PubMed Health⌕ Search

Biomedical subjects

T Kitajima

Publications and source records attributed to T Kitajima.

At least 109 records · Page 6Linked to original sources

Response of cerebral oxygen metabolism in the head-up position during laparoscopic cholecystectomy.

To clarify the influence of the head-up position on cerebral oxygen metabolism during laparoscopy with CO2 insufflation in 12 patients who underwent laparoscopic cholecystectomy, changes in the concentrations of cerebral oxyhemoglobin (HbO2), deoxyhemoglobin (Hb), total hemoglobin (total Hb) and oxidized cytochrome aa3 (Cyt aa3) were measured by use of near-infrared laser spectroscopy. Anesthesia was maintained with nitrous oxide (66%), oxygen, and sevoflurane. Pneumoperitoneum was maintained at an intraabdominal pressure of 10-12 mm Hg by use of CO2. Minute ventilation was adjusted to maintain end-tidal CO2 tension (P(ET)CO2) between 35 and 40 mm Hg during the procedure. Patients were moved from supine to the head-up (20 degree) position before intraabdominal manipulation. The concentration of HbO2 decreased significantly when patients were moved to the head-up position and 30 min thereafter. It remained significantly low after they were returned to the supine position and at the end of surgery. The concentration of Hb was unchanged during the study. Therefore, the concentration of total Hb decreased significantly when patients were moved to the head-up position, as well as 30 min thereafter. It remained significantly low after they were returned to the supine position and at the end of surgery. The concentration of Cyt aa3, however, did not change significantly during the study. These results suggest that the head-up position during laparoscopic cholecystectomy decreases cerebral HbO2 and total Hb.

Adult↗

Extracellular sodium concentration has diverse effects on the hypoxia-induced increase in intracellular Ca2+ in rat hippocampal slices.

The intracellular free Ca2+ concentration ([Ca2+]i) in the CA1 pyramidal cell layer was measured using fura-2-loaded hippocampal slices prepared from adult rats. Hypoxia (oxygen-glucose deprivation) elicited a gradual increase in [Ca2+]i in normal Krebs solution. With a high extracellular sodium concentration ([Na+]o), the hypoxia-induced response was attenuated, its onset-latency was longer and the time constant of its decay phase was shorter than in controls. In contrast, hypoxia in low [Na+]o elicited a significantly enhanced response with a short onset-latency and delayed decay phase. This exaggerated response to hypoxia in low [Na+]o was reversed by pre-incubation of the slice in low [Na+]o prior to the hypoxic insult. Some possible mechanisms and the functional significance of the observed effects of [Na+]o on the hypoxia-induced increase in [Ca2+]i are discussed, with particular emphasis on the putative participation of the glutamate transporter and the sodium-calcium exchanger in hypoxia-induced neuronal injury.

Animals↗

Lack of biliary excretion of Cd linked to an inherent defect of the canalicular isoform of multidrug resistance protein (cMrp) does not abnormally stimulate accumulation of Cd in the Eisai hyperbilirubinemic (EHB) rat liver.

A new mutant, the Eisai hyperbilirubinemic (EHB) rat, shows no inherent expression of the canalicular isoform of the multidrug resistance protein (cMrp) in the liver. It has defective biliary secretion of organic anions such as bilirubin glucuronides, bromosulfophthalein (BSP), cysteinyl leukotrienes, glutathione (GSH) and bile acid sulfate and glucuronides. When rats were injected intravenously with CdCl2, biliary excretion of Cd over 30 min was 0.28% and 0.004% of the total dose in Sprague-Dawley (SD) and EHB rats, respectively. Six SD rats and five EHB rats were fed a diet containing Cd. Bile Cd was detected at the level of 2 ng/20 min in SD rats, but not in EHB rats. There was no significant difference of hepatic Cd concentration between SD and EHB rats. Furthermore, there were no significant differences of renal and intestinal Cd, and hepatic and renal metallothionein (MT) concentrations between the SD and EHB groups. Biliary excretion of reduced-GSH for 20 min was 1.3 +/- 0.3 mg and 3.6 +/- 0.9 micrograms in SD and EHB rats, respectively. Our results suggest that hepatobiliary excretion of exogenous Cd is mediated mainly via carrier transport, including a cMrp or GSH carrier, but that the lack of the transport pathway does not contribute to abnormal accumulation of Cd in the liver.

