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Deglutition, or the act of swallowing, allows food and fluids to move through the upper gastrointestinal tract. Difficulty swallowing, known as dysphagia, causes a host of complications for patients. Fluoroscopic evaluation of dysphagia enables appropriate diagnosis and treatment. This evaluation commonly is accomplished with a swallowing dysfunction study, also known as a modified barium swallow procedure. [ABSTRACT FROM AUTHOR]

Abstract: The existence of Electrocardiography (ECG) came to light over a century ago, yet the acquisition and elicitation of non-invasive foetal electrocardiogram (fECG) is still in infancy despite mammoth advances in clinical electrocardiography, advanced Biomedical signal processing techniques and fast growing engineering technology. The acquisition of foetal ECG becomes a challenging task since it is perilous for a direct contact over the foetus. Moreover, the non-invasive abdominal ECG (aECG) measurements obtained over the surface of a maternal abdomen contains several bioelectric potentials like maternal heart activity, foetal heart activity, maternal muscle activity, foetal movement activity, generated potentials by respiration and stomach activity, and noise (thermal noise, noise generated from electrode-skin contact). The strong Maternal Electrocardiogram (mECG) along with the weak fECG in the recordings obtained from a mother is overlapping in time as well as in frequency. Hence separation of these signals cannot be accomplished by simple windowing or filtering. Over the years numerous researchers have put enormous efforts in signal processing and biomedical engineering for humanizing the foetal ECG acquisition techniques used by the physiologists. The fECG signal is a vital information source to assist physicians for precise timely decisions during labor. Some of the recently developed algorithms by researchers have given remarkable results for fECG acquisition. The focus of this paper is to review these existing algorithms for non-invasive detection and elicitation of fECG in terms of their performance and capabilities with respect to standard databases available worldwide. [Copyright &y& Elsevier]

Summary: We provide a practical review of the opportunities made available by design-unbiased stereology to estimate cell number, total volume, mean volume and mean height in the rat stomach using enterochromaffin-like cells as an example. The second example comprises estimation of the surface area of well-defined segments of rat colon and the volumes of different layers following surgery and/or treatment which may result in the atrophy or growth of the colon. The pros and cons of the stereologic designs are discussed and the pitfalls and some solutions to these are elucidated. [ABSTRACT FROM AUTHOR]

Abstract: Helicobacter pylori colonizes the gastric mucosa of half of the worlds population and persistent infection is related with an increase in the risk of gastric cancer. Adhesion of H. pylori to the gastric epithelium, which is essential for infection, is mediated by bacterial adhesin proteins that recognize specific glycan structures (Gly-R) expressed in the gastric mucosa. The blood group antigen binding adhesin (BabA) recognizes difucosylated antigens such as Lewis B (Leb), while the sialic acid binding adhesin (SabA) recognizes sialylated glycoproteins and glycolipids, such as sialyl-Lewis x (sLex). This work aimed to investigate whether these Gly-Rs (Leb and sLex) can attract and specifically bind H. pylori after immobilization on synthetic surfaces (self-assembled monolayers (SAMs) of alkanethiols on gold). Functional bacterial adhesion assays for (Gly-R)-SAMs were performed using H. pylori strains with different adhesin protein profiles. The results demonstrate that H. pylori binding to surfaces occurs via interaction between its adhesins and cognate (Gly-R)-SAMs and bound H. pylori maintains its characteristic rod-shaped morphology only during conditions of specific adhesin–glycan binding. These results offer new insights into innovative strategies against H. pylori infection based on the scavenging of bacteria from the stomach using specific H. pylori chelating biomaterials. [Copyright &y& Elsevier]

