Category: Gastrointestinal

Categories : GastrointestinalTags :

Unusual Sympathetic Nervous Activity in IBS Patients

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Photo by Andrea Piacquadio on Pexels

Using a wearable device to record nerve activity, researchers in Japan have discovered that the sympathetic nervous system of patients with irritable bowel syndrome (IBS) activated a few minutes before defecation, and persisted for a few minutes afterwards. Their results are published in the journal PLoS ONE.

Irritable bowel syndrome (IBS) is a difficult disease to treat, characterised by chronic abdominal pain related to bowel movements, of which there are four types: diarrhoeal, constipation, mixed, and unclassifiable. Patients with IBS report a reduction in quality of life and experiences of social discomfort, as they are forced to restrict their activity, such as work or travel, because of the sudden and unpredictable need to use the toilet. While there have been studies of IBS-related abnormalities in the autonomic nervous system based on 24-hour electrocardiogram measurement, until now none of them examined changes in the autonomic nervous system during bowel movements.

Associate Professor Fumio Tanaka and his research group at the Osaka Metropolitan University Graduate School of Medicine recorded the autonomic nervous system activity of IBS patients and healthy subjects using a wearable device and tracked activities such as defecation and sleep. As a result, they found that unlike healthy subjects, the sympathetic nervous system of IBS patients was activated two minutes before defecation and persisted until 9 minutes after defecation. Furthermore, the activation of the sympathetic nervous system was found to be associated with greater abdominal pain and lower quality of life.

“This research is characterised by the fact that autonomic nervous system functions are measured using a clothing-type wearable device, and that lifestyle events such as defecation and abdominal symptoms are input simultaneously in real time, using a smartphone application originally developed by our group. As a result, autonomic nervous system activity during defecation was accurately evaluated. We hope that further research will improve the quality of life of IBS patients and help elucidate the pathophysiology,” Professor Tanaka concluded.

Source: Osaka Metropolitan University

Categories : GastrointestinalTags :

Graphene Nanomaterial can Affect the Immune System

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Gut microbiome. Credit: Darryl Leja, NIH

The nanomaterial graphene oxide – used in everything from electronics to sensors for biomolecules – can indirectly affect the immune system via the gut microbiome, as shown by a study in the journal Nature Nanotechnology.

“This shows that we must factor the gut microbiome into our understanding of how nanomaterials affect the immune system,” says the paper’s corresponding author Bengt Fadeel, professor at Karolinska Institutet. “Our results are important for identifying the potential adverse effects of nanomaterial and mitigating or preventing such effects in new materials.”

Graphene is an extremely thin material, a million times thinner than a human hair. It comprises a single layer of carbon atoms and is stronger than steel yet flexible, transparent, and electrically conductive. This makes it extremely useful in a multitude of applications, including in ‘smart’ fabrics equipped with wearable electronics and as a component of composite materials, to enhance the strength and conductivity of existing materials.

With increasing use of graphene-based nanomaterials comes a need to examine how these new materials affect the body. Nanomaterials are already known to impact on the immune system, and a few studies in recent years have shown that they can also affect the gut microbiome.

The relationship between nanomaterial, gut microbiome and immunity has been the subject of this zebrafish study. The nanomaterial investigated was graphene oxide, which can be described as a relative of graphene that consists of carbon atoms along with atoms of oxygen. Unlike graphene, graphene oxide is soluble in water and of interest to medical research as, for example, a means of delivering drugs in the body.

In the study, the researchers exposed adult zebrafish to graphene oxide via the water and analysed how it affects the composition of the microbiome. They used both normal fish and fish lacking a receptor molecule in their intestinal cells called the aryl hydrocarbon receptor, commonly abbreviated as AhR, a receptor for various endogenous and bacterial metabolites.

AhR affected the gut microbiome

“We were able to show that the composition of the gut microbiome changed when we exposed the fish to graphene oxide, even at a low dose, and that the AhR also affected the gut microbiome,” says the study’s first author Guotao Peng, postdoc researcher at the Institute of Environmental Medicine at Karolinska Institutet.

