Vascular Endothelial Growth Factor Expression and Vascularity in Renal Allograft Biopsies (original) (raw)
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Pial arteriolar vasomotion changes during cortical activation in rats
Neuroimage, 2007
The oscillatory pattern of pial arterioles, i.e. vasomotion, has been described since early 1980s, but the impact of neural activation on such oscillations has never been formally examined. Sciatic nerve stimulation, a well characterized model for studying neurovascular coupling (NVC), leads to a neural activity-related increase of pial arteriolar diameter in the contralateral hindlimb somatosensory cortex. Exploiting such an experimental model, the aim of the present study was to explore vasomotion and its changes during NVC with a novel analytical approach. Indeed, to characterize oscillations, we evaluated the total spectral power in the range 0.02-2.00 Hz and subdivided this frequency interval into seven 50% overlapping frequency bands. Results indicated that only arterioles overlying the stimulated hindlimb cortex showed a significant increase of total power, unlike arterioles overlaying the whisker barrel cortex, used as control for the vascular response specificity. The total power increase was sustained mainly by marked increments in the low frequency range, with two peaks at 0.03 and 0.08 Hz, and by a wide increase in the high frequency range (0.60-2.00 Hz) in the averaged spectrum.
NEURAL CONTROL OF RENAL MEDULLARY PERFUSION
Clinical and Experimental Pharmacology and Physiology, 2004
There is strong evidence that the renal medullary circulation plays a key role in long-term blood pressure control. This, and evidence implicating sympathetic overactivity in development of hypertension, provides the need for understanding hows ympathetic nerves affect medullary blood flow(MBF).
Kidney damage causally affects the brain cortical structure: A Mendelian randomization study
eBioMedicine, 2021
Background: Alterations in the brain cortical structures of patients with chronic kidney disease (CKD) have been reported; however, the cause has not been determined yet. Herein, we used Mendelian randomization (MR) to reveal the causal effect of kidney damage on brain cortical structure. Methods: Genome-wide association studies summary data of estimated glomerular filtration rate (eGFR) in 480,698 participants from the CKDGen Consortium were used to identify genetically predicted eGFR. Data from 567,460 individuals from the CKDGen Consortium were used to assess genetically determined CKD; 302,687 participants from the UK Biobank were used to evaluate genetically predicted albuminuria. Further, data from 51,665 patients from the ENIGMA Consortium were used to assess the relationship between genetic predisposition and reduced eGFR, CKD, and progressive albuminuria with alterations in cortical thickness (TH) or surficial area (SA) of the brain. Magnetic resonance imaging was used to measure the SA and TH globally and in 34 functional regions. Inverse-variance weighted was used as the primary estimate whereas MR Pleiotropy RESidual Sum and Outlier, MR-Egger and weighted median were used to detect heterogeneity and pleiotropy. Findings: At the global level, albuminuria decreased TH (b = À0.07 mm, 95% CI: À0.12 mm to À0.02 mm, P = 0.004); at the functional level, albuminuria reduced TH of pars opercularis gyrus without global weighted (b = À0.11 mm, 95% CI: À0.16 mm to À0.07 mm, P = 3.74£10 À6). No pleiotropy was detected. Interpretation: Kidney damage causally influences the cortex structure which suggests the existence of a kidney-brain axis.
Pathophysiology of the neurovascular unit: disease cause or consequence?
Journal of Cerebral Blood Flow & Metabolism, 2012
Pathophysiology of the neurovascular unit (NVU) is commonly seen in neurological diseases. The typical features of NVU pathophysiology include tissue hypoxia, inflammatory and angiogenic activation, as well as initiation of complex molecular interactions between cellular (brain endothelial cells, astroctyes, pericytes, inflammatory cells, and neurons) and acellular (basal lamina) components of the NVU, jointly resulting in increased blood–brain barrier permeability, brain edema, neurovascular uncoupling, and neuronal dysfunction and damage. The evidence of important role of the brain vascular compartment in disease pathogenesis has elicited the debate whether the primary vascular events may be a cause of the neurological disease, as opposed to a mere participant recruited by a primary neuronal origin of pathology? Whereas some hereditary and acquired cerebral angiopathies could be considered a primary cause of neurological symptoms of the disease, the epidemiological studies showing...
