Capnography for safe use of the laryngeal mask during emergence from anesthesia.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to T Asai.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The Escherichia coli genome carries seven rRNA (rrn) operons, each containing three rRNA genes. The presence of multiple operons has been an obstacle to many studies of rRNA because the effect of mutations in one operon is diluted by the six remaining wild-type copies. To create a tool useful for manipulating rRNA, we sequentially inactivated from one to all seven of these operons with deletions spanning the 16S and 23S rRNA genes. In the final strain, carrying no intact rRNA operon on the chromosome, rRNA molecules were expressed from a multicopy plasmid containing a single rRNA operon (prrn). Characterization of these rrn deletion strains revealed that deletion of two operons was required to observe a reduction in the growth rate and rRNA/protein ratio. When the number of deletions was extended from three to six, the decrease in the growth rate was slightly more than the decrease in the rRNA/protein ratio, suggesting that ribosome efficiency was reduced. This reduction was most pronounced in the Delta7 prrn strain, in which the growth rate, unlike the rRNA/protein ratio, was not completely restored to wild-type levels by a cloned rRNA operon. The decreases in growth rate and rRNA/protein ratio were surprisingly moderate in the rrn deletion strains; the presence of even a single operon on the chromosome was able to produce as much as 56% of wild-type levels of rRNA. We discuss possible applications of these strains in rRNA studies.
The neuronal plasticity in the spinal dorsal horn induced after conditioning low-frequency stimulation of afferent A fibers, and its relationship with spinal inhibitory networks, was investigated with an optical-imaging method that detects neuronal excitation. High-intensity single-pulse stimulation of the dorsal root activating both A and C fibers evoked an optical response in the dorsal horn in transverse slices of 12- to 25-day-old rat spinal cords stained with a voltage-sensitive dye, RH-482. The optical response, reflecting the net excitation of neuronal elements along the thickness of each slice, was suppressed after a conditioning low-frequency stimulation (0.2-1 Hz for 10 min) to A fibers in the dorsal root. The degree of suppression was largest in the lamina II of the dorsal horn (48% reduction), where the majority of C fibers terminate, and much less in the deeper dorsal horn (5% reduction in laminae III-IV). The onset of suppression was somewhat slow; after the low-frequency stimulation, the magnitude of excitation gradually decreased, reached the maximum effect 30 min after the conditioning, and remained at the suppressed level for >1 h. Suppression was not observed when the low-frequency stimulation was given during a 20-min perfusion with a solution containing an NMDA-receptor antagonist, DL-2-amino-5-phosphonovaleric acid (30 microM). A brief application of an opioid-receptor antagonist, naloxone (0.5 microM), inhibited the induction, but not the maintenance, of low-frequency stimulus-induced suppression. However, treatments with the GABA(A) receptor antagonist bicuculline (1 microM) and the glycine receptor antagonist strychnine (0.3 microM) did not affect suppression induction and maintenance. In conclusion, conditioning low-frequency stimulation to A fibers interferes with the afferent-induced excitation in the dorsal horn. The low-frequency stimulation-induced suppression is maintained by a reduction of glutamatergic excitatory transmissions in the dorsal horn, not by an enhanced inhibition. Activation of the spinal opioid-mediated system by low-frequency stimulation, but not the inhibitory amino acid-mediated system, is necessary to initiate robust suppression. The long-term depression of afferent synaptic efficacy onto excitatory interneurons likely takes the primary role in the robust suppression of neuronal excitation in the dorsal horn.
We studied the prevalence of dementing disorders in a rural municipality of Japan (Hanazono-mura), using a door-to-door two-phase design. In phase 1, the Hasegawa's Dementia Scale-Revised was applied as a screening test to all subjects aged 65 years and older (n = 201). Among subjects screened positive, 17 were diagnosed with dementia in phase 2. The prevalence (cases/100 aged 65 years and older) was 8.5 for all types of dementia, 3.5 for Alzheimer's disease, 3.0 for vascular dementia, and 2.0 for other dementia (including mixed dementia). The prevalence of dementia was slightly but consistently higher in men than women at all ages. The overall prevalence was higher in women for Alzheimer's disease and in men for vascular dementia.
