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This study aimed to update cost-effectiveness and public health impact estimates of the two-dose recombinant zoster vaccine (RZV) compared with no vaccination against herpes zoster (HZ) in the Japanese population aged 65 years. List price of the vaccine and latest RZV efficacy and waning estimates were incorporated.A multicohort static Markov model with a cycle length of 1 year was used to follow a hypothetical cohort of one million people aged 65 years over their remaining lifetime (base case). Age-stratified vaccine efficacy and waning rates were updated on the basis of the latest clinical trial data (interim ZOE-LTFU; NCT02723773). First-dose coverage was assumed at 40%, and second-dose compliance was assumed at 95%. Costs and outcomes were discounted at 2% annually, and the incremental cost-effectiveness ratio (ICER) was calculated from payer and societal perspectives. The societal perspective considered productivity loss due to suffering HZ, or due to suffering HZ and time required for vaccination. Sensitivity analyses explored the overall uncertainties in the model. Scenario analyses for Japanese adults aged 50, 60, 70, 80, ≥ 50, and ≥ 65 years (main scenario) were conducted. An ICER below ¥5-6 million/quality-adjusted life-year (QALY) was considered cost-effective.RZV was estimated to prevent 71,423 HZ cases and 15,858 post-herpetic neuralgia (PHN) cases per million people aged 65 years compared with no vaccine in Japan. The ICER was ¥4,205,515 from a payer perspective and was most sensitive to assumptions regarding vaccine efficacy waning, proportion of patients with HZ developing PHN, and HZ incidence. From societal perspectives, ICERs were ¥3,854,192 (productivity loss from suffering HZ only) and ¥4,622,212 (productivity loss from suffering HZ and time required for vaccination). Overall, the results were considered robust under extensive sensitivity and scenario analyses.Vaccination against HZ with RZV is cost-effective compared with no vaccination in Japanese adults aged 65 years.

Adjuvanted vaccines are recommended for administration through an intramuscular route. The Centers for Disease Control and Prevention (CDC) has recommended the anterolateral thigh using a 22 - 25-G 25-mm (1 inch) needle for infants, injected at a 90° into the skin surface, and using a 16 mm (5/8 inch) for newborns. Appropriate needle lengths may differ depending on racial backgrounds. In the present study, the thickness of the epidermis and lengths from the skin surface to the muscle fascia and bone were measured using ultrasonic echograms in order to determine suitable needle lengths for Japanese infants aged 2, 3, 4, 5, 6, and 12 - 15 months old. The thickness of the epidermis was 1.44 - 1.54 mm (95% CI), and the lengths from the skin surface to the muscle fascia and bone were 11.52 - 12.28 mm (95% CI), and 25.66 - 26.93 mm (95% CI), respectively, at the anterolateral thigh. At the center of the deltoid muscle, skin thickness was similar to that at the thigh, furthermore the lengths from the skin surface to the muscle fascia and bone were 8.49 - 9.10 mm (95% CI), and 17.38 - 18.31 mm (95% CI), respectively. The lengths from the skin surface to the muscle fascia and bone were 1 - 2 mm shorter in 2-month-old infants than those in older generations. Therefore, the appropriate needle length for intramuscular injections in Japanese infants was 16 mm (5/8 inch) at any age and sites, and with 25 mm (1 inch) needles at a 90° angle being associated with the risk of over-penetration.

This phase III, randomized, open-label, multicenter study (NCT01027845) conducted in Japan assessed the immunogenicity, safety, and reactogenicity of 10-valent pneumococcal nontypeable Haemophilus influenzae protein D conjugate vaccine (PHiD-CV, given intramuscularly) co-administered with diphtheria-tetanus-acellular pertussis vaccine (DTPa, given subcutaneously). Infants (N=360 ) were randomized (2:1) to receive either PHiD-CV and DTPa (PHiD-CV group) or DTPa alone (control group) as 3-dose primary vaccination (3-4-5 months of age) and booster vaccination (17-19 months of age). Immune responses were measured before and one month after primary/booster vaccination and adverse events (AEs) were recorded. Post-primary immune responses were non-inferior to those in pivotal/efficacy European or Latin American pneumococcal protein D-conjugate vaccine studies. For each PHiD-CV serotype, at least 92.6% of infants post-primary vaccination and at least 97.7% of children post-booster had pneumococcal antibody concentrations ≥0.2 μg/ml, and at least 95.4% post-primary and at least 98.1% post-booster had opsonophagocytic activity (OPA) titers ≥8 . Geometric mean antibody concentrations and OPA titers (except OPA titer for 6B) were higher post-booster than post-priming for each serotype. All PHiD-CV-vaccinated children had anti-protein D antibody concentrations ≥100 EL.U/ml one month post-primary/booster vaccination and all were seroprotected/seropositive against each DTPa antigen. Redness and irritability were the most common solicited AEs in both groups. Incidences of unsolicited AEs were comparable between groups. Serious AEs were reported for 47 children (28 in PHiD-CV group); none were assessed as vaccine-related. In conclusion, PHiD-CV induced robust immune responses and was well tolerated when co-administered with DTPa in a 3-dose priming plus booster regimen to Japanese children.

