No abstract available.
Head* ; Orthognathic Surgery* ; Posture* ; Prognathism*

PURPOSE: DNA mismatch repair gene is responsible for hereditary nonpolyposis colorectal cancer. But it is not well known its role in sporadic colorectal cancer patients. We analysed normal hMSH2, hMLH1 protein expression in colorectal adenocarcinoma tissues and corresponding normal tissues to find out the role of mismatch repair gene in sporadic colorectal cancer by Western blotting. METHODS: Normal hMSH2 and hMLH1 protein expression was studied on 25 colorectal cancer and corresponding normal tissue by Western blot with hMSH2 and hMLH1 monoclonal antibody. Normal protein band was expressed on 100 kD in hMSH2 and 87 kD in hMLH1. SW480 and LoVo cell line was used as positive and negative control for hMSH2 and LoVo and SW480 as positive and negative for hMLH1. And we analysed the relation between the hMSH2, hMLH1 protein expression and clinicopathological parameters. RESULTS: It was 2 cases (8%) that both hMSH2 and hMLH1 protein expression was not observed. Three cases (12%) were negative for hMSH2 and 2 cases (8%) for hMLH1. One or both hMSH2, hMLH1 protein expression was not observed in 7 cases (28%) in total. There was no correlation for proximal occurrence (25% vs 35%), young age (37.5% vs 23.5%) and lymph node metastasis (50% vs 47%). But poorly and mucinous differentiation was regarded as having relation with negative expression of hMSH2 and hMLH1 (50% vs 17.6%) but not significant statistically. CONCLUSION: Sporadic colorectal cancer with negative expression of normal hMSH2 and hMLH1 protein showed no relation to younger age, proximal site preference and lymph node metastasis. But it was suggested that mismatch repair gene protein was involved in cancer cell differentiation in sporadic colorectal cancer.
Adenocarcinoma ; Blotting, Western ; Cell Differentiation ; Cell Line ; Colorectal Neoplasms* ; Colorectal Neoplasms, Hereditary Nonpolyposis ; DNA Mismatch Repair ; Humans ; Lymph Nodes ; Mucins ; Neoplasm Metastasis

PURPOSE: Bile acids (especially deoxycholate) was known to be toxic and mutagenic on colon epithelium. They proposed at least four mechanisms for the bile acid toxicity. It is the one of these mechanisms that bile acid inhibits the xenobiotic metabolizing enzyme activity (esp glutathione S-transferase, GST). So we measured the cytosolic GST level of colon carcinoma cell lines after deoxycholate exposure whether or not the deoxycholate lowered the cytosolic GST activity. METHODS: Three colon cancer cell lines (LoVo, SW480, HT29) were used for this study. We calculated the cellular toxicity by MTS method. And cytosolic GST activity was measured according to the method as Habig described. For total GST activity, 2.5 mM 1-chloro-2,4-dinitrobenzene was used for substrate, and measured as absorbance in 340 nm. RESULTS: Basal cytosolic GST level for LoVo, SW480, HT29 cell line was 514.59+/-27.01, 291.63+/-38.44 and 344.58+/-47.92 nmol/min/mg cytosol protein. GST level did not changed significantly after 5 days culture without DCA. But GST level was decreased significantly to 128.63+/-21.35, 134.33+/-41.76 and 163.10+/-22.73 nmol/min/mg cytosol protein each cell line after 5 days deoxycholate exposure (p<0.005). CONCLUSION: Cytosolic GST level was lowered significantly after deoxycholate exposure for 5 days. One of the mechanisms of bile acid toxicity for colon cancer cell is proposed to inhibit cytosolic GST activity.
Bile ; Bile Acids and Salts ; Cell Line* ; Colon* ; Colonic Neoplasms* ; Cytosol* ; Deoxycholic Acid* ; Dinitrochlorobenzene ; Epithelium ; Glutathione Transferase* ; Glutathione* ; HT29 Cells ; Humans

