No abstract available.
Osteoporosis* ; Spondylolisthesis*

Objective: Individuals with borderline personality disorder (BPD) commonly have a favorite person (FP), whom they are heavily emotionally attached to and dependent on. This study aims to identify and illustrate the patterns of destructive FP relationships based on actual experiences described by those with BPD. Methods: A data mining process was conducted using raw data collected from online communities, such as blogs and social networks. An in-depth review of the information to better understand the natural course of the FP relationship was also conducted. Results: Individuals with BPD form an intense and insecure attachment toward their FP, from which they enormously suffer. FPs can be their friends, romantic or life partners, or family members. As their feelings go beyond their control, being increasingly obsessed with their FP, they make their FP gradually lose hope in continuing the relationship and want to quit trying to fulfill their needs. The relationship finally ends when the FP stops being responsible for meeting their expectations and eventually drifts away. Conclusion This study suggests that certain FPs, distinctively named Teddy Bear Person, may behave in a particular manner to increase the likelihood of the FP relationship becoming more destructive. Moreover, the rejection sensitivity model should be discussed to understand their dysfunctional interaction.

For the estimation of the proliferative activity, related to the biologic behaviour, malignant potential, and prognosis, of human thyroid tumors, PCNA(proliferating cell nuclear antigen) immunohistochemical staining was performed on paraffin-embedded sections of 9 normal thyroid tissues, 9 adenomatous goiters, 9 follicular adenomas, 4 Hurthle cell tumors, 12 papillary carcinomas, 4 follicular carcinomas, and 3 anaplastic carcinomas. The results were as follows: 1) The PCNA labeling indices in adenomatous goiter, follicular adenoma, and Hurthle cell tumor were 1.1, 1.5, and 2.4, respectively. They were significantly higher than the labeling index in normal thyroid. 2) The PCNA labeling indices in papillary carcinoma and follicular carcinoma were 3.5 and 4.4, respectively. They were significantly higher than the labeling indices in adenomatous goiter and follicular adenoma, but there was no significant difference between papillary and follicular carcinoma. 3) The PCNA labeling index in anaplastic carcinoma, 14.1, was significantly higher than those in benign and other malignant tumors. According to the results, the PCNA labeling index was well correlated with the malignant potential of a tumor. So the PCNA immunohistochemical staining is thought to be a useful method for the evaluation of the malignant potential and prognosis of a tumor.
Humans

BACKGROUND: We evaluated 1) the sequential changes of angiotensin-converting enzyme (ACE) mRNA expression in lung (main site for circulating ACE synthesis) and left ventricle, and 2) whether such expression is modified by ACE inhibitor or angiotensin II receptor blocker treatment after acute myocardial infarction (MI) in rats. METHODS: Placebo, captopril (2 g/liter drinking water) or TCV-116 (10 mg/kg/day gavage) was administered 3 days before left coronary occlusion and continued for 6 weeks. At 1, 3 and 6 weeks after operation, hemodynamic measurement was performed and pulmonary and myocardial ACE mRNA expression was analyzed by quantitative RT-PCR using rcRNA as an internal standard. RESULTS: Mean BP and LVEDP increased in untreated rats compared with captopril- and TCV-116-treated rats (post-MI 6week, p<0.05). Pulmonary ACE mRNA increased in acute phase (post-MI 1 week, max. 1.4 fold, p<0.05 vs. pre-MI) and returned to pre-MI value thereafter. In contrast, cardiac ACE mRNA expression showed slightly decreasing tendency in acute phase, and was increased up to 1.6 fold in chronic phase after MI (post-MI 3 and 6weeks, p<0.05 vs. pre-MI). No changes in pulmonary ACE gene expression were found with RAS blockade. However, in acute phase after MI, cardiac ACE mRNA increased with both captopril and TCV-116 treatment (post-MI 24hour and 1week, max. 2 fold, p<0.05 vs. untreated group). CONCLUSION: 1) In contrast to the pulmonary ACE mRNA that is activated in acute phase, the cardiac ACE mRNA is activated in chronic phase after MI. 2) RAS blockade does not affect the change of pulmonary ACE expression, but modulate the change of cardiac ACE expression after MI.
Animals ; Captopril ; Coronary Occlusion ; Drinking ; Gene Expression* ; Heart Ventricles ; Hemodynamics ; Lung* ; Myocardial Infarction* ; Myocardium* ; Peptidyl-Dipeptidase A ; Rats ; Receptors, Angiotensin ; RNA, Messenger

BACKGROUND: Epidural anesthesia is becoming an increasingly important aspect of anaesthetic practice because it has many advantages. To achieve the appropriate sedation, various methods have been described. The authors applied the ketamine for this purpose in subanesthetic dose and compared with the midazolam that has been most commonly used for intravenous sedation. METHODS: Fifty-seven adult patients undergoing lower abdominal and extremity surgery who were receiving epidural anesthesia were randomely enrolled into this clinical study. They were allocated to three groups to receive only normal saline (group C), midazolam 0.05 mg/kg (group M) and ketamine 0.5 mg/kg midazolam 0.05 mg/kg (group K) in normal saline 10ml, respectively. Hemodynamic and respiratory measurements were recorded at baseline, 1 minute, 3 minute, 5 minute, 10 minute, 20 minute and 30 minute after sedation. The degree of sedation was assessed by a blinded observer using sedation score. RESULTS: There were no significant differences for hemodynamic and respiratory parameters, but decrements of arterial pressure at 1 minute after sedation were most remarkable in the group M. Sedation was satisfactorily achieved by combination of ketamine and midazolam without significant emergence reaction. CONCLUSIONS: The combination of ketamine and midazolam was judged to be suitable alternative for sedation during epidural anesthesia.
Adult ; Anesthesia, Epidural* ; Arterial Pressure ; Extremities ; Hemodynamics ; Humans ; Ketamine* ; Midazolam*

