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Biomedical subjects

M Miyazaki

Publications and source records attributed to M Miyazaki.

At least 307 records · Page 17Linked to original sources
PubMed1998

Inhibition of growth of MDA-MB-231 human breast cancer xenografts in nude mice by bombesin/gastrin-releasing peptide (GRP) antagonists RC-3940-II and RC-3095.

Bombesin or gastrin-releasing peptide (GRP) may act as autocrine growth factors and play a role in the initiation and progression of breast cancer. We investigated the effect of bombesin/GRP antagonists RC-3095 and RC-3940-II on the growth of the MDA-MB-231 oestrogen-independent human breast cancer cell line xenografted into female nude mice. Bombesin/GRP antagonists, RC-3095 and RC-3940-II, were administered subcutaneously twice daily at a dose of 10 micrograms for 5 weeks. The growth of MDA-MB-231 tumours was inhibited during the treatment, as shown by a reduction in tumour volume. RC-3940-II and RC-3095 significantly decreased the final tumour volume by 72.4% and 57.7%, respectively, and greatly reduced tumour weights. RC-3940-II also significantly increased tumour doubling time and appeared to be more effective than RC-3095 in inhibiting the growth of MDA-MB-231 breast cancers. Serum gastrin and insulin-like growth factor-I (IGF-I) levels in animals treated with RC-3095 or RC-3940-II showed no significant changes as compared with controls. There was a significant decrease in the number of binding sites for epidermal growth factor (EGF), as well as bombesin, in tumour cells after chronic treatment with RC-3095 or RC-3940-II, which might be related to inhibition of tumour growth. Reverse transcription polymerase chain reaction, followed by Southern blot analysis, also showed a reduction in the expression of mRNA for EGF receptors in the group treated with RC-3940-II. Our findings suggest that bombesin/GRP antagonists such as RC-3095 or RC-3940-II could be considered for endocrine therapy for oestrogen-independent breast cancers, but further investigations are necessary.

Animals↗
PubMed1998

A hypertensive father, but not hypertensive mother, determines blood pressure in normotensive male offspring through body mass index.

This investigation was to assess the role of genetic loading of hypertensive parents in the determination of blood pressure (BP) in their normotensive offspring. The medical check-up data from 7279 Japanese university students aged 19.22 +/- 0.01 years were analysed of which 641 students had only one hypertensive parent with or without hypertensive grandparents, and from this number 609 cases were available for the present analysis. The BP in the students having only one hypertensive parent were in the normotensive range, but was significantly higher than in those students without hypertensive relatives. Analyses of the data from the students having only one hypertensive parent revealed that systolic BP (SBP) and body mass index (BMI) were higher in the male than in the female students. In addition, there were no differences in BP and BMI between the male students with a hypertensive father and the male students having a normotensive father. However, multivariate analyses revealed that BMI was an independent predictor of SBP solely in the male students having a hypertensive father, but not in the male students having a normotensive father. Such a relationship between BMI and BP determination was not observed in the female students with one hypertensive parent. It is suggested that there are different mechanisms for the determination of BP in normotensive offspring of hypertensive parents, and genetic loading of a hypertensive father plays a critical role in the determination of BP through BMI.

Adolescent↗
PubMed1998

Plasma concentration of cytokine antagonists in patients with infection following liver resection.

