No abstract available.

Conflicting results have been reported, as to whether or not wound repair is influenced following treatment with low doses of prednisolone, insulin, or thyrotrophic hormone. The present studies were undertaken to evaluate and compare the influence of above hormones on the wound repair process and their target organs in rats at different times after operation. The influence of the above hormones were observed as measurement of the tensile strength of healing skin incisions and the histologic finding of the wound sites and the target organs staining with H-E, PAS, and Masson's trichrome method. Saline 0. 1 ml were injected daily intramusculary in control group: prednisolone acetate 0. 2ml (4mg/kg/day) in prednisolone treated group: regular zinc insulin 0.1 ml(1.5IU/kg/day) in insulin treated group; thyrotrophin 0.1 ml (0.4IU/kg/day) in TSH trcated group. The observation period wer at 4th day, 7th day, 14th day and 21st day of post-operation. The results were as follows: 1. Prednisolone treated group: (1) The tensile strength were decreased at 4th and 7th day than control groups, but there were no statistically significant difference at 14th and 21st day from control group. (2) In histologic findings of the wound sites at 4th and 7th day, the repair processes were suppressed, but at 14th and 21st day, there were no difference from control group. (3) In histologic finding of adrenal cortex, the atrophic changes was observed from early stage. 2. Insulin treated group: (1) There were no statistical difference from control group in tensile strength at each observation period. (2) In histologic findings of the wound sites, the pictures of the repair processes were similar with control group at each observation period. (3) Atrophic change of islets of Langerhans in pancreas was observed at each observation period. 3. TSH treated group: (1) The tensile strength were increased at 4th, 7th, and 14th day than control group, but there was no statistical difference at 21st day frorn control group. (2) In histologic findings of the wound sites, the repair processes were aecelerated at 4th and 7th day than control group, but there were no defferences at 14th and 21st day from control group. (3) Hyperplastic change of acini in thyroid gland was observed through entire observation period.
Adrenal Cortex ; Animals ; Insulin ; Islets of Langerhans ; Pancreas ; Prednisolone ; Rats ; Skin ; Tensile Strength ; Thyroid Gland ; Thyrotrophs ; Thyrotropin ; Wounds and Injuries* ; Zinc

No abstract available.
Lymphocytes* ; T-Lymphocyte Subsets* ; Thyroid Gland*

No abstract available.
Aged* ; Humans

Fabricating human organs with tissue engineering and stem cells may be an alternative to current suboptimal therapies for treatment of malfunction or loss of human tissues or organs. From the tissue engineering's perspective, the patients are expected to be treated with new tissues or organs reconstructed with transplanted cells. The cells for tissue engineering could be somatic cells derived from the patients themselves, other individuals, or animals. Another valuable cell source would be stem cells. Embryonic stem cells retain the pluripotency to differentiate into every cell type of human organs, but ethical issues remain to be addressed. Adult stem cells may solve these ethical issues and immune rejection, but have limitation in differentiation into all ranges of tissue-specific cell types. Tissue engineering typically employs scaffolds fabricated from synthetic or natural biomaterials to engineer a new functional tissue from cells. The configuration of the biomaterials guides the structure of a regenerated tissue by defining a three-dimensional space. Appropriate combination of tissue engineering with stem cells shows a promise to fabricate human organs or tissues that can be utilized for patients in the near future.
Adult Stem Cells ; Animals ; Artificial Organs ; Biocompatible Materials ; Embryonic Stem Cells ; Ethics ; Humans ; Stem Cells* ; Tissue Engineering*

No abstract available.
Thinking*

BACKGROUND: The renin-angiotensin system (RAS) plays a crucial role in pathophysiology of congestive heart failure and ventricular remodeling after myocardial infarction (MI). There are two components, systemic and local, in RAS. There has not been a study to analyze differentially the sequential changes of systemic and local RAS after MI. The aim of this study was to analyze the sequential change of the expression of angiotensinogen mRNA, the first component of the renin-angiotensin system, in liver and non-infarcted myocardium in rats after myocardial infarction. METHOD: Female Sprague-Dawley rats (body weight 200-250 g) were subjected either to left coronary artery occlusion or to sham operation. And the rats were sacrificed at 1, 4, 18, 24 hours, 3 days, 2, 3 weeks. Hemodynamic measurement was performed and RNA was extracted from various tissues including liver and ventricle for the analysis of the expression of the angiotensinogen mRNA by northern blot analysis or RT-PCR. RESULTS: Coronary artery ligation resulted in comparable infarct sizes among rats at 3 weeks after MI and was accompanied by significant increases of LVEDP (preMI 11+/-2 vs postMI 21+/-3 mmHg, n=4). Systolic arterial pressure was reduced in animals with infarction (preMI 130+/-15 vs postMI 90+/-10 mmHgn n=4). The liver angiotensinogen mRNA levels increased at 4, 18, 24 hours after myocardial infarction and decreased at 3rd day to control values (Angiotensinogen/GAPDH;preMI 1.35+/-0.20 vs postMI 5.97+/-0.25, max 4-fold, n=3). After sham operation, the liver angiotensinogen mRNA levels increased also at 4, 18, 24 hours, but in a less degree (Angiotensinogen/GAPDH;preop. 2.15+/-1.17 vs postop. 3.41+/-1.76, max 1.5-fold, n=3). In contrast to the liver, small amounts of angiotensinogen mRNA were detectable in normal left ventricle of rat with RT-PCR. The myocardial angiotensinogen mRNA levels decreased transiently in acute phase after MI, and recovered at 3-day after MI and increased further afterwards upto 3rd month after MI. CONCLUSION: The angiotensinogen in liver was activated early during acute phase after MI and decreased toward normal as the stable state was achieved. In contrast to the circulating RAS that was activated in acute phase after MI, the local RAS in heart was activated in chronic phase after MI.
Angiotensinogen* ; Animals ; Arterial Pressure ; Blotting, Northern ; Coronary Vessels ; Female ; Gene Expression ; Heart ; Heart Failure ; Heart Ventricles ; Hemodynamics ; Humans ; Infarction ; Ligation ; Liver* ; Myocardial Infarction* ; Myocardium* ; Rats* ; Rats, Sprague-Dawley ; Renin-Angiotensin System ; RNA ; RNA, Messenger* ; Ventricular Remodeling

The hemodynamic aspects of cerebral arteriovenous malformations(AVM) are currently the subject of increasing interest. Recently developed methods such as Doppler sonography, Xenon-enhanced Computed tomography Cerebral blood flow(CT CBF), single photon emission computed tomography(SPECT), and position emission tomography(PET) have promoted a more dynamic diagnostic and therapeutic approach to the complicated problem related to surgery of AVM. In this article, the literatures concerning the hemodynamics of cerebral AVM were reviewed.
Arteriovenous Malformations ; Hemodynamics* ; Intracranial Arteriovenous Malformations*

No abstract available.
Urinary Bladder*

No abstract availalbe.
Severe Acute Respiratory Syndrome*