Effects of zerumbone on chronic gastritis remain unclear. The purpose of this study was to investigate the mechanism of the protective effect of zerumbone on the treatment of chronic gastritis in rats. The animal models of chronic gastritis in rats were established, and the surface damage of gastric mucosa was observed by gross anatomy; the changes of gastric mucosal tissue and surface morphology were observed by pathological sections of gastric mucosal tissues; the expressions of heme oxygenase-1 (HO-1) and nuclear factor E2-related factor 2 (Nrf-2) proteins of gastric mucosal tissues in each group were detected by western blot analysis; the activities of superoxide dismutase (SOD) and catalase (CAT) as well as the contents of reduced glutathione (GSH) and malondialdehyde (MDA) in gastric mucosal tissues were detected by kits. The results indicated that zerumbone could significantly relieve red and swelling as well as erosion of the gastric mucosal tissues in rats with chronic gastritis; ...
Several studies indicate that naturally occurring antioxidants exert protective biochemical effects in a number of biological experimental systems. In particular, phenolic antioxidants, which are widely distributed in vegetable foods, are considered to play an important role in the prevention of oxidative damage in living systems.32 Because generation of ROS in the stomach greatly contributes to the damaging effect exerted by a number of ulcerogens,2-4 we sought to investigate whether APE prevented oxidative stress induced injury to cultured gastric mucous cells in vitro, under conditions independent of acid secretion or systemic factors, including blood flow.. Our data indicate that APE counteract the damaging effect of X-XO generated ROS in gastric epithelial cells and that this protective effect seems to be mainly attributable to the major components of APE (that is, CAT and CA). This effect is associated with permeation of gastric cells by apple phenolic compounds and seems to be due to ...
The human stomach normally contains high levels of bioactive nitric oxide (NO). This NO derives from salivary nitrate (NO3-) that is converted to nitrite (NO2-) by oral bacteria and thereafter non-enzymatically reduced in the acidic gastric lumen to NO. Nitrate is a common component in vegetables, and after ingestion it is absorbed in the small intestine. Interestingly, circulating nitrate is then concentrated by the salivary glands. Hence, intake of nitrate-rich vegetables results in high levels of NO in the stomach. The physiological effects of the high concentration of NO gas normally present in the gastric lumen have been hitherto unknown, and the present investigations were therefore conducted to address this issue.. NO produced in the gastric lumen after nitrate ingestion increased gastric mucosal blood flow and the thickness of the firmly adherent mucus layer in the stomach. The blood flow and mucus layer are essential defense mechanisms that protect the mucosa from luminal acid and ...
The purpose of this investigation was to study cell proliferation kinetics in human gastric mucosa. Biopsies were taken from the antral and fundic part of the stomach through a fibre-gastroscope and incubated in culture medium containing a DNA-precursor (3-H-thymidine). Autoradiographs were prepared by the dipping technique. The number of labelled cells and the total number of cells in all cross sections of foveolae containing one or more labelled cells were counted. The labelling index (LI), which is defined as the percentage of labelled cells in the progenitor cell region, was estimated. When only cross sections with labelled cells are taken into consideration, the labelling index will be a little overestimated. In order to reduce this error a formula for correction was worked out. Thirty-six patients with different gastric diseases were studied. The observer error was minimal, and the results were highly reproducible. It was not possible to demonstrate any correlation between the labelling ...
The gastric mucosa is constantly exposed to conditions that would normally be damaging to living cells. A complex defensive system has evolved that involves multiple mechanisms arranged in a laminar fashion, that as a whole constitute the gastric mucosal barrier to acid. As antisecretory therapy becomes perfected, more attention has been focused on these defensive components of the gastric mucosal barrier in disease. Recently, our laboratory has developed a means of measuring intracellular pH (pH,sub,i,/sub,), mucosal blood flow, acid secretion, surface cell acidification rate, and acid secretion simultaneously ,i,in vivo,/i,. This system has enabled our laboratory to explore how the different components of the gastric mucosal barrier interact so as to protect the pH,sub,i,/sub, of the surface cells under a variety of conditions. Analysis of these studies has revealed a significant inverse correlation between the initial fall in pH; of surface cells during luminal acid exposure and the thickness ...
