The value of frequent positioning of treatment field in radiotherapy of esophageal cancer]

Since 1983 a clinical trial of proton beam radiotherapy has been conducted at the Proton Medical Research Center (PMRC) of the University of Tsukuba. We have made it a rule to do field localization by X-ray pictures before each treatment. For this purpose we have developed a localize-verify system consisting of a fluoroscopic unit and a real time digital image processing device. By using this system as well as X-ray films, field placement errors or corrected distance at field localization were measured in 11 patients with esophageal cancers. Measurements of corrected distances on a total of 177 localization attempts disclosed that correction by > 5 mm was necessary in 30.6% and by > 10 mm in 10.2% of all localization attempts. Corrected distances appeared to increase with age, possibly because the skin becomes looser and ambulatory status tends to be more limited in older patients. Field placement corrections of more than 5 mm were required in 66.7% of 60 localizations in patients > 80 years old. Two patients in whom the anatomical positions of the esophagus were easily movable are presented. The following common characteristics of these patients were considered high risk factors: they were more than 80 years old; lesions were located in the lower esophagus; and they had T1 tumors. These findings suggested that frequent positioning and verification of treatment fields are necessary in the accurate treatment of esophageal cancers, especially those in high-risk patients.     

Treatment of central giant cell lesions using bisphosphonates with intralesional corticosteroid injections

ABSTRACT: Central giant cell lesions are benign intraosseous proliferative lesions that have considerable local aggressiveness. Nonsurgical treatment methods, such as intralesional corticosteroid injections, systemic calcitonin and interferon have been reported. Recently, bisphosphonates have been used to treat central giant cell lesions. A case of a 36-year-old male with a central giant cell lesion crossing the mandibular midline was treated with intralesional corticosteroids combined with alendronate sodium for the control of systemic bone resorption. The steroid injections and the use of bisphosphonates were stopped after seven months when further needle penetration into the lesion was not possible due to new bone formation. After two years, the bony architecture was near normal, and only minimal radiolucency was present around the root apices of the involved teeth. The patient was followed up for four years, and panoramic radiography showed areas of new bone formation. Thus far, neither recurrence nor side effects of the medication have been detected.     

Dissecting aneurysm of the anterior cerebral artery with later development of collateral circulation: a case report

Intracranial dissecting aneurysm (DA) is much less frequent than berry aneurysm. Such dissection involves mostly the vertebral and basilar arteries, followed by the internal carotid and middle cerebral arteries. DA of the anterior cerebral artery (ACA) is relatively rare and little is known about its natural Development. Only 23 cases have been reported previously. Our present patient, a 44-year-old man, suddenly developed paresis of the left leg while bathing. Diffusion magnetic resonance imaging indicated an area of high signal intensity in the territory of the ACA. Angiography on day 3 following onset showed a DA involving the left A2 segment. Antiplatelet therapy was administered. Further luminal narrowing in the lesion was demonstrated by repeat angiography on day 17. Occlusion of the distal A2 segment was demonstrated together with sufficient collateral supply on day 41. Symptoms resolved completely. DA of the ACA usually presents with ischemic attacks. Its etiology remains uncertain, and its natural course is unclear. Surgical intervention is recommended for patients with intracranial hemorrhage, while non surgical therapies have achieved good outcomes in ischemic cases.     

Patulous eustachian tube following otitis media

Loss of weight, dehydration, pregnancy, fatigue, and otitis media are among the factors proposed as causes of a patulous eustachian tube, but true details remain obscure. We studied patients who developed a patulous eustachian tube following otitis media and discuss the relationship between these 2 conditions. Subjects were 12 patients diagnosed with otitis media at our department who later developed a patulous eustachian tube. The initial middle ear disease progressed from acute otitis media to otitis media with effusion in 2, acute otitis media in or acute mastoiditis in 1 each, and otitis media with effusion in the remaining 8 patients. Seven patients evidenced a low body mass index (BMI), weight loss, and underlying disease, but 5 with a patulous eustachian tube following otitis media did not. We retrospectively analyzed 119 patients diagnosed with a patulous eustachian tube in our department for whether they had been diagnosed by an ENT physician as having otitis media, i.e., acute otitis media or otitis media with effusion. Some 42 (35.3%) had a history of otitis media. At acute otitis media or otitis media with effusion, the tympanic cavity becomes inflamed, accompanied by inflammation of the eustachian tube mucosa and a stenotic tendency. Healing from otitis media is accompanied by decreased eustachian tube mucosa inflammation. We surmise that, depending on how inflammation disappears, fibrosis of the eustachian tube mucosa occurs, leading to a pathologically patulous eustachian tube. Many aspects of the causation of this condition remain unclear, but we surmised that in patients with earlier otitis media, a pathological patulous eustachian tube develops during resolution of inflammation. Our findings indicate the involvement of otitis media as a causative factors in a patulous eustacian tube.     

Effects of a low dose of indapamide, a diuretic, given daily or every-other-day on blood pressure and metabolic parameters.