BACKGROUND: The interactions between endogenous cytokine antagonists, surgical injury and perioperative infection are poorly understood. METHODS: Perioperative plasma concentrations of soluble tumour necrosis factor receptor p55 (STNFR p55), interleukin (IL) 1 receptor antagonist (IL-1ra) and IL-6 were measured by immunoassay in 29 consecutive patients undergoing liver resection. RESULTS: Plasma concentrations of STNFR p55, IL-1ra and IL-6 showed a striking increase immediately after operation (day 0) and on postoperative day 1. STNFR p55 concentrations correlated significantly with operating time (P< 0.05); IL-1ra levels with operating time, blood loss and weight of resected liver (P < 0.05); and IL-6 concentrations with operating time and blood loss (P< 0.05). Eight of the 29 subjects developed postoperative infections, of whom four had positive cultures of enteric organisms. Plasma STNFR p55 and IL-6 concentrations were significantly higher in the infected group than in the uninfected group (P < 0.05). STNFR p55 and IL-6 concentrations on day 0 differentiated between the two groups with a diagnostic accuracy of 79 and 83 per cent respectively. CONCLUSION: These results suggest that STNFR p55, IL-1ra and IL-6 are produced during operation in response to surgical stress. This production of STNFR p55 and IL-6 may be enhanced further by intraoperative bacterial translocation. Measurement of plasma STNFR and IL-6 concentrations may predict the development of postoperative infectious complications.

Adult↗
PubMed1998

Pituitary-dependent expression of the testicular angiotensin II receptor and its subtypes in rats.

Angiotensin II (AT2) has been implicated in the growth and/or differentiation of its target tissues. In the present study, testicular AT2 receptor and its subtypes in hypophysectomized rats were examined using quantitative in vitro autoradiography and Northern blot analysis in an attempt to determine possible involvement of pituitary hormones in their expression. Prepubescent (3 weeks of age) male Sprague-Dawley rats underwent hypophysectomy or sham operation. From 10 days thereafter, they were treated with vehicle, growth hormone, human chorionic gonadotrophin or human menopausal gonadotrophin for 10 days. Testicular AT2 receptors were labelled with 125I-[Sar1,Ile8] AT2 and differentiated into its subtypes (AT1 and FAT2) according to their susceptibility to AT1 (losartan, 5 microM) and AT2 (CGP42112B, 1 microM) antagonists. Hypophysectomy led to a marked increase in AT2 receptor concentration (sham-operated rats: 0.7 +/- 0.2 fmol/mg protein, hypophysectomized rats: 2.5 +/- 0.6 fmol/mg protein, mean +/- SEM, n = 11-12, p < 0.01) with predominant occurrence of AT1 receptors. Both human chorionic gonadotrophin and human menopausal gonadotrophin decreased testicular AT2 receptor concentration, whereas growth hormone did not affect AT2 receptor expression. Northern blot analysis revealed both testicular AT1 and AT2 receptor mRNA expression to be significantly increased after hypophysectomy and reduced by gonadotrophin treatment. These results suggest that the expression of testicular AT2 receptors is regulated by pituitary gonadotrophins and that AT2 may play a role in testicular growth and/or differentiation.

Angiotensin II↗
PubMed1998

Expression of endothelial and inducible nitric oxide synthase in human glomerulonephritis.

The presence of nitric oxide (NO) in the kidney has been implicated in the pathogenesis of human glomerulonephritis. However, the exact type of glomerular cells that express NO synthase (NOS) and the NOS isoform involved in the local production of NO has not been identified in the human diseased kidney. We examined the expression of three isoforms of NOS, inducible NOS (iNOS), endothelial NOS (eNOS) and brain NOS (bNOS) in the renal tissue of patients with IgA nephropathy (IgAN, N = 10), lupus nephritis (LN, N = 5), membranous nephropathy (MN, N = 5) and minimal change nephrotic syndrome (MCNS, N = 5). Sections were immunostained and the correlation between the expression of each NOS and the degree of glomerular injury in that section was also examined. Normal portions of surgically resected kidneys served as controls. eNOS was present in glomerular endothelial cells and endothelium of cortical vessels in the control and diseased kidneys. iNOS was localized in mesangial cells, glomerular epithelial cells and infiltrating cells in the diseased glomeruli, whereas immunostaining for iNOS was hardly detected in control kidneys. In addition, the expression pattern of eNOS in each glomerulus was the reverse of that of iNOS. In IgAN and LN, the extent of staining for eNOS correlated negatively with the degree of glomerular injury, while the extent of staining for iNOS correlated positively with the degree of glomerular injury in the same tissues. bNOS was not detected in normal or nephritic glomeruli. Our results indicate the presence of a NO pathway in human diseased kidney, and suggest that NO derived from eNOS and iNOS may be involved in the progression of renal diseases and that NO derived from each NOS may play an important role in different way in human inflamed glomeruli.