Guarda Foto stock di Crosssection Of The Gastric Or Stomach Epithelium Showing The Numerous Gastric Pits On The Surface Of The Mucosa Sem. Cerca foto premium ad alta risoluzione su Getty Images.
TY - JOUR. T1 - Cholecystokinin secretagogue-induced gastroprotection. T2 - Role of nitric oxide and blood flow. AU - West, Sonlee D.. AU - Helmer, Kenneth S.. AU - Chang, Lily K.. AU - Cui, Yan. AU - Greeley, George H.. AU - Mercer, David W.. PY - 2003/3/1. Y1 - 2003/3/1. N2 - This study was done to examine the role of CCK in gastric mucosal defense and to assess the gastroprotective roles of nitric oxide and blood flow. In rats, the CCK secretagogues oleate and soybean trypsin inhibitor augmented gastric mucosal blood flow and prevented gastric injury from luminal irritants. Type A CCK receptor blockade negated CCK secretagogue-induced gastroprotection and exacerbated gastric injury from bile and ethanol but did not block adaptive cytoprotection. CCK secretagogue-induced gastroprotection and hyperemia were negated by nonselective nitric oxide synthase (NOS) inhibition (nG-nitro-L-arginine methyl ester) but not by selective inducible NOS inhibition (aminoguanidine). Gastric mucosal ...
Stomach mucosa. Light micrograph (bottom left) and computer illustration (top right) of the lining of the stomach, known as the mucosa. The stomach is a muscular sac involved in storage and digestion of food. The surface of the mucosa consists of simple columnar cells (dark purple in micrograph) that secrete mucus. The mucus protects the stomach lining from digestive acids and enzymes that act on food in the stomach. Beneath the columnar cells are gastric pits, the glands that make the acids and enzymes needed to digest food. - Stock Image F016/8749
The balance of protective and aggressive factors in the gastric mucosal barrier is an important consideration in gastrointestinal diseases (4). Gastric acid, pepsin, and external stimuli are known aggravating factors of gastric mucosal cells, while microcirculatory system, HCO3−, prostaglandins, epidermal growth factor synthesis, and epithelial cell reconstitution are gastro-protective factors that maintain integrity of the gastric mucosal layer. Obviously, there are several viewpoints in association with the effect of ethanol on gastric mucosal cells. However, the main pathogenesis of ethanol-induced gastritis is vascular damage followed by mucosal cell-hypoxia, -degeneration, and -necrosis, respectively. The decline of anti-oxidant level and over production of oxygen free radicals especially super-oxide and hydrogen peroxide, are also link to ethanol-induced gastric injury and play a crucial role to further induce gastric inflammatory response. In addition, ethanol itself destroys gastric ...
Using a novel optical technique, polarization-gated spectroscopy, our group detected an early increase in blood supply (EIBS) prior to any morphological manifes...
Gastric mucosa of BALB/c mouse infected with H. pylori for 1 week. Significant infiltration of inflammatory cells is not seen. H & E stain. Original magnifi
The cytology of gastric mucosa: Smears and sections were obtained from various labelled points on the mucosal surface of 25 freshly-excised stomachs, and the ap
The involvement of cAMP as a second messenger for histamine-induced H+ secretion was studied in a physiologically active, in vitro preparation of piglet gastric mucosa. During the first 5--10 min of stimulation with either histamine or the cAMP phosphodiesterase inhibitor 3-isobutyl-1,4-methylxanthi …
Gastrointestinal diseases often do not cause much discomfort, and felt a slight indigestion after eating. Any irregularities in the digestive organs indicate changes in the frequency and character of stool.. The presence of any of these symptoms may indicate pathological conditions, to identify which will help timely survey. Sometimes these symptoms to report breaches of the mucosa of the body, so doctors do not recommend ignore them.. ...
Isolation and characterization of a gene expressed mainly in the gastric epithelium, a novel member of the ep37 family that belongs to the βγ-crystallin superfamily (1998 ...