A 65-year-old woman presented with pain in her throat and neck. Thin-section computed tomography (CT) revealed an air-filled lesion at the right paratracheal region and two narrow connections to the trachea. Flexible bronchoscopy showed four diverticula 4-5 cm below the vocal cords in the right lateral part of the trachea. Consistent with the CT findings, two of the diverticula were deep. A radiological barium swallow study and an esopagogastroduodenal endoscopic examination revealed no abnormalities. We therefore believe that her right paratracheal air cyst is an extension of a tracheal diverticulum. Right-sided paratracheal air cysts at the level of the thoracic inlet are a common finding on CT and should not be confused with pneumomediastinum in order to avoid unnecessary examinations or treatments.

Background. Pulmonary spindle cell carcinoma is a rare lung cancer which was first classified in 1999 by the World Health Organization (WHO). Case. A 70-year-old man was admitted to our hospital because of bloody sputum, right-side chest and back pain, and an abnormal lung shadow. He was originally given a diagnosis of poorly differentiated non-small cell lung carcinoma based on cytology. The tumor had invaded the bones, and the patient received radiotherapy and chemotherapy, both of which were ineffective. The cancer progressed and he died 5 months later. An autopsy revealed that the cancer was sarcomatoid carcinoma (subgroup, spindle cell carcinoma) according to the 2004 WHO classification of tumors. It was difficult to distinguish the carcinoma from sarcomatoid mesothelioma by pathological examination alone. Initial chest computed tomography had showed a lung mass that led to the diagnosis of sarcomatoid carcinoma. The cause directly leading to his death was respiratory failure caused by diffuse alveolar damage. Conclusion. Pulmonary spindle cell carcinoma is believed to have a poor prognosis and is sometimes difficult to distinguish from sarcomatoid mesothelioma. Additional study of cases is needed to confirm this disease entity and to develop better treatments.

A 39-year-old man with dyspnea was revealed to have severe pneumothorax and received partial resection of the left upper lobe after unsuccessful drainage. Necrotizing epitheloid granuloma was found in the resected lung and Mycobacterium fortuitum was detected from the lesion. Chemotherapy with levofloxacin and clarithromycin was started one year after surgery because of the newly found nodular shadow near the lesion. The case experienced pyothorax due to pulmonary tuberculosis three years before and Mycobacterium avium pleuritis one year before this episode. Three-time mycobacterial pleural infection in three years seems to be uncommon. Furthermore this is the first report of pneumothorax associated with pulmonary Mycobacterium fortuitum infection.

Significant evidence has been provided for the pathophysiological involvement of the β 2 -adrenergic receptor ( ADRB2 ) in hypertension. Among ADRB2 polymorphisms identified to date, 2 amino acid substitutions, Arg16Gly and Gln27Glu, and a promoter variant, T-47C, are considered functionally important. In particular, Arg16Gly was shown to be associated with hypertension in black and white subjects. To investigate the relevance of ADRB2 polymorphisms to hypertension, we undertook an extensive association study in a Japanese population. An association was tested in 2 ways. First, a case-control study was conducted in 842 hypertensive and 633 normotensive subjects. In addition to the overall comparison between case and control groups, each was stratified by body mass index and compared with an independent panel of 525 diabetic subjects. Second, ANOVA and multivariate analyses were performed to test the significance of an association between ADRB2 genotype and the level of blood pressure within the entire population except for 395 subjects who had been under treatment for hypertension. Although no significant association was observed for Arg16Gly and T-47C, 2 analytical methods indicated a marginal association ( P =0.01 to 0.04) between the Glu27 variant and lower blood pressure levels. Given such a normotensive propensity, the odds ratio for Glu27 versus Gln27 allele frequencies was estimated to be 0.74, with a wide confidence interval (95% CI, 0.55 to 0.99) reflecting the low Glu27-allele frequency (6% to 8%) in Japanese. There were no apparent confounding influences of obesity and diabetes on the postulated association. Our data suggest that 3 ADRB2 polymorphisms tested are unlikely to confer principal genetic susceptibility for hypertension in the Japanese population. However, further investigation is warranted to clarify the relevance of ADRB2 polymorphisms to blood pressure regulation.