The researchers have also generated zebrafish larvae that completely lack a natural gut microbiome, which makes it possible to study the effects of individual microbiome components, in this case butyric acid (a fatty acid), which is secreted by certain types of gut bacteria. Butyric acid is known to be able to bind to AhR.

Doing this, the researchers found that the combination of graphene oxide and butyric acid gave rise to so-called type 2 immunity in the fish. The effect turned out to be dependent on the expression of AhR in the intestinal cells.

“This type of immunity is normally seen as a response to parasitic infection. Our interpretation is that the gut immune response can handle graphene oxide in a similar way to how it would handle a parasite,” says Guotao Peng.

Using an advanced method for mapping the immune cells, the researchers were also able to show that a component of the immune system called innate lymphoid cells are found in zebrafish larvae.

“This shows that the zebrafish is a good model for studying the immune system, including the primitive or innate immune system,” says Bengt Fadeel.

Source: Karolinksa Institutet

Categories : Gastrointestinal Obstetrics & GynaecologyTags :

Even in Remission, IBD is a Risk Factor for Preterm Birth

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Photo by Jonathan Borba on Unsplash

Inflammatory bowel disease is a risk factor for giving birth preterm even when in apparent disease remission, according to a study published in the journal eClinicalMedicine. If corroborated, the results may eventually affect recommendations for women with ulcerative colitis wishing to conceive.

Inflammatory bowel disease (IBD) is chronic inflammatory disease with a prevalence of approximately 0.5%. IBD, which includes ulcerative colitis and Crohn’s disease, and – unlike irritable bowel syndrome (IBS) – causes visible damage to the mucosa lining the intestines. IBD is characteristic for its recurrent tendency for symptoms to relapse, followed by periods of remission.

Onset of IBD commonly occurs at age 15–30, so questions about its impact on pregnancy and the foetus are common. IBD has previously been linked to negative birth outcomes, such as preterm birth (< 37 weeks of pregnancy), mainly in women showing signs of active disease.

Also, women without obvious IBD activity often have microscopic inflammation in the intestinal mucosa. Until now, however, it has been unknown whether even microscopic inflammation may be associated with risks in pregnancy.

Higher risk of preterm birth

The present study, shows that microscopic inflammation in IBD, especially ulcerative colitis, is linked to an elevated risk of giving birth prematurely.

Among babies born to women with microscopic inflammation due to IBD, 9.6% were preterm, while 6.5% of children were born preterm to women without microscopic inflammation of IBD. This corresponds to a relative risk increase of 46 percent. Microscopic inflammation was not clearly associated with other adverse pregnancy outcomes, such as growth restriction.

The results are based on register data on women in Sweden, diagnosed with IBD in 1990–2016, in whom information was available on the microscopic appearance of the intestine shortly before pregnancy. The study included 1223 children of women with microscopic IBD inflammation of the intestine and 630 children of women with IBD but with microscopically healed intestinal mucosa.

Through register linkages, data were also retrieved from several national health registers, such as the Swedish Medical Birth Register and the Swedish Quality Register for Inflammatory Bowel Desiease (SWIBREG).

Prospect of new treatment targets

“Our results suggest that IBD treatment aimed at not merely alleviate symptoms of IBD, but also microscopically heal the intestine, can reduce the risk of giving birth preterm,” sayd first author and corresponding author is Karl Mårild, associate professor of paediatrics at Sahlgrenska Academy, University of Gothenburg. “If our results hold up in future studies, they may therefore be the basis for recommendations to confirm microscopic healing before pregnancy, to reduce such risks.”

“Even a modestly increased relative risk of preterm birth is important, given that preterm birth can greatly affect the child’s health in both the short and the long term. Preterm birth is still one of the most common causes of death for children under the age of five in Sweden,” Karl Mårild concludes.