Acetylglucosamine↗

Formation of recombinant human procollagen I heterotrimers in a baculovirus expression system.

The present study describes the production of human procollagen I in a baculovirus expression system. Recombinant baculovirus carrying pro alpha1(I) or pro alpha2(I) cDNA was constructed and infected to Sf9 cells. Full-length pro alpha1(I) or pro alpha2(I) chains were synthesized by the cells infected with either of the recombinant viruses. The pro alpha1(I) chains formed pepsin-resistant homotrimers stabilized by interchain disulfide bonds, a small proportion of which was secreted into the culture medium. The pro alpha2(I) chains were not linked into trimers by disulfide bonds and failed to form stable triple helices, although some chains were suggested to exist as dimers or unstable trimers in which only two chains were linked by disulfide bonds. In spite of their non-helicity, the pro alpha2(I) chains were secreted at a higher rate than the pro alpha1(I) chains. Sf9 cells simultaneously synthesized both pro alpha1(I) and pro alpha2(I) chains when the cells were co-infected with the two recombinant viruses. Pepsin-treatment of the product clearly demonstrated the production of procollagen I heterotrimers composed of two pro alpha1(I) chains and one pro alpha2(I) chain, homotrimers of the pro alpha1(I) chains being negligible. This expression system appears to offer a unique means of studying the mechanism of chain association and secretion during procollagen biosynthesis.

Baculoviridae↗

Comparison of stellate ganglion block with intravascular infusion of prostaglandin E1 on brachial artery blood flow in dogs.

We sought to determine whether sympathetic blockade or infusion of prostaglandin E1 (PGE1) is better for vasodilation. We measured brachial artery blood flow (BABF) in 10 mongrel dogs using an ultrasonic time flowmeter to compare the effects of stellate ganglion block (SGB) and intravascular infusion of PGE1. The experimental protocol was designed as follows: 1) intravenous (IV) infusion of PGE1 at a rate of 10 ng x kg(-1) x min(-1) for 10 min, 2) IV infusion of PGE1 at a rate of 150 ng x kg(-1) x min(-1) for 10 min, 3) intraarterial infusion of PGE1 at a rate of 0.1 ng x kg(-1) x min(-1) for 10 min, 4) SGB with 0.5% mepivacaine 1.0 mL was used as a sympathetic blockade. These procedures were successively performed on each dog. Mean arterial pressure (MAP), heart rate (HR), and BABF were measured before and after each procedure for 40 min. MAP and HR did not change significantly after the procedures. BABF increased significantly after IV infusion of PGE1 150 ng x kg(-1) x min(-1), intraarterial infusion of PGE1 and SGB, reaching maximums of 157%, 174%, and 171% 10 min after IV infusion of PGE1 150 ng x kg(-1) x min(-1), intraarterial infusion of PGE1 and SGB compared with the prevalues, respectively. These data indicate that sympathetic blockade may produce the same vasodilation as IV infusion of PGE1 150 ng x kg(-1) x min(-1) and intraarterial infusion of PGE1 0.1 ng x kg(-1) x min(-1). Intravascular infusion of PGE1 could provide clinically equivalent vasodilation without the complications associated with SGB.

Alprostadil↗

The effect of epidural saline injection on analgesic level during combined spinal and epidural anesthesia assessed clinically and myelographically.

