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Pathological Implications (pathological + implication)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

The noradrenaline plasma concentration and its gradient across the lung

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 8 2000
Marenzi
Background We investigated the lung contribution to circulating noradrenaline (NA) homeostasis. Evaluation of the transpulmonary NA gradient, related to the NA amount entering the lungs, is potentially important, mainly regarding clinical conditions, such as congestive heart failure (CHF), that are associated with excessive circulating NA. Materials and methods 15 moderate (group 1) and 15 severe (group 2) CHF patients, and 10 normal individuals had determination of NA transpulmonary gradient in the baseline and during rise (exercise, in normals and group 1) or fall (withdrawal from plasma by ultrafiltration, in group 2) of plasma NA. Results NA gradient (pg mL,1) at rest was 30 ± 3 in normals, 21 ± 6 in group 1 and 5 ± 8 in group 2. Increase of NA concentration in the mixed venous blood with exercise was paralleled by depression of the transpulmonary gradient. Pulmonary arteriovenous difference disappeared when NA entering the lungs averaged 1300 pg mL,1. In group 2, ultrafiltration lowered NA in the mixed venous blood from 1225 ± 213 to 718 ± 182, which caused transpulmonary gradient to increase from 5 ± 8 to 22 ± 9. Conclusions Transpulmonary gradient of NA diminishes when NA entering the lungs increases, and 1300 pg mL,1 in the pulmonary artery is, both in patients and normal subjects, the level at which gradient disappears; which likely reflects cessation of NA uptake or achievement of a balance between lung uptake and production. This may have physiological and pathological implications. [source]

Angiogenesis in the female reproductive organs: pathological implications

INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 4 2002
Lawrence P. Reynolds
Summary. The female reproductive organs (ovary, uterus, and placenta) are some of the few adult tissues that exhibit regular intervals of rapid growth. They also are highly vascular and have high rates of blood flow. Angiogenesis, or vascular growth, is therefore an important component of the growth and function of these tissues. As with many other tissues, vascular endothelial growth factors (VEGFs) and fibroblast growth factors (FGFs) appear to be major angiogenic factors in the female reproductive organs. A variety of pathologies of the female reproductive organs are associated with disturbances of the angiogenic process, including dysfunctional uterine bleeding, endometrial hyperplasia and carcinoma, endometriosis, failed implantation and subnormal foetal growth, myometrial fibroids (uterine leiomyomas) and adenomyosis, ovarian hyperstimulation syndrome, ovarian carcinoma, and polycystic ovary syndrome. These pathologies are also associated with altered expression of VEGFs and/or FGFs. In the near future, angiogenic or antiangiogenic compounds may prove to be effective therapeutic agents for treating these pathologies. In addition, monitoring of angiogenesis or angiogenic factor expression may provide a means of assessing the efficacy of these therapies. [source]

Role of EG-VEGF in human placentation: Physiological and pathological implications

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 8b 2009
Pascale Hoffmann
Abstract Pre-eclampsia (PE), the major cause of maternal morbidity and mortality, is thought to be caused by shallow invasion of the maternal decidua by extravillous trophoblasts (EVT). Data suggest that a fine balance between the expressions of pro- and anti-invasive factors might regulate EVT invasiveness. Recently, we showed that the expression of the new growth factor endocrine gland-derived vascular endothelial growth factor (EG-VEGF) is high in early pregnancy but falls after 11 weeks, suggesting an essential role for this factor in early pregnancy. Using human villous explants and HTR-8/SVneo, a first trimester extravillous trophoblast cell line, we showed differential expression of EG-VEGF receptors, PKR1 and PKR2, in the placenta and demonstrated that EG-VEGF inhibits EVT migration, invasion and tube-like organisation. EG-VEGF inhibitory effect on invasion was supported by a decrease in matrix metalloproteinase (MMP)-2 and MMP-9 production. Interference with PKR2 expression, using specific siRNAs, reversed the EG-VEGF-induced inhibitory effects. Furthermore, we determined EG-VEGF circulating levels in normal and PE patients. Our results showed that EG-VEGF levels were highest during the first trimester of pregnancy and decreased thereafter to non-pregnant levels. More important, EG-VEGF levels were significantly elevated in PE patients compared with age-matched controls. These findings identify EG-VEGF as a novel paracrine regulator of trophoblast invasion. We speculate that a failure to correctly down-regulate placental expression of EG-VEGF at the end of the first trimester of pregnancy might lead to PE. [source]

Nitric oxide in the lower urinary tract: physiological and pathological implications

BJU INTERNATIONAL, Issue 5 2000
F.H. Mumtaz
First page of article [source]

Heparan Sulfate Accumulation with A, Deposits in Alzheimer's Disease and Tg2576 Mice is Contributed by Glial Cells

BRAIN PATHOLOGY, Issue 4 2008
Paul O'Callaghan
Abstract Amyloid ,-peptide (A,) plaques, one of the major neuropathological lesions in Alzheimer's disease (AD), can be broadly subdivided into two morphological categories: neuritic and diffuse. Heparan sulfate (HS) and HS proteoglycans (HSPGs) are codeposits of multiple amyloidoses, including AD. Although HS has been considered a limiting factor in the initiation of amyloid deposition, the pathological implications of HS in A, deposits of AD remain unclear. In this study, immunohistochemistry combined with fluorescence and confocal microscopy was employed to gain deeper insight into the accumulation of HS with A, plaques in sporadic and familial AD. Here we demonstrate that HS preferentially accumulated around the A,40 dense cores of neuritic plaques, but was largely absent from diffuse A,42 plaques, suggesting that A,42 deposition may occur independently of HS. A codeposition pattern of HS with A, deposits in Tg2576 mice was also examined. We identified the membrane-bound HSPGs, glypican-1 (GPC1) and syndecan-3 (SDC3), in glial cells associated with A, deposits, proximal to sites of HS accumulation. In mouse primary glial cultures, we observed increased levels of GPC1 and SDC3 following A, stimulation. These results suggest that HS codeposits with A,40 in neuritic plaques and is mainly derived from glial cells. [source]