Search PubMed⌕ Search

Biomedical subjects

I Fukuda

Publications and source records attributed to I Fukuda.

At least 73 records · Page 4Linked to original sources
PubMed1996

[Aortic valve injury due to blunt trauma--treatment in acute phase].

Aortic valve injury due to blunt trauma is rare and often difficult to diagnose. Therefore, most reported cases are operated on months or years after initial injury. Reported below is the case of a 55-year-old male, who was involved in a head-on collision with a bus. He was transported to Tsukuba Medical Center by ambulance, 34 minutes after the accident. The patient presented acute shock without obvious evidence of hemorrhaging. On physical examination a murmur was detected. The murmur was evaluated by Doppler echocardiography and revealed aortic regurgitation. On further physical examination he had gross hematuria and intratracheal bleeding. Computerized tomography (CT) showed evidence of contusions to his lungs, liver, and kidneys. The individual was diagnosed with an aortic valve injury, causing aortic insufficiency. It was necessary to continuously monitor the patients' hemodynamic state, assessing when conditions to operate were most favorable. However, in the hyper-acute phase the bleeding is difficult to control. We waited for his platelet count to recover before operating on the fifth day. When the patient underwent valve repair using extracorporeal circulation (ECC), aprotinin was added to the procedure. The surgery revealed a large laceration on the right coronary cusp of the aortic valve. Repair to the valve was impossible, so replacement of the aortic valve was required. A Carbomedics mechanical valve (phi 21 mm) was inserted. The patient did well after surgery, and eventually returned to work. To date, in Japan, there are eleven such cases of aortic valve injury on file. However, this is the first reported case that involved operating during the acute phase. This case demonstrates that, with careful evaluation of coexisting injuries and control of bleeding, successful treatment of aortic valve injury using ECC is possible, even in the acute phase.

Aortic Valve↗
PubMed1995

The structure of the core polyol of the ether lipids from Sulfolobus acidocaldarius.

The major ether-type lipid structures of Sulfolobus acidocaldarius (ATCC33909) were composed of caldarchaeol and calditoglycerocaldarchaeol. However, the characterization by nuclear magnetic resonance spectroscopy and mass spectrometry showed that the structure of calditol in calditoglycerocaldarchaeol is not nonitol, 2-(1',2',3'-trihydroxypropyl)1,2,3,4,5,6-hexahydroxyhexane, but 2-hydroxymethyl-1-(2,3-dihydroxypropoxy)2,3,4,5-cyclopentanetet raol with an ether linkage in the molecule. Such an intermolecular ether linkage was resistant to BCl3 treatment, but nonresistant to 57% HI degradation treatment conducted at 100 degrees C for 60 h, producing 2-hydroxymethyl-1,2,3,4,5-cyclopentanepentaol from calditol as reaction product. Further, it was confirmed that the structure of calditol is essentially a derivative of glycerol, and hydrocarbon chains were conjugated to the glycerol-like site in the structure. The calditol with an ether linkage in the molecule suggested an important role regarding the properties of heat-resistance and acid-resistance observed in Sulfolobales.

Acetylation↗
PubMed1995

Identification of a novel virulence gene, virA, on the large plasmid of Shigella, involved in invasion and intercellular spreading.

A novel virulence gene (virA) was identified upstream of the virG gene on the large plasmid of Shigella flexneri 2a YSH6000. Characterization of virA mutants infecting MK2 epithelial cell monolayers revealed that their invasive capacity was decreased to less than one fifth of the wild-type level. Nevertheless, the bacteria were capable of expressing and secreting IpaB, IpaC and IpaD proteins. The virA mutants were also impaired in their ability to spread intercellularly, since the bacteria gave rise to a small number of foci in a focus-plaque-forming test with MK2 cells. Although virG expression was slightly decreased in the virA mutants, introduction of a cloned virG gene into a virA mutant, N1945, failed to restore spreading ability. Although, introduction of a cloned virA gene into N1945 restored invasiveness and spreading ability, the reduced virG transcription level was not affected, indicating that the reduced virG expression in virA mutants does not play a major role in defective intercellular spreading. The nucleotide sequence of the virA region revealed that the virA gene was located 528 bp upstream of the virG gene, in the opposite orientation. The deduced amino acid sequence of the VirA protein indicated a 44.7 kDa protein with no homology to known proteins. The VirA protein was secreted into the culture supernatant, a process that required the Mxi and Spa loci. The expression of virA was under the control of the virB gene, the positive regulator of the ipa, mxi and spa operons. These results indicate that virA is a new member of the invasion regulon directed by virB and that the VirA function is involved in invasion and intercellular spreading.

