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Biomedical subjects

K Nishiwaki

Publications and source records attributed to K Nishiwaki.

At least 19 recordsLinked to original sources

A marked decrease in heart rate variability associated with junctional rhythm during anesthesia with sevoflurane and fentanyl.

Heart rate variability (HRV) was investigated using a new technique for time series analysis combining the maximum entropy method and non-linear least squares method -- the 'MemCalc method' -- in patients undergoing general anesthesia with sevoflurane and fentanyl for elective surgery. As the occurrence of junctional rhythm coincided with the measurement of these variables in two patients, we successfully evaluated the entropy, low (LF) and high (HF) frequency component of the HRV during junctional rhythm and found that the occurrence of junctional rhythm is associated with marked decreases in the entropy, LF and HF of HRV. When evaluating autonomic control of the heart using HRV analysis, the decrease in HRV caused by the occurrence of junctional rhythm must be taken into account.

Adult↗

Severe hypertension after stellate ganglion block.

Haemodynamic effects may occur after stellate ganglion block (SGB) arising from autonomic imbalance and local anaesthetic infiltration to barosensitive areas. We report seven patients who developed severe hypertension (systolic arterial pressure >200 mm Hg) after SGB in our pain clinic service. We postulate that diffusion of the local anaesthetic along the carotid sheath may produce vagal blockade causing unopposed sympathetic activity as a result of attenuation of the baroreceptor reflex. We recommend close monitoring of arterial pressure measurement in patients who received SGB.

Adult↗

CD2+ acute promyelocytic leukemia is associated with leukocytosis, variant morphology and poorer prognosis.

The T cell-lineage marker CD2 is sometimes expressed in acute promyelocytic leukemia (APL), and CD2 expression is reported to correlate with some clinical characteristics. However, the significance of CD2 expression in APL has not been fully elucidated. We evaluated CD2 expression in APL treated by the same treatment strategy in a single institute, and whether it had any special characteristics. Among 29 APL, 6 were positive for CD2. Patients with CD2+ APL tended to have a higher leukocyte count than CD2- APL (34.5 +/- 13.1/l vs. 6.8 +/- 2.1/l), morphological characteristics as variant-APL (50 vs. 0%). They also showed poor clinical prognosis. The CR rate of CD2- APL was 87.0% while that of CD2+ APL was 50 %. The mortality was 13.0 and 66.7%, respectively, and the survival rate was significantly lower in CD2+ APL. CD2 expression was proven to be a risk factor associated with death in addition to the morphological characteristics of variant-APL and leukocytosis. These results indicated that CD2 expression might have a significant impact on the prognosis of APL. Whether CD2+ APL should be characterized as a special clinical entity should be discussed in a larger patient population.

Adult↗

CED-12/ELMO, a novel member of the CrkII/Dock180/Rac pathway, is required for phagocytosis and cell migration.

The C. elegans genes ced-2, ced-5, and ced-10, and their mammalian homologs crkII, dock180, and rac1, mediate cytoskeletal rearrangements during phagocytosis of apoptotic cells and cell motility. Here, we describe an additional member of this signaling pathway, ced-12, and its mammalian homologs, elmo1 and elmo2. In C. elegans, CED-12 is required for engulfment of dying cells and for cell migrations. In mammalian cells, ELMO1 functionally cooperates with CrkII and Dock180 to promote phagocytosis and cell shape changes. CED-12/ELMO-1 binds directly to CED-5/Dock180; this evolutionarily conserved complex stimulates a Rac-GEF, leading to Rac1 activation and cytoskeletal rearrangements. These studies identify CED-12/ELMO as an upstream regulator of Rac1 that affects engulfment and cell migration from C. elegans to mammals.

Adaptor Proteins, Signal Transducing↗

[Perioperative management of a patient with purpura fulminans syndrome due to protein C deficiency].

