Biomedical subjects

H Kato

Publications and source records attributed to H Kato.

At least 55 records · Page 3Linked to original sources

PubMed2005

The co-existence of an aberrant origin of the right subclavian artery and a coronary myocardial bridge.

We encountered the co-existence of an aberrant origin of the right subclavian artery and a myocardial bridge on the left anterior descending coronary artery in the cadaver of an 80-year-old Japanese woman during the course of educational dissection at Nagoya City University Medical School. We document the precise gross anatomical findings with some morphometric measurements. Neither an aberrant origin of the right subclavian artery nor the cardial myocardial bridge is a very rare anomaly, but a case of both anomalies being found in the same body is very rare. We believe this is the first report of the simultaneous occurrence of these two anomalies.

Aged↗

PubMed2004

Evaluation of genitofemoral nerve block, in addition to ilioinguinal and iliohypogastric nerve block, during inguinal hernia repair in children.

BACKGROUND: Ilioinguinal and iliohypogastric (IG-IH) nerve block has been widely used in children undergoing inguinal hernia repair. This technique may provide insufficient analgesia for intraoperative management as the inguinal region may receive sensory innervation from genitofemoral nerve. We proposed that addition of a genitofemoral nerve block might improve the quality of analgesia. METHODS: Ninety-eight children undergoing inguinal hernia repair were assigned randomly to receive either IG-IH nerve block (Group I) or IG-IH and genitofemoral nerve blocks (Group II). Systolic arterial pressure (SAP) and heart rate (HR) were recorded before surgery (control), after skin incision, at sac traction and at the end of surgery. Postoperative analgesic requirements and incidence of complications were recorded until discharge. RESULTS: At sac traction, SAP and HR were significantly higher in Group I (P<0.05), and the incidence of episodes of increased HR was also significantly higher in Group II (29 vs 12%, respectively, P<0.05). There were no significant differences in SAP and HR at other time points, postoperative analgesic requirements or incidence of complications between the groups. CONCLUSIONS: The benefit of the additional genitofemoral nerve block to IG-IH nerve block was limited only to the time of sac traction without any postoperative effect. This suggests there is little clinical benefit in the addition of a genitofemoral nerve block.

Analgesics↗

PubMed2004

An immunohistochemical study of TIMP-3 expression in oesophageal squamous cell carcinoma.

Tissue inhibitor of metalloproteinase-3 (TIMP-3) inhibits the activity of matrix metalloproteinase, which may play an important role in carcinoma invasion and metastasis. We have investigated the relationship between TIMP-3 reduction and clinicopathological factors in oesophageal squamous cell carcinoma (ESCC). We examined tissue specimens that had been removed from 90 patients with thoracic oesophageal cancer who had undergone surgery between 1983 and 2001. Immunohistochemical staining was performed by the standard streptavidin-biotin method. Immunostaining of TIMP-3 was seen in the cytoplasm of cancer cells and normal oesophageal epithelial cells, particularly in cells located in shallow areas of the tumour. TIMP-3 preserved (+), moderate (+/-), and reduced (-) cases accounted for 30, 27, and 33 of the 90 patients, respectively (33, 30, 37%). Significant correlations were observed between TIMP-3 expression and depth of tumour invasion (P=0.001), number of lymph node metastases (P=0.003), infiltrative growth pattern (P=0.003), and disease stage (P=0.005). The survival rates of patients with TIMP-3 (-) cancer were significantly lower than those of patients with TIMP-3 (+) and TIMP-3 (+/-) cancer (P=0.0003). The mean 5-year survival rates of patients with TIMP-3 (+), (+/-), and (-) were 50, 58, and 21%, respectively. In conclusion, decreased expression of TIMP-3 protein correlates with invasive activity and metastasis. This makes the prognosis for patients with cancer that has lost TIMP-3 significantly less favourable than that for patients with cancer that has maintained TIMP-3.

Adult↗

PubMed2004

Pitavastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, reduces hippocampal damage after transient cerebral ischemia in gerbils.

Pitavastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, is a potent cholesterol-lowering drug that reduces the risk of myocardial infarction and stoke. In this study, we examined its neuroprotective effects against hippocampal CA1 neuronal damage following transient cerebral ischemia in gerbils. Forebrain ischemia was induced by occlusion of bilateral common carotid arteries for 5 min. Pitavastatin, at a dose of 3, 10 or 30 mg/kg, was administered orally twice a day for 5 consecutive days and transient cerebral ischemia was induced in mice 1 h after the last treatment with pitavastatin. Histopathological observations showed that neuronal damage to the hippocampal CA1 neurons, which was observed 5 days after ischemia in animals, was prevented by pitavastatin treatment. Immunohistochemical staining for copper/zinc superoxide dismutase (SOD) and manganese SOD decreased in the hippocampal CA1 sector of gerbils 2 days after ischemia when histological neuronal destruction was not yet found, but was clearly observed in pitavastatin-treated animals. These results indicate that pitavastatin can protect dose-dependently against ischemia-induced neuronal damage and that the mechanism of the neuroprotection may be related to the preservation of SODs, especially copper/zinc-SOD. This in part explains how pitavastatin therapy, which targets free radicals, has beneficial effects against disorders including ischemic stroke.

Animals↗

PubMed2004

Value of positron emission tomography in the diagnosis of recurrent oesophageal carcinoma.

BACKGROUND: Positron emission tomography (PET) with [18F]fluorodeoxyglucose (FDG) might be useful for staging oesophageal squamous cell carcinoma (SCC). FDG-PET may be more accurate than computed tomography (CT) in diagnosing lymph node metastasis. This retrospective study compared the ability of FDG-PET and CT to diagnose recurrent oesophageal carcinoma. METHODS: Fifty-five patients with thoracic oesophageal SCC who had undergone radical oesophagectomy were studied. The accuracy of FDG-PET and CT in detecting recurrence during follow-up was calculated using data from the first images generated by either modality that suggested the presence of recurrent disease. Lesions deemed to be equivocal on these scans were considered as positive for recurrence. RESULTS: Twenty-seven of the 55 patients had recurrent disease in a total of 37 organs. Locoregional recurrence was observed in 19 patients (35 per cent). Distant recurrent disease occurred in 15 patients (27 per cent) in 18 organs. Six patients had recurrence in the liver, four in the lung, six in bone and two in distant lymph nodes. FDG-PET showed 96 per cent sensitivity, 68 per cent specificity and 82 per cent accuracy in demonstrating recurrent disease. The corresponding values for CT were 89, 79 and 84 per cent. The sensitivity of FDG-PET was higher than that of CT in detecting locoregional recurrence, but its specificity was lower because of FDG uptake in the gastric tube and thoracic lymph nodes. In distant organs the sensitivity of PET in detecting lung metastasis was lower than that of CT, but its sensitivity for bone metastasis was higher. CONCLUSION: FDG-PET has a larger field than CT. Combined PET-CT would appear to be an appropriate modality for the detection of recurrent oesophageal cancer.

Adult↗

PubMed2004

Expression of heat-shock protein Hsp60 correlated with the apoptotic index and patient prognosis in human oesophageal squamous cell carcinoma.

