Search PubMed⌕ Search

Biomedical subjects

Y Kuroda

Publications and source records attributed to Y Kuroda.

At least 145 records · Page 8Linked to original sources

Laparoscopic lower anterior resection is equivalent to laparotomy for lower rectal cancer at the distal line of resection.

BACKGROUND: Procedures that involve resection of the distal rectum challenge the current limitations of laparoscopic technology, because of lack of compact articulating stapling instruments. METHOD: We improve the procedure with the aid of a Lap disk, an abdominal wall sealing device that was developed for hand-assisted manipulation. A linear stapler capable of changing its stop angle is inserted through the disk, and the rectum is transected by the disk during a second pneumoperitoneum. RESULTS: The transection line becomes equivalent to that obtained with laparotomy. CONCLUSION: This new technique made laparoscopic lower anterior resection possible to transect the lower rectum in the same way as is done with laparotomy.

Abdominal Muscles↗

Chairpersons' opinions regarding quality control of surgical faculty performance in Japanese academic surgery departments.

BACKGROUND: The governance and power structure of the department of surgery depends to a large extent on the chairperson's decisions in Japanese medical schools. This paper reports the current collective opinions of surgery department chairpersons regarding the quality assessment of surgical faculty performance. METHODS: Surveyed were 78 chairpersons of general surgery departments from 72 Japanese medical schools. Chairpersons were questioned about administrative and organizational decision making: rank order requirements for full-time surgical faculties, coordination of staff for surgical operations, and performance outcome measures. RESULTS: In all, 68 (87%) chairpersons responded. When selecting surgical faculties, publishing competence (45%) and collaborative personality (44%) were the two foremost concerns of chairpersons. Teaching experience (0%) and board certification (2%) showed the lowest rate for the first priority among the 6 elements listed. The operator was mainly decided by the chairperson (63%) whereas the rest of the operative team members were decided by either the chairperson (28%), a specialty team (38%), or attending surgeons (32%). Thirty-three chairpersons (49%) of 68 respondents used the morbidity and mortality conference as the only available approach for assessing surgical performance on a regular basis, whereas the remaining half did not have routine outcome measures. CONCLUSIONS: The results of this study indicate that surgery department chairpersons deemed collaborative personality and publishing competence the two major requirements for candidates of surgical faculties. Although the morbidity and mortality conference is currently the only available approach for assessing surgical performance, the majority of chairpersons felt that outcome measures should be based on more objective and structured criteria.

Academic Medical Centers↗

Tumor necrosis factor, tumor necrosis factor receptors type 1 and 2, lymphotoxin-alpha, and HLA-DRB1 gene polymorphisms in human T-cell lymphotropic virus type I associated myelopathy.

We studied tumor necrosis factor (TNF), lymphotoxin-alpha (LT-alpha), and TNF receptors type 1 (TNFR-1) and type 2 (TNFR-2) gene polymorphisms as well as HLA class II DRB1 alleles in Japanese patients with human T-cell lymphotropic virus type I (HTLV-I) associated myelopathy (HAM) (n = 51), patients with adult T-cell leukemia/lymphoma (ATL) (n = 48), asymptomatic HTLV-I carriers (n = 50), and HTLV-I seronegative, normal controls (n = 112). There were significant differences between HAM patients and normal controls in the distributions of TNF promoter region polymophism at position --857, the LT-alpha gene NcoI polymorphism, and the T-G substitution in exon 6 of the TNFR-2 gene. The distribution of the NcoI polymorphism of the LT-alpha gene was also significantly different between HAM patients and asymptomatic HTLV-I carriers. In contrast, we failed to detect any difference in the frequency of DRB1, TNF promoter at position --1031, --863, or the TNFR-1 promoter --383 polymorphism. The results suggest that the TNF/LT-alpha gene region within the HLA class III of chromosome 6 and the TNFR-2 gene region located on chromosome 1p36 might contribute to susceptibility to HAM, and that aberrant expression or function of these cytokines and the receptor could be involved in the development of HAM.

Alleles↗

Long-term potentiation induction--a synaptic catch mechanism released by extracellular phosphorylation.

