Canalicular adenoma of the buccal mucosa: a case report with computed tomography and magnetic resonance imaging.
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Publications and source records attributed to Hiroyuki Yamada.
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UNLABELLED: We reported a case of thyroglossal duct cancer, which metastasized to the bilateral cervical lymph nodes. The cervical lymph node metastases were detected in the upper portion of the neck. According to the results obtained in the preoperative fine needle aspiration cytology, the lymph node metastases were classified as group V and a diagnosis of papillary carcinoma was made. The preoperative studies with 123I revealed no concentration in the submittal tumor. In our surgical procedure, bilateral supraomohyoid neck dissection was added to excision of the tumor. CONCLUSION: In view of the fact that thyroglossal duct cancer metastasized bilaterally to cervical lymph nodes in the present case, we experienced an extremely rare case.
To investigate the role of TLR in the development of murine tuberculosis in vivo, TLR2 and TLR6 knockout (KO) mice were infected with Mycobacterium tuberculosis by placing them in the exposure chamber of an airborne infection apparatus. Both TLR2 and TLR6 KO mice survived until sacrifice at 12 weeks after infection. Infected TLR2 KO mice developed granulomatous pulmonary lesions with neutrophil infiltration, which were slightly larger in size than those in wild-type mice. Pulmonary levels of the mRNAs for inducible nitric oxide synthase (iNOS), TNF-alpha, TGF-beta, IL-1beta, and IL-2 were significantly lower, but levels of the mRNAs for IL-4 and IL-6 were higher, than in wild-type (WT) mice. No significant difference was recognized in cytokine mRNA expression between TLR2 KO and WT mice at 12 weeks after infection. DNA binding by NF-kappaB was low in TLR2 KO mice. On the other hand, TLR6 KO mice were not different from WT mice in terms of pulmonary histopathology, mRNA expression and CFU assay. Therefore, TLR2 does not play an essential role in the pathogenesis of murine tuberculosis, although it is important for defense against mycobacterial infection.
MyD88 is an adaptor protein that plays a major role in TLR/IL-1 receptor family signaling. To understand the role of MyD88 in the development of murine tuberculosis in vivo, MyD88 knockout (KO) mice aerially were infected with Mycobacterium tuberculosis. Infected MyD88 mice were not highly susceptible to M. tuberculosis infection, but they developed granulomatous pulmonary lesions with neutrophil infiltration which were larger than those in wild-type (WT) mice (P < 0.01). The pulmonary tissue levels of mRNA for iNOS and IL-18 were slightly lower, but levels of mRNA for IL-1 beta, IL-2, IL-4, IL-6, IL-10, IFN-gamma, and TGF-beta were higher in MyD88 KO mice. IFN-gamma, TNF-alpha, IL-1 beta, and IL-12 also were high in the sera of MyD88 KO mice. There were no statistically significant differences in the expression of TNF-alpha, IL-12, and ICAM-1 mRNA between MyD88 KO and WT mice. Thus, MyD88 deficiency did not influence the development of murine tuberculosis. NF-kappa B activity was similar in the alveolar macrophages from the lung tissues of MyD88 KO and WT mice. Also, there may be a TLR2-specific, MyD88-independent IL-1 receptor/TLR-mediated pathway to activate NF-kappa B in the host defense against mycobacterial infection.
A 27-year-old male visited the outpatient clinic of our hospital with the chief complaints of fever, right chest pain and shortness of breath. He was admitted to our hospital for detailed examination of the right hydrothorax. The pleural effusion obtained by thoracocentesis was exudative and negative for Mycobacterium tuberculosis. Since the titer of adenosine deaminase in the pleural effusion was abnormally high, antitubercular therapy was started under suspicion of tuberculous pleuritis. Thereafter, the patient's subjective symptoms and blood parameters improved. Necrotic tissues were obtained by pleural biopsy using the Cope needle. In order to make a definitive diagnosis, pleural biopsy was performed thoracoscopically. White tubercular lesions with a smooth surface were sparsely distributed on the pleura. Histopathologically, these lesions were characterized by central areas of caseous necrosis surrounded by epithelial cells and Langhans' giant cells. Therefore, they were considered to be granulomatous lesions. The patient was given a diagnosis of idiopathic tuberculous pleuritis, and was treated with four antitubercular drugs in combination. His clinical signs subsided, and he was discharged. This case indicates that the examination of the inside of the pleural cavity with a flexible bronchoscope, instead of thoracoscope, under local anesthesia is useful to diagnose patients having tuberculous pleuritis.
