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食品成分で血管拡張作用を示す一酸化窒素（NO）を産生する亜硝酸塩と臨床的に汎用されているジヒドロピリミジン系のカルシウム拮抗薬の併用投与による血圧と、それぞれの成分の体内動態に対する相互作用について検討した。SD系雄性ラットに一酸化窒素合成阻害剤（L-NAME）を3 週間投与し、内因性NO産生不足高血圧ラットを作成した。本ラットに亜硝酸塩（経口投与）とニフェジピン（腹腔内投与）を単独、または併用投与し60分間の血圧を測定した。さらに、血液中の亜硝酸イオンと硝酸イオン量、およびニフェジピン濃度をHPLC法により測定した。その結果、血圧は両成分とも投与量依存的な効果を示し、併用投与では血圧降下作用が増強した。その際の、血中ニフェジピン濃度は単独と併用で有意差を認めなかった。しかし、血漿中の亜硝酸イオンは単独に比べ併用投与でTmaxの遅延とCmaxの増加が認められた。以上のことから、亜硝酸塩とニフェジピンの併用は血圧に対して相互作用を示すことが明らかになった。また、この相互作用はニフェジピンが亜硝酸塩（または、亜硝酸塩から生成されたNO）の代謝や消失に影響を与えたことによる薬物動態学的な相互作用であることが示唆された。

Background and aims Direct measurement of arginine vasopressin (AVP) via immunoassays is not widely conducted, mainly because of technical constraints. Liquid chromatography–tandem mass spectrometry (LC/MS/MS) has been widely used as the gold standard in clinical chemistry. Here, we aimed to develop an MS-based assay to determine human plasma AVP and compare the results with those obtained using a conventional immunoassay. Materials and methods We developed a protocol using triple quadrupole MS coupled with LC for the measurement of human plasma AVP. Analytical evaluations of the method were performed, and the results obtained using LC/MS/MS and radioimmunoassay (RIA) were compared. Results The lower limit of quantification (LLOQ) for plasma AVP obtained using LC/MS/MS and RIA were 0.2 and 0.4 pg/mL, respectively. Although there was a weak overall correlation between the results obtained using the two different methods, the RIA results did not agree with the LC/MS/MS results, particularly at low concentrations. Conclusions AVP detection through RIA is not satisfactory compared with that using LC/MS/MS. Diagnostic values of direct AVP measurements must be evaluated based on the results obtained via sensitive and accurate MS-based methods rather than those obtained through RIA.

Bardet-Biedl syndrome (BBS; OMIM #209900) is a pleiotropic genetic disorder, or ciliopathy, with autosomal recessive inheritance [1].

Adefovir dipivoxil (ADV) is effective for hepatitis B virus (HBV) infection; however, ADV may provoke renal injury resulting in osteomalacia, and this side effect is seldom recognized until bone fractures emerge. We herein present a 66-year-old woman with HBV infection who received ADV for 6 years. Although she exhibited no sign of bone fractures, her urinary β-2 microglobulin (β2MG) level increased to 83,837 μg/L and scintigraphy revealed minimal fractures of the third rib. ADV was subsequently reduced and her urinary β2MG rapidly fell to 3,637 μg/L. Conversely, her urinary N-acetyl-β-D-glucosaminidase, and serum phosphate, alkaline phosphatase levels did not respond.