BACKGROUND AND PURPOSE: Despite technical advances in endovascular and microsurgical treatment, patients with aneurysmal subarachnoid hemorrhage still have a high mortality and morbidity rate. To improve the treatment results in patients with aneurysms, we must better understand the pathophysiology of cerebral aneurysms and the mechanisms leading to their rupture. Therefore, we studied the pathological differences between unruptured and ruptured aneurysms. METHODS: Ruptured (n=44) and unruptured (n=27) aneurysms were obtained at surgery. The aneurysmal endothelium was scored from 0 (normal) to 5 (complete disruption) by using a scanning electron microscope. The aneurysmal wall was evaluated by immunohistochemical methods. The wall structure was scored from 1 (dense collagen and rich, smooth muscle cells) to 5 (hyaline-like structure). The degree of inflammatory cell invasion into the wall was also scored from 0 (very few cells) to 3 (many cells). RESULTS: Ruptured aneurysms manifested significant endothelial damage (score of 3.7 versus 0.8; Mann-Whitney U test, P<10(-3)), significant structural changes of the wall (3.7 versus 1.7, P<10(-5)), and significant inflammatory cell invasion (2.2 versus 0.8, P<10(-4)) compared with unruptured aneurysms. There was a significant correlation between the score for wall structure and the score for inflammatory cell invasion (Rs=0. 63; Spearman rank correlation test, P<10(-5)). The pathophysiology of several symptomatic unruptured aneurysms was similar to that of ruptured aneurysms. CONCLUSIONS: We conclude that the pathophysiology of unruptured, asymptomatic and ruptured aneurysms is different. The wall of ruptured aneurysms was found to be fragile, possibly because macrophage infiltration into the aneurysmal wall resulted in loss of smooth muscle cells and in degradation of matrix proteins.
Fas-ligand (FasL) is a member of the tumor necrosis factor family and transmits apoptotic cell death signal by binding to its receptor, Fas. FasL is expressed on the cell surface of activated T-cell and natural killer (NK) cell. It has been shown that the FasL can be released from the cell surface by metalloproteinase. The serum soluble FasL (sFasL) is increased in some patients with NK cell lymphoma/large granular lymphocytic leukemia. We have recently seen a patient with recurrent B-cell lymphoma accompanied with an increased serum sFasL level after autologous peripheral blood stem cell transplantation. The sFasL was markedly decreased with the tumor regression induced by the chemotherapy. We present here the first case of an elevated serum sFasL level associated with B-cell lineage malignancy and discuss the possible clinical value of sFasL.
We reported a case of peduncular hallucination after aneurysmal subarachnoid hemorrhage (SAH). The patient underwent endovascular embolization of an intracranial aneurysm using the Guglielmi detachable coils (GDCs) 9 days after SAH. On the 11th day, she reported visual hallucination: a maggot was on the ceiling, or a soldier who wore green clothes was standing by a locker. The hallucination was vivid, well-formed and associated with insomnia, suggesting peduncular hallucination. A computed tomographic (CT) scan revealed small infarctions of right frontal lobe, which were not responsible for the visual hallucination. Hyperdynamic therapy relieved the visual hallucination 23 days after SAH. It was conceivable that vasospasm was the cause of the infarction and visual hallucination. Only 4 cases with peduncular hallucination after SAH were reported in conjunction with vasospasm. The symptom may be concealed by disturbance of consciousness. Visual hallucination should be considered as a sign of cerebral vasospasm, and an appropriate treatment should be done at right time.