In this study, Albis (containing ranitidine, sucralfate, and bismuth) prevented the gastric mucosal injury provoked by long-term use of ASA. There was no development of peptic ulcer in either of the groups during the study period. This might be due to the study period being too short to allow peptic ulcer to develop by the use of low-dose ASA. However, gastric mucosal injury measured by the MLS developed, but was reduced by concomitant use of Albis. Although several studies have reported the efficacy of PPIs or H2RAs in the prevention of peptic ulcer and gastric mucosal injury caused by ASA, there is no report of the efficacy of fixed-dose combination of H2RA, sucralfate, and bismuth [3,7,11,14-17]. This is the first prospective trial to evaluate the efficacy of combination of H2RA, sucralfate, and bismuth for the prevention of peptic ulcer or gastric mucosal injury due to long-term use of lowdose ASA ...
TY - JOUR. T1 - Ii-CS on gastric epithelial cells interacts with CD44 on T cells and induces their proliferation. AU - Barrera, C. A.. AU - Chan, T.. AU - Crowe, S. E.. AU - Ernst, P. B.. AU - Reyes, Victor. PY - 2003. Y1 - 2003. KW - CD44. KW - Gastric epithelial cell. KW - H. pylori. UR - http://www.scopus.com/inward/record.url?scp=0038579613&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0038579613&partnerID=8YFLogxK. M3 - Article. VL - 987. SP - 285. EP - 287. JO - Annals of the New York Academy of Sciences. JF - Annals of the New York Academy of Sciences. SN - 0077-8923. ER - ...
We have shown that contact with H. pylori rapidly activates ERK1, ERK2, p38, JNK p46, and JNK p54 MAP kinases in AGS gastric epithelial cells. We also find that H. pylori cag+ strains are more potent than cag− strains in inducing MAP kinase activation. Differential MAP kinase activation by cag+ and cag−H. pylori strains is particularly evident for JNK phosphorylation and appears to be dependent upon genes within the cag pathogenicity island. Inhibitors of p38 and MEK1 MAP kinases prevent H. pylori-induced IL-8 production. However, p38 and MEK1 MAP kinase activity do not appear to be essential for H. pylori-induced NF-κB activation.. H. pylori has adapted to interact specifically with gastric-type epithelial cells. H. pylori infection is limited to areas of the gastrointestinal tract that are lined by gastric epithelium, and the bacterium is known to activate several gastric epithelial cell signaling events. Previous studies have shown that adherence of H. pylori to AGS gastric epithelial ...
The isolation of Helicobacter pylori from the human gastric mucosa in 1982 and the demonstration of its involvement in gastritis, peptic ulcer disease and gastric adenocarcinomas have radically changed our perception of these diseases. H. pylori is a small, spiral, gram-negative bacillus that appears to inhabit the mucous layer overlying the gastric epithelial cells in humans. It produces a potent urease, which, by producing ammonia, may help to neutralize gastric acid, but the mechanism by which the bacteria produces gastric inflammation is not clear as it does not invade the mucosa. Development of atrophy and metaplasia of the gastric mucosa are strongly associated with H. pylori infection. Oxidative and nitrosative stress in combination with inflammation plays an important role in gastric carcinogenesis. More. Last updated: 25 Janury 2008. ...
Ethanol, after intragastric administration, penetrates deeply into the gastric mucosa because of high lipid solubility and, at concentrations of 50-100%, causes microvascular damage and hemorrhagic lesions (23, 34, 37, 38, 41). Ethanol-induced injury to the gastric mucosa is a time-related process in which disruption or exfoliation of the gastric surface epithelium is followed by necrosis of deeper mucosal layers, including the mucosal proliferative zone and the microvasculature (23,37, 38, 41). Angiogenesis is a prerequisite for the healing of ethanol-induced deep gastric mucosal damage. Our previous study has shown that ethanol-induced injury to gastric mucosa triggers an angiogenic response as well as an increase in bFGF, a known angiogenic factor, in the mucosa bordering necrosis (36, 39).. The present study demonstrates for the first time that ethanol-induced injury to the gastric mucosa activates VEGF gene expression as reflected by increases in VEGF at both the transcriptional and ...