Background Ectopic adrenocorticotropic hormone (ACTH) syndrome (EAS) is caused by tumours releasing ACTH. Ectopic ACTH-producing tumour regression is rarely induced using steroidogenesis inhibitors. We presented a case of EAS in which ACTH production by a lung tumour was reduced by metyrapone (MTP) and also reviewed previous cases of ectopic ACTH production suppressed via steroidogenesis inhibition. Case presentation A 71-year-old female with general fatigue, central obesity and impaired glucose tolerance was diagnosed with Cushing’s syndrome due to elevated ACTH (192.9 pg/mL; normal range, 7.2–63.3 pg/mL), cortisol (73.1 μg/dL; 6.4–21.0 μg/dL) and 24-h urinary free cortisol (UFC) (6160 μg/day; 11.2–80.3 μg/day) levels. Chest computed tomography identified a solid 26.6 × 22.9 × 30.0 mm tumour with a cavity in the upper lobe of the left lung. There was no adrenal gland enlargement. Tumour markers were not significantly elevated; ACTH levels were not suppressed by 8-mg dexamethasone. A corticotropin-releasing hormone stimulation test revealed blunted ACTH response (basal ACTH, 204.6 pg/mL; highest ACTH level during the 120-min stimulation test, 214.0 pg/mL). She was diagnosed with EAS due to a lung lesion. MTP treatment was started to reduce cortisol production. ACTH levels and cortisol and UFC levels were normalised and the ACTH-producing lung tumour was ablated after MTP treatment. In several reported cases, plasma ACTH levels reduced during steroidogenesis inhibitor treatment for EAS. Among the 10 patients, three cases of pheochromocytoma, one of thymic carcinoid and one of islet cell carcinoma were reported. In four cases, the tumour was not detected. In our case, the pathology of the lung tumour was unknown because of lack of tumour cells in biopsy. The patients were treated with ketoconazole (KTZ) and/or MTP and exhibited ACTH and cortisol/UFC suppression, but tumour regression was observed only in our case. Conclusion MTP and/or KTZ may reduce ACTH and cortisol production. The tumour spontaneously regressed after MTP treatment, indicating that MTP may reduce the tumour size without surgery. The mechanisms of therapeutic effects of steroidogenesis inhibitors and prognosis of spontaneous remission should be elucidated further via molecular biology studies. Electronic supplementary material The online version of this article (10.1186/s12902-018-0246-2) contains supplementary material, which is available to authorized users.

Thymic carcinoid in multiple endocrine neoplasia type 1 (MEN 1) is previously reported as a non-ACTH producing tumor. The present case is a 39-year-old man with mortal outcome from thymic carcinoid and Cushing's syndrome with high plasma ACTH. The symptom was first observed at age 29 and was relieved after extended thymectomy, with reduction of ACTH level. The tumor was positive for ACTH, Grimelius silver staining and Chromogranin A. The finding of primary hyperparathyroidism, pituitary adenoma, and a novel germline nonsense mutation (W423X) established the diagnosis of MEN 1. Cushing's syndrome due to ACTH producing thymic carcinoid should be also considered as one phenotype of the MEN 1 spectrum.

NO-1886 is a lipoprotein lipase (LPL) activator. Administration of NO-1886 results in an increase in plasma high-density lipoprotein cholesterol (HDL-C) and a decrease in plasma triglyceride (TG) levels. The aim of this study was to ascertain whether NO-1886 improves fatty liver caused by high-fat feeding in streptozotocin (STZ)-induced diabetic rats. Administration of NO-1886 resulted in increased plasma HDL-C levels and decreased TG levels without affecting total cholesterol and glucose levels in the diabetic rats. NO-1886 dose-dependently decreased liver TG contents and cholesterol contents, resulting in improvement of fatty liver. NO-1886 also reduced plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) that accompany fatty liver. The liver cholesterol contents were inversely correlated with plasma HDL-C levels (r = -0.5862, P

Background : It has been shown that restless legs syndrome (RLS) in adults may be linked to abnormalities in iron stores. Whether reduced iron stores play a role in children is not clear. Methods : We evaluated the status of iron stores and sleep in three teenagers who presented with severe sleep onset insomnia, subjective sleep latency exceeding 60 min and excessive daytime sleepiness. Results : The three teenagers were found to have RLS and laboratory evaluation confirmed reduced body stores of iron with a low percent iron saturation (mean value 9.7%) and a low serum ferritin level (mean value 17 μg/l). None had marked anemia. The three patients were treated with oral iron for 4–5 months. As a group they had an increase in percent iron saturation (from a mean of 9.7 to 22.7%) and serum ferritin (from a mean of 17 to 27 μg/l) and a marked reduction of the symptoms of RLS, with mean subjective sleep latency decreasing from 143 to 23 min, sleep efficiency increasing from 75.7 to 84.0% and the number of periodic movements per hour of sleep decreasing from 20.5 to 10.5. Interpretation : These findings support the hypothesis that abnormal iron stores or metabolism may result in RLS causing insomnia in teenagers. We recommend evaluation of iron status including serum iron, total iron binding capacity and ferritin levels in teenagers with chronic insomnia of unexplained origin even when anemia is mild or absent.