Purpose: To determine the proportion of critically ill adults developing impaired gastrointestinal transit (IGT) using a clinically pragmatic definition, its associated morbidity and risk factors. Materials and Methods: Critically ill adult patients receiving enteral nutrition for .72 hours and mechanically ventilated for .48 hours were prospectively identified. IGT was defined as absence of a bowel movement for .3 days, treatment for constipation, and one of the following: (1) radiologic confirmed ileus, (2) feed intolerance, (3) abdominal distention, or (4) gastric decompression. Results: One thousand patients were screened, and 248 were included for analysis. Fifty patients (20.1%; 95% confidence interval, 15.1-25.6%) developed IGT persisting for 6.5 ± 2.5 days. Patients with IGT had longer lengths of intensive care unit stay and were less likely to reach nutrition targets compared to patients without IGT or traditional definitions of constipation. Daily opioid use and pharmacological constipation prophylaxis were identified risk factors for IGT. Conclusion: Traditional definitions of constipation or ileus in intensive care unit patients are simplistic and lack clinical relevance. Pragmatically defined IGT is a common complication of critical illness and is associated with significant morbidity. Future interventional studies for IGT in critically ill adults should use a more clinically relevant definition and evaluate energy deficits and lengths of stay as clinically relevant outcomes. [ABSTRACT FROM AUTHOR]

Abstract: Objective: To compare Knodell and HAI scores in patients with wild type and pre-core/core promoter mutant CHB to see if there is any difference in severity of liver injury between these two types of HBV. Methods: We did percutaneous liver biopsies of 155 CHB patients. Of them 102 (65.8%) were infected wild type HBV and the rest 53 (34.2%) were infected with pre-core/core promoter mutant CHB. Results: 11/53 (20.8%) patients with pre-core/core promoter mutant CHB had moderate to severe CH (HAI score 8-18). In contrast, moderate to severe CH was seen in 19/102 (18.6%) patients with wild type CHB. Fibrosis score was >2 in 15/53 (28.3%) pre-core/core promoter mutant CHB as opposed to 20/102 (19.6%) patients with wild type CHB. Conclusions: The study shows that pre-core/core promoter mutant HBV produces more severe histological liver disease compared to wild type HBV. [Copyright &y& Elsevier]

Abstract: Objective: To investigate the correlation between the gastric mucosal cell proliferation and low-concentration alcohol intake in a chronic drinking rat model, and to investigate the possible role of ROS/BMK1 pathway in this process. Methods: SD rats were randomly divided into 4 groups: control group, administered with tap water; ethanol group, with 6% ethanol in the drinking water; quercetin group, with quercetin (100 mg/kg) by intragastric gavage twice a day; ethanol+quercetin group, administered with quercetin combined with 6% ethanol. The cell proliferation in rat gastric mucosa was analyzed by flow cytometery and proliferating cell nuclear antigen (PCNA) immunohistochemical staining. Activation of ERKs and BMK1 was evaluated by the expression and phosphorylation of these kinases using Western Blot analysis. Results: Compared to the controls, the cell proliferation in gastric mucosa of rats exposed to the ethanol for 7 d was enhanced, and the activation of BMK1 was also increased in this period. Otherwise quercetin, as a free radical scavenger, attenuated increased cell proliferation and activation of BMK1 in rat stomach treated with ethanol. However, no changes of ERKs expression and phosphorylation occurred in the rats in all groups. Conclusion: These results suggested that the ROS and BMK1 activation may be a central mechanism, which underlies cell proliferation in rat gastric mucosa stimulus with the chronic low-concentration ethanol. [Copyright &y& Elsevier]