Permeable endothelium and the interstitial space of brain
Cellular and molecular neurobiology, 2000
1. Fenestrated vessels can be reversibly induced in brain by agents that stimulate urokinase production. This plasminogen activator, like vascular endothelial growth factor and metalloproteinases, is secreted by tumor cells and may account for induction of fenestrated vessels. Why only some of the brain's barrier vessels are converted to fenestrated vessels is unknown. 2. The structures responsible for the filtering of solutes by fenestrated vessels may be the same as those of continuous, less permeable vessels: the glycocalyx on the surfaces of the endothelial cells and the subendothelial basal lamina. 3. Solutes leaving the cerebral ventricles immediately enter the interstitial clefts between the cells lining the ventricles. A fraction of a variety of solutes, injected into CSF compartments, is retained by subendothelial basal lamina, from which the solutes may be released in a regulated way. 4. The brain's CSF and interstitial clefts are the conduits for nonsynaptic volum...
Relationship between vascular factors and white matter low attenuation of the brain
Acta Neurologica Scandinavica, 1993
To study the relationship between vascular factors and white matter low attenuation of the brain (WMLA), computer tomography findings of 25 1 patients were re-interpreted. Clinical data on patients were collected from the hospital records. It was possible to obtain sufficient clinical data on 204 patients who were included in the study. WMLA changes, on computer tomography, were found in 51.5% of patients. WMLA was most commonly present in patients with vascular (69.8%) and combined (69.2%) dementia. The occurrence of WMLA did not differ between patients with Alzheimer's disease (26.7 %) and those without dementia (35.9%). Arterial hypertension, coronary heart disease, or diabetes were not associated with WMLA. Heart failure and orthostatic hypotension, were found to be more commonly present in patients with than in those without WMLA (34.0% vs 14.3%, p = 0.0012; 10.0% vx 2.0%, p = 0.036). Both systolic and diastolic low blood pressure values were associated with WMLA unlike hypertensive blood pressure values. Atrial fibrillation in electrocardiography was associated with WMLA, while neither left ventricular hypertrophy nor myocardial infarction was. When several explanatory variables were adjusted by logistic regression analysis, age, heart failure, and systolic blood pressure below 130 predicted WMLA. In conclusion, the association between WMLA and vascular factors with hemodynamic significance suggests that cerebral hypoperfusion may contribute to the genesis of WMLA.
PLOS ONE, 2016
Renal tubulointerstitial injury often leads to interstitial fibrosis and tubular atrophy (IF/TA). IF/TA is typically assessed in the renal cortex and can be objectively quantitated with computerized image analysis (IA). However, the human medulla accounts for a substantial proportion of the nephron; therefore, medullary scarring will have important cortical consequences and may parallel overall chronic renal injury. Trichrome, periodic acid-Schiff (PAS), and collagen III immunohistochemistry (IHC) were visually examined and quantitated on scanned whole slide images (WSIs) (N = 67 cases). When tuned to measure fibrosis, IA of trichrome and Trichrome-PAS (T-P) WSIs correlated for all anatomic compartments (among cortex, medulla, and entire tissue, r = 0.84 to 0.89, P all <0.0001); and collagen III deposition correlated between compartments (r = 0.69 to 0.89, P <0.0001 to 0.0002); however, trichrome and T-P measures did not correlate with collagen deposition, suggesting heterogeneous contributions to extracellular matrix deposition. Epithelial cell mass (EPCM) correlated between cortex and medulla when measured with cytokeratin IHC and with the trichrome red portion (r = 0.85 and 0.66, respectively, all P < 0.0001). Visual assessment also correlated between compartments for fibrosis and EPCM. Correlations were found between increasing medullary inner stripe (IS) width and fibrosis in all of the tissue and the medulla by trichrome morphometry (r = 0.56, P < 0.0001, and r = 0.48, P = 0.00008, respectively). Weak correlations were found between increasing IS width and decreasing visual assessment of all tissue EPCM. Microvessel density (MVD) and microvessel area (MVA) measured using a MVD algorithm applied to CD34 IHC correlated significantly between all compartments (r = 0.76 to 0.87 for MVD and 0.71 to 0.87 for MVA, P all < 0.0001). Overall, these findings demonstrate the interrelatedness of the cortex and medulla and the importance of considering the renal parenchyma as a whole.
Journal of Neurology, Neurosurgery, and Psychiatry, 1972
Book reviews and serum pherograms in a number of inflammatory, neoplastic, and demyelinating disorders with brief accompanying case details. Changes in the CSF protein pattern found in meningitis of varying aetiology and radiculitis are attributed largely to selective alteration of blood-brain barrier permeability. Certain changes in post-albumin and transferrin bands are of interest and deserve further study. However, in general, the data do not provide any fresh information of diagnostic importance. The problem of CSF immunoglobulins in multiple sclerosis receives only scant mention. Brain proteins and CSF enzymes do not appear to have been considered in relation to the abnormal pherograms. The standard of production and illustration is high and there is a useful bibliography with full titles. The introductory sections on electrophoretic technique and the blood-brain barrier are lucid and would be of value to students.