No abstract available.
Urinary Retention*

No abstract available.
Pancreatitis, Chronic*

BACKGROUND AND OBJECTIVES: The atherosclerotic plaque in the thoracic aorta has been considered as potential source of cerebral embolization. The aim of this study was to evaluate the relation of atherosclerotic plaque burden and aortic distensibility by combined transesophageal echocardiography(TEE) and acoustic quantification(AQ) in patients with cerebral infarction without cardiac origin of emboli. METHODS: The maximal intimal-medial thickness and distensibility of descending thoracic aorta using TEE (a 7.5 MHz multiplane transducer, Hewlett Packard Sonos 2500) and AQ were prospectively measured in 36 patients(mean age ; 61+/-9 years) with cerebral infarction without cardiac origin of emboli and compared with 87 controls(mean age ; 56+/-11 years) without history of cerebral infarction. After the quality of the short-axis images of the aorta was optimized, a software of AQ was activated and gain controls were adjusted. A region of interest was mannually traced around the descending thoracic aorta and then integrated software was used to compute and instantaneously display arotic lumen area as a function of time. Maximal and minimal cross sectional area and fraction area change were calculated as an average from five consecutive heart cycle. RESULTS: There were no statistically significant differences between two groups in gender, hyperlipidemia and smoking, but hypertension and diabetes were more common in the cerebral infarction group. The atherosclerotic intimal-medial thickness above grade 3 was found in 13(36.1 %) out of 36 patients with cerebral infarction and 15(17.2%) out of 87 controls(p<0.05). Aortic areas normalized for body surface area were not statistically different between patients and normal controls, but there were significant differences for elastic indices except compliance. Patients with cerebral infarction had a lower fractional area change(5.7+/-3.2% vs. 7.8+/-4.1%, p<0.05) and higher stiffness index(12.2+/-7.7 vs. 8.0+/-5.1, p<0.05) compared with control group. There was an inverse relationship between the aortic intimal-medial thickness and the fractional area change of descending aorta(r=-0.380, p<0.01). CONCLUSION: The data suggest that the aortic distensibility noninvasively measured by TEE and AQ predicts the atherosclerotic burden. Thus the aortic distensibility may be an additive risk factor for cerebral infarction.
Acoustics* ; Aorta ; Aorta, Thoracic ; Body Surface Area ; Cerebral Infarction* ; Compliance ; Heart ; Humans ; Hyperlipidemias ; Hypertension ; Plaque, Atherosclerotic ; Prospective Studies ; Risk Factors ; Smoke ; Smoking ; Transducers

BACKGROUND AND OBJECTIVES: The atherosclerotic plaque in the thoracic aorta has been considered as potential source of cerebral embolization. The aim of this study was to evaluate the relation of atherosclerotic plaque burden and aortic distensibility by combined transesophageal echocardiography(TEE) and acoustic quantification(AQ) in patients with cerebral infarction without cardiac origin of emboli. METHODS: The maximal intimal-medial thickness and distensibility of descending thoracic aorta using TEE (a 7.5 MHz multiplane transducer, Hewlett Packard Sonos 2500) and AQ were prospectively measured in 36 patients(mean age ; 61+/-9 years) with cerebral infarction without cardiac origin of emboli and compared with 87 controls(mean age ; 56+/-11 years) without history of cerebral infarction. After the quality of the short-axis images of the aorta was optimized, a software of AQ was activated and gain controls were adjusted. A region of interest was mannually traced around the descending thoracic aorta and then integrated software was used to compute and instantaneously display arotic lumen area as a function of time. Maximal and minimal cross sectional area and fraction area change were calculated as an average from five consecutive heart cycle. RESULTS: There were no statistically significant differences between two groups in gender, hyperlipidemia and smoking, but hypertension and diabetes were more common in the cerebral infarction group. The atherosclerotic intimal-medial thickness above grade 3 was found in 13(36.1 %) out of 36 patients with cerebral infarction and 15(17.2%) out of 87 controls(p<0.05). Aortic areas normalized for body surface area were not statistically different between patients and normal controls, but there were significant differences for elastic indices except compliance. Patients with cerebral infarction had a lower fractional area change(5.7+/-3.2% vs. 7.8+/-4.1%, p<0.05) and higher stiffness index(12.2+/-7.7 vs. 8.0+/-5.1, p<0.05) compared with control group. There was an inverse relationship between the aortic intimal-medial thickness and the fractional area change of descending aorta(r=-0.380, p<0.01). CONCLUSION: The data suggest that the aortic distensibility noninvasively measured by TEE and AQ predicts the atherosclerotic burden. Thus the aortic distensibility may be an additive risk factor for cerebral infarction.
Acoustics* ; Aorta ; Aorta, Thoracic ; Body Surface Area ; Cerebral Infarction* ; Compliance ; Heart ; Humans ; Hyperlipidemias ; Hypertension ; Plaque, Atherosclerotic ; Prospective Studies ; Risk Factors ; Smoke ; Smoking ; Transducers

No abstract available.