Amino Acid Sequence↗
PubMed1995

Cleavage of Shigella surface protein VirG occurs at a specific site, but the secretion is not essential for intracellular spreading.

The large plasmid-encoded outer membrane protein VirG (IcsA) of Shigella flexneri is essential for bacterial spreading by eliciting polar deposition of filamentous actin (F-actin) in the cytoplasm of epithelial cells. Recent studies have indicated that VirG is located at one pole on the surface of the bacterium and secreted into the culture supernatant and that in host cells it is localized along the length of the F-actin tail. The roles of these VirG phenotypes in bacterial spreading still remain to be elucidated. In this study, we examined the surface-exposed portion of the VirG protein by limited trypsin digestion of S. flexneri YSH6000 and determined the sites for VirG processing during secretion into the culture supernatant. Our results indicated that the 85-kDa amino-terminal portion of VirG is located on the external side of the outer membrane, while the 37-kDa carboxy-terminal portion is embedded in it. The VirG cleavage required for release of the 85-kDa protein into the culture supernatant occurred at the Arg-Arg bond at positions 758 to 759. VirG-specific cleavage was observed in Shigella species and enteroinvasive Escherichia coli, which requires an as yet unidentified protease activity governed by the virB gene on the large plasmid. To investigate whether the VirG-specific cleavage occurring in extracellular and intracellular bacteria is essential for VirG function in bacterial spreading, the Arg-Arg cleavage site was modified to an Arg-Asp or Asp-Asp bond. The virG mutants thus constructed were capable of unipolar deposition of VirG on the bacterial surface but were unable to cleave VirG under in vitro or in vivo conditions. However, these mutants were still capable of eliciting aggregation of F-actin at one pole, spreading into adjacent cells, and giving rise to a positive Sereny test. Therefore, the ability to cleave and secrete VirG in Shigella species is not a prerequisite for intracellular spreading.

Amino Acid Sequence↗
PubMed1995

Appropriate intravenous doses of L-thyroxine and magnesium in a thyroidectomized patient with thyroid and parathyroid carcinomas receiving total parenteral nutrition during acute necrotizing pancreatitis.

A totally thyroidectomized patient with thyroid and parathyroid carcinomas, which had developed after neck irradiation in childhood, became hypercalcemic due to pulmonary metastases. The hypercalcemia was ameliorated by intermittent iv administration of bisphosphonate for 3.5 years, but this gradually became refractory to the bisphosphonate treatment. After right thoracotomy for resection of pulmonary metastases, acute necrotizing pancreatitis developed. The patient was therefore placed on total parenteral nutrition supplemented with T4 and a restricted dose of magnesium. Thyroxine(T4) (30 micrograms/day, iv) was not sufficient to maintain euthyroidism, but a higher dose (60 micrograms/day) elicited mild hyperthyroidism to the same extent as that elicited by an oral dose of 100 micrograms/day. The present case showed that the appropriate iv dose of T4 in this thyroidectomized patient with acute pancreatitis was about 60% of the oral dose. Furthermore, bisphosphonates (pamidronate and alendronate) and magnesium depletion were very effective in controlling the hypercalcemia.

Acute Disease↗
PubMed1995

[Anesthetic management of a patient with microcephaly associated with cerebral atrophy].

We describe the management of a 35-year-old female with microcephaly, cerebral atrophy especially in frontal lobes, dwarfism and severe mental retardation. The patient underwent open reduction of fracture of the humerus neck suffered from traffic accident. Authors could not find any article on the anesthetic management of microcephaly but could locate some about mentally retarded patients claiming the difficulty in anesthetic induction as well as emergence and frequent incidence of convulsions. We anesthetized the patient with modified NLA with nitrous oxide-oxygen and interestingly very small doses of fentanyl (1.7 micrograms.kg-1) were required. The anesthetic and surgical courses were uneventful. The patient emerged immediately with intravenously administered naloxone and flumazenil with no excitement nor convulsion. We conclude that fentanyl is the drug of choice for mentally retarded patient with microcephaly and smaller doses per kg.weight are sufficient for orthopedic surgery.