Source: University of Gothenburg

Categories : Gastrointestinal NeurologyTags :

Mapping the Neural Pathways for Vomiting after Eating Infected Food

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Photo by Kyle Glenn on Unsplash

The urge to vomit after eating contaminated food is the body’s natural defensive response to get rid of bacterial toxins. However, exactly how the brain initiates the response has remained a mystery. Now, researchers have mapped out the detailed neural pathway of the defensive responses from the gut to the brain in mice. The study, published in the journal Cell, could help scientists develop better anti-nausea medications for cancer patients who undergo chemotherapy.

Many foodborne bacteria produce toxins in the host after ingestion. After sensing their presence, the brain will initiate a series of biological responses, including vomit and nausea, to expel the substances and develop an aversion toward foods that taste or look the same.

“But details on how the signals are transmitted from the gut to the brain were unclear, because scientists couldn’t study the process on mice,” says Peng Cao, the paper’s corresponding author at the National Institute of Biological Sciences in Beijing. Rodents cannot vomit, so scientists have been studying vomit in other animals like dogs and cats, but these animals are not comprehensively studied and thus failed to reveal the mechanism of nausea and vomiting. However, Cao and his team noticed that while mice don’t vomit, they retch – meaning they also experience the urge to vomit without throwing up.

The team found that after receiving Staphylococcal enterotoxin A (SEA), which is a common bacterial toxin produced by Staphylococcus aureus that also leads to foodborne illnesses in humans, mice developed episodes of unusual mouth opening. Mice that received SEA opened their mouths at angles wider than those observed in the control group, where mice received saline water. Moreover, during these episodes, the diaphragm and abdominal muscles of the SEA-treated mice contract simultaneously, a pattern seen in dogs when they are vomiting. During normal breathing, animals’ diaphragm and abdominal muscles contract alternatively.

“The neural mechanism of retching is similar to that of vomiting. In this experiment, we successfully build a paradigm for studying toxin-induced retching in mice, with which we can look into the defensive responses from the brain to toxins at the molecular and cellular levels,” Cao says.

In mice treated with SEA, the team found the toxin in the intestine activates the release of serotonin, a type of neurotransmitter, by the enterochromaffin cells on the lining of the intestinal lumen. The released serotonin binds to the receptors on the vagal sensory neurons located in the intestine, which transmits the signals along the vagus nerves from the gut to a specific type of neurons in the dorsal vagal complex – Tac1+DVC neurons – in the brainstem. When Cao and his team inactivated the Tac1+DVC neurons, SEA-treated mice retched less compared with mice with normal Tac1+DVC neuron activities.

In addition, the team investigated whether chemotherapy drugs, which also induce defensive responses like nausea and vomiting in recipients, activate the same neural pathway. They injected mice with doxorubicin, a common chemotherapy drug. The drug made mice retch, but when the team inactivated their Tac1+ DVC neurons or serotonin synthesis of their enterochromaffin cells, the animals’ retching behaviours were significantly reduced.

Cao says some of the current anti-nausea medications for chemotherapy recipients, such as Granisetron, work by blocking the serotonin receptors. The study helps explain why the drug works.

“With this study, we can now better understand the molecular and cellular mechanisms of nausea and vomiting, which will help us develop better medications,” Cao says.

Next, Cao and his colleagues want to explore how toxins act on enterochromaffin cells. Preliminary research shows that enterochromaffin cells don’t sense the presence of toxins directly. The process likely involves complex immune responses of damaged cells in the intestine.

“In addition to foodborne germs, humans encounter a lot of pathogens, and our body is equipped with similar mechanisms to expel these toxic substances. For example, coughing is our body’s attempt to remove the coronavirus. It’s a new and exciting field of research about how the brain senses the existence of pathogens and initiates responses to get rid of them.” Cao says, adding that future research may reveal new and better targets for drugs, including anti-nausea medicines.

Source: ScienceDaily

Categories : Cancer GastrointestinalTags :

Diverticular Disease Linked to Cancers outside the Gastrointestinal System

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Anatomy of the gut
Source: Pixabay CC0

In a large-scale study of cancer among 75 000 patients with a diagnosis of diverticular disease and colorectal histopathology, researchers have reported an elevated cancer risk in patients with diverticular disease. Their findings were published in the Journal of the National Cancer Institute.

