[Blepharitis, hordeolum, abscess in the lids].
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Abscess↗
Biomedical subjects
K Kitagawa
Publications and source records attributed to K Kitagawa.
Characteristic feature of oxygen cost at simulated laboratory triathlon test in trained triathletes.
BACKGROUND: The present study was carried out in order to investigate the respiratory and circulatory features during a simulated laboratory triathlon test in trained triathletes. METHODS EXPERIMENTAL DESIGN: Sixteen male triathletes were divided into superior (n = 8) and slower triathletes (n = 8) according to their race time. These subjects performed both maximal exercise tests and a simulated laboratory triathlon test (ST). The latter test consisted of flume-pool swimming for 30 min, ergometer cycling for 75 min and treadmill running for 45 min as a continuous task. The exercise intensity was 60% of VO2 max during swimming, cycling and running, respectively. RESULTS: In slower triathletes, VO2, minute ventilation (VE), heart rate (HR) and temperature of external auditory canal were increased from an earlier stage compared with those in superior athletes. The percent increase (delta) of VO2, VE and HR between the 10th and last min of cycling and running stages in superior triathletes were significantly smaller than those in slower athletes. The oxygen cost (oxygen uptake/running velocity) of running stage was significantly lower in superior triathletes (0.220 +/- 0.020 ml.kg-1.m-1) compared with slower athletes (0.264 +/- 0.014 ml.kg-1.m-1). CONCLUSIONS: These results suggest that superior triathletes performed ST more economically than slower athletes and had excellent thermoregulatory adaptation.
Analysis of Variance↗
[Five cases of cerebral and/or cerebellar embolism after insertion of a heparin-coated catheter from the left thoracoacromial artery].
We reported five cases of cerebral and/or cerebellar embolism after insertion of a heparin-coated catheter from the left thoracoacromial artery for multiple liver metastases. They were one patient with multiple liver metastases from the angiosarcoma of the scalp, and 4 others with gastrointestinal cancer liver metastases. The first case suffered a cerebeller embolism just after removal of a catheter that had been obstructed. In this case, it is possible that the thrombus quickly migrated into a cranial vessel from around the catheter. In the others with patent catheters, the cerebral embolisms occurred more than a month after insertion of the catheters. In the latter cases, it is thought that embolisms did not occur because of catheter insertion maneuver. However, a thrombus that grew around the catheter migrated into the left common carotid artery or the left vertebral artery. The anti-coagulation therapy should be considered for prophylactic treatment.
Aged↗
[Microcirculatory derangement and apoptosis in ischemia-reperfusion injury].
This study was undertaken to clarify the involvement of microcirculatory failure and apoptosis in the pathophysiology of cerebral ischemia using ICAM-1 knockout mice (K/O) and BCL-2 transgenic mice, respectively. In both permanent and transient focal ischemia, infarcted size of cerebral cortex in ICAM-1 K/O mice was significantly smaller than that in wild type mice. Microcirucaltaory disturbance in the cerebral cortex after permanent and transient focal ischemia was mitigated in ICAM-1 K/O mice compared with that in wild type mice. However, the number of granulocytes in the infarcted tissue was similar between K/O and wild mice, and neutrophil depletion in K/O mice showed further reduction of cortical infarction after transient focal ischemia. In contrast, neuronal overexpression of BCL-2 in mice showed protective effect on selective neuronal death observed in the hippocampus after transient global forebrain ischemia for 12 min. The present study supported the notion that (1) microcirculatory disturbance mediated through interaction of ICAM-1 and leukocytes played an important role in expansion of cerebral infarction after focal ischemia and (2) apoptosis inhibited in part by overexpression of BCL-2 was involved in selective neuronal vulnerability after transient global ischemia.
Animals↗
Antiserum against Cl- pump complex recognizes 51 kDa protein, a possible catalytic unit in the rat brain.