The study investigated whether patients hospitalized for unstable angina pectoris (UAP), who subsequently develop complete coronary thrombosis (acute transmural myocardial infarction (AMI)) despite medical treatment, exhibit platelet hyperaggregability in an assay system that does not employ agonist stimulation. The study comprised 89 patients with UAP (Braunwald type B). Unfractionated heparin and nitrate were administered to all patients via continuous intravenous drip together with aspirin taken orally. Citrated platelet-rich plasma (230-250 × 103/μl) was obtained on admission and again, in some patients, following the AMI. Platelet aggregability was measured in an optically modified cone-plate viscometer that enables the detection of platelet aggregation without agonist stimulation. A continuous shear rate of 1,200/s was employed. Of the 89 patients, 85 were finally stabilized, while 4 developed an AMI accompanied by persistent ST-segment elevation with increased levels of plasma creatine kinase within 3 h after starting the treatment. The extent of platelet aggregation on admission was significantly greater in these 4 patients compared with the 85 who were stabilized (87.8±6.8%, n=4 vs 26.8±9.1%, n=85; mean ± SD). These data suggest that platelet hyperaggregability mediated mainly by fibrinogen binding to the activated glycoprotein IIb/IIIa complex occurs before a complete thrombotic occlusion and this evaluation may provide important information before the onset of myocardial infarction. (Jpn Circ J 2001; 65: 279 - 282)

A 76-year-old HTLV-I-positive male with acute cerebellar ataxia was suffering from dyspnea on exertion. Chest CT suggested interstitial pneumonitis. Methylprednisolone pulse therapy improved his symptoms and chest CT findings. Twelve months after discharge, when the prednisolone dose was tapered to 5 mg every other day, his lung lesion recurred. The lesion responded initially to steroid therapy. However, hypoxemia intractable to steroid pulse therapy developed and the patient died of respiratory failure. The autopsy revealed diffuse alveolar hemorrhage with no finding of vasculitis. This is the first case report of diffuse alveolar hemorrhage in an HTLV-I carrier.

Immunoglobulin (Ig) production by human B cells in thymus-independent (TI) and -dependent (TD) immune response against Staphylococcus aureus was investigated in vitro. Highly purified human peripheral B cells were cultured either in the presence of formalinized Cowan I strain Staphylococcus aureus (SAC) or with anti-CD3 stimulated T cells, and Ig content in supernatants was analyzed after 10 days of culture by specific sandwich ELISA. When activated with SAC in the absence of T cells, B cells produced minimal amounts of Ig. In the presence of interleukin-2 (IL-2) or supplemental recombinant CD40 ligand plus IL-2, Ig production by SAC-induced B cells was dramatically enhanced. When cultured with T cells stimulated with low concentrations of anti-CD3 or when cultured with smaller numbers of T cells, B cells produced large amounts of Ig, whereas T cells stimulated with higher concentrations of anti-CD3 or large numbers of T cells failed to induce effective Ig secretion by B cells. These findings suggest that TI immune response against Staphylococcus aureus is strongly enhanced in the presence of activated T cells in an antigen non-specific manner, indicating its critical role in the local humoral immune defense. Moreover, it is indicated that the secretion of Ig induced by TD antigens participates in the immune defense against Staphyloccocus aureus dependent on activated T cell/B cell ratio or an impact of CD3 stimulation on T cells.

Background Current methods of angiography cannot provide images of arteries measuring Methods and Results Microangiography was performed in the normal and the ischemic limb 4 weeks after the excision of the femoral artery. In the normal limb, up to the fourth branches of the iliac and/or femoral arteries (diameter Conclusions The small collateral artery network was angiographically visualized with a resolution limit

A 53-year-old man developed bilateral pleural effusion with respiratory failure. The amylase level in the pleural effusion was elevated. He had neither abdominal symptoms nor abdominal physical findings. Abdominal computed tomography (CT) also showed no abnormalities. Magnetic resonance cholangiopancreatography (MRCP) was non-diagnostic, but endoscopic retrograde cholangiopancreatography (ERCP) and subsequent CT showed a fistula connecting the pancreatic duct with the right pleural cavity. The pleural effusion was refractory to drug therapy, leading to the need for surgical intervention. The pathological findings revealed chronic pancreatitis without pseudocysts. The elevated pancreatic amylase in the pleural effusion offered an important clue to the correct diagnosis.

