The gastric motor function in gastric cancer and its correation of c-kit density in circular muscle layer

1998 ◽  
Vol 114 ◽  
pp. A818
Author(s):  
HJ Park ◽  
JH Kim ◽  
SI Lee ◽  
JK Kang ◽  
IS Park
Keyword(s):  
Gastric Cancer ◽  
Motor Function ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Circular Muscle Layer ◽  
Gastric Motor Function

scholarly journals First reported case of per anal endoscopic myectomy (PAEM): A novel endoscopic technique for resection of lesions with severe fibrosis in the rectum

2017 ◽  
Vol 05 (03) ◽  
pp. E146-E150 ◽  
Author(s):  
David Rahni ◽  
Takashi Toyonaga ◽  
Yoshiko Ohara ◽  
Francesco Lombardo ◽  
Shinichi Baba ◽  
...  
Keyword(s):  
Longitudinal Muscle ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Rectal Tumor ◽  
Resection Margins ◽  
Submucosal Layer ◽  
Longitudinal Muscle Layer ◽  
Circular Muscle Layer ◽  
Tunneling Method ◽  
Severe Fibrosis

Background and study aims A 54-year-old man was diagnosed with a rectal tumor extending through the submucosal layer. The patient refused surgery and therefore endoscopic submucosal dissection (ESD) was pursued. The lesion exhibited the muscle retraction sign. After dissecting circumferentially around the fibrotic area by double tunneling method, a myotomy was performed through the internal circular muscle layer, creating a plane of dissection between the internal circular muscle layer and the external longitudinal muscle layer, and a myectomy was completed.The pathologic specimen verified T1b grade 1 sprouting adenocarcinoma with 4350 µm invasion into the submucosa with negative resection margins.

scholarly journals The transwall gradient across the mouse colonic circular muscle layer is carbon monoxide dependent

2010 ◽  
Vol 24 (10) ◽  
pp. 3840-3849 ◽  
Author(s):  
L. Sha ◽  
G. Farrugia ◽  
D. R. Linden ◽  
J. H. Szurszewski
Keyword(s):  
Carbon Monoxide ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Circular Muscle Layer

Cholinergic nerve-mediated excitation in the guinea pig choledochoduodenal junction activated by distension

1994 ◽  
Vol 267 (5) ◽  
pp. G938-G946 ◽  
Author(s):  
F. Vogalis ◽  
R. R. Bywater ◽  
G. S. Taylor
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Action Potential ◽  
Action Potentials ◽  
Discharge Rate ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Circular Muscle Layer ◽  
Circular Layer ◽  
Longitudinal Layer

The electrical basis of propulsive contractions in the guinea pig choledochoduodenal junction (CDJ), which are triggered by distension, was investigated using intracellular microelectrode recording techniques. The isolated CDJ was placed in a continuously perfused tissue chamber at 37 degrees C. Membrane potential was recorded from smooth muscle cells in either the ampulla or in the upper CDJ (upper junction) regions, which were immobilized by pinning. Distension of the upper junction (20-30 s) by increasing intraductal hydrostatic pressure (mean elevation: 2.0 +/- 0.3 kPa, n = 13) triggered "transient depolarizations" (TDs: < 5 mV in amplitude and 2-5 s in duration) and action potentials in the circular muscle layer of the ampulla. The frequency of TDs in the ampulla was increased from 2.2 +/- 0.2 to 15.9 +/- 2.2 min-1 (n = 13) during distension. Simultaneous impalements of cells in the longitudinal and circular muscle layers in the ampulla revealed that subthreshold TDs in the circular layer were associated with an increased rate of action potential discharge in the longitudinal layer. Atropine (Atr; 1.4 x 10(-6) M) and tetrodotoxin (TTX; 3.1 x 10(-6) M blocked the distension-evoked increase in TD frequency, without affecting the frequency of ongoing TDs. The sulfated octapeptide of cholecystokinin (1-5 x 10(-8) M) increased the amplitude of TDs recorded in the circular muscle layer of the ampulla and increased action potential discharge rate. In separate recordings, radial stretch of the ampulla region increased the rate of discharge of action potentials in the smooth muscle of the upper junction.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of transmural field stimulation in isolated muscle strips from human esophagus

1990 ◽  
Vol 258 (3) ◽  
pp. G344-G351 ◽  
Author(s):  
A. Tottrup ◽  
A. Forman ◽  
P. Funch-Jensen ◽  
U. Raundahl ◽  
K. E. Andersson
Keyword(s):  
Longitudinal Muscle ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Isometric Tension ◽  
Field Stimulation ◽  
Platinum Electrodes ◽  
Longitudinal Muscle Layer ◽  
Circular Muscle Layer ◽  
Human Esophagus ◽  
40 Hz

Smooth muscle strips representing longitudinal and circular muscle layers of the esophagogastric junction (EGJ) and esophageal body (EB) of the human esophagus were prepared. The strips were mounted in organ baths and isometric tension was recorded. Square wave stimulation was applied through platinum electrodes. Only responses abolished by tetrodotoxin (TTX) were considered neurogenic. Strips taken from longitudinal muscle layers of the EB and EGJ contracted during field stimulation. The responses evoked were abolished by atropine, and optimal frequency of stimulation was 40 Hz. In strips taken from the circular muscle layer of the EB, a contraction occurred after cessation of the stimulus. Atropine inhibited 90% of this response; the optimal stimulation frequency was 40 Hz. When a tone was induced in strips from this layer, a TTX-sensitive relaxation was seen during field stimulation. During stimulation of strips from the EGJ circular muscle layer, which was the only preparation developing spontaneous active tone, a relaxation was seen. A small contraction followed after termination of the stimulus. The relaxation, which was nonadrenergic, noncholinergic, reached maximum at 10 Hz. Atropine inhibited 40% of the contraction. The results suggest that in the longitudinal muscle layer of the human lower esophagus field stimulation causes postganglionic nerves to release transmitter(s) acting on muscarinic receptors. The responses of circular muscle layers seem to be mediated through release of at least two transmitters.