Abstract: The secretions of the gastro-intestinal tract and associated organs enable the food that we eat to be broken down into small molecules available for absorption. For each secretion it is necessary to understand: its function and composition; how it is formed; and how secretion is controlled. In this article secretions from the salivary glands and stomach are considered. Most secretions flow into the lumen of the tract (mouth, stomach lumen), with the exception of hormones such as gastrin and histamine, which are secreted into the interstitium and blood. Saliva is concerned with: protecting the mouth against microorganisms and ulceration; facilitating swallowing; and initiating digestion of starches. It is produced from three pairs of glands that secrete mucus and an alkaline ionic solution containing an amylase, ptyalin. The primary ionic secretion is modified along the salivary duct, the extent of which depends on flow rate: at low rates ion reabsorption produces a hypotonic solution, as flow rate increases the solution approaches isotonicity. Flow rate is controlled by the autonomic nervous system, predominantly the parasympathetic branch. Gastric secretions contain: mucus to protect the stomach wall; acid as hydrochloric acid (HCl) to kill remaining microorganisms and initiate hydrolysis of food; an inactive proteolytic enzyme pepsinogen and hormones (gastrin and histamine); as well as the only essential molecule intrinsic factor, which binds vitamin B12 for later absorption in the ileum. Gastric pits in the mucosa have specialized cells to produce mucus, acid and intrinsic factor (parietal cells) and pepsinogen (chief cells). Specialized G-cells produce gastrin through interacting neural (acetylcholine), paracrine (histamine) and endocrine (gastrin-dependent) controls; enterochromaffin cells produce histamine. Acid secretion is also regulated by interacting acetylcholine, histamine and gastrin-dependent pathways, with the vagus nerve having a prominent regulatory role. Gastric secretions occur in three phases: cephalic, gastric and intestinal – the regulatory processes behind these phases are considered in this article. [Copyright &y& Elsevier]

Background & Aims: Helicobacter pylori–induced gastric epithelial cell (GEC) apoptosis is a complex process that includes activation of the tumor suppressor p53. p53-mediated apoptosis involves p53 activation, bax transcription, and cytochrome c release from mitochondria. Apurinic/apyrimidinic endonuclease-1 (APE-1) regulates transcriptional activity of p53, and H pylori induce APE-1 expression in human GECs. H pylori infection increases intracellular calcium ion concentration [Ca2+]i of GECs, which induces APE-1 acetylation. We investigated the effects of H pylori infection and APE-1 acetylation on GEC apoptosis. Methods: AGS cells (wild-type or with suppressed APE-1), KATO III cells, and cells isolated from gastric biopsy specimens were infected with H pylori. Effects were examined by immunoblotting, real-time reverse-transcription polymerase chain reaction, immunoprecipitation, immunofluorescence microscopy, chromatin immunoprecipitation, mobility shift, DNA binding, and luciferase assays. Results: H pylori infection increased [Ca2+]i and acetylation of APE-1 in GECs, but the acetylation status of APE-1 did not affect the transcriptional activity of p53. In GECs, expression of a form of APE-1 that could not be acetylated increased total and mitochondrial levels of Bax and induced release of cytochrome c and fragmentation of DNA; expression of wild-type APE-1 reduced these apoptotic events. We identified a negative calcium response element in the human bax promoter and found that poly (adenosine diphosphate-ribose) polymerase 1 recruited the acetylated APE-1/histone deacetylase-1 repressor complex to bax nCaRE. Conclusions: H pylori–mediated acetylation of APE-1 suppresses Bax expression; this prevents p53-mediated apoptosis when H pylori infect GECs. [Copyright &y& Elsevier]

Tests of gastric neuromuscular function are used to evaluate patients with symptoms referable to the upper digestive tract. These symptoms can be associated with alterations in the rates of gastric emptying, impaired accommodation, heightened gastric sensation, or alterations in gastric myoelectrical function and contractility. Management of gastric neuromuscular disorders requires an understanding of pathophysiology and treatment options as well as the appropriate use and interpretation of diagnostic tests. These tests include measures of gastric emptying; contractility; electrical activity; regional gastric motility of the fundus, antrum, and pylorus; and tests of sensation and compliance. Tests are also being developed to improve our understanding of the afferent sensory pathways from the stomach to the central nervous system that mediate gastric sensation in health and gastric disorders. This article reviews tests of gastric function and provides a basic description of the tests, the methodologies behind them, descriptions of the physiology that they assess, and their clinical utility. [Copyright &y& Elsevier]