Adult↗
PubMed1998

Expression of decay accelerating factor mRNA and complement C3 mRNA in human diseased kidney.

BACKGROUND: Decay accelerating factor (DAF), a product of mesangial cells in vitro, is expressed on the surface of cells and is a candidate for the focal suppression of complement activation. It is not clear at present whether the levels of expression of DAF and intrarenal C3 synthesis correlate with the level of tissue injury. METHODS: Immunohistochemistry for DAF and C3 and nonradioactive in situ hybridization with digoxigenin-labeled oligonucleotide probe for DAF and C3 mRNA were performed in 22 tissue samples of kidneys from patients with IgA nephropathy (IgAN), 6 with membranous nephropathy (MN), 6 with lupus nephritis (LN), and five normal kidneys. RESULTS: In the normal kidney, DAF was confined to the juxtaglomerular apparatus and little or no C3 was detected; however, a few glomerular cells were positive for DAF mRNA but no C3 mRNA positive cells were detected. In diseased kidneys, DAF and C3 as well as their mRNAs were detected in mesangial cells, tubular cells and infiltrating cells. Glomerular epithelial cells and Bowman's capsule cells contained little or no DAF and C3 but were positive for their mRNAs. The mean percentages of mesangial cells positive for DAF and C3 mRNAs were 49.3 +/- 11.5% and 50.7 +/- 10.3% in IgAN, and 17.0 +/- 6.3% and 19.4 +/- 9.0% in MN, respectively. The percentage of mesangial cells positive for DAF and C3 mRNAs among intraglomerular cells correlated positively with the degree of mesangial proliferation and glomerular sclerosis in IgAN. In contrast, in LN the percentage of glomerular cells positive for DAF mRNA correlated negatively with the degree of glomerular injury, while the percentage of cells positive for C3 mRNA did not change with the progression of the disease. The ratio of C3 mRNA/DAF mRNA of glomerular cells correlated with the degree of glomerular injury in both IgAN and LN. In the tubulointerstitium, the percentage of cells expressing mRNA, and C3 mRNA/DAF mRNA radio correlated with the degree of tubular atrophy and interstitial broadening in both IgAN and LN. CONCLUSIONS: We conclude that DAF and C3 mRNAs are synthesized in human diseased kidneys, and that a balance between locally synthesized DAF and C3 may be important in the progression of glomerulonephritis.

Adult↗
PubMed1998

Effects of mild (33 degrees C) and moderate (29 degrees C) hypothermia on cerebral blood flow and metabolism, lactate, and extracellular glutamate in experimental head injury.