We purified Cl- pump in the rat brain and obtained 520 or 580 kDa protein complexes which consisted of 62, 60, 55 and 51 kDa proteins. An antiserum against 520 kDa protein complex recognized 51 kDa protein in both 520 and 580 kDa complexes, and reduced both Cl(-)-ATPase and Cl(-) pump activities. Such an immunoreactive 51 kDa protein was found in the brain, spinal cord and kidney. When incubated with [gamma-(32)P]ATP, the protein complex yielded phosphorylated 51 kDa protein, the label being hydroxylamine-sensitive and increased in the presence of Cl- and/or an inhibitor of Cl- pump, ethacrynic acid. Thus, the antibody appears to recognize a possible catalytic subunit of Cl- pump, 51 kDa protein, in the rat.
Adenosine Triphosphatases↗
Remarkable diversity of proteolipid proteins in fish.
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Amino Acid Sequence↗
CI-ATPase and Na+/K(+)-ATPase activities in Alzheimer's disease brains.
The enzyme activities and the protein levels of Cl(-)-ATPase and Na+/K(+)-ATPase were examined in Alzheimer's disease (AD) brains. Cl(-)-ATPase and Na+/K(+)-ATPase activities in AD brains (n = 13) were significantly lower than those in age-matched control brains (n = 12). In contrast, there was no significant difference in anion-insensitive Mg2(+)-ATPase activity between the two groups. Western blot analysis revealed that the protein levels of Cl(-)-ATPase, Na+/K(+)-ATPase and neuron specific Na+/K(+)-ATPase alpha3 isoform were also significantly reduced in AD brains, while the amount of protein disulfide isomerase, one of the house keeping membrane proteins, was not different between the two groups. The data first demonstrated that Cl(-)-ATPase and Na+/K(+)-ATPase are selectively impaired in AD brains, which may reduce the gradients of Na(+), K(+) and Cl(-) across the cell membranes to cause excitotoxic cellular response and the resulting neuronal death.
Adenosine Triphosphatases↗
A helix-turn-helix structure unit in human centromere protein B (CENP-B).
CENP-B has been suggested to organize arrays of centromere satellite DNA into a higher order structure which then directs centromere formation and kinetochore assembly in mammalian chromosomes. The N-terminal portion of CENP-B is a 15 kDa DNA binding domain (DBD) consisting of two repeating units, RP1 and RP2. The DBD specifically binds to the CENP-B box sequence (17 bp) in centromere DNA. We determined the solution structure of human CENP-B DBD RP1 by multi-dimensional 1H, 13C and 15N NMR methods. The CENP-B DBD RP1 structure consists of four helices and has a helix-turn-helix structure. The overall folding is similar to those of some other eukaryotic DBDs, although significant sequence homology with these proteins was not found. The DBD of yeast RAP1, a telomere binding protein, is most similar to CENP-B DBD RP1. We studied the interaction between CENP-B DBD RP1 and the CENP-B box by the use of NMR chemical shift perturbation. The results suggest that CENP-B DBD RP1 interacts with one of the essential regions of the CENP-B box DNA, mainly at the N-terminal basic region, the N-terminal portion of helix 2 and helix 3.
Amino Acid Sequence↗
Regulation of the PepT1 peptide transporter in the rat small intestine in response to 5-fluorouracil-induced injury.
BACKGROUND & AIMS: The oligopeptide transport system of the small intestine is resistant to mucosal injury. The mechanism of this resistance was investigated by examining the activity level and expression of the peptide transporter PepT1 in the intestine of rats treated with 5-fluorouracil. METHODS: The expression and localization of PepT1 were examined by immunoblot analysis of brush border membrane vesicles and immunohistochemical analysis of intestinal sections with PepT1-specific rabbit polyclonal antibodies. Also, Northern blot analysis was used for the expression of PepT1 messenger RNA (mRNA). RESULTS: Although the amounts of sucrase and an Na+-dependent glucose transporter protein in intestinal vesicles decreased markedly after 5-fluorouracil treatment, the amount of PepT1 protein remained largely unaffected. Immunohistochemical analysis also showed that the PepT1 immunoreactivity level was preserved in the brush border membrane of the remaining villi of 5-fluorouracil-treated rats. Levels of amino acid, glucose, and phosphate transporter mRNAs were profoundly depressed in 5-fluorouracil-treated animals, whereas the level of PepT1 mRNA conversely increased. CONCLUSIONS: The resistance of intestinal peptide transport to tissue injury may be attributable to increased synthesis of PepT1 rather than to a change in the kinetic properties of the residual absorbing cells.