An obese 23-year-old man with sleep-disordered breathing and primary pulmonary hypertension (PPH) had been administered oral beraprost sodium, anticoagulant warfarin, and home oxygen therapy, at another hospital as treatment for the PPH, but he had not experienced any symptomatic improvement. The patient had a body mass index of 32.4kg/m 2 , and complained of fatigue, shortness of breath on exertion, excessive daytime sleepiness, and snoring. Arterial blood gas analysis showed a PaO 2 and a PaCO 2 of 70.9 and 31.2mmHg, respectively. A polysomnographic study revealed central sleep apnea with an apnea-hypopnea index (AHI) of 29.7 episodes/h. The patient showed improvement of daytime sleepiness after starting nocturnal nasal bilevel positive airway pressure (BiPAP) therapy for the central sleep apnea, but his pulmonary hypertension, measured in the daytime, worsened. The patient died suddenly while walking to the bathroom in the morning 1 month after initiation of BiPAP therapy. It is necessary to consider the possibility of sudden death when nasal BiPAP therapy is given to a PPH patient with central sleep apnea.

The effect of pituitary adenylate cyclase-activating polypeptide (PACAP) on arginine vasopressin (AVP) release was investigated in conscious rats. Intracerebroventricular (i.c.v.) administration of PACAP raised the plasma AVP concentration in a dose-dependent manner (50-500 pmol/rat), and the maximum effect was obtained at 5 min after the administration. This AVP-releasing effect was not due to a fall of blood pressure, increase of plasma Na or decrease of plasma volume, all of which are known to stimulate AVP release. PACAP had little effect on blood pressure at a low dose, but at higher doses increased it. Vasoactive intestinal peptide (VIP), which is homologous to PACAP, also raised the plasma AVP concentration by i.c.v. injection. An antagonist for VIP receptor, [Lys, Pro, Arg, Tyr]-VIP inhibited the VIP-induced increase of plasma AVP, but had little effect on PACAP-induced increase of plasma AVP. These results suggest that PACAP stimulates AVP release, via specific receptors which are distinct from VIP receptors.

Previous neuroanatomical studies have revealed a localization of galanin in several nuclei in the brain stem which are involved in the hemodynamic control of arginine vasopressin (AVP) release. The present study, therefore, investigates the contribution of endogenous galanin to the plasma volume-mediated control of AVP release in conscious rats. Injection of synthetic rat galanin (12.5-50 pmol/rat) into the cisterna magna (i.c.s.) suppressed plasma AVP increased by polyethylene glycol-induced hypovolemia (2.45 +/- 0.24 pg/ml at 50 pmol/rat vs. the vehicle group 5.72 +/- 0.69 pg/ml, p0.01). In contrast, when plasma AVP was suppressed by isotonic plasma volume expansion, immunoneutralization of endogenous galanin by antigalanin-antibody i.c.s. significantly reversed the suppression (1.02 +/- 0.07 pg/ml vs. vehicle group 0.63 +/- 0.05 pg/ml, p0.01) without altering the mean arterial blood pressure. These results suggest that endogenous galanin is physiologically involved in the plasma volume-mediated control of AVP release through an inhibitory action on this pathway.

We studied histologic findings of age-related change in the posterior pituitary gland focusing specifically on abnormal deposition of tau protein. Posterior pituitary glands from a total of 201 patients with mean age of 72, range 15 to 100 years, were dissected at autopsy, and semiquantitative analysis of tau protein deposition in the posterior pituitaries was performed. We confirmed that tau protein deposition in the posterior pituitary appears histologically as either a 'thread-like' or 'dot' form. In double staining using an anti-neurofilament antibody and Gallyas-Braak staining, Gallyas-Braak-positive structures were located in the neurite. The grade and the frequency of tau protein deposition were increased in accord with aging. An interrelation was observed between tau protein deposition in the brain and that in the posterior pituitary. In tauopathy diseases, tau protein deposition in the posterior lobe is advanced compared to that in non-tauopathy diseases. The level of tau protein deposition in the hypothalamus was compared semi-quantitatively with that in the posterior pituitary, and the levels correlated well. We suggest that in the posterior pituitary of elderly people, high frequency of occurrence of deposition of abnormal tau protein in the neurites may cause dysfunction of the pituitary gland.