PURPOSE: Protein C is a vitamin K-dependent anticoagulant and homozygous protein C deficiency is a rare fatal thrombotic disease. This report describes the perioperative management of homozygous protein C deficiency in a patient who underwent a total of three surgical procedures under general anesthesia and the successful use of activated protein C concentrate. CLINICAL FEATURES: A female baby, who developed disseminated intravascular coagulation and purpura fulminans shortly after birth, was diagnosed as purpura fulminans syndrome due to homozygous protein C deficiency. At one month of age, she suffered bilateral retinal detachment and glaucoma due to retinal hemorrhage. After marked improvement of her condition after administration of activated protein C concentrate, she underwent a left iridectomy and implantation of a Broviak catheter under general anesthesia. Her intraoperative course was uncomplicated but, on postoperative day four, she presented another episode of massive cutaneous necrosis and gangrene. Activated protein C concentrate was administered again, with good results. She underwent replacement of a Broviak catheter at four months of age, and right iridectomy for glaucoma at eight months. Both were uneventful. CONCLUSION: The perioperative management of homozygous protein C deficiency and purpura fulminans requires appropriate measures for thromboembolic prophylaxis. Sufficient iv fluid administration is necessary. Attention should be paid to decrease the risk of tissue compression such as that associated with positioning, blood pressure cuff, and endotracheal intubation, which may cause necrosis over pressure points. Replacement therapy with activated protein C concentrate appears safe and effective. The anesthetic management is reviewed and discussed.

Anesthesia, General↗

A putative GDP-GTP exchange factor is required for development of the excretory cell in Caenorhabditis elegans.

The Caenorhabditis elegans excretory cell extends tubular processes, called canals, along the basolateral surface of the epidermis. Mutations in the exc-5 gene cause tubulocystic defects in this canal. Ultrastructural analysis suggests that exc-5 is required for the proper placement of cytoskeletal elements at the apical epithelial surface. exc-5 encodes a protein homologous to guanine nucleotide exchange factors and contains motif architecture similar to that of FGD1, which is responsible for faciogenital dysplasia. exc-5 interacts genetically with mig-2, which encodes Rho GTPase. These results suggest that EXC-5 controls the structural organization of the excretory canal by regulating Rho family GTPase activities.

Amino Acid Sequence↗

A metalloprotease disintegrin that controls cell migration in Caenorhabditis elegans.

In Caenorhabditis elegans, the gonad acquires two U-shaped arms by the directed migration of its distal tip cells (DTCs) along the body wall basement membranes. Correct migration of DTCs requires the mig-17 gene, which encodes a member of the metalloprotease-disintegrin protein family. The MIG-17 protein is secreted from muscle cells of the body wall and localizes in the basement membranes of gonad. This localization is dependent on the disintegrin-like domain of MIG-17 and its catalytic activity. These results suggest that the MIG-17 metalloprotease directs migration of DTCs by remodeling the basement membrane.

Amino Acid Sequence↗

Heart rate variability during massive hemorrhage and progressive hemorrhagic shock in dogs.

PURPOSE: To investigate the sequential changes in heart rate (HR), autonomic nervous activity presented by the spectral analysis of heart rate variability (HRV), hemodynamics and metabolism during massive hemorrhage and progressive hemorrhagic shock in dogs. METHODS: Twelve dogs were subjected to acute massive hemorrhage until mean arterial pressure (MAP) reached 50 mm Hg. Then bleeding was stopped and they were allowed to reach a plateau phase. They were divided, post hoc, into bradycardic or tachycardic groups according to their HR response to the acute massive hemorrhage. After reaching a plateau phase, the dogs were further bled to keep their MAP around 50 mmHg (progressive hemorrhagic shock). Their heart rate power spectra were quantified into low-frequency (LF) (0.04-0.15 Hz) and high-frequency (HF) (0.15-0.4 Hz) components. RESULTS: In the bradycardic group, both LF and HF increased after massive hemorrhage, but during progressive hemorrhagic shock these components decreased while HR increased. In the tachycardic group, LF increased after massive hemorrhage, but during progressive hemorrhagic shock LF decreased with continuous suppression of HF CONCLUSION: Massive hemorrhage caused two types of HR response: bradycardia and tachycardia. The HRV profile showed differential autonomic characteristics, and could be a valuable tool in assessing various degrees of hemorrhagic shock.