Animals↗
Plant defense-related enzymes as latex antigens.
BACKGROUND: Latex allergy is an increasing hazard to people who frequently come into contact with latex products. Of interest concerning this immediate-type allergy is the cross-reactivity to various vegetable foods and pollen. Despite its high prevalence, no adequate explanation has been provided for the cross-reactive antigens. OBJECTIVE: We have hypothesized that a series of plant defense-related proteins act as latex allergens, as well as vegetable food allergens. To evaluate this hypothesis, hydrolytic enzymes that are very likely to take on defensive roles in rubber trees were examined for their antigenicity. METHODS: By applying chromatographic procedures, defense-related enzymes were separated from nonammoniated latex (NAL). Their antigenicity was examined by immunoblotting and ELISA with sera containing IgE antibodies to crude latex proteins. RESULTS: Three kinds of hydrolytic enzymes (basic beta-1,3-glucanases [35, 36.5, and 38 kd], a basic chitinase/lysozyme [29.5 kd], and an acidic esterase [44 kd]) were separated from NAL. They were recognized by IgE antibodies from a significant number of patients allergic to latex. The basic beta-1,3-glucanases and the acidic esterase were also strongly recognized by IgE antibodies from several atopic subjects who were allergic to various vegetable foods rather than latex products. CONCLUSION: It was ascertained that the three defense-related enzymes separated from NAL constituted part of the latex antigens. Taking together the well-known serologic or immunologic relationships and amino acid sequence similarities of defense-related proteins coming from phylogenetically distant plant species, we can suspect their universal antigenicity and cross-reactivity.
Chitinases↗
Alterations of Bcl-2 family proteins precede cytoskeletal proteolysis in the penumbra, but not in infarct centres following focal cerebral ischemia in mice.
Apoptosis has drawn attention in ischemic neuronal death recently. However, studies of apoptosis in cerebral ischemia have concentrated largely in DNA fragmentation, a late phase in apoptotic nuclei, at the expense of possible primary ischemic targets at the subcellular level and of upstream apoptotic signalling. To assess those issues, we used an intraluminal middle cerebral artery occlusion model in mice with or without reperfusion, and examined sequential changes of Bcl-2 family proteins modulating apoptotic signalling immunohistochemically and studied nuclear DNA fragmentation, to compare their chronology in relation to the development of infarct as detected by loss of microtubule-associated protein-2, an early marker of cytoplasmic damage. In the centre of the lesion, Bax protein increased and Bcl-2 and Bcl-x proteins decreased after loss of microtubule-associated protein-2 antigenicity occurred, but at the border of the lesion, the former changes preceded loss of microtubule-associated protein-2 antigenicity. Additionally, close morphologic analysis of DNA fragmentation in situ indicated that transient ischemia predominantly induced apoptotic cells but permanent ischemia produced necrosis of cells in the centre of the lesion. The contrasting cell death mechanisms, apoptosis and necrosis, are selectively involved in the pathology of cerebral ischemia, depending on its severity.
Animals↗
Cerebral ischemia after bilateral carotid artery occlusion and intraluminal suture occlusion in mice: evaluation of the patency of the posterior communicating artery.
Cerebral ischemia models using mice have drawn increasing attention, particularly because of the availability of transgenic animals. However, the variability of intracranial vasculature at the circle of Willis in mice can influence the degree of ischemia in both the bilateral common carotid artery (CCA) occlusion and intraluminal suture occlusion models. We have developed a method to predict the extent of the anastomosis between carotid and vertebrobasilar circulation in three mouse strains (C57BL/6, CBA, and DBA/2) by measuring cortical microperfusion with laser Doppler flowmetry during a 1-minute occlusion of both CCA. When animals showed residual cortical microperfusion of less than 12% during bilateral CCA occlusion, the mice showed absence of functional anastomosis, developed ATP depletion in the frontal cortex during occlusion, and had ischemic neuronal death in the hippocampus and caudoputamen after occlusion for 15 minutes and recirculation for 7 days. Furthermore, those mice exhibited decreased local cerebral blood flow and associated ischemic neuronal death in the hippocampus, within the territory supplied by the posterior cerebral artery, with the intraluminal suture occlusion model. The current study demonstrates the need for assessment of intracranial vasculature in each animal by measuring cortical microperfusion during temporary occlusion of both CCA, no matter whether cerebral ischemia is produced by bilateral CCA occlusion or intraluminal suture occlusion in transgenic mice.
