No abstract available.

Bcl-2 oncoprotein is being localized to mitochondria and interfering with programmed cell death (apoptosis) independent of promoting cell division in the lymphoid and nonlymphoid cells. The bcl-2 oncoprotein expression has been reported in follicular lymphomas as well as in diffuse non-Hodgkin's lymphoma, leukemia and a variable propotion of Hodgkin's lymphoma cases. Recent evidence suggests that some lymphomas protected from apoptosis is conferred through expression of Epstein-Barr virus(EBV) latent membrane protein which turn to cause upregulation of bcl-2. To define the role of the bcl-2 oncoprotein and EBV in lymphoid malignancy, we tried immunohistochemical studies with anti-bcl-2 antibody and In situ hybridization (ISH) with EBV-encoded small nuclear RNAs(EBER) in the paraffin embedded sections of 46 non-Hodgkin's lymphoma (NHL) cases and 20 Hodgkin's lymphoma (HL) cases. Bcl-2 oncoprotein expression was found in 37 of 46 cases (80%) of NHL with relatively strong cytoplasmic staining, and in 14 of 20 cases (70%) of HL with weak cytoplasmic staining in limited small numbers of RS, Hodgkin and lacunar cells. The widespread presence of bcl-2 oncogene in many different types of both NHL and HL supports that the extended cell survival through overexpression of bcl-2 gene protein may be a growth advantage of neoplastic lymphoid cells. In the ISH analysis for EBV, the presence of EBV was detected in 17 of 20 cases (85%) of HL, compared to 6 of 44 cases(13.6%) of NHL. It appears to be no direct correlation between overexpression of bcl-2 oncoprotein by neoplastic lymphoid cells and the presence of EBV in NHL but it seems to be a definite association between EBV and HL.

No abstract available.
Animals ; Carbohydrate Metabolism* ; Hindlimb Suspension* ; Hindlimb* ; Insulin* ; Muscle, Skeletal* ; Rats* ; Receptor, Insulin*

No abstract available.
Lymphangioma*

The androgen insensitivity syndrome is a heterogeneous disorder with a wide spectrum of phenotypic abnormalities, ranging from complete female to ambiguous forms that more closely resembles males. Mutations of the androgen receptor gene are responsible for a variable degree of impaired androgen action. The complete androgen insensitivity syndrome is characterized by normal female external appearance in spite of the normal male karyotype 46XY with testes and normal testosterone production and metabolism. This is transmitted by X-linked recessive manner. Wolffian duct does not develop. However, m llerian development does not occur in presence of antim llerian hormone activity. Recently we experienced a case of complete androgen insenditirity syndrome. We reported a case with concerned literatures.
Androgen-Insensitivity Syndrome* ; Female ; Humans ; Karyotype ; Male ; Metabolism ; Receptors, Androgen ; Testis ; Testosterone ; Wolffian Ducts

No abstract available.
Aged* ; Humans

BACKGROUND: Although the efficacy of morphine in a neuropathic pain state is somewhat controversial, intrathecally administered morphine reversed the mechanical allodynia in a previous animal study. Using a behavioral test, we investigated the mechanism of the antiallodynic action of intrathecal morphine by administering opioids, alpha2 adrenergic and cholinergic receptor antagonists in a rat model of neuropathic pain induced by a spinal nerve ligation injury. METHODS: Male Sprague Dawley rats were prepared with a tight ligation of the left lumbar 5th and 6th spinal nerves and insertion of a chronic lumbar intrathecal catheter. Morphine 1 microgram was administered intrathecally to attenuate the mechanical allodynia. Naloxone 10 microgram, yohimbine 30 microgram, prazosin 30 microgram, atropine 10 microgram, pirenzepine 10 microgram, and methoctramine 10 microgram was administered intrathecally before and after the injection of morphine in order to investigate the reversal of an increased allodynic threshold by morphine. The allodynic thresholds for the left hindpaw withdrawal to von Frey hairs were assessed and converted to %MPE. RESULTS: A reduction of mechanical allodynia by intrathecal morphine was produced. Naloxone pretreatment, but not posttreatment, reversed the antiallodynic effect of intrathecal morphine (P < 0.01). All alpha2 adrenergic and cholinergic receptor antagonists used here did not reverse it. CONCLUSIONS: The results suggest that the reversal mechanism of mechanical allodynia by intrathecal morphine appears to be mediated mostly by the opioid receptor system, but not the alpha2 adrenergic and cholinergic receptor systems, at the spinal level in a rat model of a spinal nerve ligation injury.
Analgesics, Opioid ; Animals ; Atropine ; Catheters ; Cholinergic Antagonists ; Hair ; Humans ; Hyperalgesia ; Ligation* ; Male ; Models, Animal ; Morphine* ; Naloxone ; Neuralgia* ; Pirenzepine ; Prazosin ; Rats, Sprague-Dawley ; Receptors, Opioid ; Spinal Nerves* ; Yohimbine

Myasthenia gravis is an autoimmune disorder, caused by the presence of anti-ac- etylcholine receptor antibody or acetylcholine-receptor deficiency and involved neuro- muscular endplate. The clinical course and outcome of myasthenia gravis are variable during pregnancy. The special caution and adequate management for myasthenic mother and myasthenia gravis occurred newborn of myasthenic mother are essential for good perinatal outcomes. We experienced a case of myasthenia gravis associated with pregnancy who underwent cesarean section. We present this case with a brief review of literatures.
Cesarean Section ; Female ; Humans ; Infant, Newborn ; Mothers ; Myasthenia Gravis* ; Myasthenia Gravis, Neonatal ; Pregnancy*

Leiomyoma of the female urethra is a very rare condition. A case of the leiomyoma arised from paraurethral area, between the urethra and vaginal wall in thirty seven-year-old female is presented. The weight of mass was 50g and 7X4x5cm. in size. That was enucleated surgically and confirmed as a leiomyoma histologically.
Female* ; Humans ; Leiomyoma* ; Urethra

No abstract available.
Diskectomy*