Obstructive sleep apnea syndrome (OSAS) often accompanies obesity and diabetes mellitus. This study was performed to investigate the prevalence of glucose intolerance and to determine independent predictors for insulin resistance in patients with OSAS.A cross-sectional study of 679 OSAS patients with an apnea-hypopnea index (AHI)or=5/h and 73 controls subjects (AHI5/h) was done in a tertiary university-based medical center. They were assessed by nocturnal polysomnography and underwent an oral glucose tolerance test.The prevalence of diabetes mellitus in OSAS patients was higher than that of the control group (25.9% vs. 8.2%, p0.001) and 424 patients (62.4%) received a new diagnosis of impaired glucose tolerance or diabetes mellitus. The very severe OSAS group (AHIor=45/h) had significantly higher homeostasis model assessment of insulin resistance (HOMA-IR) and HOMA beta-cell function than the other OSAS groups (AHI45/h) and the control group. In a logistic regression model adjusting for potential confounders: age, AHI, minimum SpO(2) and body mass index (BMI), only BMI was associated with insulin resistance (HOMA-IR3) (odds ratio: 1.272, 95% confidence interval 1.206-1.343, p0.0001).Glucose intolerance was more common in patients with OSAS. Insulin resistance was associated not with AHI but rather with BMI.

The effect of centrally administered galanin on arginine vasopressin (AVP) release was investigated in conscious rats. Intracerebroventricular injection of porcine galanin suppressed hypertonic saline-induced increase in plasma AVP in a dose-dependent manner (12.5–100 pmol/rat) at 10 min after the injection. Pretreatment with subcutaneous injection of naloxone ( 1 mg 100 g b.wt. ) partially blocked the galanin-induced effect on plasma AVP. These results suggest that central galanin inhibits osmotically stimulated AVP release and endogenous opioids are, at least in part, involved in the mechanism.

We examined the effects of gamma-aminobutyric acid (GABA) and naloxone, a potent opioid antagonist, on arginine vasopressin (AVP) secretion in conscious rats in order to study the relationship of GABA and endogenous opioid peptides in the regulation of AVP secretion. Intracerebroventricular administration of GABA caused a time- and dose-dependent decrease in the plasma concentration of AVP that was elevated by hypertonic saline injection, whereas it did not affect the basal AVP. Pretreatment with naloxone (10 mg/kg) significantly attenuated the inhibitory effect of GABA (100 micrograms) on AVP release. These results suggest that GABA produces an inhibition of AVP release stimulated by hypertonic saline, and that this inhibitory effect may be mediated at least in part by the endogenous opioid systems.

It has been demonstrated that hyperprolactinemia is sometimes present even in patients with idiopathic diabetes insipidus (DI). In this study, we examined the responses of serum prolactin (PRL) to hypertonic saline infusion and TRH injection in 11 patients with idiopathic DI diagnosed by clinical examinations. Serum sodium in these patients (147.5 +/- 3.2 mEq/L) was significantly higher at baseline than in normal subjects (139.7 +/- 2.4 mEq/L). The plasma arginine vasopressin (AVP) level was significantly lower in DI (0.42 +/- 0.24 pg/ml) at baseline than in normal subjects (2.53 +/- 1.03 pg/ml). However, the serum PRL level in both groups did not differ significantly except in one patient with idiopathic DI (35.6 ng/ml). There was no significant correlation between the basal serum sodium and basal serum PRL in either group. After an infusion of hypertonic saline, the serum sodium level gradually increased to 155.6 +/- 3.4 mEq/L in DI and to 146.5 +/- 4.3 mEq/L in the normal subjects. However, this increase did not affect PRL secretion in either group. PRL response to TRH was essentially normal in all patients with idiopathic DI. These results indicate that the secretion of PRL is not generally affected by chronic mild hypernatremic hypovolemia in the patients with idiopathic DI.

