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To clarify the relationship between dose-volume histogram (DVH) parameters and radiation pneumonitis (RP) after surgery in cases of non-small cell lung cancer (NSCLC) treated with induction concurrent chemoradiotherapy (CCRT). Patients with NSCLC treated with induction CCRT (chemotherapy: cisplatin and docetaxel; radiotherapy: 2.0 Gy fractions once daily for a total of 46 Gy) before surgery were reviewed. We calculated the percentage of lung volume receiving at least 20 Gy (V20) and the mean lung dose (MLD) for the total lung volume and the lung remaining after resection. Factors affecting the incidence of RP at grade 2 or higher (≥ G2 RP) were analyzed. Eighteen of 49 patients (37%) experienced ≥G2 RP. The V20 and MLD for the lung remaining after resection (V20r and MLDr) were significant predictors according to the multivariate analysis (p=0.007 and 0.041, respectively). The incidence of ≥G2 RP was 8% in patients with V20r

To investigate the relation between thrombolysis in myocardial infarction (TIMI) frame count (TFC) and coronary blood flow velocity (CBFV) parameters reflecting the degree of microvascular injury in patients with acute myocardial infarction.TFC and CBFV were measured after primary coronary angioplasty in 103 consecutive patients with their first anterior wall acute myocardial infarction. TFC correlated inversely with the averaged peak velocity (r = -0.43, p0.0001). However, TFC did not correlate significantly with diastolic deceleration time and with the averaged systolic peak velocity (r = -0.16, p = 0.22, and r = -0.23, p = 0.16, respectively). The patients were divided into two groups according to presence (35 patients) or absence (68 patients) of systolic flow reversal. There was no significant difference in TFC between the two groups (29 (16) v 25 (13), p = 0.20).These findings suggest that the TFC reflects epicardial CBFV. However, it is not accurate enough to assess the degree of microvascular injury after primary coronary angioplasty.

Purpose Mastermind-like domain containing 1 (MAMLD1) is a causative gene for the fetal development of male external genitalia. Almost 10% of patients with both severe and non-severe hypospadias exhibit mutations of MAMLD1. The aim of this work was to determine whether polymorphisms of MAMLD1 are a genetic risk factor for hypospadias. Material and methods This study included 150 hypospadias with a range of severities and 150 controls. Direct sequencing of the MAMLD1 coding exons and their flanking splice sites was performed. In silico secondary and tertiary structure prediction and accessibility of changed amino acids were evaluated using JPred, Netsurf and PHYRE software. Functional studies of the transactivation of haplotypes on Hes3 promoter were performed in vitro using cDNAs of missense variants of MAMLD1. Results The p.P286S polymorphism was identified in 17/150 patients and 12/150 controls (11.3% vs. 8.0%, p = 0.32). The p.N589S polymorphism was identified in 22/150 patients and 12/150 controls (14.6% vs. 8.0%, p = 0.068). The double polymorphism (S-S haplotype) was present in 16/150 patients and 6/150 controls (10.6% vs. 4.0%, p = 0.044, OR = 2.87, CI from 1.09 to 7.55). The association of polymorphisms consistently revealed a modification in the structure prediction or amino acid accessibility in all three in silico models. The P286S, N589S and P286S + N589S proteins did not exhibit reduced transactivating activity on Hes3 promoter. Conclusion Polymorphisms of MAMLD1 gene are frequent in patients with hypospadias. Although no change in transactivation was noted on Hes3 promoter, the in silico studies and the significantly increased incidence of the S-S haplotype in hypospadiac patients raise the hypothesis of a particular susceptibility conferred by these variants.

