Facial nerve is subject to injury at any point in the course from the cerebral cortex to the motor end plate in the face, so many etiologic varieties of facial paralysis may be encountered, including trauma, viral infection and the idiopathic. Authors have studied 39 cases of facial paralysis which had experienced of treatment in our department from March, 1996 to March, 1997 at Dong San Medical Center. The results obtained are as follows : 1) The highest age incidence showed 10 cases(24.6%) in 3rd decade 2) Among the total of 39 cases, male were 21 cases(53.8%) and female were 18cases(46.2%). 3) At the involved side, left side were 19 cases(48.7%) and right side were 18 cases(46.2%). 4) The causes of facial paralysis were; idiopathic (Bell's palsy) in 19 cases(48.7%) infectious in 6 cases(15.4%) neoplastic in 6 cases(15.4%) traumatic in 5 cases(12.9%) metabolic in 2 cases(5.1%) congenital in 1 cases(2.6%) 5) In time interval between onset of symptom and treated initial date, 26 cases(66.7%) in below 10 days and 8 cases(20.5%) in 11-20 days 6) Correlation of recovery rate according to the treated duration did not differ significantly 7)Result after treatment were satisfactory
A 5-year-old, spayed female Maltese dog presented with generalized multifocal pruritic erythema and alopecia for a month. Initial skin biopsy suggested cutaneious histiocytosis. The dog had been treated with the immunosuppressive therapy for a month, but multifocal erythematous patches and plaques were newly observed. Direct imprint smear of cutaneous lesions suggested a lymphoma and rebiopsy was performed. Microscopic examination demonstrated a round cell tumor with epitheliotrophism to the epidermis and adnexal structures. The neoplastic round cells were strongly positive for CD3 yet negative for CD79a, indicting the tumor was cutaneous epitheliotropic T-cell lymphoma. After 2 cycles of oral administration of lomustine ($70mg/m^2$, once every 2-3 weeks), only partial response was observed. Alternative chemotherapy with gemcitabine ($500mg/m^2$, 30-minute IV infusion, once every week) was initiated. A total 3 cycles of gemcitabine failed to control the progression of disease, and the dog was euthanized on Day 69 after the 1st lomustine treatment.
Ga-67 citrate scan has been requested for detection or follow-up of inflammatory or neoplastic disease. Visualization of Ga-67 citrate in the kidneys at 48 and 72 hr post injection is usually interpreted as evidence of renal pathology. But precise mechanisms of abnormal Ga-67 uptake in kidneys were unknown. We undertook a study to determine the clinical value of Ga-67 citrate imaging of the kidneys in 68 patients with primary or secondary nephropathy confirmed by renal biopsy and 66 control patients without renal disease. Renal uptake in 48 to 72 hr images was graded as follows: Grade 0=back-ground activity:1=faint uptake greater than background;2=definite uptake, but less than lumbar vertebrae; 3=same uptake as lumbar vertebrae, but less than liver; 4=same or higher uptake than liver. The results were as follows. 1) 42 of 65 (62%) patients with noninfectious nephritis showed grade 2 or higher Ga-67 renal uptake but only 10 percent of control patients showed similar uptake. 2) In 14 patients with systemic lupus erythematosus, 8 of 9 (89%) patients with lupus nephritis exhibited marked renal uptake 3) 36 of 41 patients (88%) with combined nephrotic syndrome showed Grade 2 or higher renal uptake. 4) Renal Ga-67 uptake was correlated with clinical severity of nephrotic syndrome determined by serum albumin level, 24 hr urine protein excretion and serum lipid levels. 5) After complete remission of nephrotic syndrome, renal uptake in all 8 patients who were initially Grade 3 or 4, decreased to Grade 1 or 0. In conclusion, we think that the mechanism of renal Ga-67 uptake in nephrotic syndrome might be related to the pathogenesis of nephrotic syndrome. In systemic lupus erythematosus, Ga-67 citrate scan is useful in predicting renal involvement.