Inflammatory myofibroblastic tumor (IMT) is a space occupying lesion which is composed of myofibroblasts, plasma cells, and lymphocytes. IMT of the maxillary sinus is rare and its etiology is unknown. We present a case of inflammatory myofibroblastic tumor occurring in the right maxillary sinus of a 57-year-old woman. Radiologically, this tumor was interpreted as malignant neoplasm. On histologic examination, bundles of spindle cells were admixed with inflammatory cells including mature plasma cells and lymphocytes. On the basis of the immunohistochemical findings and ultrastructural features, we recognized that the intervening spindle cells were myofibroblasts. We discussed etiology and prognostic factors of this tumor.
Female ; Humans ; Lymphocytes ; Maxillary Sinus* ; Middle Aged ; Myofibroblasts* ; Plasma Cells

No abstract available.
Fever*

The etiological and precipitating factors, clinical features and outcomes of 48 patients over the age of 17 years with generalized major motor status epilepticus were studied. Eleven patients were regarded to have idiopathic epilepsy and the other thirty-seven had symptomatic epilepsy due to intracranial infection, cerebrovascular diseases, cerebral tumors, cerebral trauma, metabolic disorders, unknown and others. Most frequent causes were intracranial infection including nonspecific inflammatory granuloma, cerebral cysticercosis, viral encephalitis and sequela of previous meningitis. The major single precipitating factor of the status was abrupt discontinuation of antiepileptic drugs and this accounted for 57% of the status in 30 patients with previous seizures. Other factors were upper respiratory infection, alcohol intake and physical exhaustion. In 18 patients without history of previous seizure, only six had obvious precipitating factors. Among 48 patients, sixteen patients showed primary generalized tonic-clonic status and the remaineder had generalized tonic-clonic status with focal onset. Twenty-five patients (78%) in the latter group had apparent causes and brain C.T. scans revealed structural lesions in 68% of 28 patients in the latter group. Therefore it is suggested that patients showing the status with focal onset must be screened with laboratory studies as fully as possible, including brain C.T. In 41 patients who had no apparent ifectious process, the episodes of status were accompanied by hyperthermia (69%) and transient leukocytosis (65%). In 16 of them, cerebrospinal fluid was examined and a status-induced cererbrospinal fluid pleocytosis was observed in 3 patients. Forty-two patients in this series recoverd without neurological sequelas from the status and three had some sequelae at the time of discharge, including disturbances of recent memory, calculation, judgement and emotion. Three patients (6%) who died from the status were having idiopathic epilepsy, viral encephalitis or subarachnoid hemorrhage, respectively.
Anticonvulsants ; Brain ; Cerebrospinal Fluid ; Cysticercosis ; Encephalitis, Viral ; Epilepsy ; Fever ; Granuloma ; Humans ; Leukocytosis ; Memory ; Meningitis ; Precipitating Factors ; Seizures ; Status Epilepticus* ; Subarachnoid Hemorrhage

Background : It has been suggested that thrombospondin (TSP) is a p53-dependent negative regulator of tumor angiogenesis. TSP expression and localization in hepatocellular carcinomas (HCCs) and its association with overexpression of p53 protein were investigated. Methods : TSP-1 and -2 expressions were examined in 40 HCC specimens by immunohistochemical staining and in 4 HCC cell lines by Western blotting. In addition, p53 protein expression and microvessel density (MVD) were correlated with the TSP expression. Results : Strong immu- nopositivity for TSP-1 was observed in fibroblasts, vascular endothelial cells, and some vas- cular smooth muscle cells of the stroma in 18 cases (45%), and in tumor cells in 3 cases (7.5%) of 40 cases of HCC. Immunoreactivity for TSP-2 was observed in only the sinusoidal lining cells of the tumor in 15 cases (46%), and in tumor cells in 2 cases (6%) of 32 cases of HCC. TSP-1 expression was inversely correlated with MVD (p=0.028), but TSP-2 expression did not show any correlation with MVD. Although p53 was overexpressed in 17 cases, there was no significant correlation between TSP and p53 expressions. None of the HCC cell lines expressed TSP-1 or -2. Conclusions : These findings indicate that TSP-1 is mainly derived from nonparenchymal cells, and may decrease tumor angiogenesis in HCC.
Angiogenesis Inhibitors ; Blotting, Western ; Carcinoma, Hepatocellular* ; Cell Line ; Endothelial Cells ; Fibroblasts ; Microvessels ; Myocytes, Smooth Muscle ; Thrombospondin 1 ; Thrombospondins

No abstract available.
Congenital Hypothyroidism*