Animals↗
Deficiency of intercellular adhesion molecule 1 attenuates microcirculatory disturbance and infarction size in focal cerebral ischemia.
Recent evidence has shown crucial roles for cell-adhesion molecules in inflammation-induced rolling, adhesion, and accumulation of neutrophils in tissue. Intercellular adhesion molecule-1 (ICAM-1) is one of these adhesion molecules. Previous studies have shown marked reduction in the size of infarction after focal cerebral ischemia by depletion of granulocytes and administration of the antibody against ICAM-1. In the present study we investigated the role of ICAM-1 in the size of ischemic lesions, accumulation of granulocytes, and microcirculatory compromise in focal cerebral ischemia by using ICAM-1-knockout mice. Ischemic lesions were significantly mitigated in knockout mice after permanent and transient focal ischemia, even though the number of granulocytes in the infarcted tissue was almost the same between knockout and wild-type mice. Depletion of granulocytes further decreased the size of ischemic lesions after transient focal ischemia in ICAM-1-knockout mice. Microcirculation was reduced after focal ischemia, but it was better preserved in the cerebral cortex of knockout mice than that of wild-type mice. The present study demonstrated that ICAM-1 played a role in microcirculatory failure and subsequent development and expansion of infarction after focal cerebral ischemia. However, it is highly unlikely that ICAM-1 played a key role in accumulation of granulocytes after focal cerebral ischemia.
Animals↗
Mixtures of trifluoroethanol or hexafluoroisopropanol and dimethylformamide are not of general applicability for peptide condensations catalyzed by trypsin.
Mixtures of a good hydrogen bond donor, 2,2,2-trifluoroethanol (TFE) or 1,1,1,3,3,3-hexafluroisopropanol, and an acceptor, dimethylformamide (DMF) (1:1, v/v), containing 4% buffer have been described as adequate solvent systems for trypsin-catalyzed peptide fragment condensations [Mihara et al. (1993) Int. J. Pept. Protein Res. 41, 405]. Thus, we decided to study the behaviour of trypsin in such solvent systems. We investigated whether this protease would efficiently catalyze condensations between fragments derived from an analogue of the gp-41 capsid protein of HIV virus or from cholecystokinin-22. None of the reactions carried out yielded the desired condensation products. However, when Fmoc-NLQNLDPSHR-OH and cholecystokinin-12 (H-ISDRDYMGWMDF-NH2) were used as substrates, the last had its R-D peptide bond hydrolyzed producing cholecystokinin-8. The proteolytic activity of this enzyme measured against a fluorogenic peptide derivative was 50 times lower in DMF/TFE containing 5% of aqueous phase than in buffer. Steady-state fluorescence studies in DMF/TFE buffer were performed to examine the structure of this protease in these media. Steady-state spectra obtained with increasing proportions of these two organic solvents in buffer showed that the emission intensities built up. Quenching studies with iodide revealed that the Io/I ratio (where Io and I are the fluorescence emission intensities in the absence and presence of quencher, respectively) changed from 1.2 in aqueous media to 2.2 in DMF/TFE (1:1, v/v) containing 11% 0.2 M Tris-HCl buffer, pH 8.0, for 0.5 M iodide. The complete data indicated a higher exposure of tryptophan residues to the quencher in organic media, probably because of the partial unfolding of the enzyme.
Amino Acid Sequence↗
Early lens changes seen in patients with atopic dermatitis applying image analysis processing of Scheimpflug and specular microscopic images.