Proceedings of the Korean Society of Applied Pharmacology
/
2002.07a
/
pp.113-113
/
2002
Phylogenetically conserved Bcl-2 family proteins play a pivotal role in the regulation of apoptosis from virus to human. Members of the Bcl-2 family consist of antiapoptotic proteins such as Bcl-2, Bcl-xL, and Bcl-w, and proapoptotic proteins such as BAD, Bax, BOD, and Bok. It has been proposed that anti- and proapoptotic Bcl-2 proteins regulate cell death by binding to each other and forming heterodimers. A delicate balance between anti- and proapoptotic Bcl-2 family members exists in each cell and the relative concentration of these two groups of proteins determines whether the cell survives or undergoes apoptosis. Mcl-1 (Myeloid cell :leukemia-1) is a member of the Bcl-2 family proteins and was originally cloned as a differentiation-induced early gene that was activated in the human myeloblastic leukemia cell line, ML-1 . Mcl-1 is expressed in a wide variety of tissues and cells including neoplastic ones. We recently identified a short splicing variant of Mcl-1 short (Mcl-IS) and designated the known Mcl-1 as Mcl-1 long (Mcl-lL). Mcl-lL protein exhibits antiapoptotic activity and possesses the BH (Bcl-2 homology) 1, BH2, BH3, and transmembrane (TM) domains found in related Bcl-2 proteins. In contrast, Mcl-1 S is a BH3 domain-only proapoptotic protein that heterodimerizes with Mcl-lL. Although both Mc1-lL and Mcl-lS proteins contain BH domains fecund in other Bcl-2 family proteins, they are distinguished by their unusually long N-terminal sequences containing PEST (proline, glutamic acid, serine, and threonine) motifs, four pairs of arginine residues, and alanine- and glycine-rich regions. In addition, the expression pattern of Mcl-1 protein is different from that of Bcl-2 suggesting a unique role (or Mcl-1 in apoptosis regulation. Tankyrasel (TRF1-interacting, ankyrin-related ADP-related polymerasel) was originally isolated based on its binding to TRF 1 (telomeric repeat binding factor-1) and contains the sterile alpha motif (SAM) module, 24 ankyrin (ANK) repeats, and the catalytic domain of poly(adenosine diphosphate-ribose) polymerase (PARP). Previous studies showed that tankyrasel promotes telomere elongation in human cells presumably by inhibiting TRFI though its poly(ADP-ribosyl)action by tankyrasel . In addition, tankyrasel poly(ADP-ribosyl)ates Insulin-responsive amino peptidase (IRAP), a resident protein of GLUT4 vesicles, and insulin stimulates the PARP activity of tankyrase1 through its phosphorylation by mitogen-activated protein kinase (MAPK). ADP-ribosylation is a posttranslational modification that usually results in a loss of protein activity presumably by enhancing protein turnover. However, little information is available regarding the physiological function(s) of tankyrase1 other than as a PARP enzyme. In the present study, we found tankyrasel as a specific-binding protein of Mcl-1 Overexpression of tankyrasel led to the inhibition of both the apoptotic activity of Mel-lS and the survival action of Mcl-lL in mammalian cells. Unlike other known tankyrasel-interacting proteins, tankyrasel did not poly(ADP-ribosyl)ate either of the Mcl-1 proteins despite its ability to decrease Mcl-1 proteins expression following coexpression. Therefore, this study provides a novel mechanism to regulate Mcl-1-modulated apoptosis in which tankyrasel downregulates the expression of Mcl-1 proteins without the involvement of its ADP-ribosylation activity.
Primary malignant neoplasm of the pericardium is very rare, Neoplastic involvement of the pericardium may result in rapidly developing hemorrhagic effusion. A 30-year-old male who occasionally suffered from chest tightness was referred to our hospital under the diagnosis of unstable angina. He presented with acute chest pain and severe dyspnea that had developed one day previously. The diagnostic investigations such as echocardiography, chest CT and magnetic resonance image suggested cardiac tamponade that was caused by rupture of the pericardial teratoma. An operation to remove the tumor and effusion was performed. The pericardial mass was completely excised, and the result of the frozen biopsy favored malignancy. The final pathologic report was malignant fibrosarcoma of the pericardium and no malignant cells were found on the cytology of the pericardial effusion. The patient had a smooth postoperative course and was referred to another hospital for additional radiation therapy. We report here on this case of cardiac tamponade that was caused by primary pericardial fibrosarcoma, and this required urgent diagnosis and surgical management.
The most significant direct role of estrogen in vivo is its ability to elicit receptor-mediated cellular proliferation in mammalian target tissues. However, the mechanism by which exogenously added estrogen causes the neoplastic transformation of renal cortical cells is yet to be uncovered. The present study was designed to evaluate interaction of $17{\beta}-estradiol\;(E_2)$ with epidermal growth factor (EGF) and insulin-like growth factor-I (IGF-I) on proliferation and $P_i$ uptake in primary cultured rabbit renal proximal tubular cells in phenol red-free, hormonally defined-medium. $[^3H]-thymidine$ incorporation increased markedly by about 133% and 141% more in the presence of $10^{-9}\;and\;10^{-6}\;M\;E_2$, respectively, than that of control. Cell count was 162% and 143% greater in the presence of $10^{-9}\;and\;10^{-6}\;M\;E_2$ , respectively, compared with control. Among all time points examined, there was an increase in $[^3H]-thymidine$ incorporation in the presence of $10^{-9}\;M\;E_2$ at day 9 or 13, respectively. However, $E_2$ ($10^{-9}\;M$) significantly drove up cell count to 160% of that of control at day 13, while it had a slight but statistically insignificant effect at day 9. $E_2-induced$ stimulation of $[^3H]-thymidine$ incorporation was completely reversed by $E_2$ antagonists (progesterone or tamoxifen). $E_2$ ($10^{-9}\;M$) or EGF ($10^{-8}\;M$) significantly stimulated $[^3H]-thymidine$ incorporation by 144% and 154% of control. $E_2$ plus EGF was synergistic on $[^3H]-thymidine$ incorporation (204% of control), while $E_2$ plus IGF-I showed a slight but no significant synergistic effect. Cell number also displayed similar pattern. $E_2$ ($10^{-9}\;M$) significantly stimulated $P_i$ uptake to 134% of control. $E_2$-induced stimulation of $P_i$ uptake was partially reversed by $E_2$ antagonists. EGF or IGF-I ($10^{-8}\;M$) significantly also increased $P_i$ uptake to 132% or 129% of control. $E_2$ plus EGF had synergistic effect on $P_i$ uptake, while $E_2$ plus IGF-I did not. In conclusion, $E_2$ may act not only directly interaction with its receptors but also indirectly as a modulator of EGF in proliferation and $P_i$ uptake of primary cultured rabbit renal proximal tubular cells.
