Comparison of quality of life and psychological distress in patients with tongue cancer undergoing a total/subtotal glossectomy or extended hemiglossectomy and free flap transfer: a prospective evaluation.

The aim of this study was to assess changes in the quality of life and psychological distress of patients with tongue cancer undergoing total/subtotal glossectomy (TG) or extended hemiglossectomy (HG) and free flap transfer. Differences between the two groups were compared using the Short Form 8-Item Health Survey (SF-8) and Hospital Anxiety and Depression Scale (HADS). Of the 43 patients with tongue cancer, 24 (56%) underwent TG and 19 (44%) underwent HG. The general health and social functioning scores in the SF-8 and depression in the HADS were significantly worse in the TG group than in the HG group at 12 months after surgery, indicating that patients in the TG group may experience social isolation and psychological distress, and have difficulty in employability even 12 months after surgery. In contrast, all items of the SF-8 in the HG group were nearly equal to those in the general population. Due to the extensive psychological impact on patients with tongue cancer who are planned for an extended resection, curative surgery with free flap transfer and multidisciplinary psychiatric support are essential to improve quality of life and manage psychological distress.

Field test of quantum key distribution in the Tokyo QKD Network.

A secure communication network with quantum key distribution in a metropolitan area is reported. Six different QKD systems are integrated into a mesh-type network. GHz-clocked QKD links enable us to demonstrate the world-first secure TV conferencing over a distance of 45km. The network includes a commercial QKD product for long-term stable operation, and application interface to secure mobile phones. Detection of an eavesdropper, rerouting into a secure path, and key relay via trusted nodes are demonstrated in this network.

Histopathological manifestations of membranoproliferative glomerulonephritis and glomerular expression of plasmalemmal vesicle-associated protein-1 in a patient with polycythemia vera.

Only a few cases of various glomerulonephropathies have been reported in patients with polycythemia vera. We report the case of a 72-year-old female with polycythemia vera in whom renal biopsy examination showed membranoproliferative glomerulonephritis (MPGN)-like lesion and glomerular expression of plasmalemmal vesicle-associated protein-1 (PV-1), a marker of glomerular capillary remodeling after injury. Prior to admission to our hospital for nephrotic syndrome, she had received hydroxyurea and phlebotomy. On admission, she was hypertensive with pretibial edema, hepatosplenomegaly, massive proteinuria (6.14 g/day), low serum albumin (2.9 g/dl), high fibrinogen, fibrin/fibrinogen degradation products and thrombomodulin levels, but with normal serum creatinine and complement levels. Microscopic examination of a renal biopsy demonstrated MPGN-like features with double contour and mesangial interposition. Electron microscopy showed subendothelial deposits, platelets attached to glomerular capillary walls and fibrin deposition. Immunofluorescence study identified IgM deposition along part of the capillary wall and mesangium. CD42b-positive platelets and megakaryocytes were detected in glomerular capillaries, accompanied with increased expression of platelet-derived growth factor receptor b and thrombomodulin in the mesangium and glomerular capillary, respectively. PV-1 was expressed along the glomerular capillary. Anti-platelet and anticoagulant combination therapy, together with the use of anti-hypertensive agents and hydroxyurea, resulted in improvement of the nephrotic syndrome. The findings suggested that activated platelets, enhanced coagulation state and endothelial damage may contribute to glomerulonephropathy associated with polycythemia vera.

Interaction of functional FCER2 promoter polymorphism and phenotype-associated haplotypes.

Low-affinity IgE receptor gene (FCER2) rs3760687 polymorphism was found to be associated with differential binding affinity of transcription factors Sp1 and Sp3 leading to altered transcriptional activity. Haplotypic interaction of functional FCER2 polymorphisms (rs28364072, rs2228137 and rs3760687) might potentially provide a background for genotype-phenotype associations previously observed for some rather non-functional FCER2 variants.

Oral medicine psychiatric liaison clinic: study of 1202 patients attending over an 18-year period.