Cellular stress response and apoptosis are two highly conserved mechanisms for maintaining homeostasis. Hsp60 and Hsp90 have been shown to play pro- and anti-apoptotic roles, respectively. Our present study examined whether there is a correlation between the expression of Hsp60 and Hsp90, clinical parameters, the apoptotic index (AI), and the prognosis of patients with oesophageal squamous cell carcinoma (ESCC). We immunohistochemically stained cells for Hsp60, Hsp90, and single-stranded DNA (ssDNA), which acts as an apoptotic marker. In normal oesophageal epithelium tissue, Hsp60 and Hsp90 were expressed in the cytoplasm and membrane from the basal cell layer to the supra-basal cell layers. Hsp60 and Hsp90 positive stainings (+) were found in 63 of 123 cases (51%) and 62 of 123 cases (50%), respectively. There was no correlation between Hsp60 and Hsp90 expression levels and any of the clinical parameters examined. The five-year survival rate for ESCC patients with Hsp60 (+) expression was significantly higher than for those patients with Hsp60 (-) expression (P=0.0371). Five-year survival rates of patients with Hsp60 (+) and (-) were 49% and 33%, respectively. By contrast, Hsp90 expression failed to predict patient prognosis (P=0.7965). The high-AI group did not have a significantly better prognosis than the low-AI group (P=0.2218). Statistical analysis showed a significant correlation between the expression of Hsp60 and AI in ESCC patients (P=0.008). Thus, the five-year survival rate for the high-AI/Hsp60 (+) group was statistically significantly better than for the other groups (P=0.0281). The results obtained in this study indicate that positive Hsp60 expression is a good prognostic indicator. This may be due to its role as a chaperone in contributing to the induction of apoptosis. These data suggest that Hsp60 expression correlates with the AI and patient prognosis in human ESCC.

Adult↗

PubMed2004

Implication of spinal protein kinase C in the suppression of morphine-induced rewarding effect under a neuropathic pain-like state in mice.

We previously demonstrated that spinal protein kinase C (PKC) is involved in the development of a neuropathic pain-like state induced by sciatic nerve ligation, and the morphine-induced rewarding effect is attenuated by sciatic nerve ligation in rodents. Here we first investigated whether sciatic nerve injury could change the activity of a conventional PKC (cPKC) and an atypical PKC isoform PKCzeta in the mouse spinal cord. The second experiment was to investigate whether direct inhibition of spinal PKC by intrathecal (i.t.) administration of a specific PKC inhibitor, 2-[8-[(dimethylamino)methyl]-6,7,8,9-tetrahydropyrido[1,2-a]indol-3-yl]-3-(1-methyl-1H-indole-3-yl)maleimide (RO-32-0432), could affect the rewarding effect induced by morphine following sciatic nerve ligation in mice. We found here that the activities of both cPKC and PKCzeta in the spinal cord were clearly increased following sciatic nerve ligation. Furthermore, i.t. administration of RO-32-0432 reversed a long-lasting pain-like syndrome as indicated by thermal hyperalgesia following sciatic nerve ligation in mice. These data provide direct evidence that activated cPKC and PKCzeta in the spinal cord may contribute to the development and maintenance of neuropathic pain. In the present study, we confirmed that the morphine-induced place preference was significantly suppressed by sciatic nerve ligation. It should be mentioned that i.t. pretreatment with RO-32-0432 significantly reversed the attenuation of morphine-induced rewarding effect following sciatic nerve ligation. These results suggest that activation of PKCs, including cPKC and PKCzeta, within the spinal cord is directly responsible for the attenuation of the morphine-induced rewarding effect under a neuropathic pain-like state following sciatic nerve ligation in mice.

Analgesics, Opioid↗

PubMed2004

Outcome of surgery for small cell lung cancer -- response to induction chemotherapy predicts survival.

BACKGROUND: The role of surgery for local control of small cell lung cancer (SCLC) is controversial. METHODS: Sixty-nine consecutive patients who underwent complete resection of SCLC in our hospital were reviewed. The patients included 62 men and 7 women. Clinical stage at the time of diagnosis was c-stages IA and B in 29, c-stages IIA and B in 12, c-stage IIIA in 21, and c-stage IIIB in 7. RESULTS: Thirty-two patients received induction chemotherapy, and 37 patients underwent initial surgery. The overall response rate to induction chemotherapy was 71.9 %. The survival rate stratified by clinical stage at the time of diagnosis was 48.9 % for c-stage I, 33.3 % for c-stage II, 20.2 % for c-stage IIIA, and 0 % for c-stage IIIB. Downstaging after induction chemotherapy conferred a survival benefit. Survival after lobectomy or bilobectomy was better than after pneumonectomy. Patients who received adjuvant chemotherapy survived longer than patients who did not. CONCLUSIONS: Surgery combined with chemotherapy is a therapeutic option in selected patients with SCLC. Pathologic nodal status and response to induction chemotherapy are predictors of survival.

