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Biomedical subjects

J Grande

Publications and source records attributed to J Grande.

At least 19 recordsLinked to original sources
PubMed2001

Inflammatory myofibroblastic tumour of the larynx.

A case of inflammatory myofibroblastic tumour of the larynx in a 74-year old man is reported. The lesion presented as a polypoid tumour arising in the left true vocal fold. The patient died of non-tumour-related causes and the autopsy showed persistence of the laryngeal tumour. Multicentricity and distant metastases were not detected. The literature about this entity and its differential diagnosis is reviewed and briefly commented upon.

Actins↗
PubMed2000

[A matter of heart--two examinations of the same heart with a sixty year interval].

The 20th of May 1869, Professor Emanuel Winge used a human heart as an exhibit at a meeting of The Medical Society in Christiania. This heart was later conserved and kept in the museum of the Institute of Pathology. Sixty years later, one of Winge's successors, Professor Francis Harbitz, used the very same heart, also at a meeting of The Medical Society. Harbitz had then confirmed Winge's hypothesis of 1869, that the endocarditis of this heart was due to a bacterial infection. This article contemplates the disparity between the "scientific gazes" of Winge and Harbitz, and why Harbitz was able to convert Winges hypothesis of 1869 into a scientific discovery in 1929.

Cardiology↗
PubMed1999

The Banff 97 working classification of renal allograft pathology.

BACKGROUND: Standardization of renal allograft biopsy interpretation is necessary to guide therapy and to establish an objective end point for clinical trials. This manuscript describes a classification, Banff 97, developed by investigators using the Banff Schema and the Collaborative Clinical Trials in Transplantation (CCTT) modification for diagnosis of renal allograft pathology. METHODS: Banff 97 grew from an international consensus discussion begun at Banff and continued via the Internet. This schema developed from (a) analysis of data using the Banff classification, (b) publication of and experience with the CCTT modification, (c) international conferences, and (d) data from recent studies on impact of vasculitis on transplant outcome. RESULTS: Semiquantitative lesion scoring continues to focus on tubulitis and arteritis but includes a minimum threshold for interstitial inflammation. Banff 97 defines "types" of acute/active rejection. Type I is tubulointerstitial rejection without arteritis. Type II is vascular rejection with intimal arteritis, and type III is severe rejection with transmural arterial changes. Biopsies with only mild inflammation are graded as "borderline/suspicious for rejection." Chronic/sclerosing allograft changes are graded based on severity of tubular atrophy and interstitial fibrosis. Antibody-mediated rejection, hyperacute or accelerated acute in presentation, is also categorized, as are other significant allograft findings. CONCLUSIONS: The Banff 97 working classification refines earlier schemas and represents input from two classifications most widely used in clinical rejection trials and in clinical practice worldwide. Major changes include the following: rejection with vasculitis is separated from tubulointerstitial rejection; severe rejection requires transmural changes in arteries; "borderline" rejection can only be interpreted in a clinical context; antibody-mediated rejection is further defined, and lesion scoring focuses on most severely involved structures. Criteria for specimen adequacy have also been modified. Banff 97 represents a significant refinement of allograft assessment, developed via international consensus discussions.

Acute Disease↗
PubMed1998

Redox regulation of renal DNA synthesis, transforming growth factor-beta1 and collagen gene expression.

