[A case of spontaneous submucosal hematoma of the esophagus].
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
T Matsui
Publications and source records attributed to T Matsui.
[Multicentric Castleman's disease with lymphoid interstitial pneumonia and polyneuropathy].
A 51-year-old woman was admitted to a local hospital because of pneumonia, and received a diagnosis of cervical lymphadenopathy, anemia, and hyperimmunoglobulinemia with suspected multicentric Castleman's disease (MCD). At the age of 53 she was transferred to our hospital because of numbness and muscle weakness. Polyclonal hyperimmunoglobulinemia was observed, and biopsy specimens of lymph node tissue revealed infiltration of plasma cells in the interfollicular areas, thus leading to a diagnosis of MCD. A chest computed tomography scan revealed diffuse nodular shadows in all lung fields, and a transbronchial lung biopsy disclosed infiltration of plasma cells in the alveolar septa. Together, these findings indicated lymphoid interstitial pneumonia (LIP). Polyneuropathy was diagnosed by neurological examination and nerve conduction studies. Treatment with prednisolone and cyclophosphamide was ineffective against LIP probably because the patient had coexising pulmonary fibrosis. Since pulmonary complications of MCD determine its prognosis, their early detection and treatment are essential.
Castleman Disease↗
[Disseminated carcinomatosis of the bone marrow occurring 11 years after subtotal gastrectomy for gastric cancer].
A 44-year-old man was admitted to our hospital because of purpura, increased serum alkaline phosphatase, and thrombocytopenia. He had undergone subtotal gastrectomy for gastric cancer 11 years earlier. A biopsy specimen of the bone marrow revealed metastatic mucin-forming, moderately differentiated adenocarcinoma. Because the primary tumor was not detected in any other organ, the gastric cancer the patient was treated for 11 years earlier was suspected as the primary tumor. Microangiopathic hemolytic anemia and disseminated intravascular coagulation developed during the clinical course, and the patient deteriorated despite treatment with anticoagulants. Finally, he died of pulmonary carcinomatous lymphangitis. Autopsy revealed a small number of adenocarcinomatous cells in the lymphoduct of the remaining stomach in spite of its mucosa being intact. We concluded that the bone marrow was infiltrated by cancer cells which originated in the stomach 11 years before. It is unclear why adenocarcinoma cells remained dormant for as long as 11 years in the gastric lymphoduct and bone marrow.
Adenocarcinoma↗
[A case of linear sebaceous nevus syndrome associated with a cerebrovascular anomaly].
We report a 34-year-old woman with linear sebaceous nevus syndrome and dolichomegalic artery. The patient was admitted to our hospital for evaluation of a headache and fever. Neurological examination revealed no focal sign except neck stiffness. She had had sebaceous nevi on the left side of her head, cheek and neck since she was born. A cranial CT scan showed high signal intensity in the subarachnoid space. Cranial MRI showed a dolichomegalic artery. The patient's past history included many episodes of headache and fever since her first decade of life and she had been diagnosed five times with cerebrovascular disease. At the present admission, subarachnoid hemorrhage was diagnosed and treated. The patient improved and was discharged on the 21st day. Linear sebaceous nevi are associated with many types of anomalies, but we found no other reported cases of linear sebaceous nevus syndrome associated with a cerebrovascular anomaly. This case suggests that a patient with sebaceous nevi who presents with headache and fever should be examined with careful attention to the cerebrovascular system.
Adult↗
Isolation of a highly metastatic cell line to lymph node in human oral squamous cell carcinoma by orthotopic implantation in nude mice.
To isolate a variant cell line with increased lymph node metastasising potential from human oral squamous cell carcinoma (SCC) we performed in vivo selection using orthotopic implantation in nude mice. Human oral SCC cells (HSC-3) were injected orthotopically into the tongue of nude mice. After 3 weeks their cervical lymph nodes were excised and the tumour cells metastasised to the lymph nodes were isolated and injected into the tongue of nude mice again, this procedure was performed three times. The resultant cells, designated as HSC-3-M3, metastasised to cervical lymph nodes in 90% of mice, while parental HSC-3 cells metastasised in only 30% of mice after injection into the tongue. HSC-3 and HSC-3-M3 cell lines which have the same origin but different lymphatic metastatic capacities could be a useful model system for studying mechanisms involved in lymph node metastasis of human oral SCC.
Animals↗
[A case of leiomyosarcoma of the jejunum with postoperative hepatic encephalopathy].