Adult↗
PubMed1995

[A repair of the aortic pseudoaneurysm after ascending aortic grafting in acute type A dissection--a case report].

A postoperative pseudoaneurysm of the ascending aorta is reported. The patient was a 73-year-old female with a history of graft replacement of the ascending aorta for acute type A dissection 5 years ago. She was referred to our hospital because of chest pain. Preoperative radiographic examination revealed a large pseudoaneurysm of the ascending aorta close to the distal anastomotic site of the graft as well as an aneurysm of transverse arch. During surgery, the pseudoaneurysm originated from a intimal defect in the aortic wall 1 cm distal to the suture line. It is suggested that the pseudoaneurysm was caused by a clamp injury during the initial operation. Replacement of the ascending aorta and transverse arch was successfully performed under selective cerebral perfusion. We should keep the clamp injury in mind when we apply an aortic clamp to a fragile dissected aorta.

Acute Disease↗
PubMed1995

[A case of unresectable gastric cancer responding to combined therapy with intraperitoneal cisplatinum administration and continuous intravenous infusion of 5-fluorouracil].

A 41-year-old woman diagnosed as gastric cancer with peritoneal dissemination was admitted for operation. Exploratory laparotomy was done and a reservoir was implanted with intraperitoneal catheter. At the operation, CDDP (100 mg) was administered intraperitoneally. Four days after the operation, continuous intravenous infusion of 5-FU (250 mg) was carried out. CDDP was administered every four weeks for 6 times and 5-FU continuously for 194 days. Grade 2 toxicity (nausea, vomiting) was noted without myelosuppression and renal disturbance. The general condition of the patient was fairly improved. PS (performance status) improved from Grade 3 to Grade 1. Combined therapy with repeated intraperitoneal CDDP administration and continuous intravenous infusion of 5-FU is effective and safe for gastric cancer with peritoneal dissemination based on biochemical modulation.

Adult↗
PubMed1994

Absence of p53 mutations and various frequencies of Ki-ras exon 1 mutations in rat hepatic tumors induced by different carcinogens.

Mutations of p53 and Ki-ras exon 1 were investigated in rat hepatic lesions induced by four kinds of hepatocarcinogenic protocols: continuous feeding of 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB), daily intraperitoneal injection of aflatoxin B1 (AFB1), and the Solt and Farber regimen (Nature 236:701-703, 1976), in which diethylnitrosamine (DEN) or nitrosomethylurea (NMU) was used as initiating agents. DNA from microdissected tissue sections was amplified by the polymerase chain reaction (PCR) directly using primers for p53 exons 5-8 and Ki-ras exon 1 and analyzed for mutations by denaturing gradient gel electrophoresis (DGGE) or constant denaturant gel electrophoresis (CDGE). One or both of the p53 PCR primers were located within introns to prevent amplifying the p53 processed pseudogenes. In a total of 59 hepatocellular carcinomas (HCCs), no p53 aberrations were detected, indicating that p53 mutations are not very important in rat hepatic carcinogenesis. On the other hand, Ki-ras codon 12 mutations were found at low frequency in HCCs, hyperplastic foci, and cholangiofibroses induced by 3'-Me-DAB and by AFB1 but not in the lesions induced by the Solt and Farber regimen. Although Ki-ras codon 12 mutations are generally infrequent in rat hepatic tumors, their incidence thus appears to vary depending on the carcinogen used for their induction.

Animals↗
PubMed1994

Identification and characterization of a chromosomal virulence gene, vacJ, required for intercellular spreading of Shigella flexneri.