Growth and injury represent recurrent and related themes in the study of progressive renal disease. We have previously demonstrated that a prooxidant diet, one deficient in antioxidants, selenium and vitamin E, induces renal enlargement, proteinuria, mild tubulointerstitial disease and diminished glomerular filtration rate (GFR). Our present study represents continued examination of these processes. We demonstrate that these diets increase thymidine incorporation into DNA and net DNA content in renal tissue, and induce expression of the mRNA for the proto-oncogene, c-myc, and the histone, H2b. We localize increased DNA synthesis as occurring mainly in the distal renal tubular epithelium. These deficient kidneys also exhibit interstitial expansion that parallels the pattern of DNA synthesis in that both processes are more prominent in the medulla than in the cortex. mRNAs for collagens I, III and IV in conjunction with transforming growth factor-beta1 (TGF-beta1) are up-regulated in the kidney in rats maintained on the deficient diet. In complementary in vitro studies, the exposure of rat kidney fibroblasts, NRK 49F cells, to noncytolytic doses of hydrogen peroxide, induces collagen III, collagen IV and TGF-beta1 mRNA. Induction of these genes is also observed in mesangial cells so exposed to noncytolytic doses of hydrogen peroxide. A final aspect of our study was the examination of renal generation of hydrogen peroxide and the profile of the hydrogen peroxide-degrading enzymes. Deficient kidneys exhibit increased mitochondrial generation of hydrogen peroxide independent of oxygen consumption but in conjunction with suppression of glutathione peroxidase mRNA and activity. Lipid peroxidation was increased twofold in the cortex and medulla of the deficient kidneys. Surprisingly, catalase activity, measured in the cortex and medulla, and whole kidney catalase mRNA were also reduced in rats maintained on the antioxidant deficient diet, effects that may further compromise the clearance of hydrogen peroxide. These changes in catalase represent an adverse response to this dietary deficiency, and may be relevant to decreased catalase activity described in chronic renal insufficiency. Thus, a chronic prooxidant state, with features that mimic those of clinical uremia, increases DNA synthesis of renal tubular epithelium, induces mRNA expression for collagens I, III and IV in conjunction with the mRNA for the fibrogenic cytokine, TGF-beta1. Oxidants also induce collagen III, collagen IV and TGF-beta1 mRNA in vitro.

Animals↗
PubMed1996

[Polymer microparticles for right and left heart echocardiography and imaging myocardial perfusion after peripheral vein injection].

It is conceivable that a stable ultrasound contrast agent could be used for reproducible right and left heart echocardiography and myocardial visualization after intravenous injection. Microparticles from different polymers and preparation procedures were screened in six dogs leading to one superior agent with reproducible high quality echo contrast in doses of 1 mg/kg. This special agent is based on condensates of aspartic acid, ethanolamine and decanoic acid. Out of this material particles were formed with an average diameter of 2 micrometers. The easily suspendable particles were used for the following studies in a dose of 1 mg/kg intravenously in eight pigs. Maximal video intensity averaged 116 +/- 42 relative intensity units (IU) in the right, 137 +/- 42 IU in the left ventricle, 42 +/- 7 in the normally perfused and 11 +/- 2 in the hypoperfused myocardium after circumflex ligature. The area under the intensity curve was 1942 +/- 100 IUxs in the right, 2452 +/- 1291 IUxs in the left ventricle, 518 +/- 124 in the normally perfused and 202 +/- 94 in the hypoperfused myocardium after circumflex ligature. There was no change of heart rate, central arterial or pulmonary artery pressure during and after the injections. There was also no loss of echo intensity during the passage of contrast material through the heart due to systolic pressure. The described agent can be used for the opacification and ultrasonic visualization of the right and left heart as well as normally and hypoperfused myocardium without visible side-effects in animal studies.

Animals↗
PubMed1993

Arnold-Chiari malformation associated with sleep apnea and central dysregulation of arterial pressure.

The natural history of symptomatic adult type I Arnold-Chiari (ACM1) malformation is variable. Patients with this condition frequently develop corticospinal and sensory deficits, together with cerebellar signs and lower cranial nerve palsies in various combinations. In the present report we describe a patient with ACM1 in whom sleep apnea together with disturbances in the central regulation of arterial pressure were a major component of the symptomatology. These paroxysmal blood pressure changes has not been previously reported. The decompression of our patient's medulla, which contains the primary respiratory centers and baroreceptors, resulted in a marked improvement and indicate that the origin may have been on a central basis.

Arnold-Chiari Malformation↗
PubMed1993

Transforming growth factor-beta 1 induces collagen IV gene expression in NIH-3T3 cells.