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The oxyntic, or parietal cell has two characteristic membrane systems. The mammalian intracellular canaliculi are specialized networks of narrow channels lined with numerous microvilli. The other common to al1 oxyntic cells is the tubulovesicles, a system of tubules and vesicles. The tubulovesicular compartment is drastically depleted during maximal gastric acid secretion and this is coincident with an increase in the cell surface membrane area. A plausible explanation of this process is the fusion and transfer of tubulovesicular membranes to the plasma membrane. However, for many years there was no convincing evidence of the connections between these two membrane systems. How the tubulovesicular membranes transform into plasma membrane without demonstrable connections has been an enigma to electron microscopists. Recent ultra-high resolution scanning electron microscopic observations on the rat oxyntic cell treated with aldehyde-osmium-aldehyde method revealed that in the resting stage, the tubulovesicles were isolated spherical vesicles. But after tetragastrin stimulation, they were interconnected by slender connecting tubules forming a tubulovesicular network. Then this network was fused to the intracellular canaliculus at relatively few points. These connections between the tubulovesicles and luminal surface membrane was also demonstrated in the frog oxynticopeptic cells. In this review, these membrane transformations as well as changes of the H+/K+-ATPase, the lectin binding glycocalyx and the cytoskeleton during secretion will be illustrated and discussed.

A simultaneous operation was successfully performed on a 70-year-old man with recurrent aortic arch aneurysm and squamous cell carcinoma of the lung. Via a left thoracotomy, left lower lobectomy with lymph node resection was performed, and via the same incision, aneurysmectomy with graft replacement was performed under the hypothermic cerebral circulatory arrest. The patient was readmitted because of brain metastasis 10 months later, and died 11 months postoperatively. The present report suggests that selected cases of thoracic aortic aneurysm with malignant tumor are safely able to undergo simultaneous operations. This is the first report in Japan of aortic arch aneurysmectomy and lobectomy performed during the course of one operation.

In 1988 the authors surveyed all the teaching hospitals in Japan to evaluate the present status of postgraduate medical education (PGME); they received responses from 67 (84%) of the university and 172 (89%) of the non-university teaching hospitals. It was found that a large proportion of residents had spent two years in a residency without having had a single experience of some of the basic clinical skills. Consequently the residents' confidence in their abilities to perform these skills was low. The residents at the university hospitals, in particular, had had fewer experiences and were less confident about their clinical skills than were the residents at the non-university hospitals. The lack of standard and minimum requirements for PGME in Japan may be the cause of the poor level of acquisition of clinical skills of residents during PGME. Other possible causes are the tendency in Japanese medical society to attach greater importance to academic attainment than to clinical competence and the excessive gravitation of residents toward university hospitals. The authors suggest their results show the necessity to improve the training in basic clinical skills in PGME in Japan, especially in university hospitals.

A neurofibroma originated from the intrathoracic vagal nerve was presented. A 26-year-old male was found to have an abnormal shadow in the right chest filed on a routine examination. He was complicated with Von Recklinghausen's disease and showed multiple "cafe au lait" spots over his extremities and trunk but no subcutaneous mass. A block resection of the mass was carried for the mediastinal tumor. The tumor was arising from the right intrathoracic vagal nerve which located just below the origin of recurrent nerve and was measured 3 X 3 X 6 cm. Histological examination of the specimen revealed neurofibroma. His postoperative course was uneventful. A brief review in Japan was made on 22 cases collected from the literature.

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X-linked nonspecific mental retardation (MRX) has a frequency of 0.15% in the male population and is caused by defects in several different genes on the human X chromosome. Genotype-phenotype correlations in male patients with a partial nullisomy of the X chromosome have suggested that at least one locus involved in MRX is on Xp22.3. Previous deletion mapping has shown that this gene resides between markers DXS1060 and DXS1139, a region encompassing approximately 1.5 Mb of DNA. Analyzing the DNA of 15 males with Xp deletions, we were able to narrow this MRX critical interval to approximately 15 kb of DNA. Only one gene, VCX-A (variably charged, X chromosome mRNA on CRI-S232A), was shown to reside in this interval. Because of a variable number of tandem 30-bp repeats in the VCX-A gene, the size of the predicted protein is 186-226 amino acids. VCX-A belongs to a gene family containing at least four nearly identical paralogues on Xp22.3 (VCX-A, -B, -B1, and -C) and two on Yq11.2 (VCY-D, VCY-E), suggesting that the X and Y copies were created by duplication events. We have found that VCX-A is retained in all patients with normal intelligence and is deleted in all patients with mental retardation. There is no correlation between the presence or absence of VCX-B1, -B, and VCX-C and mental status in our patients. These results suggest that VCX-A is sufficient to maintain normal mental development.