The data comes from the ESPRESSO cohort, which covers all histopathology reports from Sweden’s 28 pathology departments. Through linkage with the Swedish national patient register, researchers identified patients with diverticular disease. Diverticular disease can present through gastrointestinal bleeding, but also through diverticulitis when patients may have fever, nausea and abdominal pain. Previous research has focused on colorectal cancer development in diverticular disease but less has been know about cancer development elsewhere. The researchers found a 33% increased risk of overall cancer in Swedish patients with diverticular disease.

“This is the first nationwide cohort study to demonstrate that diverticular disease is associated with an increased, long-term risk of overall cancer”, says first-author Wenjie Ma from Massachusetts General Hospital. “Diverticular disease is associated with an increased risk of specific cancers, including liver cancer and lung cancer.”

She also adds that “Given the high prevalence of diverticular disease, our results highlight the need for awareness for cancer, not only for colorectal cancer, in patients with diverticular disease.”

Patients with diverticular disease had significantly increased overall cancer incidence (24.5 vs 18.1 cancer cases per 1000 person-years). After adjusting for covariates, these rates corresponded to 1 extra cancer case in 16 individuals with diverticular disease followed for ten years.

“There has been a lot of research on extraintestinal cancer in other bowel disorders such as inflammatory bowel disease (IBD) and celiac disease, but less is known about diverticular disease”, says senior author Jonas F Ludvigsson, professor at Karolinska Institutet.

“These data suggest that patients with diverticular disease are at increased risk of other cancers than colorectal cancer, but it should also be emphasized that the absolute risk for cancer was moderate”, adds Ludvigsson. “I hope other researchers are inspired by our findings and explore the biological mechanisms underlying the association between diverticular disease and cancer”, he concludes.

Source: Karolinska Institutet

Categories : GastrointestinalTags :

Pain-sensing Neurons Protect the Gut from Damage

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Photo by Andrea Piacquadio on Pexels

Neurons that sense pain protect the gut from inflammation and associated tissue damage by regulating the microbial community living in the intestines, according to a study from Weill Cornell Medicine researchers.

The study, published in Cell, found in a preclinical model that pain-sensing neurons in the gut secrete a molecule called substance P, which appears to protect against gut inflammation and related tissue damage by boosting the population of beneficial microbes in the gut. The researchers also found that these pain-sensing nerves are diminished in number, with significant disruptions to their pain-signaling genes, in people who have inflammatory bowel disease (IBD).

“These findings reshape our thinking about chronic inflammatory disease, and open up a whole new approach to therapeutic intervention,” said study senior author Dr David Artis at Weill Cornell Medicine.

The study’s first author, DrWen Zhang, added: “Defining a previously unknown sensory function for these specific neurons in influencing the microbiota adds a new level of understanding to host-microbiota interactions.”

IBD covers two distinct disorders, Crohn’s disease and ulcerative colitis. It is typically treated with drugs that directly target elements of the immune system. Scientists now appreciate that gut-dwelling bacteria and other microbes also help regulate gut inflammation.

As Dr Artis’s laboratory and others have shown in recent years, the nervous system, which is ‘wired’ into most organs, appears to be yet another powerful regulator of the immune system at the body’s barrier surfaces. In the new study, Dr Artis and his team specifically examined pain neurons that innervate the gut.

These gut-innervating pain neurons, whose cell bodies sit in the lower spine, express a surface protein called TRPV1, which serves as a receptor for pain-related signals. TRPV1 can be activated by high heat, acid, and the chili-pepper compound capsaicin, for example – and the brain translates this activation into a sense of burning pain. The researchers found that silencing these TRPV1 receptors in gut nerves, or deleting TRPV1-expressing neurons, led to much worse inflammation and tissue damage in IBD mouse models, whereas activating the receptors had a protective effect.