Patients with orofacial pain and discomfort often suffer from psychiatric disorders. However, few studies involving a large sample have examined the diagnostic results of patients with orofacial pain or discomfort in relation to psychiatric disorders. The purpose of this study was to summarize and clarify the characteristics and demographic data of 1202 patients attending the psychiatric liaison clinic at Aichi Gakuin University Hospital. Psychiatric diagnosis was performed by psychiatrists for all patients, based on the Diagnostic and Statistical Manual of Mental Disorders, fifth edition. Among the 1202 patients, 992 (82.5%) were female. The average age of the patients was 57.2±15.0years. The predominant broad categories of orofacial pain and discomfort seen were burning mouth syndrome (n=484, 40.3%), persistent idiopathic facial pain (n=258, 21.5%), and oral dysesthesia (n=215, 17.9%). The predominant broad categories of psychiatric diagnoses seen were somatic symptoms and related disorders (n=934, 77.7%) and depressive disorders (n=76, 6.3%). Among the 934 patients with somatic symptoms and related disorders, 678 had a somatic symptom disorder with predominant pain. The results confirmed that most patients with orofacial pain and discomfort were middle-aged and elderly women suffering from a somatic symptom disorder with predominant pain.

Primary hyperparathyroidism caused by parathyroid-targeted overexpression of cyclin D1 in transgenic mice.

The relationship between abnormal cell proliferation and aberrant control of hormonal secretion is a fundamental and poorly understood issue in endocrine cell neoplasia. Transgenic mice with parathyroid-targeted overexpression of the cyclin D1 oncogene, modeling a gene rearrangement found in human tumors, were created to determine whether a primary defect in this cell-cycle regulator can cause an abnormal relationship between serum calcium and parathyroid hormone response, as is typical of human primary hyperparathyroidism. We also sought to develop an animal model of hyperparathyroidism and to examine directly cyclin D1's role in parathyroid tumorigenesis. Parathyroid hormone gene regulatory region--cyclin D1 (PTH--cyclin D1) mice not only developed abnormal parathyroid cell proliferation, but also developed chronic biochemical hyperparathyroidism with characteristic abnormalities in bone and, notably, a shift in the relationship between serum calcium and PTH. Thus, this animal model of human primary hyperparathyroidism provides direct experimental evidence that overexpression of the cyclin D1 oncogene can drive excessive parathyroid cell proliferation and that this proliferative defect need not occur solely as a downstream consequence of a defect in parathyroid hormone secretory control by serum calcium, as had been hypothesized. Instead, primary deregulation of cell-growth pathways can cause both the hypercellularity and abnormal control of hormonal secretion that are almost inevitably linked together in this common disorder.

Molecular genetic and immunohistochemical study of autosomal recessive Alport's syndrome.

A DNA analysis of autosomal type IV collagen alpha3 and alpha4 chain genes (COL4A3 and COL4A4) and an immunohistochemical study of type IV collagen alpha1 to alpha6 chains were performed in an inbred family with autosomal recessive Alport's syndrome (AS). A linkage study using polymorphic markers around the COL4A3/COL4A4 genes clearly differentiated the affected patients from healthy individuals. These patients were homozygous for all markers analyzed, whereas their parents were heterozygotes. Because of the large size of both the genes and the heterogeneous range of the mutations of these genes, linkage analysis by using highly polymorphic markers is still the method of choice in genetic counseling for autosomal recessive AS, as well as for the X-linked form. Although the distribution of alpha1 and alpha2 chains in the index patient and her affected sister were normal, the alpha3 and alpha4 chains were completely defective in the renal basement membrane (BM). The alpha5 chain could be found in Bowman's capsular basement membrane (BCBM) but not in the glomerular basement membrane (GBM). In addition, our study showed, for the first time, that the alpha6 chain in BCBM is spared in this form of AS. This abnormal pattern of type IV collagen could be a useful tool for differentiation of the autosomal recessive type from the X-linked type of AS.

Plasma and urine levels of adrenomedullin and proadrenomedullin N-terminal 20 peptide in chronic glomerulonephritis.

