No abstract available.
Hepatitis B virus* ; Hepatitis B* ; Hepatitis*

No abstract available.
Hepatitis B virus* ; Hepatitis B* ; Hepatitis*

PURPOSE: This study evaluated the treatment effectiveness and proper radiation dose of helical tomotherapy (HT) in spine oligometastases from gastrointestinal cancers. MATERIALS AND METHODS: From 2006 to 2010, 20 gastrointestinal cancer patients were treated with HT for spine oligometastases (31 spine lesions). The gross tumor volume (GTV) was the tumor evident from magnetic resonance imaging images fused with simulation computed tomography images. Clinical target volume (CTV) encompassed involved vertebral bodies or dorsal elements. We assumed that the planning target volume was equal to the CTV. We assessed local control rate after HT for 31 spine metastases. Pain response was scored by using a numeric pain intensity scale (NPIS, from 0 to 10). RESULTS: Spine metastatic lesions were treated with median dose of 40 Gy (range, 24 to 51 Gy) and median 5 Gy per fraction (range, 2.5 to 8 Gy) to GTV with median 8 fractions (range, 3 to 20 fraction). Median biologically equivalent dose (BED, alpha/beta = 10 Gy) was 52 Gy10 (range, 37.5 to 76.8 Gy10) to GTV. Six month local control rate for spine metastasis was 90.3%. Overall infield failure rate was 15% and outfield failure rate was 75%. Most patients showed pain relief after HT (93.8%). Median local recurrence free survival was 3 months. BED over 57 Gy10 and oligometastases were identified as prognostic factors associated with improved local progression free survival (p = 0.012, p = 0.041). CONCLUSION: HT was capable of delivering higher BED to metastatic lesions in close proximity of the spinal cord. Spine metastases from gastrointestinal tumors were sensitive to high dose radiation, and BED (alpha/beta = 10 Gy) higher than 57 Gy10 could improve local control.
Disease-Free Survival ; Gastrointestinal Neoplasms ; Humans ; Magnetic Resonance Imaging ; Neoplasm Metastasis ; Radiotherapy, Intensity-Modulated ; Recurrence ; Spinal Cord ; Spine ; Treatment Outcome ; Tumor Burden

Although a number of remedies like corticosteroids, retinoids, griseofulvin, PUVA, cyclosporine, antibiotics, dapsone, cyclophosphamide, surgery, methotrexate, radiation therapy, antimalarial drugs, psychotharapy and psychiatric medications have been used to treat lichen planus, there were no specific methods until now. We report herein an interesting case of lichen planus in which complete healing was achieved by griseofulvin administration. The patient was a 54-year-old male who for 3 months had variouly sized and shaped, flat-topped, scaly, violaceous papules and plaques on the whole of his body. We confirmed the patients disease as lichen planus by a histopathologic examination of a skin biopsy specimen and gave him 500mg ultramicronized griseofulvin daily in divided dosages. After 12 weeks of the medication nearly all of the skin lesions were regressed, and by 14 weeks all skin lesions had disappeared leaving hyperpigmentation. Up to now, l9 months after discontinuation of the medication, no recurrence of the disease has been noted.
Adrenal Cortex Hormones ; Anti-Bacterial Agents ; Antimalarials ; Biopsy ; Cyclophosphamide ; Cyclosporine ; Dapsone ; Griseofulvin* ; Humans ; Hyperpigmentation ; Lichen Planus* ; Lichens* ; Male ; Methotrexate ; Middle Aged ; Recurrence ; Retinoids ; Skin