A 6-year-old female Shih-tzu dog was referred with left elbow joint mass associated with weight bearing lameness. Ultrasonography demonstrated an encapsulated hyperechoic mass at the left elbow joint. Radiography was performed on elbow joint, chest, and abdomen, but there was no evidence of metastasis. Clinicopathologic examination revealed the existence of neoplastic cells with anisocytosis, pleomorphism and increased nuclear-cytoplasmic ratio. The left forelimb was amputated for cure. Histopathological examination diagnosed the mass as a malignant peripheral nerve sheath tumor. During the 4 weeks follow-up, the patient showed full remission and adopted to walk with remaining three legs. Thereafter, the tumor recurred after 5 months of first surgery at the operation site and other two cutaneuos regions. Cytology test revealed the mesenchymal originated tumor cells with malignancy. These tumors were surgically removed and histopathological examination of the resected tissue revealed the recurrence of primary tumor and metastasis. Metronomic therapy with cyclophophamide (10 mg/$m^2$, PO, sid) and piroxicam (0.3 mg/kg, PO, sid) had been adopted for 5 months. At 26 months of follow up after the first surgery, the dog alive with satisfactory quality of life. Aggressive surgical resection with metronomic chemotherapy should be the most effective treatment for malignant peripheral nerve sheath tumor.
A seven-year-old, castrated male Basset hound weighing 21.1 kg was presented for investigation of anorexia, lethargy, weight loss, melena and vomiting for 4 months. In laboratory findings, microcytic hypochromic anemia was identified, and other results were within a normal reference range. On the plain radiographs, soft tissue opacity was increased in the descending duodenal region; and on the contrast radiographs, ulcerative changes were identified in the entire segment of descending duodenum. Ultrasonographic findings included increased duodenal wall thickness and duodenal wall layering was lost. Endoscopy revealed irregular mucosal surface and luminal narrowing of the descending duodenum. There was concentrically thickened descending duodenum on the computed tomography. And the wall of the descending duodenum showed heterogenous enhancement after contrast agent injection. On histopathological findings, both chronic inflammation with mucosal proliferation and neoplastic changes with multiple small glandslike structures invading into the submucosa were identified. Based on these findings, presented case was diagnosed as an annular form duodenal adenocarcinoma. After 13 months of supportive medical treatment, the patient was expired. The purpose of this case report was to describe the duodenal adenocarcinoma in a dog.
A 3-year-old intact female hedgehog (Atelerix albiventris) was presented for evaluation of mandibular swelling. Fine needle aspiration of swollen mandibular was performed and smears were stained with Romanowsky type stain for cytological evaluation. Smears were highly cellular with predominance of variably shaped keratinized or non keratinized squamous cells with low numbers of spindloid to abnormally elongated cells. Cytologic impression was squamous cell carcinoma. The mass was surgically removed for histological examination. Microscopically tortuous and anastomosing delicate to broad pegs and nests of neoplastic squamous epithelial cells were supported by a moderate collagenous and spindloid fibroblast stroma. Tumor cells had moderate anisocytosis and mild anisokaryosis and range from moderately to well keratinized, with areas of intratumoral acantholysis accompanied by mixed stromal lymphoplasmacytic, neutrophilic inflammation. The mitotic index is 2-3 per high-power field. Tumor cells were expanding the subcutis subjacent to the layer of skeletal muscle and incorporating the osseous tissue fragments. The final diagnosis was squamous cell carcinoma. The patient survived three months after surgery without any further medical treatments.
A 4-year-old female beagle with progressive exophthalmos and which had a neoplastic mass with diameter of 1.4 cm in the left lower ocular adnexa. Histologically, the mass was composed of hyper-plastic lobules and tubular structures separated by fibrous septum. The well differentiated sebaceous gland forming various sized lobules, and infiltration of mast cells and mononuclear inflammatory cells were observed. Apical decapitation secretion of these tubular structures with basophilic materials in their lumen showed mild sebaceous gland metaplasia. Immunohistochemical studying, cell groups were positive in ${\alpha}-SMA$ and vimentin. The primary tumor was diagnosed as adenocarcinoma originated from moll gland and meibomian gland of the eyelid, and the infiltrating intraocular neoplasm was diagnosed as a malignant mixed tumor.
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