on drperlmutter.comMessaoudi M, Violle N, Bisson JF, Desor D, Javelot H, Rougeot C. Beneficial psychological effects of a probiotic formulation (Lactobacillus helveticus R0052 and Bifidobacterium longum R0175) in healthy human volunteers. Gut Microbes 2011; 2:256-61. Page on tandfonline.comBenton D, Williams C, Brown A (2007) Impact of consuming a milk drink containing a probiotic on mood and cognition. Eur J Clin Nutr 61(3):355–361. Page on researchgate.netKennedy PJ, Clarke G, O’Neill A, Groeger JA, Quigley EM, Shanahan F, et al. Cognitive performance in irritable bowel syndrome: evidence of a stress-related impairment in visuospatial memory. Psychol Med 2013:1–14. Cognitive performance in irritable bowel syndrome: evidence of a stress-related impairment in visuospatial memoryTillisch K et al (2013) Consumption of fermented milk product with probiotic modulates brain activity. Gastroenterology 144:1394–1401. Consumption of Fermented Milk Product With Probiotic Modulates Brain ActivityDavis KD et al (2008) Cortical thinning in IBS: implications for homeostatic, attention, and pain processing. Neurology 70(2):153–154.Ellingson BM et al (2013) Diffusion tensor imaging detects microstructural reorganization in the brain associated with chronic irritable bowel syndrome. Pain 154(9):1528–1541. http://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC3758125&blobtype=pdfKassinen, A., Krogius-Kurikka, L., Makivuokko, H., Rinttila, T., Paulin, L., Corander, J., Malinen, E., Apajalahti, J., Palva, A., 2007. The fecal microbiota of irritable bowel syndrome patients differs significantly from that of healthy subjects. Gastroenterology 133, 24–33. Page on researchgate.netMalinen, E., Rinttila, T., Kajander, K., Matto, J., Kassinen, A., Krogius, L., Saarela, M., Korpela, R., Palva, A., 2005. Analysis of the fecal microbiota of irritable bowel syndrome patients and healthy controls with real-time PCR. Am. J. Gastroenterol. 100, 373–382.Schiano, T. D. Treatment options for hepatic encephalopathy. Pharmacotherapy 30, S16–S21 (2010)).Morgan MY. The treatment of chronic hepatic encephalopathy. Hepatogastroenterology 1991; 38:377-87.Morgan MY, Blei A, Grüngreiff K, Jalan R, Kircheis G, Marchesini G, et al. The treatment of hepatic encephalopathy. Metab Brain Dis 2007; 22:389-405.Bajaj, J.S., Gillevet, P.M., Patel, N.R., Ahluwalia, V., Ridlon, J.M., Kettenmann, B., Schubert, C.M., Sikaroodi, M., Heuman, D.M., Crossey, M.M., Bell, D.E., Hylemon, P.B., Fatouros, P.P., Taylor-Robinson, S.D., 2012a. A longitudinal systems biology analysis of lactulose withdrawal in hepatic encephalopathy. Metab. Brain Dis. 27, 205–215.Bajaj, J. S. et al. Linkage of gut microbiome with cognition in hepatic encephalopathy. Am. J. Physiol. Gastrointest. Liver Physiol. 302, G168–G175 (2012). Page on physiology.orgBajaj, J.S., Hylemon, P.B., Ridlon, J.M., Heuman, D.M., Daita, K., White, M.B., Monteith, P., Noble, N.A., Sikaroodi, M., Gillevet, P.M., 2012b. Colonic mucosal microbiome differs from stool microbiome in cirrhosis and hepatic encephalopathy and is linked to cognition and inflammation. Am. J. physiol. Gastrointest. Liver Physiol. 303, G675–G685. Page on physiology.orgCollins, Stephen M., Michael Surette, and Premysl Bercik. "The interplay between the intestinal microbiota and the brain." Nature Reviews Microbiology 10.11 (2012): 735-742.Coury DL, Ashwood P, Fasano A, Fuchs G, et al.2012.Gastrointestinal conditions in children with autism spectrum disorder: developing a research agenda. Pediatrics 130: S160–8. Page on www.aipro.infoFinegold SM, Molitoris D, Song Y, Liu C, Vaisanen ML, Bolte E, et al. Gastrointestinal microflora studies in late-onset autism. Clin Infect Dis 2002; 35(Suppl 1):S6-16. Page on bacteriaandautism.comParracho, H.M., Bingham, M.O., Gibson, G.R., McCartney, A.L., 2005. Differences between the gut microflora of children with autistic spectrum disorders and that of healthy children. J. Med. Microbiol. 54, 987–991. Page on ncims.comSandler RH, Finegold SM, Bolte ER, Buchanan CP, Maxwell AP, Väisänen ML, et al. Short-term benefit from oral vancomycin treatment of regressive-onset autism. J Child Neurol 2000; 15:429-35. PMID:10921511; Short-Term Benefit From Oral Vancomycin Treatment of Regressive-Onset Autism.Finegold SM. Therapy and epidemiology of autism- -clostridial spores as key elements. Med Hypotheses 2008; 70:508-11. Page on bacteriaandautism.comSong Y, Liu C, Finegold SM. Real-time PCR quantitation of clostridia in feces of autistic children. Appl Environ Microbiol 2004; 70:6459-65. Real-Time PCR Quantitation of Clostridia in Feces of Autistic ChildrenWang, L. et al. Low relative abundances of the mucolytic bacterium Akkermansia muciniphila and Bifidobacterium spp. in feces of children with autism. Appl. Environ. Microbiol. 