Animals↗

[Recovery from pancytopenia and liver dysfunction after administration of thiamazole for hyperthyroidism].

A 45-year-old woman was referred to our hospital because of hyperthyroidism complicated by atrial fibrillation and heart failure. Laboratory data revealed pancytopenia, with a white blood cell count of 2,600/microliter, red blood cell count of 330 x 10(4)/microliter, and platelet count of 6.2 x 10(4)/microliter. The patient had normal transaminase levels, but tests for hepaplastin and cholinesterase showed values of 34% and 1.4 U/ml, respectively, indicating liver dysfunction. There was also decreased excretion of indocyanine green. After initiation of treatment with 30 mg thiamazole and 20 mg propranolol daily, the patient's thyroid function normalized and the other abnormal laboratory findings such as pancytopenia and liver dysfunction also disappeared. Pancytopenia is a rare complication of hyperthyroidism. In this case, various laboratory abnormalities were normalized by antithyroid therapy alone, indicating that the hyperthyroidism itself was closely related to the pathogenesis of pancytopenia and liver dysfunction.

Antithyroid Agents↗

Transfer function analysis of the circulation in patients undergoing sevoflurane anesthesia.

PURPOSE: The effects of sevoflurane anesthesia on the interactions between heart rate, blood pressure and respiration were assessed using transfer function analysis. METHODS: Nine ASA 1 or 2 patients undergoing elective surgery were involved. They were paralysed and their lungs were mechanically ventilated during sevoflurane anesthesia. Instantaneous heart rate (IHR) from electrocardiogram, instantaneous lung volume (ILV) by respiratory inductive plethysmography and mean blood pressure (MBP) by arterial tonometry were obtained during conscious state, and 1MAC and 2MAC of sevoflurane anesthesia. Transfer function analysis for the relationships between ILV and IHR, ILV and MBP, MBP and IHR were made for five minute periods during which the respiratory rate was varied in a standardized fashion. RESULTS: In awake patients transfer magnitudes for the relationships between ILV and IHR and between MBP and IHR in the 0.04-0.5Hz frequency band were 8.9 +/- 7.7 bpm x l(-1) and 0.95 +/- 0.44 bpm x mmHg(-1) respectively. Sevoflurane 2MAC decreased these values to 1.2 +/- 0.7 (P = 0.014) and 0.26 +/- 0.14 (P < 0.01) respectively, but phases were not affected. Neither transfer magnitudes nor phases between ILV and MBP were affected during sevoflurane anesthesia. Coherence for the relationships between ILV and IHR and between MBP and IHR were decreased during 1MAC sevoflurane anesthesia but not affected during 2MAC sevoflurane anesthesia. CONCLUSIONS: The interactions between heart rate, blood pressure and respiration were altered by sevoflurane anesthesia. These findings could be explained by the attenuation of autonomic nervous system activity.

Adult↗

Heart rate and blood pressure power spectral analysis during calcium channel blocker induced hypotension.