The patient was a 51-year-old man with Marfan syndrome who had simultaneously undergone modified Bentall operation (Carrel patch method) and coronary artery bypass grafting. Prosthetic valve endocarditis (PVE) occurred 19 months after the operation. PVE had thereafter been treated by antibiotic therapy for 3 months, but echocardiography revealed prosthetic valve detachment and aortic root pseudoaneurysm ruptured into the right ventricle which appeared to have been caused by PVE. At reoperation there were no laboratory or intraoperative findings indicative of ongoing inflammation or infection. The composite graft, therefore, didn't require replacing, and it was possible to simply re-suture the composite graft and directly close the tear. The postoperative course has been uneventful with no further evidence of endocarditis.
The intubating laryngeal mask has a potential role for tracheal intubation in patients with difficult airways, but there have been only reports of the techniques of blind tracheal intubation through the intubating laryngeal mask. The success rate of blind intubation at the first attempt may be merely 50-60% even in patients with normal airways. We report the use of the intubating laryngeal mask for tracheal intubation in three patients with difficult airways, in whom a tube was easily inserted through the laryngeal mask into the trachea either blindly, using a fiberoptic bronchoscope or using a lighted stylet.
OBJECTIVE: To elucidate the role of prolactin (PRL) produced in joints as part of the pathological response of rheumatoid arthritis (RA), we studied PRL production and prolactin receptor (PRLR) expression in RA synovium and its effects on RA synovial cell functions. METHODS: Proinflammatory cytokine and matrix metalloproteinase (MMP) production by RA synovial cells was estimated by ELISA, Western blotting analysis, and zymography. Expression of PRLR by RA synovial cells and local production of PRL were estimated by reverse transcription polymerase chain reaction and immunohistochemical staining. RESULTS: PRL enhanced RA synovial cell proliferation. Production of proinflammatory cytokine and MMP was augmented and production of tissue inhibitor of metalloproteinases (TIMP)-1 was inhibited by PRL treatment of RA synovial cells, suggesting that PRL enhances total collagenase activity in the joints. PRLR was exclusively expressed on fibroblast-like synovial cells and lymphocytes infiltrating into the synovium in patients with RA. Both synovium infiltrating T lymphocytes and, to a lesser extent, fibroblast-like synovial cells synthesized PRL, suggesting that PRL acts as a paracrine as well as autocrine activator of RA synovial cell functions. Stimulation of synovial cells by PRL induced rapid translocation of STAT-5 from cytoplasm into nuclei of RA synovial cells, suggesting that transcriptional regulation of RA synovial cell functions by PRL affects STAT-5. Inhibitors of PRL release, such as bromocriptine, inhibited proliferation of proinflammatory cytokines and collagenases by RA synovial cells. CONCLUSION: Our findings emphasize the importance of PRL, locally produced by infiltrating T lymphocytes, for aberrant synovial cell functions in RA, and suggest possible clinical application of PRL inhibitors.
Explore the source record for details and available documents.
Recently developed expandable metallic stents have been adopted to superior vena cava syndrome with good results. We inserted stents into the superior vena cava in 4 patients with superior vena cava syndrome. The results were comfortable and no complications. We should consider the stenting as the first choice for superior vena cava syndrome.
OBJECTIVE: Actarit (4-acetylaminophenylacetic acid), developed in Japan, has been shown to be effective for suppressing disease activity of rheumatoid arthritis (RA). We analyzed effects of actarit on synovial cell functions in patients with RA for insight into the clinical application of this medication. METHODS: RA primary synovial cells were co-cultured with actarit at 10(-4)-10(-7) M. Their subsequent proliferative responses and proinflammatory cytokine and matrix metalloproteinase (MMP) production at the mRNA and protein levels were measured. Effects of actarit on adhesion molecule expression were analyzed by immunofluorescence flow cytometry and cell-cell binding assay. RESULTS: Spontaneous tumor necrosis factor-alpha and interleukin 1beta secretion by primary synovial cells of patients with RA was reduced by actarit at therapeutic concentrations (10(-5)-10(-6) M). In contrast, actarit also suppressed MMP-1 production by the primary synovial cells. In addition, actarit down-regulates CD44 and intercellular adhesion molecule 1 expression on fibroblast-like synovial cell lines, and very late antigen 4 expression on CD14+ macrophage-like synovial cells resulted in the inhibition of lymphocyte adhesion to RA synovial cells. CONCLUSION: The results suggest that actarit acts on RA synovial cells to reduce cell-cell interactions with autologous synovium infiltrating lymphocytes and to inhibit proinflammatory cytokine and MMP production, leading to amelioration of symptoms of RA.