Intercellular spreading of shigellae is a prerequisite for shigellosis, although the molecular mechanisms underlying the phenomenon are still largely obscure. To elucidate some of these mechanisms, we performed random Tn10 insertion mutagenesis in Shigella flexneri YSH6000T and found a chromosomal locus in the NotI-J segment responsible for bacterial spreading. The locus affected in the mutant, designated vacJ, was neither involved in the invasion of epithelial cells nor in intracellular movement, but was required for intercellular spread. The vacJ mutant was capable of forming bacterium-containing membranous protrusions within the infected cell, but had diminished ability to move from the protrusions into the cytoplasm of the adjacent epithelial cells. Cloning and sequencing of the vacJ region indicated that the vacJ gene encoded a 28.0 kDa protein possessing a signal peptide at the N-terminus, which contained the motif characteristic of lipoproteins. The analysis of the vacJ product indicated that VacJ was exposed on the bacterial surface. The vacJ gene was distributed among shigellae and enteroinvasive Escherichia coli, and the constructed vacJ mutants failed to spread intercellularly, indicating that vacJ is a chromosomal gene essential for the pathogenicity of shigellae.

Amino Acid Sequence↗
PubMed1994

vacC, a virulence-associated chromosomal locus of Shigella flexneri, is homologous to tgt, a gene encoding tRNA-guanine transglycosylase (Tgt) of Escherichia coli K-12.

The genetic determinants required for invasion of epithelial cells by Shigella flexneri and for the subsequent bacterial spreading are encoded by the large virulence plasmid. Expression of the virulence genes is under the control of various genes on the large plasmid as well as on the chromosome. We previously identified one of the virulence-associated loci near phoBR in the NotI-C fragment of the chromosome of S. flexneri 2a YSH6000 and designated the locus vacC. The vacC mutant showed decreased levels of IpaC, and IpaD proteins as well as transcription of ipa, an operon essential for bacterial invasion (N. Okada, C. Sasakawa, T. Tobe, M. Yamada, S. Nagai, K. A. Talukder, K. Komatsu, S. Kanegasaki, and M. Yoshikawa, Mol. Microbiol. 5:187-195, 1991). To elucidate the molecular nature of the vacC locus, we cloned the vacC region from YSH6000 on a 1.8-kb SalI-BamHI DNA fragment. The nucleotide sequence of the 1,822-bp vacC clone was highly (> 98%) homologous to the tgt region of Escherichia coli K-12, which is located at 9.3 min on the linkage map. Complementation tests indicated that the vacC function was encoded by an open reading frame expressing a 42.5-kDa protein, which corresponded to the tgt gene of E. coli K-12, coding for tRNA-guanine transglycosylase (Tgt) (K. Reuter, R. Slany, F. Ullrich, and H. Kersten, J. Bacteriol. 173:2256-2264, 1991). The cloned tgt gene from E. coli K-12 restored the virulence phenotype to the vacC mutant of YSH6000. Characterization of the vacC mutant indicated that levels of VirG, a protein essential for bacterial spreading, and VirF, the positive regulator for the expression of the virG and ipaBCD operons, decreased significantly compared with those of the wild type. Similar phenotypic changes occurred in vacC mutants constructed by insertion of a neomycin resistance gene in shigellae and enteroinvasive E. coli strains, consistent with the hypothesis that the vacC (tgt) gene contributes to the pathogenicity of Shigella flexneri.

Amino Acid Sequence↗
PubMed1994

[Mitral valve replacement secondary to resection of mycotic cerebral aneurysm in acute phase of bacterial endocarditis--a case report].

We report a case of mitral valve replacement after ruptured mycotic aneurysm resection in acute phase of bacterial endocarditis. We have experienced a 68-year-old man with vegetation at the anterior leaflet of mitral valve and multiple systemic embolization. He underwent aneurysmectomy of ruptured mycotic cerebral aneurysm and embolectomy of left femoral artery eight days after subarachnoid hemorrhage. Mitral valve was replaced three days after successfully. If there was no heart failure preoperatively, valve replacement operation is recommended in acute phase of infected endocarditis or few days after cerebral aneurysmectomy.

Acute Disease↗
PubMed1993

Detection of p53 gene mutations in rat hepatocellular carcinoma cell lines by denaturing gradient gel electrophoresis.

