Tokuzen Iwamoto

Implication of ESR signals from ceruloplasmin (Cu2+) and transferrin (Fe3+) in pleural effusion of lung diseases

Pleural effusions of seven lung cancer patients (mean age; 58) and seven non-cancer patients (mean age; 49) were examined and Cu(2+) was measured in ceruloplasmin and Fe(3+) in transferrin signals by electron spin resonance (ESR) method. The variations of total Fe and Cu ions, ceruloplasmin and transferrin, proteins, neutrophil cell counts, LDH and nitrite/nitrate were also examined. The Cu(2+) peak was decreased and the Fe(3+) peak was increased in the cancer group. The interrelationship among Cu(2+), total Cu and ceruloplasmin, and among Fe(3+), total Fe and transferrin clarified that Cu(2+) and Fe(3+) are not a representative of ceruloplasmin and transferrin, respectively. The ratio of Cu(2+)/Fe(3+) in pleural effusion distinguished lung cancer from benign inflammation as a cause. The ratio of total Cu/total Fe measured by the chemical analysis method also distinguished these, but the ratio of ceruloplasmin/transferrin was unable to distinguish the cancer. In conclusion, the simple and rapid measurement of Cu(2+)/Fe(3+) by ESR effectively abstracts the variation of total ion concentrations caused by malignant disease.

Regional vulnerability to chronic hypoxia and chronic hypoperfusion in the rat brain.

The purpose of this study was to compare the pathological findings of injury induced by chronic hypoperfusion and by chronic hypoxia in rat brain. Adult male Wistar rats were divided into three groups: chronic hypoperfusion (n=5), chronic hypoxia (n=5), and normal control groups (n=5). Hypoperfusion was induced by ligation of the bilateral carotid arteries under 2.5% halothane anesthesia. Chronic hypoxia was induced by keeping the animals in a chamber with an atmosphere of 10% O(2) in N(2) for 3 weeks. Twelve weeks later (chronic hypoperfusion group) and 3 weeks later (chronic hypoxia group), the animals were sacrificed and perfused through the femoral artery with a fixative containing 4% paraformaldehyde. Hematoxylin and eosin staining was done in all sections in the three groups, and the number of normal-appearing cells was counted. Normal-appearing cells in CA3 were significantly decreased in the chronic hypoperfusion group compared with those in the chronic hypoxia group, although neurons in CA1, CA2 and CA4 in both groups were equally damaged. We concluded that the CA3 hippocampus shows different vulnerabilities to chronic hypoperfusion and chronic hypoxia, possibly owing to a difference in the kinds of glutaminergic receptors.

α2-Adrenergic-receptor response in reversible increase in hemoglobin concentration in intermittent hypoxia

We have previously shown that intermittent hypoxia (IHx, 10% O(2), 60 min/day) leads to an increase in the splenic alpha2-adrenoceptor response and results in a splenic contraction-induced reversible increase in hemoglobin concentration ([Hb]). In the present study, we determined whether IHx of shorter duration (15 min/day (15-min) and 30 min/day (30-min)), produced this phenomenon in rats. A significant increase in [Hb] during hypoxia was observed in both the groups, but its magnitude was larger in the 30-min IHx rats. Even when the cumulative exposure time (time/dayxdays) was shorter, the [Hb] increase was larger in the rats with longer daily hypoxic exposure. The alpha2-adrenoceptor antagonist yohimbine abolished the [Hb] increase of 15- and 30-min IHx. The increase in [Hb] following administration of the alpha2-adrenoceptor agonist oxymetazoline was also higher in 30-min IHx; indicating that the higher [Hb] produced by longer daily hypoxic exposure times is the result of increases in alpha2-adrenergic-receptor response of greater magnitude. In conclusion, IHx for periods as short as 15 and 30 min/day increases the splenic alpha2-adrenoceptor response and its magnitude reaches the maximum value depending on the daily hypoxic exposure time. A reversible increase in [Hb] constitutes a useful mechanism that protects organ oxygen supply during hypoxic episodes of variable duration and intensity.

Hypobaric hypoxia is not a direct dyspnogenic factor in healthy individuals at rest

Dyspnea consists of various uncomfortable respiratory sensations. It is believed that hypoxia causes dyspnea, but whether hypoxia is a direct dyspnogenic factor remains uncertain. We investigated whether hypoxia has a direct dyspnogenic effect. We evaluated changes in vital signs, arterial blood gases, SaO2, CaO2, Borg scale, and Mini-Mental State Examination in seven mountain climbers by using a hypobaric hypoxic chamber in which the barometric pressure was lowered to the simulated altitude of 4500 m. PaO2 and CaO2 both decreased significantly as the simulated altitude increased. On the other hand, Borg scale score which reflects dyspnea showed no significant difference. At the simulated altitude of 4500 m, Borg scale score was 1.5 ± 1.2 (mean ± SD), despite the presence of absolute hypoxia (PaO2, 46.8 ± 8.3T; CaO2, 16.4 ± 0.6 mL/dL). These results suggest that hypoxia is not a direct dyspnogenic factor in healthy individuals capable of breathing without restriction at rest.

Simple, rapid and automated method for detection of hyperaggregability of platelets in sleep apnea syndrome

the novel C-terminus of murine asTF is 53 amino acids larger than the C-terminus of human asTF, the C-terminus lacks homology to other known proteins and murine asTF is omnipresent in plasma and experimentally induced arterial blood clots. In addition, we show that asTF is induced during S. pneumoniae infection both in plasma and lung tissue. Although the presence of soluble TF in blood remains puzzling, we believe that our and Bogdanov’s [8] mouse data are in favor of an important biological role. Obviously, this biological role, be it stimulating thrombus growth [1] or inhibiting this process [7], needs further exploration. The relevance of asTF can be best obtained using knock-out animals for asTF or using mice that only express the splicing variant in state the art of models of blood coagulation, infection, atherosclerosis, and/or tumor growth. The finding that mice produce asTF which is omnipresent in blood clots is only a first important step toward the definitive answers.

A case of HAPE on K2 and literature review.

HAPE (High Altitude Pulmonary Edema) is a serious and fatal disease in mountains. Early diagnosis and immediate descent are important for successful treatment. One of the authors (GS), who was healthy and a well trained climber, participated in the expedition to K2 (8611 m) in 2006 and developed HAPE. Under the severe environmental condition, it was difficult to evaluate his condition in its early stage. The earliest symptoms were nonspecific for HAPE as reported in many papers. Neither had he suffered from HAPE on the previous expeditions. These facts probably delayed the diagnosis in spite of its typical onset. This is a rare case report by a medical doctor who suffered from HAPE. The present case may remind the climbers of the difficulties in diagnosing HAPE on a mountain.