Aged↗

PubMed2004

Development of a phantom compatible for MRI and hyperthermia using carrageenan gel-relationship between T1 and T2 values and NaCl concentration.

The authors developed a phantom, designated as the CAGN phantom, compatible for MRI and hyperthermia that is useful in the fundamental studies of non-invasive MR thermometry. The ingredients of this phantom are carrageenan, GdCl3 as a T1 modifier, agarose as a T2 modifier, NaCl as a conductivity modifier, NaN3 as an antiseptic and distilled water. Another phantom that was developed, the CAG phantom, has relaxation times that are adjustable to those of any human tissue. To use this phantom for electromagnetic heating, NaCl was added to change the conductivity of the phantom and clarified the relationship between the conductivity and NaCl concentration. This study examined the relationship between relaxation times and NaCl concentration of the CAGN phantom. The results showed that both T1 and T2 values were affected by NaCl and the experimental results led to the empirical formulae expressing the relationship between the relaxation rates (1/T1, 1/T2) and the concentrations of GdCl3, agarose and NaCl. The appropriate concentrations of T1 and T2 modifiers were calculated from these empirical formulae when making a specified phantom that has the required relaxation times and NaCl concentration.

Algorithms↗

PubMed2004

Development of a phantom compatible for MRI and hyperthermia using carrageenan gel--relationship between dielectric properties and NaCl concentration.

A phantom has previously been developed containing carrageenan, agarose and gadolinium chloride (called CAG phantom) for MRI with 1.5 T. T(1) and T(2) relaxation times of this phantom are independently changeable by varying concentrations of relaxation-time modifiers to simulate relaxation times of the various types of human tissues. The CAG phantom has a T(1) value of 202-1904 ms and a T(2) value of 38-423 ms, when the GdCl(3) concentration is varied from 0-140 micromol/kg and the agarose concentration is varied from 0-1.6%. A new phantom has now been developed (called CAGN phantom), made by adding an electric conductive agent, NaCl, to the CAG phantom for use in the areas of MRI and hyperthermia research. Dielectric properties of the CAGN phantom were measured and the results of experiments were expressed by the Cole-Cole equation in the frequency range of 5-130 MHz. The relationship between the conductivity of the CAGN phantom and the concentration of NaCl was expressed by a linear function in the frequency range of 1-130 MHz. The linear function involves a parameter of frequency and, when the frequency is 10 MHz, the conductivity of the CAGN phantom can be changed from 0.27-1.26 Sm(-1) by increasing the NaCl concentration from 0-0.7%. The CAGN phantom developed can be employed in basic experiments for non-invasive temperature measurement using MRI and as a loading phantom for MRI with up to 3 T.

Carrageenan↗

PubMed2004

Effect of pitavastatin against expression of S100beta protein in the gerbil hippocampus after transient cerebral ischaemia.