Structural alterations of the p53 gene were investigated in chemically induced rat hepatocellular carcinomas (HCCs), hyperplastic hepatic nodules (HPNs), and cell lines derived from rat neoplastic and normal liver cells. The mutations were detected by GC-clamped denaturing gradient gel electrophoresis using DNA that had been amplified from p53 mRNA by the reverse transcriptase-polymerase chain reaction. This method enabled us to find single-base changes within the p53 gene without using radioisotopes. The presence of mutations was subsequently confirmed by DNA sequencing. No mutations were detected in six primary HCCs and 12 HPNs induced by the Solt and Farber regimen (Nature 236: 701-703, 1976), suggesting that p53 gene mutations do not play a major role in rat hepatic carcinogenesis. However, five of seven HCC cell lines and one of two cell lines derived from normal liver cells had the mutated p53 gene and had lost the normal p53 gene. Five cell lines had a G-->T transversion at various codons, whereas one line had a 21-base deletion in exon 5. Therefore, we conclude that p53 gene mutations may occur in vitro during establishment of the cell lines or may be derived from very small populations within the primary tumors.

Adenoma↗
PubMed1993

Level of serum gastrin as a predictor of liver metastasis from colorectal cancer.

There have been no reports on the relationship between serum gastrin level and liver metastasis in human colorectal cancer. One hundred forty patients who underwent surgery for colorectal cancer (T2 or more) were enrolled in this study. Fasting serum gastrin level was determined prior to the surgery. Incidence of liver metastasis was significantly (P < 0.01) higher in patients with a serum gastrin level of > or = 150 pg/ml (37 percent; 14/38) than in those with a serum gastrin level of < 150 pg/ml (12 percent; 12/102). As for the tumors with venous invasion, liver metastasis was detected in 11 of 55 patients (20 percent) with a serum gastrin level of < 150 pg/ml; however, it was detected in 11 of 19 patients (58 percent) with a serum gastrin level of > or = 150 pg/ml (P < 0.01). These results suggest that serum gastrin serves as a useful predictor of liver metastasis from colorectal cancer and that the predictability of liver metastasis can be improved when both serum gastrin level and venous invasion are considered.

Adult↗
PubMed1993

Dermoid cyst in the middle ear.

A case of a moderate essentially low tone unilateral conductive hearing loss without a previous history of secretory otitis media in a six-year-old female patient is described. The condition was found to be due to a dermoid cyst in the tympanic cavity, which was confirmed by pathological examination of the surgically removed specimen. This is the sixth documented case of dermoid cyst in the tympanic cavity.

Child↗
PubMed1993

The absence of a surface protease, OmpT, determines the intercellular spreading ability of Shigella: the relationship between the ompT and kcpA loci.

A large plasmid-encoded protein, VirG, on the bacterial surface is essential for the spreading of Shigella by eliciting polar deposition of filamentous actin in the cytoplasm of epithelial cells. VirG expression from the large plasmid is diminished greatly when it is introduced into Escherichia coli K-12 from Shigella. In an attempt to identify factors affecting VirG expression, we found that the absence of the ompT gene, encoding outer membrane protease OmpT, restored full production of VirG protein to E. coli K-12. Conversely, upon introduction of the ompT gene of E. coli K-12 into Shigella, spreading ability was completely abolished, probably because of the proteolytic degradation of VirG protein by OmpT. Analysis of the DNA sequence of the ompT region indicated that the absence of the ompT gene occurred in Shigella and enteroinvasive E. coli strains, and that the absent DNA segment corresponded to a remnant lambdoid phage structure found in E. coli K-12, which encompasses a 21 kb DNA segment spanning from argU through to the ompT genes. Since ompT is located near purE in E. coli K-12 and a virulence locus for provoking keratoconjunctivitis in the eyes of guinea-pigs, named kcpA, is located near purE in S. flexneri, and the two loci are involved in VirG expression, the KcpA- mutants of S. flexneri 2a constructed were examined for correlation between acquisition of ompT and VirG degradation. Our data suggest that the previous recognition of a kcpA locus in S. flexneri is the result of transfer of the ompT gene from E. coli K-12, giving rise to a KcpA- phenotype. These results indicate that the lack of OmpT protease confers upon Shigella the ability to spread into adjacent epithelial cells.

Amino Acid Sequence↗