Visualizing the mucosal surface may require using forceps to hold the specimen open (Fig. 19), unlike the specimens pictured in the other gross photographs. Histology shows marked thickening and fibrosis of the lamina propria, submucosa, and muscularis propria (Fig. 20). (Compare the normal histology in Fig. ) Fig. 19 Stricture of the esophagus, fresh specimen 44 Fig. 20 Histology of stricture (H & E, ×20) B. Gorman 2 Histologic Anatomy 45 Inlet Patch The inlet patch is characterized by ectopic gastric mucosa that is surrounded by normal squamous mucosa (Fig. A b Fig. 21 (a) Inlet patch (H & E, ×40). The mucosa on the left side of this photomicrograph shows essentially normal gastric mucosa with foveolar and glandular epithelium. The mucosa on the right shows normal esophageal squamous epithelium. (b) Inlet patch (H & E, ×200). On higher power, the gastric mucosa of the inlet patch is identical to that seen in the stomach, with foveolar epithelium overlying gastric glands composed of mucus ...
Bullfrog tadpole stomachs of various metamorphic stages were examined to determine the fine-structural development of oxyntic cells and to correlate observed morphological development with the capacity to secrete HCl. It was found that in vitro tadpole stomachs can consistently be stimulated to secrete acid by stage XXIV of metamorphosis, when tail reabsorption is nearly complete. Concomitant with the appearance of HCl secretion, identifiable oxyntic cells were found in the gastric glands.. Prior to stage XXIV (stages XXI and XXII) the majority of cells present in the developing gastric glands exhibit features of cytological organization characteristic of undifferentiated cells: large nuclei, relatively scantry cytoplasm, and numerous ribosomal particles within the cytoplasmic matrix. The newly differentiated oxyntic cells of stage XXIV tadpole stomachs are recognizable by the accumulation of tubular members of the smooth-surfaced endoplasmic reticulum in the apical portion of the cells. These ...
Lawson R. Thoracoabdominal duplication cyst containing heterotopic gastric mucosa: report of a case. J Am Osteopath Assoc 1968;67(11):1292. doi: .. Download citation file:. ...
Chem Biol Interact. 2009 Aug 14;180(3):499-505. doi: 10.1016/j.cbi.2009.04.006. Epub 2009 May 3. Research Support, Non-U.S. Govt
Helicobacter pylori (H. pylori) is implicated in human gastric mucosa. Fork head box M1 (FoxM1), the key positive regulator of cell proliferation is overexpressed in gastric cancer. MicroRNAs are important post-transcriptional regulators of gene expression. In this study, we explored the effect of H. pylori infection on FoxM1 expression and possible mechanisms. The expression of FoxM1 was gradually increased in human gastric specimens from inflammation to cancer. FoxM1 was time- and concentration-dependently upregulated in gastric epithelial-derived cell lines infected with H. pylori. CagA, the key virulence factor of H. pylori, was associated with increasing FoxM1 expression. H. pylori and CagA inhibited the expression of P27Kip1 (cylcin-dependent kinase inhibitor 1B, CDKN1B) and promoted cell proliferation by upregulating FoxM1. The expression of hsa-miR-370 was decreased in human gastritis and gastric cancer. FoxM1 was directly downregulated by hsa-miR-370 in gastric cell lines. H. pylori and ...
Wound-healing of the gastric mucosa is suggested to be stimulated by hepatocyte growth factor (HGF). Polyamines are shown to contribute to repair after damage in the gastric mucosa. The present study was designed to elucidate whether HGF can stimulate wound-healing of the gastric mucosa via polyamin …
Investigations on gastric mucosal protective mechanisms are focused mainly on the local mucosal processes. Much less is known about how the central nervous system may influence the gastric mucosal defense. However, gastric mucosal protection induced by a central mechanism was described recently (Tache et al., 1994; Gyires, 1997;Guidobono et al., 1998; Kaneko et al., 1998; Yang et al., 1999). In our present study, the role of central opioid receptors was analyzed by means of selective δ- and μ-opioid receptor agonists. It was found that both the selective δ- and μ-opioid receptor agonists injected either i.c.v. or i.c. exerted protective effect against acidified ethanol-induced lesions; the rank order of potency was β-endorphin , DAGO , DADLE , deltorphin II , DPDPE following i.c.v. injection and deltorphin II , β endorphin , DPDPE , DAGO , DADLE following i.c. administration. The results suggest that activation of supraspinal δ- and μ-opioid receptors may induce gastric mucosal ...