In order to know the initial lens changes that accompany atopic dermatitis (AD), 99 patients diagnosed dermatologically to have AD without any or with slight external ocular inflammations and with no habit of rubbing the eyelid due to severe itching were examined opthalmologically. Clinically, none of them showed any cataractous changes in their eyes. For the sake of comparison with the above population, 4 AD patients with cataractous eyes, 49 renal transplantation patients who were administered steroids over a long period of time but clinically had no cataractous lenses, and 94 healthy individuals with transparent lenses were also selected as subjects. The crystalline lenses of the subjects were examined using an anterior eye segment analysis system and specular microscopy. From Scheimpflug slit images of the lens, light scattering intensity of different lens layers was measured as an indicator of lens transparency changes. The subcapsular basement membrane and changes in the lens epithelial layers were analyzed from specular images of these areas by image processing. Results and considerations from the investigations were: (1) Initial lens changes in cases with AD which may be occult cataractous findings were often detectable. (2) Cataract associated with AD can be accelerated by steroid administration or the habit of strongly rubbing the eyelid, but this may not be the original cause of cataract formation. (3) Two types of cataract are seen in patients with AD: (a) anterior subcapsular plaque formation and (b) anterior and posterior subcapsular opacity formation. The latter type, however, is also accompanied by epithelial damage from the early stage. (4) Significant numbers of patients with AD who have not yet shown manifest lens changes were found among the subjects.
Adolescent↗
Amelioration of hippocampal neuronal damage after global ischemia by neuronal overexpression of BCL-2 in transgenic mice.
BACKGROUND AND PURPOSE: Reports suggesting the involvement of apoptosis in ischemic neuronal damage have been accumulating, and protection against apoptotic death by BCL-2 has been shown in many types of cells. Overexpression of BCL-2 has been shown to reduce infarct size after focal ischemia. The purpose of the present study was to assess whether BCL-2 exerted its effect on selective neuronal vulnerability after transient global ischemia. METHODS: Transgenic mice overexpressing BCL-2 in neurons and their littermates were subjected to transient forebrain ischemia for 12 minutes, and the hippocampus was examined 7 days later with conventional histology, immunohistochemistry, and in situ terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling of fragmented DNA. RESULTS: Although both types of mice showed a similar degree of ischemic insult, transgenic mice showed a lesser degree of neuronal death together with DNA fragmentation in the hippocampus than their littermates. CONCLUSIONS: Overexpression of BCL-2 in neurons mitigates selective neuronal vulnerability in the hippocampus of transgenic mice after transient global ischemia.
Animals↗
Itch-associated response and antinociception induced by intracisternal endomorphins in mice.
Endomorphin-1 and endomorphin-2 are newly identified endogenous peptides and have high affinity and selectivity for mu-opioid receptors. The present experiments were conducted to determine whether intracisternal injection of these peptides would produce an itch-associated response and antinociception and to compare their effects to that of morphine. Endomorphin-1 and endomorphin-2 (0.3-3 nmol/mouse) elicited facial scratching characterized by bell-shaped dose-response curves with a peak effect at endomorphin-1 at 0.3 nmol/mouse and endomorphin-2 at 1 nmol/mouse. Their peak effects were inhibited by subcutaneous pretreatment with naloxone (1 mg/kg). Morphine (0.3-30 nmol/mouse) produced facial scratching, and its dose-response curve was also bell-shaped. Scratching of the body trunk, head and ears were not elicited by these doses of endomorphins and morphine. Endomorphin-1 and -2 at doses of 0.3-3 nmol/mouse produced dose-dependent antinociception, as measured with the tail-pressure test. The potency and duration of actions of these peptides were comparable to those of morphine. The results suggest that endomorphin-1 and endomorphin-2 are involved in itch-signaling and pain-inhibiting functions of the brain.
Analgesics, Opioid↗
123I-MIBG SPECT of Merkel cell carcinoma.
131I-MIBG may be useful in the detection of neuroendocrine tumours. Merkel cell carcinoma is a neuroendocrine tumour of the skin. We evaluated a patient with Merkel cell carcinoma using 123I-MIBG single photon emission computed tomography (SPECT) which demonstrated tumour accumulation of the radiotracer in the right eyelid. This result suggests that 123I-MIBG SPECT may be useful in the evaluation of Merkel cell carcinoma.
3-Iodobenzylguanidine↗