PURPOSE: To observe heart rate (HRV) and blood pressure variability (BPV) as indices of neurocirculatory responses to induced hypotension with diltiazem and/or nicardipine for hip surgery. METHODS: Thirty-six ASA I-II patients received diltiazem (group D, n = 12), nicardipine (group N, n = 12) or combination of diltiazem/nicardipine (group DN, n = 12). The intensity of HRV and BPV, was determined by spectral analysis of HRV and BPV before anesthesia (T0), just before induced hypotension (T1), and at 10 and 30 min after the start of induced hypotension (T2 and T3, respectively). The logarithmic HRV and BPV were integrated: sympathetic and parasympathetic mediated low frequency area (0.06-0.1 Hz, LF), parasympathetic related high frequency area (0.15-0.4 Hz, HF) and total frequency area (0.01-0.4 Hz). Blood loss was assessed by weighing gauzes and measuring suction. RESULTS: Group DN had less blood loss (466 +/- 46 ml, mean +/- SEM) than group D (733 +/- 100 ml, P < 0.05). Diltiazem (11.4 +/- 0.9 microg x kg(-1) x min(-1)), and combination of diltiazem (0.25 +/- 0.01 mg x kg(-1)) and nicardipine (5.9 +/- 0.9 microg x kg(-1) x min(-1)) decreased LF-HRV at T2 and T3 (P < 0.05 vs T0 and T1), while nicardipine (8.1 +/- 0.8 microg x kg(-1) x min(-1)) showed increase in LF-HRV at T2 (P < 0.05 vs T1). HF-HRV unchanged through hypotension except for a decrease in group N at T3 (P < 0.05 vs T1). There were no increases in HF-BPV, and LF-BPV, except for a diltiazem induced decrease in LF-BPV at T3 (P < 0.05 vs T0 and T1). CONCLUSION: Group D and group DN can be used for deliberate hypotension without an increase in sympathetically mediated LF-HRV.

Adult↗

Mutations affecting symmetrical migration of distal tip cells in Caenorhabditis elegans.

The rotational symmetry of the Caenorhabditis elegans gonad arms is generated by the symmetrical migration of two distal tip cells (DTCs), located on the anterior and posterior ends of the gonad primordium. Mutations that cause asymmetrical migration of the two DTCs were isolated. All seven mutations were recessive and assigned to six different complementation groups. vab-3(k121) and vab-3(k143) affected anterior DTC migration more frequently than posterior, although null mutants showed no bias. The other five mutations, mig-14(k124), mig-17(k113), mig-18(k140), mig-19(k142), and mig-20(k148), affected posterior DTC migration more frequently than anterior. These observations imply that the migration of each DTC is regulated differently. mig-14 and mig-19 also affected the migration of other cells in the posterior body region. Four distinct types of DTC migration abnormalities were defined on the basis of the mutant phenotypes. vab-3; mig-14 double mutants exhibited the types of DTC migration defects seen for vab-3 single mutants. Combination of mig-17 and mig-18 or mig-19, which are characterized by the same types of posterior DTC migration defects, exhibited strong enhancement of anterior DTC migration defects, suggesting that they affect the same or parallel pathways regulating anterior DTC migration.

Animals↗

[Participation of neuropeptide Y Y3-receptor subtype in the increase in lung vascular permeability--for therapy of respiratory failure].

In order to find some treatments for respiratory failure caused by pulmonary edema, we investigated the mechanism of neurogenic pulmonary edema. Previously, stimulation of sympathetic nerves caused an increase in pulmonary vascular permeability, possibly due to neuropeptide Y. Neuropeptide Y injected into the trachea increased lung vascular permeability dose-dependently, the ED50 of which was 0.3-1 nM. Such an effect remained even after treatment with reserpine, as well as in the presence of alpha- and beta-blockers. And norepinephrine enhanced the effect of neuropeptide Y on lung vascular permeability. These responses were almost similar to those obtained by stimulation of sympathetic nerves. Furthermore, neuropeptide Y, in fibrin-induced pulmonary edema, was localized in alveolar macrophages and alveolar spaces, amounting to approximately 200 nM in edema fluid. The value was significantly greater than that obtained in hydrostatic pulmonary edema by 10-30 times. Peptide YY, an analogue of neuropeptide Y, had no action on lung vascular permeability, whereas the effect of neuropeptide Y was inhibited by pretreatment with neuropeptide Y- 13-36, an antagonist for Y3-recetor subtype. These results suggested that neuropeptide Y enhances the lung vascular permeability via Y3-recetor subtype. Neuropeptide Y- 13-36, in fibrin-induced pulmonary edema, decreased a ratio of protein concentration in edema fluid to that in serum, indicating that neuropeptide Y actually acts a role in the development of neurogenic pulmonary edema, via an increase in lung vascular permeability.