The investigators observed that the worsened inflammation and tissue damage in TRPV1-blocked mice were associated with changes in the relative populations of different species of gut bacteria. When this altered bacterial population was transplanted into normal mice, it caused the same worsened susceptibility to inflammation and damage. By contrast, broad-spectrum antibiotic treatment could reverse this susceptibility even in TRPV1-blocked mice. This result demonstrated that TRPV1-expressing nerves protect the gut mainly by helping to maintain a healthy gut microbe population.

The scientists found strong evidence that a large part of this microbe-influencing effect of TRPV1-expressing nerves comes from a molecule the nerves secrete called substance P – which they observed could reverse, on its own, most of the harmful effects of blocking TRPV1. Experiments also suggested that the signaling between neurons and microbes was two-way – some bacterial species could activate TRPV1-expressing nerves to get them to produce more substance P.

To confirm the relevance to humans, the researchers examined gut tissue from IBD patients, and found abnormal TRPV1 and substance P gene activity as well as fewer signs of TRPV1 nerves overall.

“These patients had disrupted pain-sensing nerves, which may have contributed to their chronic inflammation,” Dr Zhang said.

Precisely how substance P exerts its effects on the gut microbe population, and how these microbes “talk back,” are questions that the researchers are now trying to answer in ongoing studies. But the results so far suggest that the next generation of anti-inflammatory drugs for IBD and other disorders could be compounds that target the nervous system.

“A lot of current anti-inflammatory drugs work in only some patients, and pharma companies really haven’t known why,” Dr Artis said. “Maybe it’s because, when it comes to chronic inflammation, we’ve been seeing only some of the picture – and now the rest, including the role of the nervous system, is starting to come into focus.”

Source: Weill Cornell Medicine

Categories : GastrointestinalTags :

Reducing the Rebleeding Risk from Obscure Gastrointestinal Bleeding

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Anatomy of the gut
Source: Pixabay CC0

In a study published in Gastrointestinal Endoscopy, clinical investigators found that the five-year risk of rebleeding in obscure gastrointestinal bleeding was found to be as high as 41.7%, but capsule endoscopy examinations and subsequent interventions substantially reduced the risk. Factors such as anticoagulant use were also found to be independent predictors of rebleeding risk.

Obscure gastrointestinal bleeding (OGIB) is defined as gastrointestinal bleeding from a source that cannot be identified on upper or lower gastrointestinal endoscopy. OGIB is considered an important indication for capsule endoscopy (CE). CE is particularly useful for the detection of vascular and small ulcerative lesions, conditions frequently associated with OGIB.

Previous studies have shown that patients with severe comorbidities have a higher rate of positive CE findings (observations of mucosal breaks, vascular lesions, tumours, or blood retention) for OGIB. Additionally, for OGIB in which the initial CE fails to identify bleeding lesions, repeated CE can detect lesions at a higher rate. However, there have been no reports with a sufficiently large number of cases on the long-term outcomes of OGIB detected by CE and the risk of rebleeding.

To fill this knowledge gap, investigators followed up on 389 patients who underwent CE as their initial small intestinal examination for OGIB and evaluated the risk of rebleeding over the long term. In addition, the team evaluated the risk of rebleeding in OGIB, in which no source of rebleeding was found in any part of the gastrointestinal tract, including the small intestine.

The overall cumulative rebleeding rate during the five years after CE was 41.7%. In patients with positive CE findings, the cumulative rebleeding rate was 48.0%. The cumulative rebleeding rate in patients who had therapeutic intervention resulting from positive CE findings was 31.8%.

Furthermore, overt OGIB, anticoagulants, positive balloon-assisted enteroscopy after CE, and iron supplements without therapeutic intervention were found to be independent predictors of rebleeding. Among the components of an index assessing the severity of complications, liver cirrhosis was an independent predictor associated with rebleeding in patients with OGIB.