The best understood form of long-term potentiation in hippocampal CA1 neurons is induced by activation of the N-methyl-D-aspartate receptor complex and subsequent activation of the intracellular second messenger systems. In addition to this intracellular mechanism, long-term potentiation can also be induced by an extracellular mechanism involving phosphorylation by ATP-ecto-protein kinase. In the present study, we hypothesize that a putative blocking molecule of the formation of long-term potentiation exists on the synaptic membrane, and examine whether ecto-protein kinases play a role in the block of long-term potentiation by phosphorylating the ecto-domains of this molecule in CA1 neurons of guinea-pig hippocampal slices. Long-term potentiation was induced by theta burst stimulation whether or not the test input was delivered to the CA1 neurons following burst stimulation. However, 5 microM K-252b, an ecto-protein kinase inhibitor, only blocked the induction of long-term potentiation when the test input was delivered during a 30-min period following burst stimulation. The results suggest that the process of formation of long-term potentiation continues independently of test synaptic input, while the block of long-term potentiation results from a combination of an interruption of the ATP-ecto-protein kinase-dependent processes and continued test synaptic input after burst stimulation. This block of long-term potentiation, which should be released by activation of ATP-ecto-protein kinase, is suggested to act as a "safety catch" for synaptic plasticity in hippocampal CA1 neurons.

Animals↗

3D-CT diagnosis for ingested foreign bodies.

Ingested foreign bodies can be hard to diagnose but cannot be missed. We report two cases where helical computed tomography (three-dimensional computed tomography) was used for the effective preoperative diagnosis (swallowed fish bone-induced perforation of sigmoid colon and a case of ileus caused by ingested PTP [press-through package]). Other traditional diagnostic methods could not identify the foreign bodies. Three-dimensional computed tomography is useful for the diagnosis of foreign body ingestion and should be used for the difficult cases.

Abdominal Pain↗

Diagnosis and natural history of isolated congenital pulmonary regurgitation in fetal life.

We describe a rare instance of isolated pulmonary regurgitation caused by a dysplastic pulmonary valve which was detected prenatally. Fetal echocardiography demonstrated severe pulmonary regurgitation, and progressive cardiomegaly because of right ventricular volume overload. After birth, conservative therapy was successful in alleviating the pulmonary vascular resistance, and the pulmonary regurgitation gradually decreased.

Adult↗

Effects of A1 and A2 adenosine receptor antagonists on the induction and reversal of long-term potentiation in guinea pig hippocampal slices of CA1 neurons.

1. Using simultaneous recordings of the field EPSP and the population spike in the CA1 neurons of guinea pig hippocampal slices, we confirmed that delivery of a high-frequency stimulation (tetanus: 100 pulses at 100 Hz) produced robust long-term potentiation of synaptic efficacy (LTP) in two independent components, a synaptic component that increases field excitatory postsynaptic potentials (EPSPs) and a component that results in a larger population spike amplitude for a given EPSP size (E-S potentiation). 2. In the same cells, reversal of LTP (depotentiation; DP) in the field EPSP and in the E-S component is achieved by delivering low-frequency afferent stimulation (LFS: 1 Hz, 1000 pulses) 20 min after the tetanus. 3. When the tetanus or LFS was applied to CA1 inputs in the presence of an adenosine A1 receptor antagonist, 8-cyclopentyltheophylline (1 microM), the field EPSP was enhances in LTP and attenuated in DP, while the E-S relationship was not significantly affected in either LTP or DP. 4. When similar experiments were performed using an A2 receptor antagonist, CP-66713 (10 microM), the field EPSP was blocked in LTP but facilitated in DP, while E-S potentiation was enhanced during both LTP and DP. 5. The results show that endogenous adenosine, acting via A1 or A2 receptors, modulates both the synaptic and the E-S components of the induction and reversal of LTP. Based on the results, we discuss the key issue of the contribution of these receptors to the dynamics of neuronal plasticity modification in hippocampal CA1 neurons.