BACKGROUND: While recent studies have implicated transforming growth factor-beta 1 (TGF-beta 1) in the development of glomerular scarring, extraglomerular matrix production is frequently associated with glomerulonephritis and is an important determinant of disease progression. TGF-beta 1 may be an important mediator of extracellular matrix synthesis, both by glomerular and extraglomerular mesenchymal cells. TGF-beta 1-mediated collagen IV gene expression was studied in two mesenchymal cell lines. Initial studies were performed utilizing NIH-3T3 cells, a fibroblast-like line derived from murine embryo that has been used to study regulation of fibrillar collagen (collagen I and collagen III) synthesis by TGF-beta 1. Additional studies were performed using normal rat kidney cells (NRK-49F). EXPERIMENTAL DESIGN: Cells were grown in medium supplemented with 0.5% calf serum for 24 hours before treatment with TGF-beta 1. RNA was isolated after the addition of varying amounts of TGF-beta 1 to the cells in culture for varying periods of time, and collagen alpha 1(IV) RNA was quantitated by filter hybridization. Transcription of the alpha 1(IV) and alpha 2(IV) collagen genes was assessed by an in vitro transcription assay. Deposition of collagen IV was identified by immunoblotting. RESULTS: Induction of alpha 1(IV) gene expression by NIH-3T3 cells and by NRK-49F cells was first seen 2 to 4 hours after TGF-beta 1 treatment, and was maximal after 12 to 18 hours. Maximal induction was observed following addition of 5 ng/ml TGF-beta 1 to NIH-3T3 cells, and following addition of 10 ng/ml of TGF-beta 1 to NRK-49F cells. In the presence of cycloheximide, TGF-beta 1 induction of alpha 1(IV) mRNA was markedly attenuated in both cell lines, suggesting that this effect of TGF-beta 1 requires protein synthesis. TGF-beta 1 increased transcription of both the alpha 1(IV) and alpha 2(IV) collagen genes by NIH-3T3 cells. CONCLUSIONS: TGF-beta 1 induces collagen IV gene expression in both NIH-3T3 cells and normal rat kidney fibroblasts (NRK-49F cells). Further studies of cytokine-mediated transcriptional regulation of collagen IV, utilizing these cell lines, may provide important information regarding the role of extraglomerular matrix production in the progression of renal disease.

3T3 Cells↗
PubMed1991

DNA content flow cytometry as a prognostic factor for node-positive breast cancer. The role of multiparameter ploidy analysis and specimen sonication.

The DNA content was analyzed in paraffin-embedded material from 167 patients with node-positive breast cancer to learn whether specimen sonication and multiparameter ploidy analysis (MPPA) (using DNA content and light scatter) could improve the strength of ploidy as a prognostic variable. Sonicated specimens were found to have fewer aggregates, a lower percentage of cells in S-phase (%S) and G2M phase than the corresponding nonsonicated specimens. The results using MPPA predicted the prognosis better because they allowed detection of small aneuploid peaks in histograms classified as diploid or tetraploid using DNA content alone. Ploidy was a significant univariate factor, and patients with tetraploid tumors had the best survival. In the multivariate analysis, if other routine factors were examined preferentially, ploidy and %S did not provide additional prognostic information for survival. This study of paraffin-embedded breast cancers suggested that sonication and MPPA may improve the ploidy analysis in certain cases and that tetraploidy may be a favorable ploidy pattern in this group.

Breast Neoplasms↗
PubMed1989

Acute effects of insulin and glucagon on hepatic casein kinase 2 in adult fed rats: correlation of the effects on casein kinase 2 with the changes in glycogen synthase activity.

Administration of insulin to adult fed rats caused an inactivation of hepatic casein kinase 2 as determined by the decrease in the activity ratio measured at a low (0.1 mg/ml) and a high (1.0 mg/ml) concentration of beta-casein. Maximal inactivation occurred 45 min after injection and the dose for half-maximal effect was 44 micrograms/kg. The effect of insulin was due to an increase in the apparent Km value for the protein substrate but the magnitude of the effect depended on the substrate used, decreasing in the order beta-casein greater than glycogen synthase much greater than whole casein. The activation of casein kinase 2 by glucagon (M. Pérez, J. Grande, and E. Itarte (1988) FEBS Lett. 238, 273-276) was also more marked with beta-casein and glycogen synthase than with whole casein. A good correlation was observed between the time- and dose-dependent activation of glycogen synthase and inactivation of casein kinase 2 promoted by insulin. Similarly, the inactivation of glycogen synthase by glucagon correlated with the activation of casein kinase 2 caused by this hormone. The possible involvement of casein kinase 2 on the mechanism(s) through which these hormones control hepatic glycogen synthase is discussed.