77, 6718–6721 (2011). Low Relative Abundances of the Mucolytic Bacterium Akkermansia muciniphila and Bifidobacterium spp. in Feces of Children with AutismWilliams, B. L., Hornig, M., Parekh, T. & Lipkin, W. I. Application of novel PCR‐based methods for detection, quantitation, and phylogenetic characterization of Sutterella species in intestinal biopsy samples from children with autism and gastrointestinal disturbances. MBio 3, e00261–e00211 (2012). Application of Novel PCR-Based Methods for Detection, Quantitation, and Phylogenetic Characterization of Sutterella Species in Intestinal Biopsy Samples from Children with Autism and Gastrointestinal DisturbancesAdams, J.B., Johansen, L.J., Powell, L.D., Quig, D., Rubin, R.A., 2011. Gastrointestinal flora and gastrointestinal status in children with autism–comparisons to typical children and correlation with autism severity. BMC Gastroenterol. 11, 22. Page on biomedcentral.comKang, D.W., Park, J.G., Ilhan, Z.E., Wallstrom, G., Labaer, J., Adams, J.B., Krajmalnik- Brown, R., 2013. Reduced incidence of prevotella and other fermenters in intestinal microflora of autistic children. PLoS One 8, e68322. Page on plosone.orgWang, L., Christophersen, C.T., Sorich, M.J., Gerber, J.P., Angley, M.T., Conlon, M.A., 2013. Increased abundance of Sutterella spp. and Ruminococcus torques in feces of children with autism spectrum disorder. Mol. Autism 4, 42. Page on biomedcentral.comGondalia, S.V., Palombo, E.A., Knowles, S.R., Cox, S.B., Meyer, D., Austin, D.W., 2012. Molecular characterisation of gastrointestinal microbiota of children with autism (with and without gastrointestinal dysfunction) and their neurotypical siblings. Autism Res. 5, 419–427. Page on researchgate.netWilliams, B. L. et al. Impaired carbohydrate digestion and transport and mucosal dysbiosis in the intestines of children with autism and gastrointestinal disturbances. PLoS ONE 6, e24585 (2011). Page on plosone.orgMing, X., Stein, T.P., Barnes, V., Rhodes, N., Guo, L., 2012. Metabolic perturbance in autism spectrum disorders: a metabolomics study. J. Proteome Res. 11, 5856– 5862.Wang, L., Christophersen, C.T., Sorich, M.J., Gerber, J.P., Angley, M.T., Conlon, M.A., 2012. Elevated fecal short chain fatty acid and ammonia concentrations in children with autism spectrum disorder. Dig. Dis. Sci. 57, 2096–2102. Page on researchgate.netYap, I.K., Angley, M., Veselkov, K.A., Holmes, E., Lindon, J.C., Nicholson, J.K., 2010. Urinary metabolic phenotyping differentiates children with autism from their unaffected siblings and age-matched controls. J. Proteome Res. 9, 2996–3004. Page on psu.eduDe Angelis M, Piccolo M, Vannini L, Siragusa S, De GA, Serrazzanetti DI, Cristofori F, Guerzoni ME, Gobbetti M & Francavilla R. (2013). Fecal microbiota and metabolome of children with autism and pervasive developmental disorder not otherwise specified. PLoSOne 8, e76993. http://www.plosone.org/article/fetchObject.action?uri=info:doi/10.1371/journal.pone.0076993&representation=PDFPennesi CM, Klein LC. Effectiveness of the gluten-free, casein-free diet for children diagnosed with autism spectrum disorder: based on parental report. Nutr Neurosci 2012;15: 85–91. Page on yimg.comKnivsberg AM, Reichelt KL, Hoien T, Nodland M. A randomised, controlled study of dietary intervention in autistic syndromes. Nutr Neurosci 2002;5:251–61. Page on researchgate.netWhiteley P, Haracopos D, Knivsberg AM, et al. The ScanBrit randomised, controlled, single-blind study of a gluten- and casein-free dietary intervention for children with autism spectrum disorders. Nutr Neurosci 2010;13:87–100. Page on www.mjrigtigkost.dkWang LW, Tancredi DJ, Thomas DW. 2011. The prevalence of gastrointestinal problems in children across the United States with autism spectrum disorders from families with multiple affected members. J Dev Behav Pediatr 32: 351–60.Kohane IS, McMurry A, Weber G, et al. The co-morbidity burden of children and young adults with autism spectrum disorders. PLoS One 2012;7:e33224. Page on plosone.orgMayer, Emeran A., David Padua, and Kirsten Tillisch. "Altered brain‐gut axis in autism: Comorbidity or causative mechanisms?." Bioessays 36.10 (2014): 933-939.Sternbach H & State R. (1997). Antibiotics: neuropsychiatric effects and psychotropic interactions. HarvRevPsychiatry 5, 214-226.Mehdi S. (2010). Antibiotic-induced psychosis: a link to D-alanine?. MedHypotheses 75, 676- 677.Abouesh, A., Stone, C. & Hobbs, W. R. Antimicrobial‐ induced mania (antibiomania): a review of spontaneous reports. J. Clin. Psychopharmacol. 22, 71–81 (2002).Thanks for the A2A, Vanessa Surian.

Why Do Our Customer Attach Us

It is super easy to use as it supports multiple languages and is best for requesting, tracking and reminding the responsible user/s to e-sign the documents or files which binds the various parties legally.

Justin Miller