The effects of mild (33 degrees C) and moderate (29 degrees C) hypothermia were investigated to determine which temperature was more effective against compression-induced cerebral ischemia. Eighteen cats were anesthetized. The animals were divided into three groups according to deep-brain temperature (control, 37 degrees C; mild hypothermia, 33 degrees C; and moderate hypothermia, 29 degrees C). Intracranial pressure (ICP) and cerebral blood flow (CBF) were monitored, the latter by hydrogen clearance. Arteriovenous oxygen difference (AVDO2) and cerebral venous oxygen saturation (ScvO2) were measured in blood samples from the superior sagittal sinus. The cerebral metabolic rate of oxygen (CMRO2) and the cerebral metabolic rate of lactate (CMR lactate) were calculated. Extracellular glutamate was measured by microdialysis. ICP was increased by inflation of an epidural balloon until CBF became zero, and this ischemia was maintained for 5 min, after which the balloon was quickly deflated. All parameters were recorded over 6 h. Evans blue was injected to examine vascular permeability changes. CBF was decreased by 56% by mild hypothermia and by 77% by moderate hypothermia. Mild hypothermia had a coupled metabolic suppression whereas moderate hypothermia significantly increased AVDO2 and decreased ScvO2, producing a low CBF/CMRO2 (relative ischemia). After balloon deflation, all three groups showed reactive hyperemia, which was significantly reduced by mild and moderate hypothermia. CBF then decreased to 50% of pre-inflation values and ScvO2 decreased (post-ischemic hypoperfusion). CBF/CMRO2, ScvO2, and AVDO2 did not differ significantly between the three groups. After balloon deflation, all three groups showed increased CMR lactate, which was significantly reduced by mild and moderate hypothermia. Extracellular glutamate increased in control animals (3.8 +/- 1.72 microM), an effect most effectively suppressed in the mild hypothermia group (1.0 +/- 0.46 microM). Damaged tissue volumes as indicated by Evans blue dye extravasation were 729 +/- 89 mm3 in control, 247 +/- 56 mm3 in mild hypothermia, and 267 +/- 35 mm3 in moderate hypothermia animals. These data suggest that mild hypothermia (33 degrees C) might be the optimal brain temperature to treat compression-related cerebral ischemia.

Animals↗
PubMed1998

Routes of hepatic metastasis of gallbladder carcinoma.

This clinicopathologic study aims to clarify routes of hepatic metastasis of gallbladder carcinoma. Nineteen liver specimens obtained by extensive hepatectomy performed for the treatment of advanced gallbladder carcinoma were analyzed. We defined hepatic metastasis as a discrete hepatic lesion separate from the primary tumor and paid special attention to portal tracts at the margins of direct hepatic invasion. Eleven early metastatic foci were demonstrated histologically in 6 cases, most commonly in segments adjacent to the gallbladder. All cases with hepatic metastasis had direct hepatic invasion. Nine of the 11 metastatic lesions were located within the portal tracts or accompanied by invasion into the portal tracts. Because they are in continuity with areas of direct hepatic invasion, the portal tracts at the invasive margin often were involved by cancer cells that spread along these tracts. These results suggest that the most important route in development of hepatic metastasis from gallbladder carcinoma is along the portal tracts after direct hepatic invasion.

Aged↗
PubMed1998

Expression of vascular endothelial growth factor and its receptors in rats with protein-overload nephrosis.

BACKGROUND: Based on the fact that vascular endothelial growth factor (VEGF) increases vascular permeability, it is speculated that VEGF might be involved in the development of proteinuria, although this remains unconfirmed. The production and site of action of VEGF remains unclear in nephrotic renal diseases. METHODS: Non-radioactive in situ hybridization was performed to examine the expression of VEGF mRNA and its receptors, flt-1 and KDR/flk-1, in a rat model of nephrosis induced by intraperitoneal injection of bovine serum albumin (BSA). Saline injected rats were served as control animals. RESULTS: Neither morphological changes nor deposition of immunoglobulin or complement were observed in our model. Proteinuria developed, reaching a maximum level in rats injected with BSA for 3 days, followed by persistent proteinuria until day 14. The expression of mRNA for VEGF and the two receptors was markedly upregulated in glomeruli of BSA-induced nephritis compared with the control group. VEGF mRNA was localized in glomerular cells, including cells in mesangium, visceral and parietal epithelial cells. In contrast, flt-1 mRNA and KDR/flk-1 mRNA were expressed on glomerular endothelial cells and cells in mesangium. The ratio of glomerular cells positive for VEGF mRNA and its receptors mRNA increased proportionately with the severity of proteinuria. Immunohistochemistry for ED-1 and proliferating cell nuclear antigen showed no significant increase in infiltrating macrophage or cellular proliferation. CONCLUSIONS: Our results suggest that altered glomerular expression of VEGF and its receptors is not associated with proliferation of endothelial cells, but rather with proteinuria in BSA-induced nephritis in rats. VEGF may play a different role in different renal diseases.