AIM AND METHODS: We investigated the immunohistochemical alterations of S100beta-, S100-, glial fibrillary acidic protein (GFAP)- and isolectin B4-positive cells in the hippocampus after 5 min of transient cerebral ischaemia in gerbils. We also examined the effect of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor pitavastatin against neuronal damage in the hippocampal CA1 sector after ischaemia. RESULTS: Severe neuronal damage was observed in the hippocampal CA1 pyramidal neurons from 5 days after ischaemia. GFAP-positive cells increased gradually in the hippocampus from 5 days after ischaemia. Five and 14 days after ischaemia, significant increases in the number of GFAP-positive cells and isolectin B4-positive cells were observed in the hippocampal CA1 and CA3 sector. Mild increases in the number of S100 and S100beta-positive cells were observed in the hippocampal CA1 sector from 1 h to 2 days after ischaemia. Thereafter, S100beta-positive cells increased in the hippocampal CA1 sector after ischaemia, whereas S100-positive cells decreased in this region. In our double-labelled immunostainings, S100 and S100beta immunoreactivity was found in GFAP-positive astrocytes, but not in isolectin B4-positive microglia. Pharmacological study showed that HMG-CoA reductase inhibitor, pitavastatin, can protect against the hippocampal CA1 neuronal damage after ischaemia. This drug also prevented increases in the number of GFAP-positive astrocytes, isolectin B4-positive microglia, S100-positive astrocytes and S100beta-positive astrocytes after ischaemia. CONCLUSION: The present study demonstrates that pitavastatin can decrease the neuronal damage of hippocampal CA1 sector after ischaemia. This beneficial effect may be, at least in part, mediated by inhibiting the expression of astrocytic activation in the hippocampus at the acute phase after ischaemia. Thus the modulation of astrocytic activation may offer a novel therapeutic strategy of ischaemic brain damage.

Animals↗

PubMed2004

Activation of integrin alpha IIb beta 3 in the glycoprotein Ib-high population of a megakaryocytic cell line, CMK, by inside-out signaling.

Affinity/avidity state of integrin alpha IIb beta 3 is regulated by intracellular inside-out signaling. Although several megakaryocytic cell lines have been established, soluble ligand binding to alpha IIb beta 3 expressed in these cells by cellular agonists has not been demonstrated. We have re-examined agonist-induced alpha IIb beta 3 activation on megakaryocytic cell lines with a marker of the late stage of megakaryocytic differentiation, glycoprotein Ib (GPIb). Activation of alpha IIb beta 3 was assessed by PAC1 and soluble fibrinogen binding to the cells. We found that alpha IIb beta 3 expressed in CMK cells with high GPIb expression was activated by a phorbor ester, phorbol myristate acetate (PMA). Although the population of the GPIbhigh cells was <0.5% of the total cells, incubation with a nucleoside analog, ribavirin, efficiently increased the PMA-reactive GPIbhigh cells. Not only PMA but also a calcium ionophore, A23187, induced alpha IIb beta 3 activation, and PMA and A23187 had an additive effect on alpha IIb beta 3 activation. Ligand binding to the activated alpha IIb beta 3 in the GPIbhigh CMK cells is totally abolished by an alpha IIb beta 3-specific antagonist, and inhibited by wortmannin, cytochalasin-D and prostaglandin E1, and the effects of these inhibitors on alpha IIb beta 3 activation in the GPIbhigh CMK cells were compatible with those in platelets. We have also demonstrated that the ribavirin-treated CMK cells express PKC-alpha, -beta, -delta and -theta, and suggested that PKC-alpha and/or -beta appear to be responsible for PMA-induced activation of alpha IIb beta 3 in CMK cells.

Alprostadil↗

PubMed2004

Protective effect of pitavastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, on ischemia-induced neuronal damage.

We investigated the neuroprotective effects of a novel 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor (pitavastatin) on ischemic neuronal damage in gerbils using immunohistochemistry. The animals were allowed to survive for 14 days after 5 min of ischemia induced by bilateral occlusion of the common carotid arteries. Five days after ischemia, severe neuronal cell loss was observed in the hippocampal CA1 sector. Prophylactic treatment with pitavastatin dose-dependently prevented the hippocampal CA1 neuronal cell loss 5 days after ischemia. Immunohistochemical study did not show the change of nNOS and iNOS expression in the hippocampus except for, in a few regions, up to 1 day after ischemia. Thereafter, the expression of iNOS was observed in the hippocampal CA1 sector 5 and 14 days after ischemia. In contrast, the expression of nNOS and eNOS gradually decreased in the hippocampal CA1 sector up to 14 days after ischemia. Prophylactic treatment with pitavastatin also prevented the expression of iNOS and the decrease of eNOS expression and the number of nNOS-positive cells in the hippocampal CA1 sector 5 days after ischemia. However, prophylactic treatment with pitavastatin at a dose of 10 mg kg(-1) did not change the immunoreactivity of iNOS and nNOS in the hippocampus at an early phase after ischemia. In contrast, this drug prevented the reduction of eNOS immunoreactivity in the hippocampal CA1 neurons at an early phase after ischemia. These findings demonstrate that the HMG-CoA reductase inhibitor pitavastatin can protect hippocampal CA1 neurons after transient forebrain ischemia through up-regulation of eNOS expression in this region. Thus pharmacological modulation of eNOS expression may offer a novel therapeutic strategy for cerebral ischemic stroke.