We investigated the prevalence of metabolic syndrome in patients with obstructive sleep apnea syndrome (OSAS) referred to a tertiary university-based medical center. A cross-sectional study of patients with a definite diagnosis of OSAS was performed using new diagnostic criteria for metabolic syndrome that were designed for the Japanese population. Clinical features and comorbidities related to metabolic syndrome were compared between 819 patients with OSAS (719 men and 100 women) and 89 control subjects without OSAS. Metabolic syndrome was significantly more common in the patients with OSAS than in the controls (49.5% vs. 22.0% for men, p0.01; 32.0% vs. 6.7% for women, p0.01). Men with OSAS (apnea-hypopnea index [AHI]or =5/h) had a higher risk of metabolic syndrome compared with controls (odds ratio [OR]: 3.47; 95% confidence interval [CI]: 1.84-6.53). There was a significantly increased risk of metabolic syndrome in men with moderate OSAS (AHI: 15-29.9/h) (OR: 2.83; 95% CI: 1.42-5.66) and men with severe OSAS (AHIor =30/h) (OR: 5.09; 95% CI: 2.67-9.71). Women with OSAS (AHIor =5/h) also had an increased risk of metabolic syndrome (OR: 6.59; 95% CI: 1.47-29.38), and the risk was significantly higher in women with severe OSAS (AHIor =30/h) (OR 14.00; 95% CI: 2.93-66.82). Risk factors for metabolic syndrome differed by gender: in men, age, body mass index (BMI), and OSAS (AHIor =15/h) were significantly associated with metabolic syndrome, whereas, in women, BMI was the only risk factor for metabolic syndrome. The increase of metabolic syndrome in Japanese OSAS patients suggests that this patient population is burdened with multiple risk factors for cardiovascular disease.

Obstructive sleep apnea syndrome (OSAS) is strongly associated with cardiovascular disease which means these patients could suffer sudden death from these cardiovascular diseases, but it is a rare case that common OSAS itself causes sudden death directly. On the other hand, we never wrongly diagnose serious sleep-related breathing disorders (SBDs) such as sleep hypoventilation syndrome, OSAS patients with cardiovascular disease (i.e. ischemic heart disease, cardiac arrhythmia and cardiac failure) and bilateral vocal cord paralysis caused by multiple system atrophy as common OSAS. This section describes how to distinguish these SBDs from common OSAS.

Background Sleep-disordered breathing may adversely affect heart function, and thereby contribute to the progression of heart failure. A study was undertaken in patients with idiopathic cardiomyopathy to document the characteristics of sleep-disordered breathing. Methods and Results Thirty-five patients with a diagnosis of idiopathic cardiomyopathy, comprising 20 patients with dilated cardiomyopathy (DCM) and 15 patients with hypertrophic cardiomyopathy (HCM), underwent overnight polysomnography. Of these 35, 16 (80%) of the DCM patients and 7 (47%) of the HCM patients had sleep-disordered breathing. Central sleep apnea - hypopnea syndrome (CSAHS) was seen in 10 DCM patients, but not in the HCM patients, and obstructive sleep apnea - hypopnea syndrome (OSAHS) was seen in 6 DCM patients and 7 HCM patients. CSAHS was seen in DCM patients with a low left ventricular ejection fraction. HCM patients with OSAHS had a significantly greater body mass index (BMI) than those without OSAHS and CSAHS (27.6±3.8 vs 22.0 ±4.0 kg/m2, p

A 49-year-old man with syringomyelia and a Type I Arnold-Chiari malformation (Chiari-I) was diagnosed with growth hormone insensitivity syndrome (GHIS). He was short in stature, had high circulating levels of GH, and low circulating levels of insulin-like growth factor-I (IGF-I) and IGF binding protein-3 (IGFBP-3). His GH responses to the administration of growth hormone-releasing hormone (GHRH) and L-DOPA were normal, but his levels of IGF-I and IGFBP-3 did not increase after the administration of exogenous GH. Direct genomic DNA sequencing revealed neither a mutation nor deletion in this patient's GH receptor (GHR) gene, though one polymorphism was detected, indicating that his GHR gene was normal. This is the first reported case of an association of GHIS with syringomyelia and Chiari-I malformation.

In six patients with chronic bradydysrhythmias, polysomnographies were performed before cardiac pacemaker implantation and over the week following implantation. A patient with third-degree atrioventricular block (AVB) and two patients with sinus node dysfunction (SND) were associated with sleep-disordered breathing (SDB). Their cardiac pacemaker therapies, with the increase in the average heart rate, led to a reduction of apnea-hypopnea index and/or an improvement of Cheyne-Stokes breathing. It seems that chronic bradydysrhythmia is one of the causative factors leading to SDB.

Four of the 708 snorers (0.56%), referred to our sleep breathing disorders clinic for the past 2 years were diagnosed as having narcolepsy-cataplexy. Detecting HLA DRB1*1501/DQB1*0602 positive was informative for differentiating genuine narcolepsy from non-sleep apnea syndrome (non-SAS) hypersomnia in our clinic. A non-SAS obese boy, diagnosed as having essential hypersomnia syndrome, was found to be HLA DRB1*1502/DQB1*0601 positive. His hypocretin concentration was 206 pg/mL in the cerebrospinal fluid.