The morphologic study of noninfiltrating and infiltrating duct carcinoma of the breast disclosed profound alterations along the parenchymal-stromal junction. But fate of myoepithelial cell, changes of basement membrane and the relationship of fibroblast to myofibroblast remain uncertain. To study the morphologic changes of myoepithelial cell, basement membane and stromal fibroblast, a series of 32 not otherwise specified (NOS) type of infiltrating duct carcinoma of the breast with regional lymph node metastases was examined light microscopically after S-100 protein immunoperoxidase staining by biotinavidin system (BAS) and ultrastructurally. The results were as follows. 1) In 18 out of 32 cases, S-100 protein positive myoepithelial cells were observed individually in the parenchyma at the periphery of some carcinomatous duct-like structures or cancer cell nests. The cells were noted in 7 cases of metastatic regional lymph nodes. In 5 cases contained with 2 cases of infiltrating duct carcinoma with focal sarcomatous metaplasia, S-100 protein positive cells were seen in fibroblast-like spindle cells in stroma adjacent to cancer nests. 2) Ultrastructural features of myoepithelial cells showed significant loss of fine microfilament and hemides-mosomes and relative imcrease of coarse large filaments. Morphologic transformation of myoepithelial cells to neoplastic epithelial cells or stromal fibroblast-like spindle cells were suggested in 3 NOR type and 2 metaplastic type carcinomas. 3) The ultrastructural changes of basement membrane disclosed some variations from case to case and even within a single tumor if large number of blocks were studied. Focal destruction, splitting, segmentation and extensive loss of basement membrane arround cancer nests were noted. On the other hand, basement membrane material surrounded cancer nests or individual cancer cells irregularly. 4) Most stromal fibroblasts in infiltrating duct carcinoma had abundant rough endoplasmic reticulum with enlarged plump cytoplasm. Some of them were transformed to myofibroblasts which had perinuclear rough endoplasmic reticulum and peripheral microfilaments with dense bodies in their cytoplasm.
Neoplasm Metastasis ; Breast Neoplasms

No abstract available.
Animals ; Joints* ; Orthopedics* ; Rats*

As the clinical practice of using more than one drug at a time increase, the clinician is faced with ever-increasing number of potential drug interactions. Although many interactions have little clinical significances, some may interfere with treatment or even be life-threatening. This review provides a better understanding of drug-drug interactions often encountered in pharmacotherapy of depression. Drug interactions can be grouped into two principal subdivisions : pharmackinectic and pharmacodynamic. These subgroups serve to focus attention on possible sites of interaction as a drug move from the site of administration and absorption to its site of action. Pharmacokinetic processes are those that include transport to and from the receptor site and consist of absorption, distribution on body tissue, plasma protein binding, metabolism, and excretion. Pharmacodynamic interactions occur at biologically active sites. In this review, emphasis is placed on antidepressant medications, how they are metabolized by the P450 system, and how they alter the metabolism of other drugs. When prescribing antidepressant medications, the clinician must consider the drug-drug interactions that are potentially problematic.
Absorption ; Antidepressive Agents* ; Catalytic Domain ; Depression ; Drug Interactions* ; Drug Therapy ; Metabolism ; Plasma ; Protein Binding

As numbers of serotonin's function are so many, studies of serotonin are numerous nowadays. In the beginning, concentration of metabolites such as 5-HIAA was a key issue, but recent studies have been challenged for serotonin receptor genes and their relation to mood disoder. Serotonin transporter(5-HTT) gene is a strong candidate gene of mood disoder for following reason. Serotonin transporter is a key protein in the serogonin pathway as it regulate the concentration of serotonin in the synaptic clept and essential pathophysiology of depression is dysregulation of 5-HTT so that all antidepressants have effect of 5-HTT antagonist. The decrease of 5-HTT in the platelet and in brain of the depressive patients is much consistent results in the studies of the pathophysiology of mood disorder till now. By this, we will be able to develop simple and easy marker for diagnosis type. and treatment monitoring of depression. Many psychiatrists have sought the independent genes in relation to depression or schizophrenia. Obviously, the hereditary vulnerability contributes to etiology of mood disorders, but it is difficult to discriminate the independent genes because of many environmental factors. Moreover, in the hereditarily complex diseases such as mood disorder, the only vulnerability of gene can not sufficiently explain the etiology. In the future, to exclude the role of the gene-environmental interaction the methods such as gene transfer can be considered. in the opposite direction, by usion the gene destruction method the role of target genes can be examined. As yet the concept of the gene expression, neural plasticity, neurogenesis and etc is the elementary stage. The development of this field will help to establish the treatment strategy of chronic and refractory mood disorders.
Antidepressive Agents ; Blood Platelets ; Brain ; Depression ; Diagnosis ; Gene Expression ; Humans ; Hydroxyindoleacetic Acid ; Mood Disorders* ; Neurogenesis ; Plastics ; Psychiatry ; Schizophrenia ; Serotonin Plasma Membrane Transport Proteins ; Serotonin*

Advances in molecular biology contribute to the understanding genetic mechanism of psychiatric disorders. They have renewed hope for the discovery of disease relevant gene. However, the results somewhat confused. And we will wait for a long time for the application of gene therapy in schizophrenia. Fortunately we could classified the schizophrenia with genotypes of dopamine and serotonin receptors. It is expected that this genetic classification could provide key strategy for the therapeutic application in biological treatment for schizophrenia. The purpose of this article is to call attention of the institute participants to linkage. association. mRNA expression. genotypic classification and to the need for more systemic research. The author summarized the modified methods which were done in his laboratory in appendix.
Appendix ; Classification ; Dopamine ; Genetic Therapy ; Genotype ; Hope ; Molecular Biology* ; Receptors, Serotonin ; RNA, Messenger ; Schizophrenia