Animals↗
PubMed1988

Casein kinase 2 activity increases in the prereplicative phase of liver regeneration.

Cytosolic casein kinase activity increased up to 2-fold in the first 6 h after partial hepatectomy and then decreased to control values. This increase was due mainly to casein kinase 2, which reached maximal values at 6-8 h of liver regeneration. In contrast, casein kinase 1 showed a smaller increase at 4 h and then started to decrease reaching values of about 70% of control at 16 h. The increase in total casein kinase 2 was accompanied with an activation of the enzyme, as determined by the low/high beta-casein activity ratio assay. Administration of an acute dose of glucagon to control rats also increased the activity ratio but failed to cause any rise in total casein kinase 2 activity.

Animals↗
PubMed1988

Phosphorylation of hepatic insulin receptor by casein kinase 2.

Casein kinase 2 was able to phosphorylate the beta-subunit of hepatic insulin receptor in the presence of either ATP or GTP. Phosphorylation by casein kinase 2 was observed even in the absence of insulin, was inhibited by low heparin concentrations, and led to the incorporation of phosphate on serine and threonine residues. Casein kinase 2 phosphorylation of insulin receptor partially decreased its tyrosine kinase activity.

Adenosine Triphosphate↗
PubMed1987

Developmental changes in rat hepatic casein kinases 1 and 2.

Cytosolic histone kinase and casein kinase activities varied considerably in the late fetal and postnatal periods of liver development. Both activities showed a maximum at day 21 of gestation and decreased at birth to values close to those of adult rats. The changes in total casein kinase activity were due to variations of casein kinase 1 and casein kinase 2. Similarly the activities of both the cyclic-AMP-dependent protein (histone) kinase and the cyclic-AMP-independent histone kinase varied during development. Besides the changes in total activity, the affinity of casein kinases 1 and 2 for casein also varied in fetal and postnatal development. The Km values of casein kinase 2 increased from day 18, reached a maximum at day 20 of gestation and then started to decrease until one day after birth. In contrast the Km values of casein kinase 1 decreased from day 18, reached its lowest value at day 21 of gestation and attained values similar to those in the adult at the day of birth. Changes in this parameter were also observed when insulin (3 IU/kg) was administered by intraperitoneal injection to one-day-old rats. The Km values of casein kinase 1 decreased while those of casein kinase 2 increased after administration of this hormone. On the other hand, the Km values for ATP of casein kinases 1 and 2 as well as their apparent molecular masses and sensitivity to heparin and GTP did not significantly change during ontogeny of rat liver.

Aging↗
PubMed1987

Effect of an elastin growth substrate on cholesteryl ester synthesis and foam cell formation by cultured aortic smooth muscle cells.

Exposure of smooth muscle cells cultured on plastic or glass to hyperlipidemic serum did not result in the formation of foam cells. Since elastin binds serum lipids, and vascular smooth muscle cells are normally closely associated with elastin, we investigated the effects of an elastin substrate on lipid metabolism and on the accumulation of lipid vacuoles by rabbit aortic smooth muscle cells in culture. When cells were grown in plastic petri dishes, cholesteryl ester synthesis, as measured by [14C]oleate incorporation into cholesteryl esters, was 3 times greater in rabbit hyperlipidemic serum (HLS) than in normolipemic serum (NLS) (P less than 0.001). For cells of the same subculture grown on the elastin substrate, the synthetic rate was 6-fold greater in HLS compared to NLS (P less than 0.005). The cells grown on the elastin membranes in the presence of HLS contained large numbers of Oil red O stainable lipid vacuoles and resembled foam cells, while those grown in petri dishes and exposed to HLS showed only an occasional cell containing a few vacuoles. Pre-incubation in lipoprotein-deficient serum markedly enhanced the stimulatory effect of HLS on cholesteryl ester synthesis for cells growing in plastic petric dishes but had much less stimulatory effect on the cells growing on elastin membranes. These studies indicate that close association with elastin modulates the response of smooth muscle cells to hyperlipidemia and suggest a role for elastin in the formation of foam cells of smooth muscle origin during atherogenesis.

Animals↗