Adrenergic Uptake Inhibitors↗

[Primary myelofibrosis with fatal mesenteric arterial thromboembolism caused by antiphospholipid syndrome].

A 60-year-old woman was admitted to our hospital in February 1993 due to dizziness, dyspnea, abdominal pain, and high susceptibility to bleeding. Physical examination revealed livedo reticularis of the foot, but did not detect hepatosplenomegaly. Examination of the peripheral blood detected pancytopenia, leukoerythroblastosis, and tear-drop erythrocytes. Primary myelofibrosis (PMF) was diagnosed on the basis of bone marrow biopsy findings. Antiphospholipid syndrome (APS) was confirmed by positive response to anti-cardiolipin antibody and recurrent splenic infarction. Because of factor XIII deficiency, the patient experienced severe gingival bleeding after tooth extraction. Her condition was complicated by mesenteric arterial thromboembolism and she died of sepsis 5 years after onset. Although the incidence of immunopathy in PMF patients is high, few studies to date have focused on APS patients presenting with a variety of severe embolic symptoms. Our patient required careful monitoring due to bleeding tendency and thromboemboli.

Antiphospholipid Syndrome↗

[Anesthetic management of a patient with tracheal bronchus with one lung ventilation].

A 56-year-old-male with malignant pleural mesothelioma of the left lung underwent pneumonectomy and pleurectomy. Fiberoptic bronchoscopy was not done preoperatively. Anesthesia was induced rapidly and a double-lumen endobronchial tube was inserted. When we checked the position of the tube with a fiberoptic bronchoscope, we found that the normal right upper lobe bronchus was absent and that the inflated tracheal cuff had obstructed the right upper lobe bronchus originating above the carina. Then we changed the double-lumen endobronchial tube to a endotracheal tube with the blocker. Thereafter, the surgery was completed safely and his postoperative course was uneventful. Routine bronchoscopy is essential just after intubation and before extubation of the endobronchial tube in safe airway management. How to use a fiberoptic bronchoscope to check the position of a double-lumen endobronchial tube is also discussed.

Anesthesia, Epidural↗

Recombinant human granulocyte colony-stimulating factor (G-CSF) combined conditioning regimen for allogeneic bone marrow transplantation (BMT) in standard-risk myeloid leukemia.

We previously suggested that using a combined conditioning regimen including rhG-CSF with allogeneic BMT in refractory AML and CML in blast crisis might reduce the rate of relapse and improve disease-free survival, without any major side effects. In this study, we used the same protocol for 10 AML patients in complete remission (CR) and 6 CML patients in the chronic phase (CP). We compared disease-free survival as well as toxic side effects of the regimen with 6 AML patients in CR and 6 CML patients in CP treated with chemoradiotherapy without G-CSF. The conditioning regimen consisted of TBI and high-dose AraC. RhG-CSF was infused continuously at a dose of 5 microg/kg/day, starting 24 hr before the initial dose of total body irradiation (TBI) until the end of AraC therapy. In all 28 cases, there were no early stage deaths due to regimen-related toxicity (RRT). None of the 10 AML cases treated with the G-CSF combined regime relapsed. In 6 AML cases treated conventionally without G-CSF, one patient died of infection and another relapsed. There were no relapses in either CML group. In the combined G-CSF group, one patient died of interstitial pneumonitis 48 days after BMT, while the rest of the CML cases are still alive. There were no relapses with rhG-CSF and no serious adverse effects in terms of RRT, acute graft vs. host disease (GVHD), or leukocyte recovery.

Adult↗