Action Potentials↗

Structural study of the sodium channel inactivation gate peptide including an isoleucine-phenylalanine-methionine motif and its analogous peptide (phenylalanine/glutamine) in trifluoroethanol solutions and SDS micelles.

In order to gain insight into the gating mechanisms of Na+ channels, in particular their inactivation mechanisms, we studied the structures of the Na+ channel inactivation gate related peptide which includes the IFM (Ile-Phe-Met) motif (Ac-KKKFGGQDIFMTEEQKK-NH2; K1480-K1496 in rat brain type-IIA Na+ channels, MP-3A) and its F/Q(Gln) substituted one (MP-4A) in trifluoroethanol (TFE) solutions and sodium dodecyl sulfate (SDS) micelles using circular dichroism (CD) and 1H-NMR spectroscopies. Based on observed nuclear Overhauser effect constraints, three-dimensional structures of MP-3A and MP-4A were determined using simulated annealing molecular dynamics/ energy minimization calculations. In TFE solutions, no appreciable differences in the structure were observed using either CD or NMR spectra. In SDS micelles, however, the two peptides exhibited definitely different structures from each other. It was found that in MP-3A, residues 11488 and T1491 were spatially proximate with each other owing to hydrogen bonding between the amide proton of 11488 and the hydroxyl oxygen atom of T1491, whereas in MP-4A, F/Q substitution separated them owing to conformational changes. The solvent-accessible surfaces calculated for the structures of MP-3A and MP-4A showed that the former has a smoother interaction surface to the hydrophobic docking site than the latter. In conclusion, the conformational changes, as well as decreased hydrophobicity around the IFM motif owing to the F/Q mutation, may be one reason why F1489Q mutated channels cannot inactivate almost completely.

Amino Acid Motifs↗

Structural genomics projects in Japan.

Two major structural genomics projects exist in Japan. The oldest, the RIKEN Structural Genomics Initiative, has two major goals: to determine bacterial, mammalian, and plant protein structures by X-ray crystallography and NMR spectroscopy and to perform functional analyses with the target proteins. The newest, the structural genomics project at the Biological Information Research Center, focuses on human membrane proteins.

Animals↗

HLA-mismatched CD34-selected stem cell transplant complicated by HHV-6 reactivation in the central nervous system.

We report here a patient who suffered from PCR- confirmed human herpesvirus type 6 (HHV-6) meningoencephalitis after allogeneic purified CD34+ cell transplantation from his HLA-mismatched sibling donor, even though he had been on intense prophylaxis with i.v. ganciclovir (GCV), acyclovir (ACV) and gamma-globulin containing a specific antibody against HHV-6. Serological evaluation disclosed that both the donor and recipient had IgG antibody against HHV-6 before transplantation. His blood WBC count started to transiently increase on day 10, and all blood components had decreased by day 20. He then developed a severe headache and high blood pressure, and sporadic abnormal neurological findings including nystagmus and delirium. An analysis of cerebrospinal fluid (CSF) revealed 8 cells/microl, a glucose level of 130 mg/dl and a protein level of 201 mg/dl (normal, 50 mg/dl) on day 26. At the time, HHV-6 was detected only in CSF by a PCR-based method and he was diagnosed as having meningoencephalitis due to the local reactivation of HHV-6. Although he failed to respond to high-dose therapy with ACV (60 mg/kg/day) and gamma-globulin, the DNA of this virus disappeared from the CNS upon treatment with GCV (30 mg/kg/day) combined with the intraventricular infusion of alpha-interferon. His clinical course was further complicated with meningoencephalitis due to staphylococcus epidermidis, and he died of tentorial herniation on day 79 without the recovery of blood components. This experience may indicate that intense prophylaxis to prevent reactivation of HHV-6 in the CNS is essential for the management of such profoundly immunosuppressed patients.

Acyclovir↗

Carboxyl-terminal region conserved among phosphoinositide-kinase-related kinases is indispensable for mTOR function in vivo and in vitro.