The gastric emptying rate is a carefully regulated process consisting of different mathematically defined phases. The gastric metabolic load, as well as neural regulatory mechanisms and hormonal influences, cooperate in order to achieve a well-balanced emptying of contents from the stomach into the duodenum for absorption in the small intestine. This finely tuned regulation is primarily regulated by the release of gastrointestinal peptide hormones which serve to counteract the emptying process in the fed state and to stimulate sweeping contractions in the fasted state, most likely in order to prepare the stomach for another meal. We have found that the two peptide hormones ghrelin and glucagon-like peptide- I (GLP- I) have a great impact on the regulation of gastric emptying: ghrelin is a most potent stimulator of gastric contractions and emptying, and GLP- I profoundly inhibits this emptying process. These data suggest possibilities for governing the rate of gastric emptying as a natural step in achieving metabolic balance and control. [ABSTRACT FROM AUTHOR]

The stomach is commonly the source of chronic digestive symptoms in patients with diabetes mellitus; erratic stomach emptying may result in poor glycemic control. On the other hand, medications that mimic or enhance the function of the endogenous incretins retard gastric emptying to enhance glycemic control. In patients with obesity and type 2 diabetes, bariatric procedures alter food intake and weight; however, effects on glycemic control precede and are out of proportion with the degree of weight loss. The mechanisms responsible for the improved glycemic control after bariatric surgery are the subject of ongoing research, and include increased circulating incretins stimulated by the delivery of nutrients to the intestine, contributing to weight loss and independently to glycemic control. The stomach is not always a villain, but is an ally in patients with type 2 diabetes. [Copyright &y& Elsevier]

Yamanaka and colleagues, in a Science article currently published online, have generated induced pluripotent stem (iPS) cells from liver and stomach cells, suggesting that transcription factor-induced reprogram ming is not restricted to particular cell types (Aoi et al., 2008). These results also provide important insight into the mechanistic basis of reprogramming. [ABSTRACT FROM AUTHOR]

The authors convey their concerns on a predictive model that explains the factors that determine whether gastric inflation may occur. Topics mentioned include an early study on gastric inflation in 1961, the use of a bag-valve-mask by the respiratory therapist to prevent or minimize gastric inflation, and assessment of lower esophageal pressure during resuscitation of cardiac arrest or near-drownings.

Case report. Anatomical variations of peritoneal folds are rare. We present a peritoneal fold connecting pyloric part of stomach, right colic lexure and gall bladder observed in an adult female cadaver. Literature review shows the variant peritoneal fold can be called as cystogastrocolic fold. [ABSTRACT FROM AUTHOR]

Background & Aims: A balance between effector and regulatory T-cell (Treg) responses is required to maintain intestinal homeostasis. To regulate immunity, T cells migrate to the intestine using a combination of adhesion molecules and chemokine receptors. However, it is not known whether the migration pathways of effector cells and Tregs are distinct or shared. We sought to determine whether interaction between the chemokine receptor 9 (CCR9) and its ligand, chemokine ligand 25 (CCL25), allows effectors or Tregs to localize to chronically inflamed small intestine. Methods: By using a mouse model that develops Crohn''s-like ileitis (tumor necrosis factor Δadenosine uracyl-rich element [TNFΔARE] mice) we examined the role of CCL25–CCR9 interactions for effector and Treg traffic using flow cytometry, quantitative reverse-transcription polymerase chain reaction, immunohistochemistry, immunoneutralization, and proliferation analyses. Results: In TNFΔARE mice, expression of CCL25 and the frequency of CCR9-expressing lymphocytes increased during late-stage disease. In the absence of CCR9, TNFΔARE mice developed exacerbated disease, compared with their CCR9-sufficient counterparts, which coincided with a deficiency of CD4+/CD25+/forkhead box P3+ and CD8+/CD103+ Tregs within the intestinal lamina propria and mesenteric lymph nodes. Furthermore, the CD8+/CCR9+ subset decreased the proliferation of CD4+ T cells in vitro. Administration of a monoclonal antibody against CCR9 to TNFΔARE mice exacerbated ileitis in vivo, confirming the regulatory role of CD8+/CCR9+ cells. Conclusions: Signaling of the chemokine CCL25 through its receptor CCR9 induces Tregs to migrate to the intestine. These findings raise concerns about the development of reagents to disrupt this pathway for the treatment of patients with Crohn''s disease. [Copyright &y& Elsevier]