Proadrenomedullin N-terminal 20 peptide (PAMP) is a novel hypotensive peptide present in the precursor of adrenomedullin (AM), a vasodilative and natriuretic peptide. We examined the plasma and urinary levels of these peptides in patients with chronic glomerulonephritis (CGN). The mean plasma AM concentration of the patients with CGN did not differ from that of control subjects (4.17 +/- 0.17 v 3.87 +/- 0.21 fmol/mL, respectively), whereas urinary AM excretion was significantly less in the patients with CGN (5.96 +/- 0.95 v control, 8.93 +/- 1.02 fmol/mg of creatinine; P < 0.05). Plasma concentrations and urinary excretion of PAMP were significantly less for the patients with CGN compared with control subjects (0.91 +/- 0.08 v 1.23 +/- 0.20 fmol/mL; P < 0.05 and 25.0 +/- 3.0 v 35.0 +/- 3.6 fmol/mg of creatinine, respectively; P < 0. 05). The plasma AM concentration was negatively correlated with plasma renin activity (r = -0.58; P < 0.01) and aldosterone concentration (r = -0.40; P < 0.05). Urinary excretions of AM and PAMP showed significant correlations with urine excretion of sodium (r = 0.39; P < 0.05 and r = 0.49; P < 0.01, respectively). These findings suggest that AM and PAMP may have roles in the regulation of sodium in patients with CGN.

Fractional myocardial flow reserve (FFRmyo) after coronary intervention as a predictor of chronic restenosis.

The angiographic assessment of coronary stenosis has many limitations, especially after coronary intervention. To determine the physiologic significance of such lesions, we measured the mean translesional pressure gradients at rest (P1), those during hyperemia induced by intracoronary administration of papaverine (12 mg in the left and 8 mg in the right coronary artery) (P2), and fractional myocardial flow reserve (FFRmyo) which is derived from the ratio of the mean distal coronary pressure and aortic pressure during hyperemia. Our objective was to determine the relations among P1, P2, and FFRmyo and restenosis as potential predictors of chronic restenosis. The grouped study consisted of 32 patients with ischemic heart disease scheduled to undergo intervention. The distal coronary pressure was measured using a 0.014 inch pressure monitoring wire (Pressure Guide, Radi Medical Systems, Uppsala, Sweden). The guidewire was advanced through the lesional segment. The mean percent diameter stenosis (%DS) was 67.9 +/- 13.3% before intervention and 22.9 +/- 15.3% after intervention. The mean P2 (9.9 +/- 5.3 mmHg) was significantly higher than the mean P1 (4.5 +/- 3.6 mmHg; p < 0.0001). There was no correlation of P1, P2 or FFRmyo with the %DS after intervention. Follow-up angiography (after 6 months) performed on all patients revealed restenosis (%DS > or =50%) in four patients (12.5%). There was no correlation between P1 and the %DS at the follow-up angiography, but the relation between P2, FFRmyo and the %DS at the follow-up angiography was significant (r = 0.599, p < 0.01; r = 0.703, p < 0.0001, respectively). As a measurement of P2, FFRmyo is useful for the determination of the endpoint of intervention in consideration of prevention of restenosis. A new endpoint may be established after further evaluation in a greater number of patients.

[Inhibitory effect of prior panretinal photocoagulation on experimental iris neovascularization].

We could produce iris neovascularization experimentally in rhesus monkey eyes, by occlusion of the major retinal vessels of the retina and persistent ocular hypotony. We confirmed that panretinal photocoagulation inhibits development of iris neovascularization. We evaluated the effect of panretinal photocoagulation one month before occlusion of major retinal vessels with secondary iris neovascularization in 3 monkey eyes. Rubeosis iridis appeared on day 5 and disappeared on day 14 after retinal vessel occlusion. Histologically, the newly formed vessels near the iris surface showed fenestrations and protruded into the anterior chamber. The endothelial cells were flat and similar to matured vessels. These findings were in sharp contrast to our previous experiments with panretinal photocoagulation after rubeosis iridis became manifest. The findings also showed that retinal scarring by preceding panretinal photocoagulation did not completely inhibit the iris neovascularization.

[A morphological study of experimental intravitreal proliferative tissues].

Experimental tractional retinal detachments in rabbits' eyes was produced several weeks following aspiration of vitreous gels through a posterior small window of the eye wall. Histological examination showed that intravitreal proliferative tissues contained many fibroblasts, derived from the optic disc a small amount of migrated RPE, macrophages and other cells associated with proliferative tissues, Glial cells also grew especially at the epi-retina, causing shrinkage of the sensory retina. Vitreous neovascularization deriving from the retinal vessels was also found in these proliferative tissues. Our experimental data indicated that the extent of proliferative tissues mainly depend upon the amount of vitreous loss and vitreous hemorrhage, and the duration of retinal detachment. This experiment may be useful as an animal model of vitreous neovascularization.