“If capsule endoscopy can be used to properly diagnose and lead to therapeutic intervention, the risk of rebleeding can be reduced,” concluded study leader Dr Otani. “Even if the endoscopy does not detect any lesions, adequate follow-up is necessary. Here at Osaka Metropolitan University, we have been utilising this tool clinically since its early days and have accumulated some of the world’s leading clinical data. This study revealed a high rebleeding rate in OGIB patients and clarified the effects of rebleeding predictors and therapeutic intervention. We have high expectations that this will lead to better medical care in the future.”

Source: Osaka Metropolitan University

Categories : Diet and Nutrition GastrointestinalTags :

Non-nutritive Sweeteners Impact Human Glycaemic Responses

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Since the late 1800s, non-nutritive sweeteners have been used to provide sweetness without sugar. Long been believed to have no effect on the human body, researchers reporting in the journal Cell now challenge this notion by finding that these sugar substitutes are not inert, and, in fact, some can alter human consumers’ microbiomes and thereby their glycaemic responses – albeit in a highly individualised fashion.

Previous research has already found found that non-nutritive sweeteners affected the microbiomes of mice in ways that could impact their glycaemic responses, something which the same researchers now investigated in humans.

To address this important question, the research team carefully screened over 1300 individuals for those who strictly avoid non-nutritive sweeteners in their day-to-day lives, and identified a cohort of 120 individuals. These participants were broken into six groups: two controls and four who ingested well below the FDA daily allowances of either aspartame, saccharin, stevia, or sucralose.

“In subjects consuming the non-nutritive sweeteners, we could identify very distinct changes in the composition and function of gut microbes, and the molecules they secret into peripheral blood. This seemed to suggest that gut microbes in the human body are rather responsive to each of these sweeteners,” said senior author Eran Elinav, an immunologist and microbiome researcher. “When we looked at consumers of non-nutritive sweeteners as groups, we found that two of the non-nutritive sweeteners, saccharin and sucralose, significantly impacted glucose tolerance in healthy adults. Interestingly, changes in the microbes were highly correlated with the alterations noted in people’s glycaemic responses.”

To prove the microbiomes were responsible, the researchers transferred microbial samples from the study subjects to mice that have been raised in completely sterile conditions, with no microbiome of their own.

“The results were quite striking,” explained Elinav. “In all of the non-nutritive sweetener groups, but in none of the controls, when we transferred into these sterile mice the microbiome of the top responder individuals collected at a time point in which they were consuming the respective non-nutritive sweeteners, the recipient mice developed glycaemic alterations that very significantly mirrored those of the donor individuals. In contrast, the bottom responders’ microbiomes were mostly unable to elicit such glycaemic responses,” he added. “These results suggest that the microbiome changes in response to human consumption of non-nutritive sweetener may, at times, induce glycaemic changes in consumers in a highly personalised manner.”

Elinav says that he expects the effects of the sweeteners will vary across individuals because of how unique our microbiomes are. “We need to raise awareness of the fact that non-nutritive sweeteners are not inert to the human body as we originally believed. With that said, the clinical health implications of the changes they may elicit in humans remain unknown and merit future long-term studies.”

“In the meantime, we need to continue searching for solutions to our sweet tooth craving, while avoiding sugar, which is clearly most harmful to our metabolic health,” says Elinav. “In my personal view, drinking only water seems to be the best solution.”

Source: Science Daily

Categories : GastrointestinalTags :

Body Posture, Stomach Motility Affect Oral Pill Bioavailability

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While oral administration of a pill or capsule is a simple and cheap route, it is also the most complex way for the human body to absorb an active pharmaceutical ingredient, due to the stomach environment’s influence on bioavailability. Using highly detailed computer simulations, researchers have now found that stomach motility and posture (leaning right, left or backwards) significantly affect bioavailability.

The rate of dissolution and gastric emptying of the dissolved active pharmaceutical ingredient (API) into the duodenum is modulated by gastric motility, physical properties of the pill, and the contents of the stomach. This results in varying rates of pill dissolution and nonuniform emptying of the drug into the duodenum and, occasionally, gastric dumping in the case of modified-release dosage. Current in vitro procedures for assessing dissolution of oral drugs do not simulate this process well.