Inbred mice differ in their abilities to control the growth of Mycobacterium tuberculosis in the lung and can as a result be regarded as either resistant or susceptible strains. In this study we report that the SWR mouse is both highly susceptible and in addition appears incapable of establishing a characteristic state of chronic disease after low-dose aerosol infection. In comparison to C57BL/6 mice, SWR mice were unable to contain the bacterial load in the lungs, resulting in progressive fatal disease. Histologic analysis of the lung tissue revealed evidence of a florid inflammatory cell response in the SWR mice leading to degeneration and necrosis and consolidation of a large percentage of the lung surface area. Digestion of infected lungs and analysis by flow cytometry demonstrated an initially similar but eventually higher number of lymphocytes accumulating in the SWR mice. Additionally, in contrast to the C57BL/6 mice, SWR mice had a significantly lower percentage of CD4 T cells in the lungs showing evidence of proliferation and positive intracellular staining for gamma interferon during the first two months of infection, and a lower percentage of both CD4 and CD8T cells exhibiting differentiation to an effector/memory phenotype during the first month of infection. We propose that further investigation of the SWR mouse may provide a new animal model for immunocompetent individuals apparently unable to effectively control the growth of M. tuberculosis in the lung.
Esophageal speech is the first choice for vocal rehabilitation in laryngectomized patients. However, shunt speech is a needed alternative for patients who cannot succeed at esophageal speech. Many kinds of voice prostheses, with good results, have been reported. Provox was selected for 15 laryngectomized patients who were treated in our department. Voice rehabilitation was successful in 13 patients. However, removal of the prosthesis was required in one patient because of stomal stenosis. Voice rehabilitation was not successful in one patient who exhibited esophageal stenosis. The rate of voice rehabilitation was not influenced by the extent of surgery, the dose of radiation, etc.. The maximum phonation time was more than 10 minutes in the 13 patients who succeeded at shunt speech. Prosthetic rehabilitation was requested by two patients who had been successful at esophageal speech. These results suggest that prosthetic voice rehabilitation may be indicated for a wide range of conditions.
Dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) gene expressions in metastatic colorectal cancer have been reported to be predictive parameters for the efficacy of fluoropyrimidine-based chemotherapy. In this study, we investigated the association between both DPD and TS expressions in primary colorectal tumor and the antitumor effect in patients with metastatic colorectal cancer when treated with a fluoropyrimidine-based protocol. DPD and TS expressions were measured by reverse transcription-PCR in surgically resected materials of primary colorectal tumors from 37 patients who went on to receive oral treatment of uracil and tegafur and leucovorin for either synchronous or metachronous metastatic diseases. Relative mRNA amounts of DPD or TS were expressed as the ratios of targeted gene to glyceraldehyde-3-phosphate dehydrogenase reverse transcription-PCR products. Median values of DPD mRNA expressions were 0.30 and 0.65 for responding tumors and nonresponding ones, respectively, with a statistical significance (P < 0.0001). No responding tumor had a DPD mRNA expression >/= 0.5. A total of 19 tumors had low DPD mRNA expressions of <0.5, and 63% of them showed response. There was no responding tumor with both high DPD and high TS (TS mRNA expression >/= 1.0). However, the response rate was 75% in tumors with both low DPD and low TS. The median survival time was 16.3 months in patients with both low DPD and low TS versus 8.4 months in patients with high DPD or high TS mRNA expression. In conclusion, the combination of DPD and TS mRNA expressions in the primary tumor might be useful as predictive parameters for the efficacy of fluoropyrimidine-based chemotherapy for metastatic colorectal cancer.
A phase I study was conducted to determine the maximum tolerated dose (MTD) and the dose limiting toxicity (DLT) of gemcitabine and irinotecan combination therapy as second line treatment in patients with advanced non-small cell lung cancer (NSCLC). Twelve patients with measurable NSCLC (age range 46-74 years; 7 males, 5 females; performance status 0 = 4, 1 = 8) who progressed or failed first-line chemotherapy were enrolled. Prior chemotherapy was platinum-based without gemcitabine or irinotecan. Gemcitabine was administered at a fixed dose of 1,000 mg/m2 after irinotecan administration, and irinotecan was administered at doses from 50 to 125 mg/m2 with an increment of 25 mg/m2, both on day 1 and 8. Chemotherapy was repeated every 3 weeks. Grade 3/4 leukopenia occurred in three patients (25%), neutropenia in four (33%), anemia in one (8%), and thrombocytopenia in one (8%). Grade 3 nausea and vomiting was observed in three (25%), grade 2 diarrhea in one (8%), and liver dysfunction in one (8%). Other toxicities were mild. Two of the three patients at level 4 (irinotecan 125 mg/m2) experienced dose limiting toxicity: one patient experienced grade 4 leukopenia and neutropenia, and the other experienced treatment delay of more than 2 weeks. The objective response rate was 16.6% (2/12). The maximum tolerated dose in this combination therapy was gemcitabine 1,000 mg/m2 and irinotecan 125 mg/m2. The dose level of gemcitabine 1,000 mg/m2 and irinotecan 100 mg/m2 on day 1 and 8 of a 3-week cycle is recommended for a phase II study.