[Morphological study of experimental corneal neovascularization after anterior uveal ischemia].

We morphologically investigated what kinds of inflammatory cells infiltrate the corneoscleral limbus by light and electron microscopy and what manner of keratocytes and vascular endothelial cells appear at the corneal limbus, when the corneal edema was aggravated severely and clinical corneal new vessels were found initially, i.e. until three days after anterior segmental ischemia in rabbit eyes. The majority of infiltrating inflammatory cells were polymorphonuclear leukocytes and the others were lymphocytes and histiocytes etc. Peripheral keratocytes around limbal vessels were stimulated and transformed to fibroblastic cells as a result of anterior segment ischemia. Proliferating endothelial cells of comparatively minor limbal vessels invaded between corneal lamellar layers toward the corneal center. Polymorphonuclear leukocytes were often found near activated keratocytes proliferating vascular endothelial cells, hear and there. Consequently, it is considered that the stimulated polymorphonuclear leukocytes play an important role when corneal neovascularization occurs after anterior segmental ischemia.

[Effect of pan-retinal photocoagulation in iris neovascularization].

The authors were able to produce experimental rubeosis iridis in the rhesus monkey's eye on 5 days following occlusion of the major retinal vessels and persistent ocular hypotony. Histopathological examination revealed true neovascularization. This experiment attempted to see whether laser pan-retinal photocoagulation plays an inhibiting effect on the occurrence of rubeosis iridis or not. We first performed laser pan-retinal photocoagulation, and at the same time performed occlusion of the major retinal vessels and persistent hypotony to aid for rubeosis iridis. Clinically, rubeosis iridis appeared within 5 days. At 14 days, histological examination revealed vessels on the surface of the iris following pan-retinal photocoagulation treatment were covered by fibroblast and melanocyte, and their endothelial cells showed no fenestrations. This means that clinical rubeosis iridis is not true neovascularization, but dilatation of the iris vessels. Thus, it was confirmed that pan-retinal photocoagulation inhibits development of iris neovascularization.

[Morphological study of rubeosis iridis induced in animal eyes].

Rubeosis iridis was produced experimentally in rhesus monkey eyes, by means of occlusion of the major retinal vessels of the retina and persistent ocular hypotony. Clinically, rubeosis iridis was recognized 5 days after the procedure. Histopathologically, these vessels developed anteriorly to the iris surface and endothelial fenestrations showed evidence of iris neovascularization. Endothelial cells of the vessels projected toward the internal lumen and showed immaturity. Newly formed vessels originated from the stromal vessels in the iris. This method is an effective experimental model for the induction of rubeosis iridis.

[Age-related changes in Bruch's membrane in rats].

PURPOSE: We investigated rats were worth the experimental animal on the aging changes in Bruch's membrane. METHODS: We did an ultramicromorphological study on the aging changes in Bruch's membrane, in male Sprauge-Dawley rats at 1,6,12 and 27 months after their birth. RESULTS: With the aging, the basement membranes on both sides of Bruch's membrane have become thick. At 6 months of age, the basement membranes of the endothelial cells of the choriocapillaris were found to be multilayered and cracked and pseudopodia of the endothelium were also observed toward the retinal pigment epithelium. At 12 months of age, we found vacuoles in the basal portion of the retinal pigment epithelium, as well as fibrillae and a part of the process of a cell in the outer collagenous zone correspond with the portion of the multilayered and cracked basement membranes of the endothelial cells of the choriocapillaris. At the age of 27 months, the basement membranes were thicker and a basal laminar deposit was seen. Prominent changes such as disappearance of the elastic fibers and increase of the collagenous fibers and fibrillae were also seen in some portions. CONCLUSIONS: Thus, the aging changes in Bruch's membrane of rats were remarkably reinforced in accordance with the age, it were appeared these rats were worth the experimental animal.

[Changes in Bruch's membrane in experimental hypercholesteremia in rats].