Seven patients (one man and six women) with a diagnosis of pulmonary thromboembolism (PTE) were examined by polysomnography in order to clarify the relationship between sleep-related breathing disorders and PTE. In the chronic stage of PTE, sleep apnea syndrome (SAS) was recognized in two patients (a man and a woman) among the subjects. Four of the five patients without SAS showed nocturnal hypoxemia. The female predominance was different from ordinary SAS without the disease background of PTE even though PTE is accompanied by hypoxemia and pulmonary hypertension like SAS. A pathophysiological relationship between PTE and SAS was not found in this study.

The concentration of unextracted urinary arginine vasopressin (UAVP) was directly measured by high-sensitive radioimmunoassay (AVP-RIA Kit, Mitsubishi Petrochemical Co., Ltd.). Urine was diluted to eliminate interference of nonspecific substance without prior extraction. When urine aliquots were diluted in 4 to 32 fold in assay buffer, the relationship between UAVP concentration and dilution ratio corresponded exactly in a linear regression line. The elution pattern on Sephadex G-25 of UAVP immunoreactivity was identical with that of synthesized AVP. The AVP concentration in unextracted urine was not significantly different from that of extracted urine by Sep-Pak C18 column (Water Associates, Milford MA). The mean recovery of added AVP to urine specimens was 101.1 +/- 9.8% (mean +/- SD). The immunoreactivity of UAVP was not modified by either albuminuria (50 and 100 mg/dl) or glycosuria (1000 g/dl). Mean coefficients of variance between-assay and within-assay were 8.3% and 6.6% respectively. In normal subjects (n = 28), significant correlation was observed between UAVP concentration and simultaneously measured plasma AVP (r = 0.701, p less than 0.001). Moreover, AVP concentration in random urine was significantly correlated with AVP excretion in 24 hr-urine (r = 0.703, p less than 0.05, n = 9), and this suggested that random UAVP concentration may indicate daily UAVP secretion. In normal subjects, AVP concentration in random urine was widely scattered from 9.2 to 470.6 pg/mg Cr (89.5 +/- 76.4 pg/mg Cr, n = 211). In patients with diabetes insipidus (DI), UAVP concentration (1.6 to 13.0 pg/mg Cr, 6.94 +/- 2.77 pg/mg Cr, n = 25) was significantly lower (p less than 0.001) than that of normal subjects. UAVP concentration in a patient with primary polydipsia (43.2 pg/mg Cr) was not similar to that of ID but to that of normal subjects. UAVP concentration in 2 patients with SIADH was not more than that of normal subjects, indicating that random UAVP concentration is not suitable for detecting inappropriate AVP secretion. In this study, it is suggested that patients of random UAVP concentration below 13.0 pg/mg Cr should be recommended other intensive examination to diagnose DI, even though 2 normal subjects (0.9%) were incorrectly estimated as DI. In conclusion, radioimmunoassay of AVP in unextracted random urine is easy to sample and assay, and useful in screening polyuric patients.

In order to reduce ship operating costs for large oil tankers, it is effective to burn crude oil as a fuel. For this purpose, the authors have performed tests of burning many sorts of crude oil for diesel engines. The results obtained for the combustibility of crude oil with engines were good and the availability of crude oil as a fuel for diesel engines was proved. As known already, crude oil is available for boilers as a fuel. However, it has not become popular in practice on accounting the hazard of flamability by its gasified disposition. Accordingly, the authors carried out extended works for the hazard evalution in the case of using crude oil in practice and for the means of burning crude oil safely. As the results, the density of flamable gases leaked from the fuel piping was less than expectation even in the vicinity of engines.Also, it was evident that crude oil can replace residual oil as a fuel sufficiently if the proper way is taken into account

Multiple diesel engine systems combined with several medium-speed engines have been recently developed as a propulsion system for ocean-going vessels.If bunker oil can be used satisfactorily as a fuel for these medium-speed engines, the operation cost of ships would be more reduced. However, the test of bunker oil as a fuel heated up to high temperature has not been examined yet for this type diesel engine by this time.This paper describes experiments to investigate the effect of fuel temperature on combustion for diesel engines.The results present that the fuel consumption and the exhaust temperature of the engine are increased with raising fuel temperature up, on the contrary of the authors expectation.An analysis is also made of these results.