Paclitaxel and carboplatin chemotherapy is reported to be a platelet-sparing drug combination. The objective of this study was to elucidate whether docetaxel with carboplatin has a similar platelet-sparing effect. This study investigated the time-course of the changes in the platelet count and the circulating concentration of thrombopoietin (TPO), a platelet growth factor, during combination chemotherapy consisting of carboplatin and docetaxel. Eleven patients with advanced lung cancer were enrolled; 8 receiving carboplatin and docetaxel (docetaxel group), and 3 receiving carboplatin and irinotecan (irinotecan group). The time-course profiles of the platelet count and the circulating TPO concentration were determined and compared between the two groups. The platelet count decreased significantly only in the irinotecan group, and on day 15 after therapy the thrombocytopenia was pronounced in comparison with that in the docetaxel group. The circulating TPO concentration remained almost constant in the irinotecan group, with no significant increases, while that in the docetaxel group was increased significantly on day 4 (p < 0.05), day 8 (p < 0.05), and day 15 (p < 0.01) after therapy. There was also a significant difference between the docetaxel group and irinotecan group with respect to circulating TPO concentration (p < 0.05). These results suggest that docetaxel might also have a platelet-sparing effect on the anti-platelet activity of carboplatin, mediated by levels of circulating TPO concentration.
Reverse redistribution (RR) of technetium-99m tetrofosmin (TF) in patients with acute myocardial infarction (AMI) has been considered a sign of salvaged myocardium. We examined the time evolution of the RR pattern during a 6-month period and the clinical implications of RR. TF myocardial SPET was performed in 22 patients 1 week, 1 month and 3-6 months after AMI. Myocardial images were obtained 30 min and 180 min after the injection of TF. Regional uptake of TF was rated using a four-point scoring system. RR was defined as an increase of more than 1 point in the regional score on images obtained at 180 min. Echocardiography was performed to assess regional wall motion at the same time as TF imaging. RR observed at 1 week tended to disappear after 1 month and 3-6 months. The incidence of regional wall motion abnormality was reduced in patients with RR compared with that in patients with fixed defects. Recovery of abnormal regional wall motion occurred earlier in segments with disappearance of RR than in those without disappearance of RR. It is concluded that RR may reflect salvaged myocardium and that disappearance of RR may indicate earlier recovery of salvaged myocardium.
The improvement in the sensitive determination method of estradiol using HPLC with electrochemical detection is described. The improvement was due to the optimization of the potential applied to the electrode of the analytical cell and employment of a guard cell. The detection conditions were optimized from the electrochemical properties of estradiol in acidic and alkaline eluents. The employment of the guard cell drastically decreased the background noise without any reduction in the response of estradiol, and contributed to improvement in the sensitivity. The optimized method combined with pretreatment by liquid-liquid extraction was applied to the determination of estradiol in rat plasma. The detection limit of 8 pg for the standard solution and 24 pg for the plasma sample, which was about 6-8-fold more sensitive compared to the previous reports, was attained.
BACKGROUND: Determination of intratumoral dihydropyrimidine dehydrogenase (DPD) is of clinical interest because increased DPD levels can influence the tumor response to 5-fluorouracil-based chemotherapy through increased inactivation of the agent in tumor cells. METHODS: DPD messenger RNA (mRNA) levels were evaluated in 80 consecutive patients undergoing surgery for primary colorectal cancer and 12 cases of liver metastasis. RESULTS: Higher DPD mRNA levels were associated with higher pathologic classification, corresponding to the T categories (r =.267; P =.003). The DPD mRNA level was statistically higher in tumors with microscopic lymph node metastasis than in those without (P =.002). Hence, the DPD mRNA level increased in accordance with Dukes' classification (r =.387; P =.0001). The DPD mRNA level of the liver metastasis from colorectal cancer was significantly higher than that of primary lesions (P =.002). In eight patients, the DPD mRNA level of the liver metastasis was significantly higher than that of the matched primary tumor (P =.017). CONCLUSIONS: Increases of the DPD mRNA level in cancerous tissue seem to reflect tumor progression. High DPD mRNA levels in liver metastasis and advanced colorectal cancer may have clinical importance for 5-fluorouracil-based chemosensitivity.