A gene encoding adenosine-5'-triphosphate sulfurylase (AS) was cloned from the enteric protozoan parasite Entamoeba histolytica by polymerase chain reaction using degenerate oligonucleotide primers corresponding to conserved regions of the protein from a variety of organisms. The deduced amino acid sequence of E. histolytica AS revealed a calculated molecular mass of 47925 Da and an unusual basic pI of 9.38. The amebic protein sequence showed 23-48% identities with AS from bacteria, yeasts, fungi, plants, and animals with the highest identities being to Synechocystis sp. and Bacillus subtilis (48 and 44%, respectively). Four conserved blocks including putative sulfate-binding and phosphate-binding regions were highly conserved in the E. histolytica AS. The upstream region of the AS gene contained three conserved elements reported for other E. histolytica genes. A recombinant E. histolytica AS revealed enzymatic activity, measured in both the forward and reverse directions. Expression of the E. histolytica AS complemented cysteine auxotrophy of the AS-deficient Escherichia coli strains. Genomic hybridization revealed that the AS gene exists as a single copy gene. In the literature, this is the first description of an AS gene in Protozoa.
The enteric protozoan parasite Entamoeba histolytica was shown to possess cysteine synthase (CS) activity. The cDNA and genomic clones that encode two isoforms of the E. histolytica CS were isolated and characterized from a clonal strain of E. histolytica by genetic complementation of the cysteine-auxotrophic Escherichia coli NK3 with an E. histolytica cDNA library. The two types of the E. histolytica CS genes differed from each other by three nucleotides, two of which resulted in amino acid substitution. Deduced amino acid sequences of the E. histolytica CS, with a calculated molecular mass of 36721 Da and an isoelectric point of 6.39, exhibited 38-48% identity with CS of bacterial and plant origins. The absence of the amino-terminal transit peptide in the deduced protein sequences and the presence of the CS protein mainly in the supernatant fraction of the amoebic lysate after cellular fractionation suggested that the identified E. histolytica CS genes encoded cytosolic isoforms. Substrate specificity of the recombinant E. histolytica CS was similar to that of plant CS. Phylogenetic analysis indicates that the amoebic CS, first described in Protozoa, does not belong to any families of the CS superfamily, and represents a new family.
Neuronal excitation evoked after dorsal-root (DR) stimulation in the spinal dorsal horn (DH) of rats was visualized with a high-resolution optical-imaging method, and the propagation mechanism was studied. Transverse slices of the spinal cord were obtained from 2-4 week-old rats and stained with the voltage-sensitive dye RH-482. Single-pulse stimulation to the primary-afferent A fibers in the DR attached to the slice evoked a weak, brief (<10 ms) excitatory optical response in the laminae I and III-V. When the stimulus intensity and duration were increased to activate both A and C fibers, an additional, much greater, and longer-lasting (>100 ms) excitatory response was generated in the laminae I-III, most intensely in the lamina II. A treatment with excitatory amino acid (EAA) antagonists, dl-2-amino-5-phosphonovaleric acid and 6-cyano-7-nitroquinoxaline-2, 3-dione, significantly reduced the amplitude and duration of the response in the lamina II. The optical response in the antagonists-containing solution was quite similar to that recorded in a Ca2+-free solution that blocked afferent synaptic transmission. The late component (>10 ms) was, however, slightly greater than that in the Ca2+-free solution. Treatment with the ATP-receptor antagonist, suramin, had a minimal effect on the response in the presence of EAA antagonists. These results suggested that the propagation of the DR-stimulus-elicited excitation was contributed largely by EAA receptors, but also by other receptors to a much lesser extent.