Alzheimer's disease (AD) without cure remains as a serious health issue in the modern society. The major neuropathological alterations in AD are characterized by chronic neuroinflammation and neuronal loss due to neurofibrillary tangles (NFTs) of abnormally hyperphosphorylated tau, plaques of β-amyloid (Aβ) and various metabolic dysfunctions. Due to the multifaceted nature of AD pathology and our limited understanding on its etiology, AD is difficult to be treated with currently available pharmaceuticals. This unmet need, however, could be met with stem cell technology that can be engineered to replace neuronal loss in AD patients. Although stem cell therapy for AD is only in its development stages, it has vast potential uses ranging from replacement therapy to disease modelling and drug development. Current progress with stem cells in animal model studies offers promising results for the new prospective treatment for AD. This review will discuss the characteristics of AD, current progress in stem cell therapy and remaining challenges and promises in its development.
Alzheimer Disease* ; Humans ; Models, Animal ; Neurofibrillary Tangles ; Neurogenesis ; Neurons ; Pathology ; Prospective Studies* ; Stem Cells* ; Transplantation

BACKGROUND: To investigate changes of electrocardiogram (ECG) wave amplitudes in dogs with early bupivacaine-induced cardiac depression. METHODS: Bupivacaine was infused into pentobarbital-anesthetized mongrel dogs (n = 9) at a rate of 0.5 mg/kg/min for 30 min. R-wave, S-wave, T-wave amplitude in lead II and III, and cardiac output (CO) were measured every 5 min after the initiation of bupivacaine infusion. PR interval, QRS complex duration, corrected QT interval were also measured. MAP (mean arterial blood pressure), HR (heart rate), and cSvO2 (continuous mixed venous oxygen saturation) were recorded at 5 min intervals. Arterial blood gas, serum electrolytes and bupivacaine concentration were measured at 10 min intervals. The relationships between CO and ECG amplitudes, and of CO versus hemodynamic variables were compared by regression analysis. RESULTS: With bupivacaine infusion, R-wave amplitude decreased to zero and S-wave amplitude increased negatively in both leads. The best correlation with CO was seen in S-wave (r = 0.751) in lead III among the ECG parameters. CONCLUSIONS: Close monitoring of S-wave amplitude in lead III can be helpful for detecting the early Bupivacaine-induced cardiotoxicity.
Animals ; Bupivacaine ; Cardiac Output ; Depression ; Dogs ; Electrocardiography ; Electrolytes ; Hemodynamics ; Oxygen

Purpose: To compare the clinical characteristics of Vogt-Koyanagi-Harada (VKH) disease between patients with and without prodromal manifestations. Methods: We retrospectively reviewed the medical records of patients with VKH disease who were treated with systemic steroids. We grouped the patients into the incomplete type (36 eyes of 18 patients) and probable type (32 eyes of 16 patients) according to the presence of prodromal manifestations. We compared the following outcomes between groups: best-corrected visual acuity (BCVA), anterior chamber (A/C) cell, central foveal thickness (CFT), maximal subretinal fluid (SRF) height, choroidal thickness at baseline and 12 months after treatment, and recurrence rate. Results: BCVA logarithm of the minimum angle of resolution (logMAR) significantly improved from 0.37 ± 0.26 at baseline to 0.09 ± 0.17 at 12 months in the incomplete type group (p < 0.05) and from 0.35 ± 0.24 at baseline to 0.10 ± 0.18 at 12 months in the probable type group (p < 0.05); BCVA did not significantly differ between groups. Choroidal thickness significantly decreased at 12 months after treatment, compared with one week after treatment, in both groups (p < 0.05); choroidal thickness did not significantly differ between groups. There were no significant differences in clinical factors between groups, including baseline A/C cell, CFT, maximal SRF height, and recurrence rate. Conclusions No associations were found between disease type and clinical outcomes (BCVA, OCT findings, and recurrence). These data suggested that categorization of disease according to prodromal manifestations has limited usefulness in terms of clinical outcomes of VKH disease.

Adult-onset metachromatic leukodystrophy (MLD) is very rare with a combination of cognitive and behavioral symptoms and peripheral polyneuropathy. A 47-year-old man was admitted due to memory impairment, gait disturbance, dysarthria and personality changes for a period of 3 years. The arylsulfatase A level in his leukocytes was decreased. A brain MRI showed bilateral symmetrical demyelination but nerve conduction velocities (NCV) were normal. We report a very rare case of adult-onset MLD with normal NCV.
Behavioral Symptoms ; Brain ; Cerebroside-Sulfatase ; Demyelinating Diseases ; Dysarthria ; Gait ; Humans ; Leukocytes ; Leukodystrophy, Metachromatic* ; Magnetic Resonance Imaging ; Memory ; Middle Aged ; Neural Conduction* ; Polyneuropathies

