6,218 research outputs found
HT-CO2 causes slight, transient and recoverable peritoneal damages.
No full text(A) Light microscopic analysis of peritoneal alterations (from left to right, 0, 12, 24, 48, 72, 96h after HT-CO2 insufflation). The mesothelial cells detach and denuded basal lamina is apparently observed at 12 hours after HT-CO2 insufflations; (B) Scanning electron microscopic analysis of peritoneal alterations (from left to right, 0, 12, 48, 96h after HT-CO2 insufflation). The mesothelial cells detach and massive desquamations can be seen at 12 hours after HT-CO2 insufflations. However, the peritoneum recovers from 48 hours and restores to normal 96 hours later.</p
HT-CO2 significantly decreases port site metastasis.
No full text(A) Illustration of experimental setup. The location of port sites are recorded and marked. At 28 days after HT-CO2 or NT-CO2 insufflation, the marked port sites are checked for metastatic nodules. Laparotomy is performed and the port site metastases are confirmed from inside. (B) Port site metastasis forms in mice treated with NT-CO2 (arrows). The incidence of port site metastasis in NT-CO2 is 12.5% (3/24). In contrast, no port site metastases are detected in the HT-CO2 group.</p
HT-CO2 significantly suppresses peritoneal dissemination and ascites formation.
No full text(A) Macroscopic view of the intraperitoneal tumor spread. Metastatic tumor nodules can be seen growing on the mesenterium, peritoneum, greater omentum, diaphragm and the surface of the liver. The number of metastatic nodules in mice receiving HT-CO2 insufflation is significantly less than that in mice subjected to NT-CO2. (B) Ascites of mice receiving HT-CO2 treatments are significantly less than those subjected to NT-CO2 insufflation. (C) Statistical analysis of the number of peritoneal metastasis, weight of tumor nodule and ascites volume. Data are presented as means ± SD; *: Pvs NT-CO2.</p
Inhibition of native 5-HT3 receptor-evoked contractions in Guinea pig and mouse ileum by antimalarial drugs
No full textQuinine, Chloroquine and mefloquine are commonly used to treat malaria; however with associated gastrointestinal (GI) side-effects. These drugs act as antagonists at recombinant 5-HT3 receptors and modulate gut peristalsis. These gastrointestinal side effects may be the result of antagonism at intestinal 5-HT3 receptors. Ileum from male C57BL/6 mice and guinea pigs was mounted longitudinally in organ baths. Concentration-response curves for 5-HT and the selective 5-HT3 agonist 2-Me-5-HT were obtained with 5-HT (pEC50=7.57±0.33, 12) more potent (P=0.004) than 2-Me-5-HT (pEC50=5.45±0.58, n=5) in mouse ileum. There was no difference in potency of 5-HT (pEC50=5.42±0.15, n=8) and 2-Me-5-HT (pIC50=5.01±0.55, n=11) in guinea pig ileum (P>0.05). Quinine, Chloroquine or mefloquine was applied for 10 min and inhibitions prior to submaximal agonist application. In mouse ileum, quinine, chloroquine and mefloquine antagonised 5-HT-induced contractions (pIC50=4.9±0.17, n=7; 4.76±0.14,n=5; 6.21±0.2, n=4, respectively) with mefloquine most potent (P<0.05). Quinine, chloroquine and mefloquine antagonised 2-me-5-HT-induced contractions (pIC50=6.35±0.11,n=8; 4.64±0.2, n=7; 5.11± 0.22, n=6, respectively) with quinine most potent (P<0.05). In guinea-pig ileum, quinine, chloroquine and mefloquine antagonised 5-HT-induced contractions (pIC50=5.02±0.15, n=6; 4.54±0.1, n=7; 5.32±0.13, n=5, respectively) and 2-me-5-HT-induced contractions (pIC50=4.62±0.25, n=5; 4.56±0.14, n=6; 5.67±0.12, n=4, respectively) with chloroquine least potent against 5-HT and mefloquine most potent against 2-me-5-HT (P<0.05). These results support previous studies identifying anti-malarial drugs as antagonists at recombinant 5-HT3 receptors and may also demonstrate the ability of these drugs to influence native 5-HT3 receptor-evoked contractile responses which may account for their associated GI side-effects
A novel tissue microarray instrumentation:The HT-1 tissue microarrayer
No full textBackground: Tissue microarray (TMA) is a novel and useful tool to efficiently analyze gene expression in histological tissues. Aim: Cost-efficient and easy to use automated tissue arrayers will provide a better instrumentation to generate TMAs. Thus, we designed and produced our tissue microarrayer to meet these needs. Materials and Methods: The HT-1 tissue microarrayer we designed and manufactured consists primarily of four parts, including an instrument to make array pores for the recipient paraffin blocks, a punch needle, an instrument for negative-pressure embedding, and a special manipulator. By using the HT-1, 14 different TMAs were made to accommodate 312 cases of tissues and TMA sections were tested by hematoxylin-eosin (H&E) staining, in situ hybridization, and immunohistochemistry. Results: Expand: Hematoxylin and eosin staining showed that the tissue cylinders were similar, even, and in order on the slides. Most importantly, the HT-1 microarrayer can make array pores in the recipient paraffin block with a single application in seconds. The HT-1 also contains a unique negative pressure system for embedding TMA blocks. In addition, HT-1 can make tissue cylinders with the same levels and depth for equally embedded and sectioning. Conclusions: The HT-1 tissue microarrayer is a device that is simple, economical and easy to use
MatlabCode_RAM-HT
No full textThe programs reproduce reweighted atomic norm minimization based on Hankel-Toeplitz model (RAM-HT) and compare its performance with other algorithms, such as ANM-HT, RAM-T and ANM-T. More details and figures are shown in:[1] Chu Y, Wei Z, Yang Z. New reweighted atomic norm minimization approach for line spectral estimation[J]. Signal Processing, 2023, 206: 108897
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