BACKGROUND: The mammalian target of rapamycin (mTOR) belongs to the family of phosphoinositide (PI)-kinase-related kinases that includes the ataxia-telangiectasia gene product (ATM). mTOR plays a critical role in controlling translational effectors such as p70 S6 kinase alpha (p70 alpha) and eukaryotic initiation factor 4E binding protein 1 (4EBP1). RESULTS: We show that the C-terminal region of mTOR, which is highly conserved among the PI-kinase-related kinases, plays a critical role in the mTOR protein kinase activity. Deletion of the C-terminal residues did not adversely affect the expression of mTOR, but caused a nearly complete loss of the mTOR protein kinase activity toward both 4EBP1 and p70 alpha in vitro. These deletions also abolished the ability of a rapamycin-resistant mTOR mutant to rescue the activity of p70 alpha from inhibition induced by rapamycin in vivo. Furthermore, replacement of Trp2545, a conserved residue in the C-terminal region throughout the PI-kinase-related kinase family, abolished the function of the mTOR kinase, both in vivo and in vitro. However, substitution of 32 C-terminal residues of mTOR with those of ATM did not restore the mTOR function. CONCLUSIONS: These findings define an indispensable role for the noncatalytic C-terminal region of mTOR and indicate that, although this highly conserved region may be important throughout the PI-kinase-related kinase family, it is not functionally interchangeable within the family.

Amino Acid Sequence↗

Clinical significance of urokinase-type plasminogen activator activity in hepatocellular carcinoma.

BACKGROUND AND METHODS: The plasminogen activation system plays a crucial role in the process of cancer invasion and metastasis. To evaluate the most effective factor in the invasion, metastasis and prognosis of hepatocellular carcinoma (HCC), we examined urokinase-type plasminogen activator (uPA), plasminogen activator inhibitor (PAI)-1, PAI-2 and uPA activity by enzyme-linked immunosorbent assays (ELISA) in HCC tissues obtained from 46 patients. The results were compared with the patients' clinicopathological features and prognoses. RESULTS: Of the clinicopathological features, only histological portal involvement or intrahepatic metastasis, or both (INV), was significantly correlated to the disease-free survival rates (DFS; P < 0.05). The levels of uPA, PAI-1 and PAI-2 antigens were significantly associated with INV and histological grade. The DFS was not different, however, between cases with uPA, PAI-1 and PAI-2 values above and below the median. The high levels of uPA activity were closely related to INV (P < 0.001), and the activity gradually raised histological grades (P < 0.0001). The DFS was significantly different between patients with uPA activity below and above the median (0.70 ng/mL; P = 0.0092); it was also significantly different between such patients without INV (P < 0.05). CONCLUSIONS: Urokinase-type plasminogen activator activity may be the most sensitive factor affecting HCC invasion in the plasminogen activation system and a strong predictor for the recurrence of HCC. We suggest that cases with uPA activity of more than 0.70 ng/mL should be carefully followed up for possible HCC recurrence.

Adolescent↗

Beta-catenin expression in human neural cell lines following exposure to cytokines and growth factors.

Beta-catenin acts as a key mediator of the Wnt/Wingless signaling pathway involved in cell proliferation, differentiation and survival. Recent studies have shown that an unstable interaction between beta-catenin and the mutant presenilin-1 induces neuronal apoptosis, and that beta-catenin levels are decreased in the brains of patients with Alzheimer's disease (AD). Since activated microglia and astrocytes play a role in the process of neuronal degeneration in AD, the cytokine/growth factor-regulated expression of beta-catenin in human neural cell lines, including NTera2 teratocarcinoma-derived differentiated neurons (NTera2-N), IMR-32 neuroblastoma, SKN-SH neuroblastoma and U-373MG astrocytoma, was studied quantitatively following exposure to epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), brain-derived neurotrophic factor (BDNF), tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, IL-6, interferon (IFN)-gamma, transforming growth factor (TGF)-beta1, dibutyryl cyclic adenosine 3',5'-cyclic monophosphate (cAMP) (dbcAMP) or phorbol 12-myristate 13-acetate (PMA). Beta-catenin mRNA expressed constitutively in all of these cell lines was unaffected by treatment with any factors examined. In contrast, beta-catenin protein levels were reduced markedly in NTera2-N cells by exposure to dbcAMP, EGF or bFGF, and in U-373MG cells by treatment with dbcAMP or PMA, but were unaffected in any cell lines by BDNF, TNF-alpha, IL-1beta, IL-6, IFN-gamma or TGF-beta1. These results indicate that beta-catenin is expressed constitutively in human neural cells and downregulated at a protein level by a set of growth factors in a cell type-specific manner.