PURPOSE: We investigated the effect of high cholesterol diet for the aging changes in Bruch's membrane of rats. METHODS: After feeding a 4% cholesterol diet for 15 weeks to three young rats 3 months old and four aged rats 23 months old, we observed the morphological changes of Bruch's membrane by electron microscopy, and made a comparison with rats fed an ordinary diet. RESULTS: In one young rat fed a high-cholesterol diet, the endothelial basement membrane of the choriocapillaris formed multiple folds separated from the plasma membrane of the endothelium and showed lamellar thickening and crack in some areas. The elastic fiber layer in Bruch's membrane disappeared partly and some new microfibrils appeared. In one aged rat fed a high-cholesterol diet, the endothelial basement membrane of the choriocapillaris showed more lamellar thickening with lumps in some parts. Compared with rats fed an ordinary diet, rats fed a high-cholesterol diet showed thickening of the basement membrane and the changes were more severe. CONCLUSIONS: Our data indicated that high-cholesterol diet might promote age-related changes of Bruch's membrane.

[Histopathological study of trabecular meshwork after trabeculotomy in monkeys].

Trabeculotomy is a commonly indicated surgical procedure for primary open angle glaucoma and congenital glaucoma. In order to clarify the mechanisms of lowering the intraocular pressure (IOP) following the intervention, we performed this procedure in monkey eyes, and did postoperative histopathological examinations using light microscopy, and scanning and transmission electronmicroscopy for trabecular mesh work specimens incised at various time intervals up to one year after operation. Immediately after the operation, a direct communication was seen between the Schlemm's canal and the anterior chamber. Subsequently, the repairing process of trabecular tissue occurred initially in the corneoscleral and endothelial meshwork and finally in the uveal meshwork. At one year after operation the chamber angle was almost completely repaired by newly-formed trabecular tissue which was identical to the normal trabecular tissue. There was no direct communication between the Schlemm's canal and anterior chamber at that time. These results suggest that the decreased resistance for the aqueous outflow might be caused by direct communication between the Schlemm's canal and anterior chamber at an early postoperative stage, and the repairing process of the endothelial meshwork increases the resistance of aqueous outflow.

[Morphological study of corneal edema after anterior segment ischemia].

This experiment was performed to investigate the correlation between morphological changes of the corneal endothelium and clinical corneal edematous opacities after a procedure causing obstruction of bilateral long posterior ciliary arteries of the albino-rabbits. Shortly after the procedure, corneal endothelium became irregular on the anterior-chamber side and there were numerous lysosomal granules in the cytoplasm of corneal endothelial cells. On the third day, endothelial cells became necrotic and collapsed and a part of the cells peeled into the anterior chamber. Fibroblast-like cells and inflammatory cells were piled up in severely damaged areas of the endothelium. On the 11th day, the corneal endothelium developed again as a single layered structure on Descemet's membrane. It's seemed that corneal edema was induced as a result of severe damage corneal endothelium exposed to biochemical mediators such as prostaglandins released into the aqueous humor because the severity of corneal edema indicated some relation to changes in the concentration of prostaglandins in aqueous humor after anterior segmental ischemia.

[Exercise-induced acute renal failure associated with renal vasoconstriction].

Exercise-induced acute renal failure without rhabdomyolysis is not a rare condition. We experienced 6 cases (5 men and a woman) during last the 8 years. All cases complained of severe loin pain and nausea after mild to moderate exercises (for example, a track race in an athletic meeting). The elevation of serum and urinary myoglobin was undetected. In 4 of 5 patients with abdominal CT, renal patchy vasoconstriction (wedge-shaped low-density lesion) was observed. This was diagnosed as exercise-induced acute renal failure with loin pain (serum creatinine levels: 1.7-8.6 mg/dl). The renal function in 5 of the 6 cases normalized in about three weeks by fluid replacement therapy and hemodialysis support, which one patient received for 3 days. One patient required a long time for improvement of renal function and renal insufficiency persisted (serum creatinine 1.8 mg/dl). In 2 patients, the concentration of serum uric acid became very low after the recovery of renal function. These two patients were diagnosed as an isolated hyperuricosuric hypouricemia. More than half of the 6 patients had previously experienced the same episodes (loin pain and nausea) after exercise. Exercise-induced acute renal failure, probably due to renal patchy vasoconstriction, seems to be not a rare disease. The etiology of renal patchy vasoconstriction after exercises remains to be elucidated. The occurrence of acute renal failure must be taken into consideration when the youngster, especially with renal hypouricemia, complains of severe loin pain and nausea after exercise such as a track race.