Maxillary single-jaw surgery combining Le Fort I and modified horseshoe osteotomies for the correction of maxillary excess.

A modified technique of horseshoe osteotomy combined with Le Fort I osteotomy for superior and posterior repositioning of the maxilla is presented. Eight patients with maxillary excess associated with retrogenia or microgenia were treated with this technique in combination with genioplasty. The maxillary segment was repositioned a maximum of 5.0mm posteriorly and 7.0mm superiorly at point A. The mandible autorotated anterosuperiorly to achieve sound occlusion. Point B moved 2.0-10.0mm anteriorly and 5.0-10.0mm superiorly. The pogonion moved 7.0-17.0mm anteriorly in combination with genioplasty. All patients obtained sound occlusion and a good profile after the operation. Almost no skeletal relapse was observed during 1 year of postoperative follow-up. Patients with long faces with maxillary excess and retrogenia often have small, unstable condyles. In these cases, because surgical intervention to the ramus can result in postoperative progressive condylar resorption, maxillary single-jaw surgery with a horseshoe osteotomy, thereby avoiding ramus intervention, is a less invasive option.

Transgenerational transmission of radiation- and chemically induced tumors and congenital anomalies in mice: studies of their possible relationship to induced chromosomal and molecular changes.

This article provides a broad overview of our earlier studies on the induction of tumors and congenital anomalies in the progeny of X-irradiated or chemically treated mice and our subsequent (published, hitherto unpublished and on-going) investigations aimed at identifying potential relationships between genetic changes induced in germ cells and the adverse effects manifest as tumors and congenital anomalies using cytogenetic and molecular approaches. The earlier studies document the fact that tumors and congenital anomalies can be induced by irradiation or treatment with certain chemicals such as urethane and that these phenotypes are heritable i.e., transmitted to generations beyond the first generation. These findings support the view that transmissible induced genetic changes are involved. The induced rates of congenital abnormalities and tumors are about two orders of magnitude higher than those recorded in the literature from classical mutation studies with specific locus mutations. The cytogenetic studies addressed the question of whether there were any relationships between induced translocations and induced tumors. The available data permit the inference that gross chromosomal changes may not be involved but do not exclude smaller induced genetic changes that are beyond the resolution of the techniques used in these studies. Other work on possible relationship between visible chromosomal anomalies (in bone marrow preparations) and tumors were likewise negative. However, there were indications that some induced cytogenetic changes might underlie induced congenital anomalies, i.e., trisomies, deletions and inversions were observed in induced and transmissible congenital anomalies (such as dwarfs, tail anomalies). Studies that explored possible relationships between induction of minisatellite mutations at the Pc-3 locus and tumors were negative. However, gene expression analysis of tumor (hepatoma)-susceptible offspring of progeny descended from irradiated male mice showed abnormal expression of many genes. Of these, only very few were oncogenes. This lends some support to our hypothesis that cumulative changes in gene expression of many genes, which perform normal cellular functions, may contribute to the occurrence of tumors in the offspring of irradiated or chemically treated mice.

Ultrasonographic assessment of regional differences in atherosclerotic lesions in patients with hypertension, diabetes mellitus, or both.

We evaluated risk factors involved in regional differences in atherosclerotic lesions in patients with hypertension, diabetes mellitus, or both. Using ultrasonography, we examined the brachial, common carotid, and common femoral arteries in 65 hospitalized Japanese patients (15 controls, 18 patients with hypertension, 16 with diabetes mellitus, and 16 with both hypertension and diabetes mellitus). They ranged in age from 39 to 81 yr, mean 60.3 yr. The thickness of the intima-media complex of the far wall was measured, and the severity of atherosclerotic plaques was graded according to maximal lumen stenosis. The intima-media thickness in the carotid and femoral arteries was significantly greater in the hypertensive patients and the hypertensive patients with diabetes than in the controls. Severity of plaque was greater in the hypertensive patients with diabetes than in the controls. Plaque grades were higher in the carotid and femoral arteries than in the brachial artery. Multiple regression analysis revealed that age and mean blood pressure were strongly associated with the intima-media thickness in all three arteries. In the femoral artery, cigarette smoking and hyperglycemia also significantly correlated with the intima-media thickness. Plaque grades increased with age in the carotid and brachial arteries, while in the femoral artery the grade increased with cigarette smoking and serum cholesterol concentration. These findings suggest that the extent of atherosclerosis and its underlying risk factors differ among arterial sites. In addition, risk factors may partly differ according to the stage of atherosclerosis. To prevent or reverse atherosclerosis, the above differences should be taken into account.

Circadian blood pressure variation in non-insulin-dependent diabetes mellitus with nephropathy.

We studied a circadian blood pressure variation in relation to the progression of diabetic nephropathy in patients with non-insulin-dependent diabetes mellitus (NIDDM). Age, duration of diabetes, body mass index and glycemic control did not differ among the groups of patients with normo-, micro- and macroalbuminuria. None of the patients received antihypertensive drugs. There were no differences in renal and autonomic functions between normo- and microalbuminuric groups, but these functions were impaired in the macroalbuminuric group. The rise in blood pressure was more apparent in 24-h ambulatory blood pressure (AMBP), especially during night-time, as compared with casual blood pressure. Such blood pressure rise was in accordance with the progression of nephropathy. However, pulse rate did not differ among the three groups. The nocturnal fall in blood pressure was blunted in the micro- and macroalbuminuria groups, but evident in the normoalbuminuric group. In the latter, daytime systolic blood pressure (SBP) was significantly higher than night-time SBP (123 +/- 5 mmHg vs. 113 +/- 3 mmHg, P = 0.002). In contrast, in the former two groups of patients, there were no significant differences in SBP between daytime and night-time (134 +/- 9 mmHg vs. 134 +/- 9 mmHg, ns, for microalbuminuria and 159 +/- 8 mmHg vs. 165 +/- 7 mmHg, ns, for macroalbuminuria). Urinary albumin excretion was significantly correlated with night-time SBP (r = 0.48, P = 0.015), but not with daytime SBP (r = 0.30, ns).(ABSTRACT TRUNCATED AT 250 WORDS)

[A case of Weber's syndrome due to gradual expansion of a basilar bifurcation aneurysm].