慢性心不全の治療上ジギタリスと利尿薬はアンジオテンシン変換酵素阻害薬とともに現在標準的な薬物である.通常,これらを併用することが多い.ジギタリスは頻脈型心房細動を伴う慢性心不全に,利尿薬はうっ血症状を改善するためにきわめて有用である.本稿では,ジギタリスの新しい作用機序,ジギタリスの再評価,両薬の投与法と投与上の注意点,さらに両薬の限界など最近の進歩と問題点に的をしぼり解説を行った.

Objectives: Natural angiogenesis has been shown to be impaired in spontaneously hypertensive rats (SHR). The purpose of this study was to determine whether pathological angiogenesis in the setting of tissue ischemia is also impaired in SHR, and to what extent it is modified by angiotensin-converting enzyme (ACE) inhibition. Methods: Ischemia was induced in the hindlimb of SHR by excision of the femoral artery, after which the animals were randomly assigned to receive low-dose perindopril (sub-antihypertensive, 0.2 mg/kg/day), high-dose perindopril (antihypertensive, 2.0 mg/kg/day), or vehicle for 3 weeks. Wistar–Kyoto rats (WKY) with femoral artery excision served as a control group. Results: Tissue ACE activity in SHR was significantly increased compared to WKY (49.4±6.2 vs. 34.0±14.2 IU/mg, P

Abstract —The platelet aggregation that is dependent on von Willebrand factor (vWF) is important in the thrombogenesis that occurs under conditions of high shear stress, eg, during acute coronary syndromes (ACSs). A monoclonal antibody, AJvW-2, directed against the A1 domain of human vWF specifically blocks the interaction between plasma vWF and platelet glycoprotein (GP) Ib. To evaluate the association between the vWF-GPIb interaction and the enhanced shear-induced platelet aggregation (SIPA) observed in ACSs, we tested the effect of this antibody on platelet aggregation. Platelet-rich plasma was prepared from the citrated blood of 12 patients with unstable angina (UAP) and 20 patients with acute myocardial infarction (AMI) who were admitted within 3 hours of the onset of cardiac symptoms and from 18 controls. We observed the following: (1) 1.7-fold higher plasma levels of vWF and ristocetin cofactor activity in UAP patients and (2) 2.8-fold higher levels in the AMI group than in controls. Using a cone-and-plate viscometer, we measured the mean value of SIPA under high-shear conditions (108 dyne/cm 2 ) and found them to be 1.3-fold higher in the UAP group and 2.0-fold higher in the AMI group than in controls. The high SIPA in all groups was completely inhibited by 10 μg/mL AJvW-2. Under low-shear conditions (12 dyne/cm 2 ), platelet aggregation was increased only in the AMI group, but this was unaffected by AJvW-2. We observed a significant correlation in both ACS groups between high SIPA and the plasma vWF level or vWF larger multimers. These findings suggest that the vWF-GPIb interaction is important in coronary occlusion and that inhibition of this interaction (with the use of AJvW-2) may prevent further events in the coronary arteries.

Objective: Platelet aggregation has been implicated in the pathogenesis of acute coronary syndromes. Small aggregates consisting of ≤100 platelets cannot be quantified with a conventional aggregometer employing optical density. Using a recently developed aggregometer based on laser light scattering, we studied platelet aggregability in patients with acute coronary syndromes. Methods: Peripheral blood samples were obtained from 39 patients with acute myocardial infarction or unstable angina who had received no prior antiplatelet or anticoagulant therapy, to be assayed immediately using a PA-100 platelet aggregometer. Blood samples from 14 healthy volunteers were used as controls. Results: Spontaneous formation of platelet aggregates was observed only in patients with acute coronary syndromes. The size of these aggregates was small, consisting of ≤100 platelets (primary aggregation). Agonist-induced aggregation consisted of two phases. In the first few minutes, the number of small aggregates increased markedly (primary aggregation), followed by an increase in larger aggregates (secondary aggregation). The EC50 of epinephrine for primary aggregation was nearly 50 times lower in acute coronary patients than in controls ( P