To investigate the effects of the diuretic, indapamide, on blood pressure (BP) and metabolic parameters, thirty hypertensive patients were treated with 1 mg of indapamide either every day or every other day. BP, fasting plasma glucose, lipids, serum potassium and uric acid were determined at baseline and after 3 months of a stable regimen of the drug. At the termination of the study, 48-h ambulatory blood pressure monitoring (ABPM) was performed. Three patients received only indapamide, while other patients were treated in combination with additional antihypertensive medications. Patients treated with daily indapamide showed a BP reduction from 162 +/- 2.9/85 +/- 2.4 mmHg to 134 +/- 2.4/71 +/-2.6 mmHg (p < 0.001). The BP reduction was similar in those patients receiving the drug every other day (137 +/- 3.4/71 +/- 3.6 mmHg). While plasma lipids and serum potassium did not differ significantly with the intervention, uric acid increased significantly with daily treatment and normalized with every-other-day treatment. Glycosylated hemoglobin A1c (HbA1c) was not altered (5.6 +/- 0.1% vs. 5.4 +/- 0.2%), and did not differ between patients with and without diabetes mellitus. ABPM revealed an average 24-h BP of 134 +/- 3.3/75 +/- 1.7 mmHg on days in which patients received the medication and 139 +/- 4.9/78 +/- 2.6 mmHg on the intervening day without indapamide (no significant difference). These results suggest that a low dose of indapamide given every day or every other day is effective in lowering BP and does not result in metabolic derangements.     

High prevalence of equine-like G3P[8] rotavirus in children and adults with acute gastroenteritis in Thailand

Group A rotavirus (RVA) is a major cause of acute gastroenteritis in infants and young children worldwide. This study aims to clarify the distribution of G/P types and genetic characteristics of RVAs circulating in Thailand. Between January 2014 and September 2016, 1867 stool specimens were collected from children and adults with acute gastroenteritis in six provinces in Thailand. RVAs were detected in 514/1867 (27.5%) stool specimens. G1P[8] (44.7%) was the most predominant genotype, followed by G3P[8] (33.7%), G2P[4] (11.5%), G8P[8] (7.0%), and G9P[8] (1.3%). Unusual G3P[9] (0.8%), G3P[10] (0.4%), G4P[6] (0.4%), and G10P[14] (0.2%) were also detected at low frequencies. The predominant genotype, G1P[8] (64.4%), in 2014 decreased to 6.1% in 2016. In contrast, the frequency of G3P[8] markedly increased from 5.5% in 2014 to 65.3% in 2015 and 89.8% in 2016. On polyacrylamide gel electrophoresis, most (135/140; 96.4%) of the G3P[8] strains exhibited a short RNA profile. Successful determination of the nucleotide sequences of the VP7 genes of 98 G3P[8] strains with a short RNA profile showed that they are all equine-like G3P[8] strains. On phylogenetic analysis of genome segments of two representative Thai equine-like G3P[8] strains, it was noteworthy that they possessed distinct NSP4 genes, one bovine-like and the other human-like. Thus, we found that characteristic equine-like G3P[8] strains with a short RNA electropherotype are becoming highly prevalent in children and adults in Thailand.     

Heme oxygenase-1 in vascular smooth muscle cells counteracts cardiovascular damage induced by angiotensin II

Heme oxygenase (HO) is a microsomal enzyme that catalyzes the degradation of heme into biliverdin, which is subsequently reduced to bilirubin, free iron and carbon monoxide (CO), and induction of heme oxygenase-1 (HO-1) is potentially associated with cellular protection, especially against oxidative insults. Using transgenic mice that overexpress HO-1 (HO-1 Tg) specifically in vascular smooth muscle cells, we investigated the organ-protective effects of HO-1 against angiotensin II (Ang II). Following administration of Ang II and a high- salt diet for 14 days, marked intimal hyperplasia as well as inflammatory changes were observed in coronary arteries of Ang II/salt-treated wild type (Wt) mice. In Wt mice, Ang II/salt loading increased urinary excretion of 8- hydroxydeoxyguanosine (8-OHdG) and 8-lso-Prostaglandin F2 alpha. Cardiac levels of MDA and 4-HAE, markers of lipid peroxidation, and GSSG/GSH were also increased in Wt. mice after Ang II/salt loading, but not in HO-1 Tg mice. Consistently, immunostaining for both 8-0HdG, a marker of oxidative DNA damage, and 3-nitrotyrosine, the metabolites of reactive oxygen species, were apparently increased in the Ang II/salt-treated heart of Wt. mice; however, no significant changes in these responses were detected in HO-1 Tg mice after Ang II/salt loading. These data suggest that increased oxidative stress might be involved in the coronary artery changes induced by Ang II/salt loading. The evidence presented in the current study indicates that vascular HO-1 exerts its protective effect against cardiovascular damage, possibly through the inhibition of oxidative stress.     

Functional disorders of the oxidative phosphorylation system in the heart mitochondria of mice with juvenile visceral steatosis

Mice with juvenile visceral steatosis (JVS) develop remarkable cardiac hypertrophy and exhibit an increased number of mitochondria in their heart. However, the biochemical characteristics and physiological functions of these mitochondria cardiac are little known. Here we show that the respiratory activities at state 3 with glutamate plus malate or succinate in the heart mitochondria of JVS mice were greatly decreased to 47% or 77%, respectively, compared with those of control mice. The contents of cytochromes a+a(3), b, and c+c(1) in the heart mitochondria of these mice were also decreased, to 51%, 45%, and 79%, respectively, of those of the control mice. Oligomycin-sensitive ATPase activitiy in these mitochondria, however, was increased to about 2 times over that of the control mice. Surprisingly, the ATP-Pi exchange activity of the heart mitochondria of JVS mice was greatly decreased, to 35% of that of control mice. On the other hand, the expression levels of 2 subunits of H(+)-ATP synthase, i.e., coupling factor 6 and alpha subunit, in heart mitochondria from control and JVS mice were almost the same. These results indicate that the coordinate regulation of mitochondrial proliferation and gene expression for components of the oxidative phosphorylation system was markedly defective in the heart of JVS mice. Our current results also suggest the presence of a novel regulatory mechanisms of ATP synthase activities in the heart.