Animals↗
PubMed1998

Expression of VLA-4 on peripheral mononuclear cells in patients on chronic haemodialysis with carpal tunnel syndrome.

BACKGROUND: Carpal tunnel syndrome (CTS) is a major complication in long-term haemodialysis patients and is thought to be a form of haemodialysis-associated amyloidosis. CTS may be due to the deposition of amyloid as well as local inflammatory process in the carpal tunnel. Although macrophage-like cells infiltrating the tenosynovium of carpal tunnel are known to express mRNA for adhesion molecules, the level of expression of adhesion molecules on peripheral blood mononuclear cells (PBMC) in patients with CTS is unknown. METHODS: We compared the expression of very late activation antigen (VLA-4) on PBMC by flow cytometry in 14 patients on haemodialysis (6-21 years) with CTS, nine on haemodialysis (1-6 years) but without CTS and six patients on chronic ambulatory peritoneal dialysis (CAPD, 1-5 years) without CTS. RESULTS: The expression of VLA-4 on peripheral lymphocytes was not different among the groups. However, the FACScan fluorescence histogram of VLA-4 expression on peripheral monocytes showed a bimodal pattern in the CTS group, and the rate of the high intensity portion of the expressed VLA-4 on monocytes was significantly higher in CTS than other groups (P<0.05). The observed differences were not based on differences in the type of the dialysis membrane. We also examined the adhesion of PBMC to fibronectin-coated plates. The number of adherent PBMC was significantly higher in patients with CTS than in other groups (P<0.05). CONCLUSION: Our results suggest that increased expression of VLA-4 on peripheral monocytes and augmented adhesion capacity of PBMC to fibronectin may be involved in the development of CTS in haemodialysis patients.

Carpal Tunnel Syndrome↗
PubMed1998

Enhanced glomerular expression of caldesmon in IgA nephropathy and its suppression by glucocorticoid-heparin therapy.

BACKGROUND: Activation and consequent phenotypic modulation of mesangial cells is considered to play a crucial role in the process of glomerular disease progression. Caldesmon, a calmodulin and actin-binding protein, is a molecular marker of the phenotypic change in smooth-muscle cells. SUBJECTS AND METHODS: We studied whether the expression of caldesmon in mesangial cells was enhanced in the process of IgA nephropathy and whether it would be a marker of mesangial activation indicating prognostic significance in specific disease states. We performed immunohistochemical staining with anticaldesmon and alpha-smooth-muscle actin (alpha-SMA) antibodies in 32 biopsy specimens from IgA nephropathy patients and analysed them quantitatively with a computer-aided manipulator. RESULTS: The glomerular expression of caldesmon was enhanced in IgA nephropathy patients. We compared caldesmon expression with composite histological scores (cell score and matrix score), clinical parameters and expressions of alpha-SMA. There was a statistically significant correlation between the caldesmon score and the histological scores (cell score and matrix score, P<0.0001, P<0.01 respectively). Patients showing a high intensity of caldesmon expression (defined as caldesmon score > or = 35; H-group) had significantly higher urinary protein excretion than those showing a low intensity of caldesmon expression (defined as caldesmon score < 35; L-group) (1.2 +/- 1.2 g/24 h vs 0.41 +/- 0.53 g/24 h, P<0.05). Caldesmon and alpha-SMA expression had a statistically significant correlation (P<0.000). Next, 13 patients were treated with glucocorticoid-heparin for 4-8 weeks and re-biopsies were performed. After the therapy, the caldesmon and alpha-SMA scores were significantly lower than those before the therapy (P<0.01). DISCUSSION: These results suggest that the expression of caldesmon in glomeruli is associated with the progression of IgA nephropathy, and that glucocorticoid heparin therapy may reverse the phenotype of mesangial cells during the disease process of glomerulonephritis.

Actins↗
PubMed1998

Lack of correlation between the reduction of sevoflurane MAC and the cerebellar cyclic GMP concentrations in mice treated with 7-nitroindazole.