Academic Journals Database is a universal index of periodical literature covering basic research from all fields of knowledge, and is particularly strong in medical research, humanities and social sciences. Full-text from most of the articles is available. Academic Journals Database contains complete bibliographic citations, precise indexing, and informative abstracts for papers from a wide range of periodicals.
Endothelial nitric oxide synthase (eNOS) has previously been detected in the glandular part of the human gastric mucosa. Furthermore, nitric oxide (NO) has been shown to influence gastric secretion in various animal models. The present study was cond
Hydrogen has been reported to relieve damage in many disease models, and is a potential additive in drinking water to provide protective effects for patients as several clinical studies revealed. However, the absence of a dose-response relationship in the application of hydrogen is puzzling. We attempted to identify the dose-response relationship of hydrogen in alkaline electrolyzed drinking water through the aspirin induced gastric injury model. In this study, hydrogen-rich alkaline water was obtained by adding H2 to electrolyzed water at one atmosphere pressure. After 2 weeks of drinking, we detected the gastric mucosal damage together with MPO, MDA and 8-OHdG in rat aspirin induced gastric injury model. Hydrogen-dose dependent inhibition was observed in stomach mucosal. Under pH 8.5, 0.07, 0.22 and 0.84 ppm hydrogen exhibited a high correlation with inhibitory effects showed by erosion area, MPO activity and MDA content in the stomach. Gastric histology also demonstrated the inhibition of damage by
Mucosal prostaglandin E2 levels in patients with the gastric ulcer before and after their ulcers were healed. Both the antral and duodenal PG E2 are significant
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The duodenal surface epithelium shown here consists of absorptive cells with scattered goblet cells, in contrast to that of stomach which consists uniformly of surface mucous cells.. Note that Brunners glands lie beneath the muscularis mucosae, in the submucosa. Click on the rectangle for a magnified image of the intestinal epithelium, or.... ...
Dystrophic lesions of the gastric mucosa were observed to be formed and the pepsinogen content was reduced by 57% in the gastric mucosa of rats exposed to various experimental stressors...
Gastric gland: false-colour scanning electron micrograph (SEM) of the mucous membrane lining the stomach, showing the shadowy entrances to a number of gastric glands. The glands secrete gastric juice (hydrochloric acid & the enzyme pepsin) and a protective mucous, derived from the simple, columnar cells (moss-like) that comprise the mucosa. Gastric glands are formed by simple invagination or tubular ingrowth of this mucosa into the underlying layer of tissue, the lamina propria. Magnification: x300 at 6x7cm size. - Stock Image P510/0042
Definition of Ulcer Index in the Financial Dictionary - by Free online English dictionary and encyclopedia. What is Ulcer Index? Meaning of Ulcer Index as a finance term. What does Ulcer Index mean in finance?
Positive cells in gastric mucosa of ctsz2/2 (p = 0.009) and wt mice (p = 0.001). Compared to wt animals with no further increase in F4/80 positivity, ctsz2/2
BACKGROUND Antenatal exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) has been associated with renal dysgenesis in humans. METHODS These studies characterized cyclooxygenase-2 (COX-2) versus COX-1-selective inhibition on nephrogenesis in the rodent using histomorphometry, immunohistology, and in situ hybridization. RESULTS Administration of a COX-2-selective inhibitor (SC58236), started during pregnancy until weaning, significantly impaired development of the renal cortex and reduced glomerular diameter in both mice and rats. An identical phenotype was demonstrated in COX-2 -/- mice. In contrast to its effects on the developing kidney, a COX-2 inhibitor had no effect on glomerular volume in adult mice. This effect was specific for COX-2 because maternal administration of a COX-1-selective inhibitor (SC58560) did not affect renal development despite significantly inhibiting gastric mucosal prostaglandin E2 (PGE2) synthesis in pups. The expression of COX-2 immunoreactivity peaked in the first
Background Feeding alfalfa hay is often recommended for its buffering components, like protein and calcium, to prevent lesions of the gastric mucosa in horses. Until now, there has been no information...