Astrocytoma↗

Amyloid precursor protein beta-secretase (BACE) mRNA expression in human neural cell lines following induction of neuronal differentiation and exposure to cytokines and growth factors.

Recently, a novel amyloid precursor protein beta-secretase (designated BACE) was identified. Because activated microglia and astrocytes play a role in amyloidogenesis in Alzheimer's disease, the constitutive and glial cytokine/growth factor-regulated expression of BACE was studied in human neural cell lines. By reverse transcription-polymerase chain reaction (RT-PCR) analysis, BACE mRNA expression was identified in various human neural and non-neural cell lines. By northern blot analysis, the expression of BACE mRNA composed of five distinct transcripts (>8.0, 7.0, 6.0, 4.4 and 2.6 kb) was elevated markedly in NTera2 teratocarcinoma cells following retinoic acid-induced neuronal differentiation. But the levels of three major BACE mRNA species (7.0, 6.0 and 4.4 kb) were not significantly altered in NTera2-derived neurons, SK-N-SH neuroblastoma or U-373MG astrocytoma following exposure to tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6, interferon-gamma, transforming growth factor-beta1, epidermal growth factor, basic fibroblast growth factor, brain-derived neurotrophic factor, dibutyryl cyclic adenosine monophosphate or phorbol 12-myristate 13-acetate. These results indicate that BACE mRNA is expressed constitutively in human neural cells and its expression is upregulated during neuronal differentiation, but it is unlikely to be regulated by activated glia-derived cytokines and growth factors.

Alzheimer Disease↗

Cramping pain and prolonged elevation of serum creatine kinase levels in a patient with Guillain-Barré syndrome following Campylobacter jejuni enteritis.

We describe a patient with Guillain-Barré syndrome (GBS) following Campylobacter jejuni enteritis, accompanied with severe cramping pain and a marked increase in serum creatine kinase (CK) levels. Both conditions became evident three weeks after the onset of GBS and continued for longer than one month. In this patient, it is possible that rapid extensive denervation due to severe axonal degeneration of motor nerve terminals might have caused hyperexcitability in regional muscles, leading to recurrent muscle cramps and persistent release of muscular CK.

Adult↗

A valine to methionine polymorphism at codon 83 in the 8-oxo-dGTPase gene MTH1 is not associated with sporadic Parkinson's disease.

Recently, 8-oxo-7,8-dihydrodeoxyguanosine triphosphatase (8-oxo-dGTPase; MTH1), a key enzyme for preventing oxidative stress-induced DNA damage, has been found to be expressed aberrantly in the nigrostriatal dopaminergic neurones in the brains of those with Parkinson's disease (PD). A valine (Val) to methionine (Met) polymorphism at codon 83 in exon 4 of the MTH1 gene was studied in 73 patients with sporadic PD and 151 age-matched non-PD controls by PCR-RFLP analysis, to determine a possible association of this polymorphism with development of PD. The frequency of either 83Val or 83Met allele was not statistically different between PD patients (92.5% or 7.5%) and the controls (88.7% or 11.3%) (chi(2) = 1.511, P = 0.2190). The 83Met/Met homozygotes consisting of an infrequent genotype in the control population (1.3%) were not found in the PD group. The frequency of both 83Val/Met heterozygotes and 83Met/Met homozygotes combined was not statistically different between PD patients (15.1%) and the controls (21.2%), compared with that of the 83Val/Val homozygotes (chi(2) = 1.190, P = 0.2754). These results indicate that the 83Val/Met polymorphism in the MTH1 gene is not associated with an increased risk for development of sporadic PD.

Aged↗