We report a case of leiomyosarcoma of the jejunum with postoperative hepatic encephalopathy. A 60-year-old man was operated for tumor of the abdomen. He was diagnosed as leiomyosarcoma of the jejunum with disseminated peritoneal metastasis, but no liver metastasis and cirrhosis. A palliative resection of the jejunum was performed. After operation, disturbance of orientation and apraxia with electroencepharographic abnormality and hyperammonemia developed. He was diagnosed as hepatic encephalopathy without lesion of the liver, and died 11 months after surgery. We consider that the portosystemic shunt and bleeding from the digestive tract due to invasion of metastatic lesions caused hepatic encephalopathy.
Hepatic Encephalopathy↗
On the formation and reactivity of compound I of the His-64 myoglobin mutants.
Myoglobin (Mb) catalyzes various two-electron oxidations; however, ferryl porphyrin cation radical equivalent to peroxidase compound I has not been identified yet. Distal histidine mutants of sperm whale Mb (His-64 --> Ala, Ser, and Leu) afford an apparent intermediate followed by the formation of a ferryl heme (Mb-II) in the reaction with m-chloroperbenzoic acid. Because the intermediate exhibits characteristic absorption spectrum of compound I and bears two electron oxidizing equivalents above the ferric state, we have assigned the species as compound I of myoglobin (Mb-I). Although we have recently observed compound I of the F43H/H64L Mb mutant, F43H and wild type Mb react with m-chloroperbenzoic acid to give Mb-II without any accumulation of Mb-I. The results unambiguously indicate that His-64 plays a key role in destabilizing wild type Mb-I. Furthermore, Mb-I is found to be capable of performing two-electron oxidation of styrene, thioanisole, and H2O2.
Animals↗
Thermophilic F1-ATPase is activated without dissociation of an endogenous inhibitor, epsilon subunit.
Subunit complexes (alpha3beta3gamma, alpha3beta3gammadelta, alpha3beta3gammaepsilon, and alpha3beta3gammadeltaepsilon) of thermophilic F1-ATPase were prepared, and their catalytic properties were compared to know the role of delta and epsilon subunits in catalysis. The presence of delta subunit in the complexes had slight inhibitory effect on the ATPase activity. The effect of epsilon subunit was more profound. The (-epsilon) complexes, alpha3beta3gamma and alpha3beta3gammadelta, initiated ATP hydrolysis without a lag. In contrast, the (+epsilon) complexes, alpha3beta3gammaepsilon and alpha3beta3gammadeltaepsilon, started hydrolysis of ATP (<700 microM) with a lag phase that was gradually activated during catalytic turnover. As ATP concentration increased, the lag phase of the (+epsilon) complexes became shorter, and it was not observed above 1 mM ATP. Analysis of binding and hydrolysis of the ATP analog, 2',3'-O-(2,4,6-trinitrophenyl)-ATP, suggested that the (+epsilon) complexes bound substrate only slowly. Differing from Escherichia coli F1-ATPase, the activation of the (+epsilon) complexes from the lag phase was not due to dissociation of epsilon subunit since the re-isolated activated complex retained epsilon subunit. This indicates that there are two alternative forms of the (+epsilon) complex, inhibited form and activated form, and the inhibited one is converted to the activated one during catalytic turnover.
Adenosine Triphosphate↗
Nocturnal cough in patients with sputum production.
Explore the source record for details and available documents.
Bronchitis↗
G protein betagamma complex-mediated apoptosis by familial Alzheimer's disease mutant of APP.
In familial Alzheimer's disease (FAD), three missense mutations, V642I, V642F and V642G, that co-segregate with the disease phenotype have been discovered in the 695 amino acid form of the amyloid precursor protein APP. Expression of these mutants causes a COS cell NK1 clone to undergo pertussis toxin-sensitive apoptosis in an FAD trait-linked manner by activating the G protein Go, which consists of G alpha(o) and G betagamma subunits. We investigated which subunit was responsible for the induction of apoptosis by V642I APP in NK1 cells. In the same system, expression of mutationally activated G alpha(o) or G alpha(i) induced little apoptosis. Apoptosis by V642I APP was antagonized by the overexpression of the carboxy-terminal amino acids 495-689 of the beta-adrenergic receptor kinase-1, which blocks the specific functions of G betagamma. Co-transfection of G beta2gamma2 cDNAs, but not that of other G beta(x)gamma(z) (x = 1-3; z = 2, 3), induced DNA fragmentation in a manner sensitive to bcl-2. These data implicate G betagamma as a cell death mediator for the FAD-associated mutant of APP.
Alzheimer Disease↗
Cerebrospinal fluid tau levels in neurodegenerative diseases with distinct tau-related pathology.
Cerebrospinal fluid tau (CSF-tau) levels were quantified in 8 patients with frontotemporal dementia (FTD), 6 patients with progressive supranuclear palsy (PSP), 3 patients with corticobasal degeneration (CBD), and 6 patients with dementia with Lewy bodies (DLB). The CSF-tau levels were significantly increased in FTD and DLB, but not in PSP and CBD, compared to that previously reported in normal controls. Notably, the CSF-tau level in DLB was as high as that in Alzheimer's disease (AD). Our study suggests that tau may accumulate in the CSF of patients with certain neurodegenerative diseases other than AD and that measurement of CSF-tau may not distinguish AD from DLB.