We previously reported that gastrin induced PAI-2 in gastric epithelial cells via activation of PKC and RhoA, which in part triggered release of an unidentified paracrine mediator (11) . The present findings therefore extend these studies both by identification of H. pylori as a regulator of PAI-2 in gastric epithelial cells and by demonstration of the role of NFκB and of IL-8 and COX-2 as mediators of the response. It is well recognized that NFκB is activated by H. pylori and in turn leads to induction of IL-8 and COX-2 (28 , 33 , 34) . Less clear, however, are putative targets within the gastric epithelium that might mediate the progression to cancer and the integrative mechanisms that might account for differential cell signaling in tissues as complex as the gastric mucosa. The present observations indicate that PAI-2 should now be considered a putative target of NFκB activation by H. pylori. It seems, however, that the role of NFκB is limited to cells exposed directly to H. pylori and ...
The mucus-secreting columnar cells lining the luminal surface and the pits are joined near their free surfaces to each other by tight junctions (Ham l974). It is surmized that this arrangement forms one of the mechanisms by which the underlying layers are protected against luminal acid. The supranuclear portions of the cells just below their free surfaces contain dense, homogeneous, spherical or ovoid granules consisting of a type of mucigen (Bloom and Fawcett l975). Upon release into the lumen, the granules give rise to the layer of mucus that covers the luminal surface of the mucosa. In the cells of the gastric pits, the granules become progressively less abundant at deeper levels, and in the bottom of the pits they from only a thin layer immediately beneath the cell surface. Cells of this kind continue into the necks of the gastric glands. Under physiological conditions, the surface mucus cells are continuously desquamated into the lumen and are completely replaced every 3 days (Ham l974; ...
Adenosine is the endogenous agonist at all adenosine receptors. Under resting physiological conditions, adenosine levels in the interstitial fluid are between 30 and 300 nM (7). This is sufficient to activate A1, A2A, and A3 adenosine receptors whenever these proteins are abundantly expressed on the cell surface. The local adenosine level increases 10-fold during hypoxia and 100- to 1,000-fold in ischemia (7, 18, 34, 72), allowing cell responses mediated via A2BR in these settings. The pharmacological and functional studies presented here have been conducted using parietal cells obtained from normal rabbit gastric mucosa, which are representative populations of native, nontransformed primary cells at rest. They provide evidence that A2B is the adenosine receptor that is preferentially, if not exclusively, expressed on the parietal cell membrane and mediates acid production via Gs activation. Moreover, activation kinetics indicate that the A2BR might act at full power to activate acid production ...
It must be assumed that some cause is operative in certain cases preventing the healing of defects in the gastric mucosa and is inoperative in others. Even though anhemolytic streptococci are present in practically all gastric ulcers, we cannot convince ourselves that these organisms have been proven as yet to be the factor which either initiates the ulceration or prevents healing. Nevertheless, the constant presence of streptococci in this type of lesion is a suggestive fact and further experiments to determine their significance are being undertaken. ...
The most common finding in this study is an inflammatory process of the gastric mucosa - gastritis.In fact, after 20 years it is present in almost everyone.More serious is the discovery of the plague.Its danger lies in the fact that it can bleed and even to break through the wall of the stomach completely.In the event of signs of complications held emergency EGD.Gastric ulcer, among other things, is able to regenerate a more serious disease.. Much more disturbing is the discovery in the stomach cavity of a tumor process.Unpleasant discovery is also a gastric polyp.If you find something similar or just inflamed mucous area with signs of changing the structure of the doctor, most likely, with the consent of the patient will take a biopsy.Later removal of tissue samples are sent to patotsitologicheskoe research.The result will allow to say exactly what is is one or the other a modified portion of the gastric mucosa.. ...
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During the past decade, Helicobacter pylori has become recognized as one of the most common human pathogens, colonizing the gastric mucosa of almost all persons exposed to poor hygienic conditions from childhood. It also is often found, albeit with a ...
Ulcer Index Indicator was developed by Peter Martin and Byron McCann in 1987. This is a volatility indicator that measures downside risk.
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MissD wrote:Hi all - I had my band out in 2009 - put on 30kgs. So had the sleeve done in nov 2013. Obviously there was quite a lot of time to heal in that 4 yrs
When did you all stop sleeping on your stomachs? I am 10 weeks and still do, but recently it had started to be periodically uncomfortable. I am curious when people started making the switch to a new position.