OBJECTIVE: Acute suppurative thyroiditis is a disease of an infection originated from the piriform sinus via congenital fistula. The purposes of this study are the establishment of accurate and necessary examinations for the diagnosis and necessary treatment for complete remission of this disease. METHODS: We reported nine cases with acute suppurative thyroiditis who were treated by operation. Preoperative examinations and operative procedures for nine cases were investigated. RESULTS: A congenital fistula was detected in seven of nine patients preoperatively, and in all seven patients, the fistula was detected during the operation. Serum thyroglobulin was elevated in four of five patients who were examined the serum level. Ultrasonogram was performed in eight cases, and localized swelling of the thyroid lobe was observed in all cases. No inflammatory recurrence was observed in eight cases, and recurrence was observed in one case where complete fistelectomy was not performed. CONCLUSION: Measurements of serum thyroglobulin, ultrasonography, and pharyngoesophagography were useful in the diagnosis of acute suppurative thyroiditis. Complete removal of the fistula with or without affected thyroid lobe is necessary to prevent recurrent suppuration.
When monocytes were cocultured with human osteosarcoma-derived cells (HOS cells), multinucleated giant cell formation of monocytes was induced. Intriguingly, even when a filter was interposed between monocytes and HOS cells, polykaryocytes also appeared. The multinucleated giant cells have characters similar to osteoclast-like cells. These findings indicate that soluble factor(s) secreted from HOS cells play an important role in polykaryocyte formation from monocytes. Twelve cloned cells were established from HSOS-1 cells and their capacities of inducing osteoclasts were investigated. Three cloned cells inducing nos. 4 and 9 had an ability of inducing osteoclasts (multinucleated giant cells, TRAP, calcitonin receptor and c-src mRNAs, osteoresorbing activity), and three cells, including nos. 1 and 5, did not show the ability. HOS cells and the cloned cells expressed several cytokine mRNAs. M-CSF was detected in the culture fluids of HOS cells, which also expressed RANK and RANK/ODF/OPGL mRNAs. Intriguingly, HOS cells secreting a soluble osteoclast inducing factors(s) expressed TNF-alpha converting enzyme mRNA. Furthermore, OCIF/OPG inhibited HOS cell-induced osteoclastogenesis and soluble RANKL could be detected in the culture fluids of HOS cells expressing TACE, suggesting that one of soluble osteoclast-inducing factor(s) is soluble RANKL. When blood monocytes were indirectly cocultured with HSOS-1 cells or cloned no. 9 cells in the presence of OCIF for 14 days, HOS cell-mediated osteoclastogenesis was suppressed, indicating that RANK-RANKL system is involved in the HOS cell-mediated osteoclastogenesis.
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We have found that omega-hydroxy palmitic acid (16-hydroxy palmitic acid, omega-HPA) has both cell growth inhibiting and cell death inducing actions on human lung adenosquamous carcinoma cell line H596 and adenocarcinoma cell line A549. Further, these effects were dose- and time-dependent in both cell lines. However, in squamous carcinoma cell line H226, omega-HPA had no cytotoxic effect. On the other hand, in the human small cell lung carcinoma (SCLC) cell line H128, this compound showed weak cytotoxicity. The sensitivity toward omega-HPA was higher in H596 cells than in A549 cells. In both H596 and A549 cells, cell growth was inhibited to 24.4 and 9.4%, respectively, by treatment with 100 microM omega-HPA for 12 h. In the 24 h treatment cells, growth inhibition was increased to 100 and 38.1%, respectively. In cytotoxicity experiments, the number of dead cells increased with incubation times in the presence of omega-HPA: on three days incubation with 100 microM omega-HPA, viability was 0 and 13.5%, respectively, in H596 and A549 cells. Further, the fragmentation of DNA to oligonucleosomal-sized ladder fragments, which is an index of apoptosis, was observed in both cell lines on treatment with omega-HPA. Therefore, it is assumed that these cell deaths induced by omega-HPA, were apoptosis in these cell lines. Since the number of dead cells following treatment with omega-HPA decreased by treatment with omega-HPA in combination with Z-VAD-fmk, a caspase family inhibitor, it is thought that apoptotic cell death was related to caspase activity.
In order to understand the role of IRF-1 in the development of murine tuberculosis in vivo, IRF-1 knockout mice were infected with Mycobacterium tuberculosis by placing them in the exposure chamber of an airborne infection apparatus. These knockout mice developed multifocal necrotic lesions in the lung, liver and spleen tissues and died of disseminated tuberculosis within 43 days of infection. Compared with the levels in wild-type mice, the pulmonary inducible NO synthase (iNOS) mRNA expression level was significantly lower, but IL-18 and IL-6 mRNA levels were higher. There was no statistically significant difference in the expression of IFN-gamma and TNF-alpha mRNA between the IRF-1 knockout and wild-type mice. IRF-1 is indirectly responsible for iNOS mRNA expression and plays an important role in the pathogenesis of murine tuberculosis.