Cancer is considered to occur through abnormal growth and differentiation processes, in which oncogenes and tumor suppressor genes are deeply related. Cellular responses to DNA-damaging agents are believed to be critical determinants of human tumorigenesis. Cell cycle arrests and DNA repair following DNA damage require the coordination of multiple gene products that, as a whole, serve to maintain the integrity of the genome. Within the cell cycle, both G1-S and G2-M phase transitions are under constant surveillance by checkpoint genes for the protection of cells from either exogenous or endogenous DNA-damaging agents. p53 tumor suppressor gene mediates cell cycle perturbations in response to DNA damage, and play a role in cell death, genetic stability, and cancer susceptibility. Recently, gene therapy with p53 tumor suppressor gene is expected as a new effective therapeutic strategy in many kinds of cancer. By using retroviral vector system, we transduced p53 tumor suppressor gene into human osteosarcoma cells, and analysed its growth suppression and apoptosis inducing effects. Combined effects of p53 gene therapy with chemotherapeutic agent or radiation were also analysed. Titer of ecotrophic p53 retrovirus was 5.0x10/ml, and that of amphotrophic p53 retrovirus was 2.0x10/ml when NIH3T3 cells were used as target cells. Human osteosarcoma cells infected with amphotrophic p53 retroviruses showed increased p21waf1 gene expression, which acts as a major cyclin-dependent kinase inhibitor in DNA damage responses. In normal DMEM media, human skin fibroblasts infected with amphotrophic p53wt retroviruses showed very slow growing (1.7 fold increase in doubling time) and very low saturation density (50% decrease in cell density). In media containing chemotherapeutic agent, human osteosarcoma cells infected with p53wt retroviruses died rapidly; 75% of them died within 4 days and all of them died within 10 days of incubation with chemotherapeutic agent. Their DNAs were extracted and electrophoresed in agarose gel, and we identified DNA ladders characteristic of apoptotic cell death. When human osteosarcoma cells infected with p53 retroviruses were irradiated with ultraviolet light, more than 95% of cancer cells died within 1 day; whereas mock infected cells showed only less than 5% of cell death. These findings suggest that retroviral vector mediated p53 tumor suppressor gene transfer into cancer cells can suppress tumor cell growth and decrease tumor cell density effectively. These findings also suggest that effective induction of tumor cell apoptosis can be obtained when p53 gene therapy is used in combination with chemotherapy or radiotherapy.
Apoptosis ; Carcinogenesis ; Cell Count ; Cell Cycle ; Cell Cycle Checkpoints ; Cell Death ; DNA ; DNA Damage ; DNA Repair ; Drug Therapy ; Fibroblasts ; Gene Expression ; Genes, p53 ; Genes, Tumor Suppressor* ; Genetic Therapy* ; Genome ; Humans ; Oncogenes ; Osteosarcoma ; Phase Transition ; Phosphotransferases ; Radiotherapy ; Retroviridae* ; Sepharose ; Skin ; Ultraviolet Rays ; Zidovudine

Methylene blue (MB) is an effective antidote for methemoglobinemia. MB is a basic dye, yielding a blue solution. In the human body, hemoglobin is the oxygen-carrying protein including a ferrous atom. Hemoglobin is oxidized to methemoglobin (MetHb) with the ferric atom, which cannot bind to or carry oxygen. Equilibrium between hemoglobin and MetHb is approximately 99:1. Thus a healthy man can have about 1% of methemoglobinemia. The cytochrome b5 MetHb reductase pathway plays a major role in reducing MetHb to hemoglobin. The nicotin amide adenine dinucleotide phosphate (NADPH) MetHb reductase pathway is a minor reducing system of MetHb, and it needs NADPH as a cofactor. However, to the exceeding exogenous oxidative stress, the cytochrome b5 MetHb reductase pathway is soon exhausted, and the NADPH MetHb reductase pathway can be activated 4 to 5 times by the exogenous cofactor, MB. The decision to initiate MB therapy for methemoglobinemia depends on the MetHb level and the symptoms. The indication for MB therapy in a symptomatic patient is a MetHb level >20% and in an asymptomatic patient, a MetHb level >30%. Patients with comorbidities such as anemia, heart disease, pneumonia, chronic obstructive pulmonary disease, or liver cirrhosis can be candidates for MB therapy with an even lower MetHb level. The recommended initial dose of MB is 1 to 2 mg/kg. It can be repeated every 30 minutes to 1 hour. However, the dose should not exceed 7 mg/kg. A high dose of MB may induce methemoglobinemia paradoxically and also cause hemolytic anemia. Like other antidotes, MB has its own adverse effects.
Adenine ; Anemia ; Anemia, Hemolytic ; Antidotes ; Comorbidity ; Cytochromes b5 ; Heart Diseases ; Human Body ; Humans ; Liver Cirrhosis ; Methemoglobin ; Methemoglobinemia* ; Methylene Blue* ; NADP ; Oxidative Stress ; Oxidoreductases ; Oxygen ; Pneumonia ; Pulmonary Disease, Chronic Obstructive