In Physics of Fluids, researchers used a biomimetic computer simulation based on the realistic anatomy and morphology of the stomach (a ‘StomachSim’) to investigate and quantify the effect of body posture and stomach motility on drug bioavailability over the first few minutes of absoprtion.

 The simulations show that changes in posture can potentially have a significant (up to 83%) effect on the emptying rate of the API into the duodenum. A 45 degree lean to the left greatly reduced the amount of active ingredient per cycle released into the duodenum, while a lean to the right dramatically increased it over the upright case.

Similarly, the researchers found that a reduction in antral contractility associated with gastroparesis significantly reduced the dissolution of the pill as well as emptying of the API into the duodenum. The simulations show that for an equivalent motility index, the reduction in gastric emptying due to neuropathic gastroparesis is larger by a factor of about five compared to myopathic gastroparesis.

“Oral administration is surprisingly complex despite being the most common choice for drug administration,” said co-author Rajat Mittal. “When the pill reaches the stomach, the motion of the stomach walls and the flow of contents inside determine the rate at which it dissolves. The properties of the pill and the stomach contents also play a major role.

“However, current experimental or clinical procedures for assessing the dissolution of oral drugs are limited in their ability to study this, which makes it a challenge to understand how the dissolution is affected in different stomach disorders, such as gastroparesis, which slows down the emptying of the stomach.”

Together, these issues pose several challenges for the design of drug delivery.

“In this work, we demonstrate a novel computer simulation platform that offers the potential for overcoming these limitations,” said Mittal. “Our models can generate biorelevant data on drug dissolution that can provide useful and unique insights into the complex physiological processes behind the oral administration of pills.”

The researchers note that the simulation required a lot of computational time, only capturing the first few minutes of the process, and are working on faster methods to capture differences over the period of an hour.

Source: American Institute of Physics

Categories : GastrointestinalTags :

Gold Nanoparticles Ease IBD Inflammatory Symptoms

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Gold bars
Photo by Jingming Pan on Unsplash

In a Chinese study published in Fundamental Research, researchers explored a treatment for inflammatory bowel disease (IBD) using ultrasmall gold nanoparticles. Previous studies showed that these nanoclusters effectively eliminate a variety of reactive oxygen species (ROS), elevated levels of which are commonly found in the gastrointestinal tract of IBD patients.

IBD includes ulcerative colitis and Crohn’s disease, both of which tend to be debilitating, lifelong conditions that can prove fatal in severe cases. Currently, there is no cure for IBD. The main clinical treatments are drugs such as aminosalicylic acid preparations and corticosteroids, but they are often accompanied by gastrointestinal problems, anaemia, and various intestinal complications. Finding alternative, more effective options is a priority for researchers.

The team found that administering gold (Au25) nanoclusters orally to mice suffering from colitis eliminated ROS, increased antioxidant enzymes, and inhibited pro-inflammatory cytokines, without any obvious side effects. According to paper author Fei Wang of China’s The Seventh Affiliated Hospital of Sun Yat-Sen University, a reduction in the inflammation in the gastrointestinal tracts of the mice was observed within 24 hours. She added: “And the fact that these nanoclusters can be administered orally, means there is no need for invasive procedures.”

Additionally, the team found that the nanoclusters have a number of benefits when compared with natural enzymes used in traditional IBD treatments, including lower cost, better stability, mass synthesis and easier storage. Wang explained: “The storage of Au25 nanoclusters was not affected by pH, temperature or solution medium, and their good physiological stability and acid resistance meant they were easily able to access the inflamed colon. They also have good biocompatibility and chemical stability and can remove a variety of ROS.”

Wang concluded: “Au25 nanoclusters offer a promising strategy in the research field of nanomedicine therapy for IBD. We believe this study demonstrates their value as a scientific basis and experimental basis for the clinical treatment of IBD.”

Source: EurekAlert!