Background —Recent investigations have demonstrated the ability of vascular endothelial growth factor (VEGF) to augment the development of collateral arteries in vivo. In vitro studies have suggested that the use of VEGF also improves the endothelium-dependent relaxation of collaterals at the microvascular level. The purpose of this study was to determine in vivo the extent to which vasomotor responses of collateral microvessels are altered after VEGF treatment. Methods and Results —Ischemia was induced in the hindlimb of 35 rats by excision of the femoral artery. Immediately thereafter, 400 μg of a plasmid encoding VEGF or β-galactosidase (control) was transfected into limb muscles. Four weeks later, synchrotron radiation microangiography, with a spatial resolution of 30 μm, was performed to document the reactivity of collateral microvessels. Administration of the endothelium-dependent vasodilator acetylcholine failed to induce dilation of collateral microvessels in control animals. By contrast, profound dilation of collaterals was observed after acetylcholine in VEGF-treated animals. This response was evident in vessels with a linear appearance but not in those with an undulating appearance. The resulting blood flow in the ischemic limb after administration of acetylcholine in the control animals was only 64.6±17.0% of that of the contralateral normal limb, whereas blood flow was augmented to 106.1±8.4% in VEGF-treated animals ( P Conclusions —These results demonstrate in vivo that the use of VEGF restores impaired vasomotor responses in some types of collateral microvessels, which may help to provide a basis for understanding the microcirculation after therapeutic angiogenesis with VEGF.

Objective: The development of collateral microvessels following therapeutic angiogenesis with vascular endothelial growth factor (VEGF) was investigated using a new system of microangiography that employs monochromatic synchrotron radiation (SR) and a high definition video system to visualize arteries with a spatial resolution of 30 μm. Methods: Ischemia was induced in the hindlimb of 20 rats by excision of the femoral artery, followed by transfection of the plasmid (400 μg) encoding VEGF or β-galactosidase (control) into limb muscles. Microangiography was used to assess the development of collaterals in the ischemic limb four weeks after treatment. Results: Gene transfer of VEGF produced morphologically similar, but significantly more extensive, collateral networks at the microvascular level as compared with the naturally occurring collateral arteries in the control animals (angiographic score: 0.88±0.08 versus 0.54±0.05, p

The purpose of this study was to investigate the significance of ST re-elevation at reperfusion using strict criteria for patient inclusion and exclusion. Twenty-nine patients who had a first anterior infarction with single-vessel disease, successful recanalization by intracoronary thrombolysis (ICT) with urokinase, and an angiographically confirmed patent infarct-related artery after 4 weeks, were divided into three groups according to the deviation of the ST segment at reperfusion: Group A, 10 patients with sustained ST re-elevation; Group B, 10 patients with transient ST re-elevation; and Group C, 9 patients with ST reduction. Left ventricular (LV) function was evaluated from cineventriculograms performed in the 30 degrees right anterior projection 4 weeks after ICT. LV ejection fraction and regional wall motion of the infarct area, evaluated by the centerline method (SD/chords), were significantly lower in Group A (44 +/- 10%, -3.2 +/- 0.4) than in Group B (61 +/- 9%, -1.9 +/- 0.7) and Group C (60 +/- 5%, -2.0 +/- 0.4) (p0.01). Peak creatine kinase (CK) activity was significantly higher in Group A (5848 +/- 2112 IU) than in Group B (2485 +/- 1254 IU) and Group C (1889 +/- 1525 IU) (p0.05). These data suggest that a sustained ST re-elevation at reperfusion was strongly associated with marked LV dysfunction and higher peak CK activity. It was concluded that sustained, not transient, ST re-elevation associated with successful reperfusion indicates extensive myocardial damage.

The purpose of this study was to determine whether computed tomography (CT) can detect hemorrhagic infarction occurring after intracoronary thrombolytic therapy (ICT) for acute myocardial infarction (AMI). In an experimental study, 12 dogs underwent 2-4 h of left anterior descending artery (LAD) occlusion, followed by reperfusion, and infusion of contrast material into the LAD. After CT examination, the heart was cut into transverse sections. A good correlation was obtained between the CT-enhanced area and the hemorrhagic area in the sliced heart section (r = 0.895, p less than 0.001). In a clinical study, we applied CT immediately after ICT in 25 patients with AMI. In 13 of 25 patients, the CT showed post-ICT myocardial enhancement areas. To evaluate the relationship of the enhancement areas shown by CT to the viability of the myocardium, we compared enhancement areas by CT with the corresponding perfusion defect areas of Thallium-201 imaging (SPECT) one month later. There was no significant correlation between the enhancement areas and perfusion defect areas (r = 0.38, p greater than 0.1). The SPECT defect areas were consistently smaller than the CT enhancement areas. These results indicate that CT can detect hemorrhage into the myocardium after ICT, and that after ICT half the AMI patients showed hemorrhagic infarction. However, hemorrhage did not cause complete deterioration of the myocardium.