We report an 82-year-old female who developed Weber's syndrome following gradual expansion of a basilar bifurcation aneurysm. The patient first developed subarachnoid hemorrhage at the age of 78. Cerebral angiography showed an intracranial aneurysm of 1 cm diameter at the bifurcation of the basilar artery. Three years later, the patient was readmitted because both CT and MRI at that time revealed that the lumen of the aneurysm was filled with an organizing thrombus. On her third admission at the age of 82, the diameter of the aneurysm was expanded to 2.5 cm and Weber's syndrome had developed. On T2-weighted MRI, a central low-intensity area surrounded by a high-intensity zone were evident in the aneurysm, suggesting the formation of an organized or organizing thrombus. Repeated MRI examinations are useful for following the expansion of a thrombosed aneurysm.

Circadian blood pressure in patients in a persistent vegetative state.

We examined circadian variations in blood pressure, pulse rate, and other physiological variables, including hormone levels, in 16 patients in a persistent vegetative state (mean age -/+ SE; 66.1 -+/ 3.9 yr). Cerebrovascular accident was responsible for brain damage in 12 (75%) of the 16 patients. Blood pressure was measured for 24 h with an ambulatory blood pressure monitoring device. We monitored the temperature of the urinary bladder and measured urinary excretion of epinephrine, norepinephrine, 17-hydroxycorticosteroids, water, and sodium. When data were analyzed by analysis of variance, significant circadian changes were observed in body temperature and urinary excretion of hormones and sodium, but not in blood pressure or pulse rate. Individual analysis of rhythmicity using the cosinor method detected small but significant circadian variations in blood pressure and pulse rate in five of six patients who showed a simple organized response to noxious external stimuli. The disappearance of variation in blood pressure in patients in a vegetative state appeared to be related, in part, to the lack of response to external stimuli. Our findings suggest that the circadian variation in blood pressure may largely depend on external environmental factors.

Characterization of a mutant E-cadherin protein encoded by a mutant gene frequently seen in diffuse-type human gastric carcinoma.

The cell-cell adhesion molecule E-cadherin plays an essential role in the maintenance and function of epithelial tissues. Altered expression of E-cadherin has been implicated in tumor invasion. Analysis of mutations of the human E-cadherin gene in gastric carcinoma of the diffuse type has revealed that deletion of exon 8 or 9 in its cDNA appears to be predominant. In this study, we carried out structural and functional analyses of a mutant form of E-cadherin in a cell line, HSC45-M2, established from a human signet ring-cell carcinoma. Although immunohistochemical analysis showed that the mutant cadherin was localized at cell-cell contact sites as usually seen with the wild type, these cells did not form compact colonies. HSC45-M2 cells expressed aberrant E-cadherin with an m.w. larger than that of the wild type. In these cells, we found deletion of the exon 9-intron 9 boundary including the splicing donor site in E-cadherin genomic DNA. RT-PCR indicated 2 transcripts, which appeared to be caused by the splicing defect. Northern blotting, however, showed that the transcript lacking exon 9 was predominantly detected in these cells. The electrophoretic mobilities on SDS-PAGE of the mutant E-cadherin protein in HSC45-M2 cells and the protein expressed from cDNA lacking exon 9 appeared identical. Analysis of the amino-terminal region of the mutant E-cadherin protein revealed that the cadherin was capable of becoming a mature form by removal of its amino-terminal peptide. However, the mutant E-cadherin was susceptible to trypsinization in the presence of Ca(2+), which is not the case for wild-type E-cadherin, suggesting that the mutant E-cadherin frequently found in diffuse-type gastric carcinoma may have lost its Ca(2+)-binding ability, leading to disruption of the tight cell-cell association.

Evaluation of prostaglandin D2 (PGD2) as an anticoagulative agent for haemodialysis in comparison with prostaglandin E1 (PGE1).

Prostaglandin D2 (PGD2), a potent antiplatelet agent, was evaluated as an antithrombotic agent for haemodialysis in comparison with prostaglandin E1 (PGE1) and prostaglandin I2 (PGI2). When antiplatelet action was evaluated, taking the degree of associated hypotension into consideration, PGD2 was found to be superior to PGE1 and PGI2 as the latter two had the negative effect of inducing hypotension, while PGD2 had a less hypotensive effect. The suppression of the platelet function by PGD2 was observed to have only a slight influence on platelet function in systemic blood.

Regression of carotid wall thickening after corticosteroid therapy in Takayasu's arteritis evaluated by B-mode ultrasonography: report of 2 cases.

We describe 2 young Japanese female patients with active Takayasu's arteritis whose diagnosis was mainly based on the characteristic ultrasonographic finding, that is, a circumferential vascular wall thickening in common carotid arteries. Following corticosteroid therapy, serial ultrasonographic examination documented the improvement of their thickened carotid walls (in Case 1 from 1.4 to 0.5 mm after 2 months of therapy, in Case 2 from 1.5 to 0.9 mm after 9 months of therapy). These cases emphasize that ultrasonography is useful for evaluation of the therapeutic effect as well as for the diagnosis of Takayasu's arteritis in its early stage.