Systemic amyloidosis is a disease that displays deposition of insoluble polymeric protein fibrils in tissues and organs. We report here on a case of a 64-year-old woman who initially presented with multiple enlarged lymph nodes. Computed tomography showed multiple enlarged lymph nodes in the mediastinal, lower cervical, supraclavicular, axillary and abdominal areas. Excision biopsy of the cervical lymph nodes and the subsequent histopathology showed amorphous eosinophilic material deposits, and these revealed apple-green birefringence on a polarizing microscopic examination on the Congo-red stained slide. The patient was diagnosed with amyloidosis and she received chemotherapy consisting of melphalan and dexamethasone. During chemotherapy, she was diagnosed with breast cancer. After modified unilateral radical mastectomy, the dexamethasone was restarted and this therapy resulted in stable disease.
Amyloid ; Amyloidosis ; Biopsy ; Birefringence ; Breast Neoplasms ; Dexamethasone ; Eosinophils ; Female ; Humans ; Lymph Nodes ; Lymphatic Diseases ; Mastectomy, Radical ; Melphalan ; Middle Aged ; Polymers

Present study was performed to delineate the inter-relationship among neuronal death, mossy fiber sprouting (MFS) and neurogenesis in hippocampal formation of pilocarpine-treated mice. Status epilepticus was induced by intraperitoneal administration of 300 mg/kg pilocarpine in male ICR and C57BL/6 mouse. The severity of seizure was evaluated using 5 grades of Racine scales for first 4 hr after pilocarpine injection. Fluro-Jade C (FJC) staing, NeoTimm's staining and immunohistochemistry for BrdU were employed to evaluate neuronal cell death, MFS and neurogenesis, respectively. All animals in the present study induced seizures over grade 3 of Racine scale by pilocarpine injection. ICR mice show higher seizure severity (mean Racine scale; 4.37) than C57BL/6 mice do (mean Racine scale; 3.22), while the latency times for the first seizure over Racine scale grade 3 are from 15 min to 20 min and showed no difference between the 2 strains. In ICR mouse, numerous FJC-positive cells in hilus of hippocampus were detected at 4 h after pilocarpine injection, while they were not detected at that time in C57BL/6 mouse. The number of FJC-positive neuronal cells, which were densely found in the pyramidal layer of CA1, CA3 and hilus polymorphic regions of hippocampus, reached peak at 3 days after injection and then few cells were found at 7 days after injection in both strains. In control animals, BrdU positive cells in dentate subgranular layer which represent the hippocampal neurogenesis were more numerous in C57BL/6 than in ICR. The number of BrdU positive cells significantly increased at 2 days after pilocarpine injection and reached the peak at 8 days after injection and returned to control level at 15 day after injection in both strains. The percent increase of the BrdU positive cell was more prominent in ICR mouse. MFS was found at 2 weeks after the injection and the intensity of MFS was getting strong at 4 weeks after injection. There was no differences in MFS grading between 2 strains. These results suggest that there are some inter-relationships among the seizure severity, hippocampal neuronal cell death and hippocampal neurogenesis, but they don't have any significant relationships with the mossy fiber sprouting from dentate granule cells.
Animals ; Bromodeoxyuridine ; Cell Death ; Hippocampus ; Humans ; Immunohistochemistry ; Male ; Mice ; Mice, Inbred ICR ; Neurogenesis ; Neurons ; Pilocarpine ; Seizures ; Status Epilepticus ; Weights and Measures

X-linked myotubular myopathy (XLMTM) is a rare congenital muscle disorder, caused by mutations in the MTM1 gene. Affected male infants present severe hypotonia, and generalized muscle weakness, and the disorder is most often complicated by respiratory failure. Herein, we describe a family with 2 infants with XLMTM which was diagnosed by gene analysis and muscle biopsy. In both cases, histological findings of muscle showed severely hypoplastic muscle fibers with centrally placed nuclei. From the family gene analysis, the Arg486STOP mutation in the MTM1 gene was confirmed.
*Codon, Nonsense ; Humans ; Male ; Muscle Hypotonia/genetics/pathology ; Myopathies, Structural, Congenital/*genetics/pathology ; Pedigree ; Protein Tyrosine Phosphatases, Non-Receptor/*genetics