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Volume 51, Issue 1
Displaying 1-5 of 5 articles from this issue
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Misato Kashiba, Mayumi Kajimura, Nobuhito Goda, Makoto Suematsu2002 Volume 51 Issue 1 Pages 1-10
Published: 2002
Released on J-STAGE: March 27, 2009
JOURNAL FREE ACCESSThe majority of molecular oxygen (O2) consumed in the body is used as a substrate of cytochrome c oxidase to maintain oxidative phospholylation for ATP synthesis. Rest of the O2 is used for oxidative biosynthesis including synthesis of vasoactive substances such as prostaglandins and sec-ondary gaseous mediators such as nitric oxide (NO) and carbon monoxide (CO). Thus, O2 is not only used for maintenance of energy supply but also for regulating blood supply into tissues. Nitrous oxide (N2O), laughing gas for anesthesia, is generated endogenously through NO reductase in bacteria and fungi, and has recently been shown to modulate N-methyl-D-aspartic acid (NMDA) receptor function. A number of other biologically active gases could participate in regulation of cell and tissue functions. Carbon dioxide (CO2) is generated mainly through the Krebs cycle as a result of glucose oxidation and serves as a potent vasodilator, and hydrogen sulfide (H2S) synthesized through degradation of cysteine has recently been postulated to be a neuromodulater, although their receptor proteins for signaling have not been verified as a discernible molecular entity. Easy penetration allow these gases to access the inner space of receptor proteins and to execute their biological actions. These gases are generated and consumed in anaerobic bacteria through varied reactions distinct from those in mammals. This review summarizes recent information on mechanisms for gas generation and reception in biological systems.View full abstractDownload PDF (2855K) -
William Ng, Seitaro Fujishima, Masaru Suzuki, Keiji Yamaguchi, Katsuno ...2002 Volume 51 Issue 1 Pages 11-16
Published: 2002
Released on J-STAGE: March 27, 2009
JOURNAL FREE ACCESS‹Background› In Japan, emergency departments (ED) receive a large proportion of elderly patients each year. As such, injuries in the elderly are a common reason for presentation to the ED. Knowledge about the characteristics of injuries presenting to the ED would be invaluable in devising strategies to prevent injury in the elderly. ‹Objective› To analyze the characteristics of injuries in the elderly presenting to the ED and compare them with those of the younger population. ‹Setting› The ED at Keio University Hospital, a large inner city teaching hospital located in Tokyo. ‹Method› A retrospective analysis of data extracted from the ED database of the Keio University Hospital. Information regarding patients aged 65 years or above presenting with injury was analyzed and compared with those aged less than 65 years. Prehospital triage by emergency personnel was adopted as the severity of patients, namely “life-threatening” or “non life-threatening”. ‹Results› 20% of all ED presentations of elderly patients were injury related compared to 39% of non-elderly. Compared to the non-elderly, elderly patients presenting to the ED with injury were more likely to be female, sustained injury from trauma unrelated to motor vehicle accidents (MVA) and requiring hospital admission as a result of “non life-threatening” injuries. They were less likely to have injuries from MVA or burns. The number of “life-threatening” injury cases and mortality in both groups were similar. There was evidence that the number of ED presentations relating to injury is increasing in the elderly population. ‹Conclusion› Elderly injury patients are a distinct group with distinctive demographics, mechanism of injury and outcomes. This information would be useful in the planning of injury prevention programs, with particular emphasis on elderly females and MVA-unrelated trauma.View full abstractDownload PDF (492K) -
Amy G. Tsai, Marcos Intaglietta2002 Volume 51 Issue 1 Pages 17-20
Published: 2002
Released on J-STAGE: March 27, 2009
JOURNAL FREE ACCESSBlood substitutes or oxygen carrying plasma expanders were originally formulated to sim-ulate the transport properties of blood, particularly oxygen carrying capacity, viscosity, p50, and colloid osmotic pressure, under the hypothesis that blood is the most desirable fluid in volume restitution. However, changes introduced into the organism during hemorrhage adversely affect microvascular function due to reflex vasoconstriction which causes the fall of functional capillary density, and lowers tissue oxygenation, conditions that are not universally reversed with retransfusion of blood. The res-toration of microvascular function is seldom complete upon retransfusion of blood. New formulations of hemoglobin molecules in solutions whose oncotic pressure is in the range of 60-100 mmHg, p50 is about 5 mmHg, viscosity 3-4 cP, and oxygen carrying capacity in the range of 4-7g/dl equivalent he-moglobin deliver better microvascular function after resuscitation when compared to whole blood and oxygen carrying plasma