BACKGROUND: Although inhibition of nitric oxide synthase (NOS) has been reported to be antinociceptive and to reduce the threshold of general anesthesia, the mechanism of action is largely unknown. Specifically, the relation between the minimum alveolar concentration (MAC)-reducing effects of NOS inhibition and cyclic guanosine monophosphate (cGMP) concentrations in the brain has not been defined. To further characterize the effects of NOS inhibition, the authors studied the relation between the MAC of sevoflurane and the cGMP concentration of the brain after acute and chronic treatment with a neuronally selective NOS inhibitor, 7-nitroindazole (7-NI). METHODS: Sevoflurane MAC and cerebellar cGMP concentrations were determined in mice after acute intraperitoneal administration or after 1, 2, 3, and 4 days of gavage feeding of 7-NI. After acute or chronic treatment with 7-NI, the mice were separated into two groups. Sevoflurane MAC was measured by a tail-clamp method in the first group, and cerebellar cGMP concentrations were measured by enzyme-linked immunosorbent assay in the second group of the mice. RESULTS: In mice, acute intraperitoneal administration of 7-NI dose dependently decreased sevoflurane MAC and cerebellar cGMP; and 4-day-long gavage feeding with 7-NI (500 mg/ kg, every 8 h) time dependently decreased cerebellar cGMP, but sevoflurane MAC was reduced only for the first 2 days and returned to its baseline after 3 days of 7-NI feeding. CONCLUSIONS: Although an acute selective inhibition of neuronal NOS decreases sevoflurane MAC and cerebellar cGMP concentrations in mice, there was a dissociation between the two parameters during long-term neuronal NOS inhibition. There may be cGMP-independent compensatory mechanisms that mediate nociception when NOS is chronically inhibited.

Anesthetics, Inhalation↗
PubMed1998

Features of early gastric cancer detected by modern diagnostic technique.

To ascertain how the clinicopathologic features of early gastric cancer detected by current diagnostic tools had changed clinical features, we compared 711 early gastric cancer patients with 933 advanced gastric cancer patients regarding age, sex, and tumor location. We found that the proportion of early gastric cancer cases did not change according to age. However, the proportion of early gastric cancer cases in the proximal part was significantly lower than that observed in the distal part (p < 0.01). We conclude that recent diagnostic improvements have rendered age no longer a major deterrent for early detection of gastric cancer. However, a careful examination of the proximal stomach is called for because it is so hard to detect small lesions in that area.

Adult↗
PubMed1998

Roles of vascular angiotensin converting enzyme and chymase in two-kidney, one clip hypertensive hamsters.

BACKGROUND: A chymase-dependent angiotensin II-forming pathway is present in human vascular tissues; however, the role, if it plays any, of chymase in the pathogenesis of hypertension is not known. When investigating the role of chymase, it is important to recognize marked differences in vascular angiotensin II-forming systems among species. We found recently that hamsters, like humans, possess the dual angiotensin II-forming system. OBJECTIVE: To analyze the potential involvement of angiotensin converting enzyme and chymase in the pathogenesis of hypertension, and to further characterize the efficiency of angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists for the treatment of hypertension. METHODS AND RESULTS: The mean arterial pressure in the two-kidney, one clip hamster model had increased significantly 2 weeks after clipping (acute stage), reached a peak after 4 weeks, and was sustained at the high level until 32 weeks after clipping (chronic stage). Plasma renin activity increased markedly during the acute stage, but returned to the normal level during the chronic stage. Vascular angiotensin converting enzyme activity during 4-32 weeks after clipping was significantly higher than that in the control hamsters. By contrast, vascular chymase was not activated throughout the experimental period. Administrations of an angiotensin converting enzyme inhibitor, trandolapril, and an angiotensin II receptor antagonist, CV-11974, equally lowered the mean arterial pressure during the acute and chronic stages. CONCLUSIONS: Vascular angiotensin converting enzyme plays a predominant role in the maintenance of two-kidney, one clip hypertension in hamsters, which, like humans, possess a dual system of formation of angiotensin II. Vascular chymase was not involved in the pathogenesis of two-kidney, one clip hypertension in the hamster.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Functional role of chymase in angiotensin II formation in human vascular tissue.