scholarly journals Neonatal administration of tamoxifen causes disruption of myometrial development but not adenomyosis in the C57/BL6J mouse

Reproduction ◽  
2010 ◽  
Vol 139 (6) ◽  
pp. 1067-1075 ◽  
Author(s):  
Mohamed K Mehasseb ◽  
S C Bell ◽  
M A Habiba
Keyword(s):  
Smooth Muscle Actin ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Abnormal Development ◽  
Circular Muscle Layer ◽  
Receptor Modulation ◽  
Age Related ◽  
Uterine Adenomyosis ◽  
Development And Differentiation ◽  
Neonatal Administration

We previously demonstrated that in the CD-1 mouse, which exhibits a high incidence of age-related adenomyosis, neonatal exposure to tamoxifen induced premature uterine adenomyosis and was associated with abnormal development particularly of the inner myometrium. In the present study, we examined the effect of neonatal tamoxifen administration upon uterine development in the C57/BL6J mouse strain that is not known to develop uterine adenomyosis. Female C57/BL6J pups (n=20) were treated with oral tamoxifen (1 mg/kg) from age 1 to 5 days. Uteri from control and treated mice were obtained on days 5, 10, 15 and 42 of age. We examined sections histologically using image analysis and immunohistochemistry for α-smooth muscle actin (ACTA2, α-SMA), desmin, vimentin, laminin, fibronectin and oestrogen receptor-α (ESR1). Following tamoxifen exposure, all uteri showed inner myometrium thinning, lack of continuity, disorganisation and bundling. However, adenomyosis was not seen in any uterus. ACTA2 immunostaining was less in the circular muscle layer of treated mice. The temporal pattern of desmin immunostaining found in control mice was absent in tamoxifen-treated mice. There was no difference in the localisation of laminin or fibronectin between control and tamoxifen-treated groups. However, laminin immunostaining was reduced in the circular muscle layer of treated mice. Vimentin could not be detected in either group. In conclusion, our results demonstrate that the development of the inner myometrium is particularly sensitive to oestrogen antagonism, and is affected by steroid receptor modulation. Although tamoxifen induces inner myometrial changes including that of ACTA2, desmin, ESR1 and laminin expression in C57/BL6J neonatal mice similar to those induced in CD-1 mice, C57/BL6J mice did not develop premature adenomyosis. Thus, disruption of the development and differentiation of the inner myometrium cannot alone explain the development of tamoxifen-associated adenomyosis, and this must be dependent upon its interaction with strain-dependent factors.

Spontaneous and evoked inhibitory junction potentials in the circular muscle layer of mouse colon

1998 ◽  
Vol 69 (2-3) ◽  
pp. 115-121 ◽  
Author(s):  
N.J Spencer ◽  
R.A.R Bywater ◽  
M.E Holman ◽  
G.S Taylor
Keyword(s):  
Circular Muscle ◽  
Muscle Layer ◽  
Circular Muscle Layer ◽  
Mouse Colon

The sacral neural crest contributes neurons and glia to the post-umbilical gut: spatiotemporal analysis of the development of the enteric nervous system

Development ◽  
1998 ◽  
Vol 125 (21) ◽  
pp. 4335-4347 ◽  
Author(s):  
A.J. Burns ◽  
N.M. Le Douarin
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Enteric Nervous System ◽  
Myenteric Plexus ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Specific Marker ◽  
Circular Muscle Layer ◽  
Sacral Neural Crest ◽  
Antibody Labelling

The majority of the enteric nervous system is derived from vagal neural crest cells (NCC), which migrate to the developing gut, proliferate, form plexuses and differentiate into neurons and glia. However, for some time, controversy has existed as to whether cells from the sacral region of the neural crest also contribute to the enteric nervous system. The aim of this study was to investigate the spatiotemporal migration of vagal and sacral NCC within the developing gut and to determine whether the sacral neural crest contributes neurons and glia to the ENS. We utilised quail-chick chimeric grafting in conjunction with antibody labelling to identify graft-derived cells, neurons and glia. We found that vagal NCC migrated ventrally within the embryo and accumulated in the caudal branchial arches before entering the pharyngeal region and colonising the entire length of the gut in a proximodistal direction. During migration, vagal crest cells followed different pathways depending on the region of the gut being colonised. In the pre-umbilical intestine, NCC were evenly distributed throughout the splanchnopleural mesenchyme while, in the post-umbilical intestine, they occurred adjacent to the serosal epithelium. Behind this migration front, NCC became organised into the presumptive Auerbach's and Meissner's plexuses situated on either side of the developing circular muscle layer. The colorectum was found to be colonised in a complex manner. Vagal NCC initially migrated within the submucosa, internal to the circular muscle layer, before migrating outwards, adjacent to blood vessels, towards the myenteric plexus region. In contrast, sacral NCC, which also formed the entire nerve of Remak, were primarily located in the presumptive myenteric plexus region and subsequently migrated inwards towards the submucosal ganglia. Although present throughout the post-umbilical gut, sacral NCC were most numerous in the distal colorectum where they constituted up to 17% of enteric neurons, as identified by double antibody labelling using the quail-cell-specific marker, QCPN and the neuron-specific marker, ANNA-1. Sacral NCC were also immunopositive for the glial-specific antibody, GFAP, thus demonstrating that this region of the neural crest contributes neurons and glia to the enteric nervous system.

Sign in / Sign up

Export Citation Format

Share Document