expanders with transport properties similar to those of blood. The improved performance is in part due to the increased plasma viscosity which increases capillary transmural pressure which reverses capillary collapse induced during low perfusion pressures. High oncotic pres-sure reinforces this effect, since it brings more fluid into the circulation. Microvascular transport studies of the effects of resuscitation in shock show that functional capillary density is the primary determinant of survival, thus maintenance of an open and fully perfused microcirculation is more critical than insuring oxygen supply, since closed capillaries lead to the accumulation of slowly diffusing byproducts of metabolism which ultimately become toxic. The required combination of properties can be achieved by conjugating hemoglobin and polyethylene glycol. Resuscitation fluids based on hemoglobin con-taining vesicles may provide the next level of functional improvement in the formulation of volume restitution fluids since their biophysical properties can be specifically controlled through the inclusion of specialized compounds into the vesicles, and the formulation of the suspending medium.View full abstractDownload PDF (361K) -
Detlef Zillikens2002 Volume 51 Issue 1 Pages 21-28
Published: 2002
Released on J-STAGE: March 27, 2009
JOURNAL FREE ACCESSBullous pemphigoid antigen 180 (BP180, type XVII collagen) is a transmembrane hemi-desmosomal glycoprotein of basal keratinocytes that spans the lamina lucida of the dermal-epidermal junction. Five autoimmune subepidermal blistering diseases are associated with an immune response to BP180, including bullous pemphigoid (BP), pemphigoid gestationis (PG), cicatricial pemphigoid (CP), lichen planes pemphigoides (LPP), and linear IgA disease (LAD). The BP180 ectodomain consists of 15 interrupted collagen domains. The largest non-collagenous (NC) 16A domain is located next to the cell membrane. In BP, autoantibodies are directed to a tightly clustered set of epitopes located at the N-terminal 45 amino acids of the NC16A domain. However, some BP sera also react with other por-tions of the BP180 ectodomain or with the intracellular region of this protein. In PG, antibodies appear to exclusively recognize the immunodominant BP180 NC16A region. In CP, autoantibodies are directed to both the NC16A domain and the C-terminus of BP180 that projects into the lamina lucida/ lamina densa interface of the dermal-epidermal junction. In LPP, autoantibodies react with an epitope located at the C-terminus of NC16A, that is not targeted by BP or PG sera. Finally, the epidermal 97 kDa and the keratinoctye-derived 120 kDa autoantigens of LAD (LABD97 and LAD-1, respectively) have recently been identified as portions of the BP180 ectodomain. These observations demonstrate that different clinical phenotypes are associated with an autoinunune response to the same autoantigen yet the immunoglobulin subclass of the autoantibody and the epitope that is recognized may be dif-ferent.View full abstractDownload PDF (4385K) -
Jonathan D. Kaunitz, Yasutada Akiba2002 Volume 51 Issue 1 Pages 29-35
Published: 2002
Released on J-STAGE: March 27, 2009
JOURNAL FREE ACCESSMeasuring duodenal epithelial intracellular pH (pHi), blood flow and mucus gel thickness (MGT), we studied duodenal defense mechanisms in vivo so as to more fully understand the protec-tive mucosal response to luminal acid. Exposure of the mucosa to physiologic acid solutions promptly lowered pHi, followed by recovery after acid was removed, indicating that acid at physiologic concen-trations readily diffuses into, but does not damage duodenal epithelial cells. Cellular acid then exits the cell via an amiloride-inhibitable process, presumably sodium-proton exchange (NHEII). MGT and blood flow increase promptly during acid perfusion; both decrease after acid challenge and are inhib-ited by vanilloid receptor antagonists or by sensory afferent denervation. Bicarbonate secretion does not increase during acid perfusion but increases following acid challenge. Inhibition of cellular alkali uptake by anion transport inhibitors lowers pHi, and increases mucosal injury, whereas inhibition of apical alkali secretion alkalinizes pHi and diminishes injury. These observations support the following hypothesis: luminal acid diffuses into the epithelial cells, lowering pHi. Acidic pHi increases the activity of a basolateral NHE, acidifying the submucosal space and increasing cellular alkali loading. The acidic submucosal space activates capsaicin receptors on afferent nerves, increasing MGT and blood flow. With continued acid exposure, a new steady state with thickened mucus gel, increased blood flow, and a higher cellular buffering power protects the mucosa from acid injury. After acid challenge, mucus secretion, blood flow and pHi return to normal, while bicarbonate secretion increases. Through these integrated mechanisms, the epithelial cells are protected from damage due to repeated pulses of con-centrated gastric acid.View full abstractDownload PDF (3726K)
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