Aged↗
Expression of a kinase-defective Eph-like receptor in the normal human brain.
We have identified a human Eph-family protein, HEP, gene located in human chromosomal region 7q33-->q35. The deduced amino acid sequence shared primary structural properties of Eph-family receptor tyrosine kinases. However, six invariant amino acids such as a lysine in the ATP-binding site and an aspartic acid in the phosphotransfer site of a conserved catalytic domain were substituted with other amino acid residues in HEP. Thus, no intrinsic tyrosine kinase activity was detectable in the catalytic domain expressed in CHO-K1 cell transfectants. Although most kinase-defective mutants of growth factor receptors have been reported as pathogenic receptors, its transcript was abundantly expressed in normal human adult tissues. A 135-kDa HEP protein was expressed in the human brain as much as in CHO-K1 cells transfected with a HEP cDNA expression vector. HEP is the first description of a kinase-defective Eph-family protein expressed abundantly in normal human tissues.
Adenosine Triphosphate↗
Deletion of c-myb exon 9 induced by insertion of repeats.
A simple repeat was found to be inserted into exon 9 of the c-myb gene in three out of 20 bovine T lymphomas. The repeat was composed of multiple copies of a 12-nucleotide motif and had no significant homology to the sequences reported so far. Tumor cells containing the repeat expressed two kinds of c-myb mRNA: (1) are that included the repetitive sequence in exon 9, and (2) are that lacked the whole sequence of exon 9. Transfection of an expression vector containing exon and intron sequences and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis of the mRNA demonstrated that the insertion of the repeat enhanced exon skipping of the transfected minigene. These observations imply that the insertion of the repeat may enhance exon skipping of the c-myb pre-mRNA. Although the transcription-activating activity by the c-Myb with the repeat was low, that by the c-Myb without exon 9 was three- to eightfold higher than the wild-type c-Myb. These data suggest that insertion of the 12-nucleotide repeat in codon 359 may result in c-Myb proteins having high- and low-transcription-activating activity.
Animals↗
Herpes simplex virus and risk of Alzheimer's disease.
Explore the source record for details and available documents.
Aged↗
Interference of a methotrexate derivative with urinary oncopterin [N2-(3-aminopropyl)biopterin] measurement by high-performance liquid chromatography with fluorimetric detection.
We previously reported a HPLC assay method using fluorimetric detection for the simultaneous determination of urinary N2-(3-aminopropyl)biopterin (oncopterin, a natural pteridine newly found in urine from cancer patients), biopterin and neopterin. We now have observed that an unknown substance, which may be derived from methotrexate, in urine from a patient with stomach cancer interfered with the assay of oncopterin and demonstrated that oncopterin could be completely separated from the unidentified substance by HPLC using a Nucleosil 100-5SA strong cation-exchange column. Furthermore, oncopterin was not detectable by this HPLC-fluorimetric method in urine samples from patients with stomach cancer who were not treated with methotrexate. The content of urinary oncopterin from cancer patients is supposed to be very low, with less than 1 mumol/mol creatinine. The present results indicate that the peak found with elution from the C18 column was a methotrexate-derived compound and co-eluted with the analyte oncopterin.
Biomarkers, Tumor↗
Catalytic activity of the alpha3beta3gamma complex of F1-ATPase without noncatalytic nucleotide binding site.
A mutant alpha3beta3gamma complex of F1-ATPase from thermophilic Bacillus PS3 was generated in which noncatalytic nucleotide binding sites lost their ability to bind nucleotides. It hydrolyzed ATP at an initial rate with cooperative kinetics (Km(1), 4 microM; Km(2), 135 microM) similar to the wild-type complex. However, the initial rate decayed rapidly to an inactivated form. Since the inactivated mutant complex contained 1.5 mol of ADP/mol of complex, this inactivation seemed to be caused by entrapping inhibitory MgADP in a catalytic site. Indeed, the mutant complex was nearly completely inactivated by a 10 min prior incubation with equimolar MgADP. Analysis of the progress of inactivation after initiation of ATP hydrolysis as a function of ATP concentration indicated that the inactivation was optimal at ATP concentrations in the range of Km(1). In the presence of ATP, the wild-type complex dissociated the inhibitory [3H]ADP preloaded onto a catalytic site whereas the mutant complex did not. Lauryl dimethylamineoxide promoted release of preloaded inhibitory [3H]ADP in an ATP-dependent manner and partly restored the activity of the inactivated mutant complex. Addition of ATP promoted single-site hydrolysis of 2',3'-O-(2,4,6-trinitrophenyl)-ATP preloaded at a single catalytic site of the mutant complex. These results indicate that intact noncatalytic sites are essential for continuous catalytic turnover of the F1-ATPase but are not essential for catalytic cooperativity of F1-ATPase observed at ATP concentrations below approximately 300 microM.