UNLABELLED: An epidural injection of physiological saline solution after spinal anesthesia may produce a higher level of analgesia than spinal anesthesia alone because of a volume effect. The purpose of this study was to clarify the volume effect caused by epidural injection of saline after spinal anesthesia. Twenty patients undergoing combined spinal and epidural anesthesia for elective surgery whose analgesic levels did not reach the surgical regions 10 min after spinal anesthesia at the L4-5 interspace were randomly assigned to two groups. The control group (n = 10) received no epidural saline injection. The saline group (n = 10) received 10 mL of saline through an epidural catheter at the L2-3 or L3-4 interspace 10 min after spinal anesthesia. In the saline group, the levels of analgesia 15 and 20 min after spinal anesthesia were significantly higher than those in the control group (P < 0.05). Next, we examined the volume effect of epidural injection of saline with myelography using two adult volunteers. In both volunteers, the upper level of the contrast medium, which was injected in the lumbar subarachnoid space, began to increase concurrently with lumbar epidural injection of saline, reaching from L3 to L1 and from L2 to T12. The diameter of the subarachnoid space diminished to less than 25% after injection of saline. We conclude that lumbar epidural injection of saline increases the analgesic level 10 min after spinal anesthesia, probably because of a volume effect. IMPLICATIONS: In this study, using surgical patients and volunteers, we determined that a lumbar epidural injection of physiological saline solution 10 min after spinal anesthesia produces a higher analgesic level than spinal anesthesia alone because of a volume effect.

Adult↗

A field trial of oil adjuvanten trivalent Actinobacillus pleuropneumoniae vaccine.

The trivalent vaccine of A. pleuropneumoniae serotype 1, 2 and 5 (AP3V) was prepared in the oil-in-water type adjuvanten form. At an SPF farm, the vaccinated pigs were observed for their antibody response, finishing rate, and lung lesions at the time of slaughter and for injection scars. The CF titers against serotype 1, 2 and 5 started to rise after the second injection, showed the highest titer at 30 days after injection and then gradually decreased in vaccinated pigs. The finishing rate in the vaccinated group was 91.6% and that in the control group immunized with commercial vaccine was 60%. The lungs in the control pigs showed severe pneumonia with hyperemia, pleural adhesion and abscess. In contrast, vaccinated pigs showed slight pneumonia. Injection scars were not observed in vaccinated pigs 100 days after the second injection. In conclusion, the pigs immunized with AP3V were sufficiently protected against A. pleuropneumoniae infection and the trial proved to be satisfactory in the safety of the vaccine under field conditions.

Actinobacillus Infections↗

Massive uncomplicated vascular immune complex deposits in the kidney of a patient with systemic lupus erythematosus.

The case of a patient with systemic lupus erythematosus (SLE) is reported which was accompanied by renal dysfunction and massive vascular immune deposits in the kidney without active glomerular lesions. The renal biopsy showed arterioles and small arteries with circumferential periodic acid-Schiff (PAS) and Masson trichrome-positive homogenous material in the subendothelial area in the absence of thrombotic, necrotizing or inflammatory lesions. Immunofluorescence and electron microscopy examination demonstrated immune deposits in the vascular walls. Glomeruli showed only minor abnormalities with a trend to collapse. There was no improvement in renal dysfunction over a 4-year period until the patient's death, despite steroid therapy producing a decrease in disease activity. The autopsy showed similar vascular changes to those seen in the biopsy, however; glomeruli were either sclerotic or showed a trend to collapse. Massive uncomplicated vascular immune complex deposition without active glomerular lesions is rare. The present case indicates that this type of lupus vasculopathy may be a prognostic factor for the loss of renal function in SLE mediated by hemodynamic glomerular injury.

Aged↗

Ultraviolet B radiation sensitizes a murine epidermal dendritic cell line (XS52) to undergo apoptosis upon antigen presentation to T cells.