No abstract available.
Digoxigenin* ; DNA* ; Hepatitis B virus* ; Hepatitis B* ; Hepatitis*

Cutaneous smooth muscle hamartomas are benign proliferations of smooth muscle bundles within the dermis. They can be congenital or acquired, and most cases are congenital. Congenital smooth muscle hamartomas (CSMHs) usually manifest at birth as well-circumscribed, frequently hypertrichotic, hyperpigmented or skin-colored patches or plaques on trunk or extremities. We report a case of CSMH in a 10 year-old girl, who showed a localized skin-colored patch showing prominent follicular papules on the lateral aspect of her right upper arm, which were found at birth. There was no hypertrichosis and the pseudo-Darier sign was negative. This patchy follicular variant is the less common clinical type of the disease.
Arm ; Dermis ; Extremities ; Female ; Hamartoma* ; Humans ; Hypertrichosis ; Muscle, Smooth* ; Parturition

Purpose: We report a patient with presumed ischemic unilateral oculomotor nerve palsy developing after a snake bite on the right finger.Case summary: A 58-year-old male visited our emergency department complaining of right ptosis and binocular diplopia that had developed after a snake bite. He had been bitten on a finger of the right hand by an unidentified snake about 6 hours prior to symptom onset. He lacked neurological symptoms such as headache, nausea, vomiting, or an altered consciousness level. The right hand exhibited severe swelling, oozing, and inflammation. The visual acuity was 20/25 in both eyes. Ptosis was evident in the right eye. Both pupils responded normally to light and near stimulation. Extraocular examination revealed movement limitations in all right-eye gaze fields except abduction. A serological test revealed coagulopathy. Pyridostigmine was prescribed, but the ocular symptoms did not immediately improve; however, they did improve gradually during follow-up. At 8 months after the initial visit, the patient exhibited an ortho primary gaze with an adduction limitation of -1. No aberrant regeneration was apparent. Conclusions Unilateral oculomotor nerve palsy can develop after a snake bite, possibly attributable to microvascular ischemia caused by coagulopathy.

The effects of 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) on movement and tyrosine hydroxylase (TH)-immunoreactive (ir) neuronal changes in young (5~6 weeks) and aged (10~12 months) C57BL/6 mice were studied. Locomotor activity was measured during 180 minutes after a single injection of 30 mg/kg of MPTP. For immunohistochemistry both young and aged mice were injected four repeated dosages of 10 mg/kg of MPTP 12 hours apart. We counted the numbers of TH-ir cell bodies using immunohistochemical technique in substantia nigra (SN), ventral tegmental area (VTA) and locus ceruleus (LC) 7 days after the last injection of MPTP. There was a marked decrease of locomotor activity in MPTP-treated young and aged mice, and a delay in recovery of locomotor activity in MPTP-treated aged mice. In young mice, there was a decrease in the number of TH-ir cell bodies in the SN of young mice, but not in VTA or LC. In aged mice, there was a significant decrease in the number of TH-ir cell bodies in VTA as well as SN. It was concluded that aged mice were more sensitive to MPTP than young mice, and MPTP-treated aged mice a more useful animal model for studing the characteristics of Parkinson's disease.
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine* ; Aging* ; Animals ; Immunohistochemistry ; Locus Coeruleus ; Mice* ; Models, Animal ; Motor Activity ; Neurons* ; Parkinson Disease ; Substantia Nigra ; Tyrosine 3-Monooxygenase ; Ventral Tegmental Area