Adenosine Diphosphate↗
ADP-fluoroaluminate complexes are formed cooperatively at two catalytic sites of wild-type and mutant alpha3beta3gamma subcomplexes of the F1-ATPase from the thermophilic Bacillus PS3.
Addition of Al3+ and F- to the alpha3beta3gamma subcomplex of the TF1-ATPase containing MgADP in one catalytic site causes slow, complete inactivation as the ADP-fluoroaluminate complex is formed. This conflicts with the "bisite" stochastic model suggested earlier (Issartel, J. P., Dupuis, A., Lunardi, J. & Vignais, P. V. (1991) Biochemistry 30, 4726-4733] on the finding that complete inactivation of the bovine mitochondrial F1-ATPase by Al3+, F-, Mg2+, and excess ADP occurs as ADP-fluoroaluminate complexes form in two catalytic sites. When Al3+ and F- were added to alpha3beta3gamma containing MgADP in two catalytic sites, inactivation accelerated 8-fold, indicating catalytic to catalytic site cooperativity. When added to alpha3beta3gamma containing MgADP bound to one or two catalytic sites prior to addition of Al3+ and F-, phosphate inhibits formation of the ADP-fluoroaluminate complex. When introduced after adding 200 microM ADP plus Mg2+ to alpha3beta3gamma, but before adding Al3+ and F-, phosphate accelerated formation of the ADP-fluoroaluminate complex 3-fold. Sulfite accelerated formation of the ADP-fluoroaluminate complex 9-fold when 200 microM ADP plus Mg2+ was added to alpha3beta3gamma before adding Al3+ and F-. The accelerations induced by phosphate or sulfite in the presence of excess ADP and Mg2+ suggest noncatalytic to catalytic site cooperativity. When Al3+ and F- were added to the (alphaD261N)3beta3gamma subcomplex containing MgADP in a single catalytic site, the ADP-fluoroaluminate complex formed at least 10-fold more slowly than observed with wild-type under the same conditions. Therefore, the catalytic site containing MgADP recognizes the alphaD261N substitution when noncatalytic sites are empty. Cross-linking alpha to gamma or beta to gamma by oxidizing the (alphaA396C)3beta3(gammaA22C) and alpha3(betaD390C)3(gammaS90C) subcomplexes, respectively, abolishes cooperative formation of ADP-fluoroaluminate complexes in two catalytic sites. ADP-fluoroaluminate complex formation is restricted to a single catalytic site in the oxidized double mutants. The alpha3beta3delta subcomplex does not form an inhibitory ADP-fluoroaluminate complex under any of the conditions examined for the alpha3beta3gamma subcomplexes.
Adenosine Diphosphate↗
Pro-inflammatory cytokines and interleukin 6 in the renal response to bacterial endotoxin.
Pro-inflammatory cytokines, including tumour necrosis factor alpha (TNF-alpha), interleukin (IL)-1 and IL-6 are thought to play important roles in the pathophysiology of chronic kidney disorders, including glomerulonephritis. In particular, IL-6 has received considerable attention as it appears at high concentrations to promote the progression of renal disease while at lower levels may be involved in regulating repair mechanisms. As such, cytokine profiles have been examined in the kidney by either examining secretion from isolated kidney cells or quantitating plasma and urinary levels in experimental models of glomerulonephritis. To examine the cytokine responses within the kidney, without the contribution of other organ systems, we used semi-quantitive polymerase chain reaction (RT-PCR) analysis and a recently developed kidney slice culture model from tissues of mice treated with combinations of endotoxin and neutralizing antibodies against TNF-alpha. The expression of IL-6, in addition to other pro-inflammatory cytokine genes, was increased by endotoxin treatment and reduced by pretreatment with neutralizing antibodies to TNF-alpha. Immunohistochemical staining revealed that IL-6 was expressed primarily in mesangial cells. Urinary IL-6 was also increased in endotoxin-treated mice and was inhibited by treatment with neutralizing TNF-alpha antibodies. Kinetics of the kidney-specific cytokine responses indicated that increase in TNF-alpha occurred initially, followed by IL-1 beta and finally IL-6. Furthermore, addition of TNF-alpha to glomerular mesangial cells induces IL-6 secretion. Taken together, these studies indicate that, like in the liver, a cytokine response occurs in the kidney from bacterial endotoxin and that TNF-alpha acts as a primary cytokine capable of stimulating additional cytokines, including IL-6.
Animals↗