Ultraviolet B irradiation of skin leads to immunologic tolerance, rather than immunity against newly introduced Ag, by altering the function of Langerhans cells, skin-specific members of the dendritic cell (DC) family. Using the murine epidermal-derived DC line, XS52, which retains important features of resident Langerhans cells, we have tested the hypothesis that UV radiation delivers a signal leading to apoptosis. XS52 cells, when exposed to modest fluences (25-100 J/m2) of radiation, underwent apoptosis during a subsequent 6-h incubation with LPS or upon 6-h coculture with the keyhole limpet hemocyanin-specific Th1 clone HDK-1 in the presence of Ag. Specifically, XS52 cells treated in this way exhibited diminished cell viability, DNA laddering, and condensed staining of DNA. By contrast, none of these changes was induced by radiation alone, LPS alone, or coculture with T cells and Ag. Likewise, neither UV radiation plus T cells nor radiation plus Ag were sufficient to induce apoptosis, indicating that both T cells and Ag are required to induce apoptosis in the UV-sensitized cells. XS52 cells remained fully susceptible to T cell-mediated apoptosis even 16 h after irradiation, indicating the persistence of the sensitized state. These observations establish a model in which UV radiation induces a first event in which DC become sensitive to a second, apoptotic signal that is delivered by Ag-specific interaction with T cells or by LPS. We suggest that DC undergoing apoptosis deliver unusual activation signals to T cells during Ag presentation, signals that lead to cellular unresponsiveness rather than to effective immunity.

Animals↗

T cell-mediated terminal maturation of dendritic cells: loss of adhesive and phagocytotic capacities.

Dendritic cells (DC) are a specific subset of APC characterized by the potent ability to activate immunologically naive T cells. We have observed previously that the murine epidermis-derived DC line XS52 undergoes a set of profound changes upon Ag-specific interaction with T cells, including IL-1 beta secretion acquired expression of CD86, and lost expression of CD115 (CSF-1 receptor) and proliferative responsiveness to CSF-1. These changes, which appear to reflect a critical transition during Ag presentation, have been termed T cell-mediated "terminal maturation" of DC, Here we report that XS52 cells also lose their adhesive and phagocytotic capacities during this event. XS52 cells, ordinarily adhere to petri dishes and phagocytose latex heads, as has been reported for DC freshly procured from spleen and skin. Importantly, XS52 cells lose both capacities after 3 to 24 h of incubation with HDK-1 T cells (keyhole limpet hemocyanin-specific TH1 clone) or with 5S8 T cells (dinitrobenzene sulfonate specific Th0 clone) in the presence of Ag. By contrast, incubation with T cells alone or with Ag alone has minimal effects, indicating that this regulation required both T cells and Ag. With respect to mechanisms, several lines of evidence suggest this IFN-gamma, which is secreted by T cells, serves as the primary mediator in down-regulating both capacities. Our observations illustrate a unique mechanism by which responding T cells upon Ag-specific activation by DC, suppress the machinery of Ag uptake through the elaboration of IFN-gamma.

Animals↗

Cytokine-mediated communication between dendritic epidermal T cells and Langerhans cells. In vitro studies using cell lines.

Murine epidermis contains two leukocyte populations: Langerhans cells (LC), which are APC of dendritic cell (DC) lineage, and dendritic epidermal T cells (DETC), which are members of the tissue-type gamma delta T cell family. Despite close physical approximation in vivo, the extent to which LC and DETC affect each other's function has remained unknown. We addressed this question using the long term DC line XS52 and the gamma delta T cell line 7-17, both of which were established from mouse epidermis, and both of which retain important features of the resident populations from which they were derived. XS52 DC proliferated maximally when cocultured with gamma-irradiated 7-17 DETC. They also proliferated in response to culture supernatants collected from anti-CD3- or Con A-activated 7-17 DETC, but not from nonstimulated DETC. In both systems, DETC-induced XS52 DC growth was inhibited partially (up to 70%) by Abs against granulocyte/macrophage CSF (GM-CSF) or CD115 (CSF-1 receptor) and nearly completely (up to 90%) by both together. Among 28 tested cytokines, only GM-CSF, CSF-1, IL-4, and IL-13 promoted XS52 DC growth significantly. Anti-IL-4 failed to inhibit DETC-induced XS52 cell growth, and IL-4 was not detectable in DETC supernatants. Thus, we conclude that GM-CSF and CSF-1 (and perhaps IL-13) account for the DC growth-promoting activity secreted by DETC. These results suggest that during coculture, XS52 DC activate 7-17 DETC to secrete both GM-CSF and CSF-1. In fact, when cultured with XS52 DC, 7-17 DETC also elevated their expression of the gamma c receptor and acquired proliferative responsiveness to their own growth factor IL-15. We propose that LC and DETC in situ may interact with each other in a similar manner, thereby regulating their residence and function.