Animals↗

PubMed2004

Neuroprotective effect of the angiotensin-converting enzyme inhibitor perindopril in MPTP-treated mice.

The angiotensin -converting enzyme (ACE) inhibitor perindopril has been shown to exert beneficial effects on the dopaminergic system. Here, we investigated the effects of perindopril on the dopaminergic system in mice after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment, in comparison with a Ca(2+) antagonist, amlodipine. Administration of perindopril showed dose-dependent neuroprotective effects against MPTP-induced striatal dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) depletion. However, administration of amlodipine showed no significant effects on striatal dopamine depletion after MPTP treatment. In our immunohistochemical studies with antibodies against tyrosine hydroxylase (TH), microtubule-associated protein 2a, b (MAP2), dopamine transporter (DAT), parvalbumin (PV), glial fibrillary acidic protein (GFAP) and Cu/Zn-superoxide dismutase (Cu/Zn-SOD), the administration of perindopril significantly attenuated MPTP-induced substantia nigra and striatal damage. This drug also blocked the increases in GFAP-positive astrocytes in the striatum and substantia nigra after MPTP treatment. Furthermore, the administration of perindopril showed a protective effect against the intense Cu/Zn-SOD immunoreactivity in the neurons and glial cells in both the striatum and substantia nigra after MPTP treatment. These results indicated that the ACE inhibitor perindopril can protect against MPTP-induced striatal dopamine and DOPAC depletion in mice. The protective effect may be, at least in part, caused by the reduction of free radicals caused by MPTP. The present study also demonstrated that perindopril is effective against MPTP-induced neurodegeneration of the nigro-striatal dopaminergic pathway. Furthermore, our results provided further evidence that free radical scavengers may be effective in the treatment of neurodegenerative diseases such as Parkinson's disease.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed2004

Dietary protein deprivation decreases the serine phosphorylation of insulin receptor substrate-1 in rat skeletal muscle.

Evidence has shown that protein malnutrition tends to increase peripheral insulin sensitivity, but the molecular mechanism underlying this increase is not yet clear. Here we show that, in rat muscle, the state of insulin receptor (IR) substrate-1 (IRS-1), a pivotal component of the signaling pathway of the IR, changes drastically according to protein supply. After rats were fed a protein-free diet (PF) or a 12% casein diet for 1 week, their IR and IRS-1 states were analyzed by immunoblotting using various antibodies. PF slightly increased the amount of IR without affecting the state of IR tyrosine phosphorylation. In contrast, PF decreased the amount of IRS-1 and markedly increased phosphorylation of IRS-1 tyrosine residues after insulin injection. Moreover, IRS-1 in PF rats exhibited faster mobility in SDS-PAGE as well as far less phosphorylation of Ser612 and Ser307, indicating hypophosphorylation on its serine residues. Results of additional experiments using energy-restricted (pair-fed) rats and streptozotocin-induced diabetic rats suggest that dietary protein deficiency by itself alters serine phosphorylation of IRS-1, while the up-regulation of tyrosine phosphorylation requires other factors, such as a reduction in basal plasma insulin. The serine dephosphorylation followed by up-regulation of insulin-dependent IRS-1 tyrosine phosphorylation in skeletal muscle of PF rats in vivo is similar to a phenomenon observed in cultured cells under restriction of amino acids in the medium. With these findings, it could be inferred that the reduction of serine phosphorylation contributes to the sensitization of IRS-1 to IR tyrosine kinase under protein malnutrition.