radioimmunoassay により digitoxin 維持量投与中の患者118人 (男81人, 女37人) の血清 digitoxin 濃度を測定 (のべ262回) し, その臨床的意義につき検討した. さらに従来老齢者にジギタリス中毒が多いといわれているのでこの点に注目して血清濃度の面より検討を加えた. その結果,1) 中毒群の血清濃度は平均35.5ng/ml, 非中毒群のそれは平均18.4ng/mlであり両群間で明らかな有意差 を示した (P

In order to analyse the mechanism of the positive inotropic effect on the myocardium of cardiac glycosides, the author studied on the timed localization and distribution in the rat myocardial cells of the glycosides by means of electron microscopic autoradiography.Since most part of the glycosides may be lost from the tissues during the process of fixation and dehydration, the methods were studied. The radioactivity in the tissue was measured by the oxygen combustion method. Little part of the glycosides was lost when the tissues were fixed with glutaraldehyde and osmium tetraoxide, and then dehydrated with acetone series.By this method the author found most silver grains distributed in the transverse system (T system), the sarcoplasmic reticulum and the sarcolemma. This may suggest that the glycosides act upon the membraneous component.

This article presents four cases of erectile hemangioma in the masseter muscle. These four patients, age 48 female, 18 male, 17male, 21 female, had same symptoms; enlargement of masseter portion follows muscle contraction. In all of cases, the swelling lesion took many years to become large. On the clinical examination, the swellings were immediately followed by masseter muscle contraction. The size and the hardness of the swelling gradually reduced during the patient kept contract on. In case 1 and case 2, the operations were performed after injecting silicon impression materials (for dental use) into the main cavities of hemangioma. This method makes it easier to resect the tumor. Case 3 was treated by extraoral approach and case 4 resected by intraoral approach. The pathological diagnosis of the first two cases were cavernous hemangioma and the last two cases were venous hemangioma. No patient had complications and recurrence.

Clinical studies were carried out during digoxin maintenance therapy to clarify three questions concerning digitalis therapy: optimal time for blood sample collection for serum digoxin concentration (SDC), the overlapping range of SDC levels in which some patients may be intoxicated while others are not, and both resistance and sensitivity of atrial fibrillation (AF) to digitalis. The SDC curve after a single dose of digoxin or beta-methyldigoxin shows the appropriate sampling time to be at least 12 hours after the administration. The optimal time is 24 hours. The overlapping SDC range was 1.7-2.7 ng/ml. There were significant differences in CTR and ventricular rates in AF between intoxicated and non-intoxicated groups. This suggests that susceptibility to digitalis increases with the severity of underlying heart disease. Precipitating factors such as CTR should be taken into consideration, if the SDC is in the overlapping level. Digitalis resistance occurs in 6.7% of 105 patients with AF, and more frequently in hypertensive heart disease than others. Digitalis sensitivity occurs more often in the elderly and in patients with dilated cardiomyopathy. But it is not necessary to attain higher therapeutic levels for AF than for sinus rhythm. Clearly optimal digitalis therapy for AF can be best accomplished when precise clinical findings, SDC and EKG recordings are carefully monitored and used to correct treatment.

On 79 ECG tracings obtained from 31 uremic patients, the influence of serum Ca, Na, and K concentrations on the QT duration in ECG was analyzed by multiple regression technique. It was found that Ca and K had negative and Na had a positive effect on QT duration, although only the effect of Ca was reaching the statistically significant level. Since serum electrolytes had correlations with each other, they were orthogonalized and tested for significance once again. Still Na and K did not reveal significant influences by this procedure. However, the effects of Na and K on QT duration were as the same direction and magnitude as reported in older literatures.In the course of orthogonalization it was found that Ca and Na had negative influences on K. It seems that this fact presents a sound basis for the therapeutic use of Ca and Na salts in hyperpotassemia.