Animals↗

A novel mechanism of glucocorticoid-induced immune suppression: the inhibiton of T cell-mediated terminal maturation of a murine dendritic cell line.

Working with the murine epidermal-derived dendritic cell (DC) line XS52, we have observed previously that antigen-specific interaction with T cells stimulates their "terminal maturation" into fully professional DC. In this study we examined the impact of dexamethasone (DEX) on this T cell-induced event. When added to cocultures of XS52 DC and the KLH-specific Th1 clone HDK-1 in the presence of antigen, DEX at relatively low concentrations (10(-9)-10(-7) M) prevented substantially or completely each of the changes that typify terminal maturation, including (a) secretion of relatively large amounts of IL-1beta, IL-6, and TNFalpha; (b) loss of CD115 (colony-stimulating factor-1 receptor) expression and proliferative responsiveness to colony-stimulating factor-1; and (c) elevated expression of CD86 (B7-2). XS52 cells also underwent terminal maturation upon exposure to lipopolysaccharide alone, and DEX also inhibited effectively each of the same changes, indicating that DC can serve as the direct target of DEX. By contrast, DEX inhibited XS52 DC-stimulated IL-2 secretion by HDK-1 T cells, but not other changes that accompany T cell activation, including the secretion of IFNgamma and TNFalpha and the elevated expression of CD25, CD28, and CD44. These results reveal a new immunosuppressive mechanism of glucocorticoid action, that is, direct inhibition of T cell-mediated terminal maturation by DC.

Animals↗

Novel bacterial rhodopsins from Haloarcula vallismortis.

New bacterial rhodopsins of the cruxrhodopsin (cR) tribe were identified in a type strain Haloarcula vallismortis. The genes encoding a bacteriorhodopsin-like ion pump (named cR-3), a halorhodopsin-like ion pump (chR-3) and a sensor rhodopsin (csR-3) were cloned and sequenced. Together with the data for vsRII (Seidel et al., Proc. Natl. Acad. Sci. USA 92, 3036-3040 (1995); cpR-3 in our notation), the primary structures of a set of four rhodopsins are now all known only in this species. They are separated by almost the same distances in homology, suggesting that they have derived from a single ancestral rhodopsin. The degree of conservation in the amino acid sequence of each helix showed that helices C and G are relatively well conserved in all rhodopsins, whereas helices DEF are conserved especially in sensor rhodopsin-I, possibly because these helices are needed for interaction with the transducer protein (Htr).

Amino Acid Sequence↗

Expression of spicule matrix protein gene SM30 in embryonic and adult mineralized tissues of sea urchin Hemicentrotus pulcherrimus.

We have isolated a cDNA clone for spicule matrix protein, SM30, from sea urchin Hemicentrotus pulcherrimus and have studied the expression of this gene in comparison with that of another spicule matrix protein gene, SM50. In cultured micromeres as well as in intact embryos transcripts of SM30 were first detectable around the onset of spicule formation and rapidly increased with the growth of spicules, which accompanied accumulation of glycosylated SM30 protein(s). When micromeres were cultured in the presence of Zn2+, spicule formation and SM30 expression were suppressed, while both events resumed concurrently after the removal of Zn2+ from the culture medium. Expression of SM50, in contrast, started before the appearance of spicules and was not sensitive to Zn2+. Differences were also observed in adult tissues; SM30 mRNA was detected in spines and tube feet but not in the test, while SM50 mRNA was apparent in all of these mineralized tissues at similar levels. These results strongly suggest that the SM30 gene is regulated by a different mechanism to that of the SM50 gene and that the products of these two genes are differently involved in sea urchin biomineralization. A possible role of SM30 protein in skeleton formation is discussed.

Animals↗