Animals↗

PubMed2004

[True pulmonary carcinosarcoma suspected as a metastatic lung tumor].

This patient, a 53-year-old man, has underwent operation on the diagnosis of esophageal cancer 2 years ago. An abnormal shadow was detected in the left lung field and he was admitted to our hospital for further examination. On the suspicion of metastatic lung tumor by transbronchial brushing cytology, partial resection of the left lower lobe was performed. Histologically the tumor was of carcinomatous (squamous cell carcinoma and adenocarcinoma) and sarcomatous (fibrosarcoma and chondrosarcoma) elements, so the patient was diagnosed as "true" pulmonary carcinosarcoma. True pulmonary carcinosarcoma is one of the very rarest neoplasms of the lung.

Carcinoma, Squamous Cell↗

PubMed2003

High frequency of antibiotic-associated diarrhea due to toxin A-negative, toxin B-positive Clostridium difficile in a hospital in Japan and risk factors for infection.

Patients hospitalized in a hospital with a high incidence of antibiotic-associated diarrhea due to toxin A-negative, toxin B-positive (A-/B+) Clostridium difficile were retrospectively investigated to determine the clinical manifestations and risk factors for infection. Of 77 Clostridium difficile isolates obtained from 77 patients during the 1-year investigation period, 30 were A-/B+ and 47 were toxin A-positive, toxin B-positive (A+/B+). By pulsed-field gel electrophoresis analysis, 23 of the 30 A-/B+ strains were outbreak-related, suggesting nosocomial spread of a single type of bacterium, which mainly affected patients in the wards of respiratory medicine, hematology and neurology. Using regression analysis, three factors were found to be associated with infection by A-/B+ isolates: (i) exposure to antineoplastic agents ( P=0.01, odds ratio [OR]=5.1), (ii) the use of nasal feeding tubes ( P=0.008, OR=5.2), and (iii) assignment to a certain internal medicine ward ( P=0.05, OR=3.0). Between patients with Clostridium difficile-associated diarrhea caused by A-/B+ strains and those with A+/B+ strains, no statistically significant difference was found in body temperature, serum concentration of C-reactive protein, leukocyte count in whole blood, frequency of diarrhea, or type of underlying disease. These results indicate that A-/B+ strains of Clostridium difficile can cause intestinal infection in humans and they spread nosocomially in the same manner as A+/B+ strains.

Adolescent↗

PubMed2003

Characterization of a wound-inducible cytochrome P450 gene ( CYP72A29) that is down-regulated during crown gall tumorigenesis in potato tuber.

A cDNA for a putative cytochrome P450 (CYP72A29), which is down-regulated during Agrobacterium tumefaciens -mediated tumorigenesis, was isolated from potato ( Solanum tuberosumL. May Queen) tuber by differential display. Northern analysis indicated that the CYP72A29 gene was transiently up-regulated in tuber discs after a 24-h aging period, and expression gradually increased upon further incubation (up to 7 days). Inoculation of tuber discs with the non-pathogenic A. tumefaciens strain LBA4301 had a very similar effect, but inoculation with the wild-type strain A. tumefaciens A208 suppressed the accumulation of mRNA during further incubation. Furthermore, the accumulation of CYP72A29 mRNA was strongly suppressed by inoculation with mutant strains of A. tumefaciens that produce large amounts of indole-3-acetic acid. This down-regulation also occurred when the discs were treated with 2,4-dichlorophenoxyacetic acid or 1-naphthalenacetic acid. These results suggest that the expression of CYP72A29 is regulated by auxin. RT-PCR analysis revealed that the transcripts were most abundant in sprouts and eyes, less so in roots, and hardly detectable in leaves, flower buds and stems.

Agrobacterium tumefaciens↗