Recent reports suggested that human heart chymase contributed little to angiotensin (Ang) II formation in the presence of natural protease inhibitors such as alpha-antitrypsin. We studied whether chymase could contribute to Ang II formation in the presence of natural protease inhibitors in the homogenate, the extract, and slices of human vascular tissue, and whether these inhibitors affect Ang I-induced vasocontractile responses due to chymase. In the homogenate, lisinopril, chymostatin, and alpha-antitrypsin inhibited the formation of Ang II by 14, 92, and 74%, respectively. In the extract, the inhibition of Ang II formation by lisinopril, chymostatin, and alpha-antitrypsin was 18, 94, and 93%, respectively. In the slices, lisinopril and chymostatin inhibited Ang II formation by 5 and 90%, respectively. However, unlike the homogenate and the extract experiments, only 8% of the Ang II formation was suppressed by alpha-antitrypsin. In isolated human gastroepiploic artery, 30% of Ang I-induced vasoconstriction was blocked by lisinopril, and the rest was completely eliminated by a combination of lisinopril and chymostatin. On the other hand, alpha-antitrypsin was ineffective in blocking Ang I-induced vasoconstriction in the presence of lisinopril, which demonstrates that Ang II formation is dependent on chymase. These findings suggest that chymase in human vascular tissue plays a functional role in Ang II formation in the presence of natural protease inhibitors such as alpha-antitrypsin.

Angiotensin I↗
PubMed1998

Therapeutic apheresis for renal diseases.

Plasma exchange is used frequently in renal diseases for the removal of the humoral components of immune responses. Various pathological circulating factors are recognized in primary and secondary renal diseases. Recent advances in medical technology have allowed a wider clinical application of plasmapheresis in the clinical management of a variety of conditions. However, the clinical efficacy of plasmapheresis in renal diseases is still controversial. In this article, we review the therapeutic use of apheresis in different renal diseases.

Anti-Glomerular Basement Membrane Disease↗
PubMed1998

MR imaging of the inner ear: comparison of a three-dimensional fast spin-echo sequence with use of a dedicated quadrature-surface coil with a gadolinium-enhanced spoiled gradient-recalled sequence.

PURPOSE: To prospectively evaluate the sensitivity and specificity of magnetic resonance (MR) imaging in the inner ear with a long echo train, three-dimensional (3D), asymmetric Fourier-transform, fast spin-echo (SE) sequence with use of a dedicated quadrature-surface phased-array coil to detect vestibular schwannoma in the cerebellopontine angle and the internal auditory canal. MATERIALS AND METHODS: In 205 patients (410 ears) with ear symptoms, 1.5-T MR imaging was performed with unenhanced 3D asymmetric fast SE and gadolinium-enhanced 3D gradient-recalled (SPGR) sequences with use of a quadrature surface phased-array coil. The 3D asymmetric fast SE images were reviewed by two radiologists, with the gadolinium-enhanced 3D SPGR images used as the standard of reference. RESULTS: Nineteen lesions were detected in the 410 ears (diameter range, 2-30 mm; mean, 10.5 mm +/- 6.4 [standard deviation]; five lesions were smaller than 5 mm). With 3D asymmetric fast SE, sensitivity, specificity, and accuracy, respectively, were 100%, 99.5%, and 99.5% for observer 1 and 100%, 99.7%, and 99.8% for observer 2. CONCLUSION: The unenhanced 3D asymmetric fast SE sequence with a quadrature-surface phased-array coli allows the reliable detection of vestibular schwannoma in the cerebellopontine angle and internal auditory canal.

Adolescent↗