Effect of vitamin A deficiency on oxalate uptake by rat intestinal brush border membrane vesicles (BBMV) and its contribution towards urolithiasis

The intestinal uptake of [14C]oxalate, [14C]glyoxylate, and [14C]glycolate are studied in brush border membrane vesicles (BBMV) isolated from vitamin A-deficient and pair-fed control rats. The data obtained indicate that oxalate and its precursors are transported across the BBMV by passive diffusion. The intestinal uptake of glyoxylate and glycolate remains unaltered in vitamin A deficiency, while uptake rate of oxalate was significantly increased (p less than 0.01) in vitamin A-deficient rats as compared to pair-fed controls. In conclusion, the results indicate that vitamin A deficiency leads to hyperabsorption of oxalate through the gut.     

Inhibition of Calcium Oxalate Monohydrate (COM) crystal growth by pyrophosphate,citrate and rat urine

Summary An assay system for the measurement of the rate of Calcium Oxalate Monohydrate (COM) seed crystal growth in a metastable solution of calcium chloride and sodium oxalate containing traces of ¹⁴C-oxalic acid was used to assess the inhibitory activity of pyrophosphate (10^–5 M-10^–4 M), citrate (10^–4 M-10^–3 M) and urines of normal and pyridoxine deficient rats. Both pyrophosphate and citrate were strong inhibitors of COM crystal growth and caused a 50% decrease in crystal growth rate at 1.50×10^–5 M and 2.85×10^–4 M respectively. Normal rat urine strongly inhibited the COM crystal growth, while pyridoxine deficient animals showed a significant (p< 0.01) decrease in mean inhibitory activity as compared to pair-fed controls. A lowered urinary inhibitory potential accompanied with hyperoxaluria and hypercalciuria, which is known to be associated with pyridoxine deficiency, may be a contributory risk of calcium oxalate crystallization and stone formation.     

Heterotopic heart transplantation: a radiographic review

Heterotopic heart transplantation can be performed in the presence of high pulmonary vascular resistance. The authors call attention to a rare, but potentially life-saving procedure.     

A comparison of radial dose functions for 103Pd, 125I, 145Sm, 241Am, 169Yb, 192Ir, and 137Cs brachytherapy sources.

Recently, encapsulated sources of 103Pd (21 keV average), 145Sm (41 keV average), 241Am (60 keV), and 169Yb (93 keV average) have been introduced as alternatives to conventional brachytherapy sources of 125I Model 6711 (27 keV average), 125I Model 6702 (28 keV average), 192Ir (369 keV average), and 137Cs (662 keV). To illustrate the dependence of the penetrating ability of photons from brachytherapy sources as a function of photon energy, a comparison of their radial dose functions is presented. Using the ITS Monte Carlo simulation code for photon-electron transport, the radial dose functions were calculated for monoenergetic photon sources with energies in the range of 30 keV to 1 MeV. Also, similar calculations were performed using the photon spectra emitted by the encapsulated brachytherapy sources. To verify the accuracy of Monte Carlo calculations, comparisons are made with our new measured data for 241Am and existing experimental and theoretical data from other investigators. A comparison of radial dose functions indicates that for 241Am, 169Yb, 192Ir and 137Cs sources radial dose functions are close to unity for distances up to 10 cm, for 145Sm the radial dose function drops to about 0.4 at 10 cm, and for 125I and 103Pd it drops precipitously to less than 0.20 at 7 cm. At 5 cm, the measured radial dose functions for 103Pd, 125I Model 6711, 125I Model 6702, 145Sm, 241Am, and 192Ir have values of 0.09, 0.34, 0.38, 0.86, 1.12, and 0.97, respectively. While all of these radioisotopes provide adequate penetrating power for interstitial brachytherapy, only the radioisotopes emitting photons with energies greater than about 40 keV can provide adequate depth dose (that is, small or no tissue attenuation) for intracavitary irradiation. Our criterion for choice of minimum photon energy suitable for intracavitary irradiation is that the radial dose function at 5 cm should not be less than 0.90. Also, note that photons with energies around 80 keV exhibit maximum penetrating ability in solid water for distances up to 5 cm.     

Cyclophosphamide-induced cytogenetic effects in mouse bone marrow and spleen cells in in vivo and in vivo/in vitro assays

Sister chromatid exchange (SCE) and chromosomal aberration studies have been used to monitor human populations for genotoxic exposure to chemical substances. These monitoring techniques involve collection of blood and/or bone marrow from the exposed subjects and culturing cells for one or two cell cycles with various treatments in culture. The results obtained from such in vivo/in vitro studies may lead to an over- or underestimation of the damage that could occur in vivo. In the present study, which uses a mouse model, the in vivo/in vitro cytogenetic assays (SCEs and chromosomal aberrations) have been compared with similar in vivo systems in bone marrow and spleen cells treated with various doses of cyclophosphamide (CPA). The results indicate a significant difference in CPA-induced cytogenetic endpoints between in vivo and in vivo/in vitro conditions in both organs. However, linear relationships were found between CPA dose and cytogenetic end point analyzed under both conditions. Based on these results it appears that the in vivo/in vitro assay is a useful technique for indicating potential in vivo damage of chemicals.     

A potential role for beta- and gamma-crystallins in the vascular remodeling of the eye.

We demonstrate that expression of beta- and gamma-crystallins is associated with intraocular vessels during normal vascular development of the eye and also in the Nuc1 rat, a mutant in which the hyaloid vascular system fails to regress normally. Real-Time RT PCR, Western blot and metabolic labeling studies indicate an increased expression of beta- and gamma-crystallins in Nuc1 retina. The increased expression of crystallins was localized to the astrocytes surrounding the intraocular vessels. A similar pattern of crystallin expression was also observed in the retinal vessels during normal development. Cultured human astrocytes exposed to 3-nitropropionic acid, an established model of neuronal hypoxia, increased VEGF expression, as expected, but also increased expression of crystallins. Our data suggest that crystallins may function together with VEGF during vascular remodeling. Interestingly, in human PFV (persistent fetal vasculature) disease, where the hyaloid vasculature abnormally persists after birth, we show that astrocytes express both VEGF and crystallins.     

Increased venous proinflammatory gene expression and intimal hyperplasia in an aorto-caval fistula model in the rat

We hypothesized that the venous limb of an arteriovenous (AV) fistula would evince up-regulation of genes relevant to vascular remodeling along with neointimal hyperplasia and relevant histological changes. Using the aorto-caval model of an AV fistula model in the rat, we demonstrate marked up-regulation in such proinflammatory genes as monocyte chemoattractant protein-1, plasminogen activator inhibitor-1, and endothelin-1, 2 weeks after the creation of the fistula. Neointimal hyperplasia occurred in variable degrees by 5 weeks after establishing the fistula, and by 16 weeks, such neointimal hyperplasia was progressive and pronounced; at this time point, abundant extracellular matrix was also observed. Smooth muscle cells were present in the hyperplastic neointima as evidenced by staining for alpha-smooth muscle actin; ultrastructurally, smooth muscle cells with a synthetic as well as a contractile phenotype were readily observed. Accumulation of extracellular matrix in the model at 16 weeks was accompanied by increased expression of transforming growth factor-beta1 mRNA, the latter finding contrasting with the suppression of transforming growth factor-beta1 mRNA observed in this model at 2 weeks. In summary, we describe marked up-regulation in proinflammatory genes and progressive neointimal formation in the venous vasculature in an AV fistula model in the rat. We suggest that such alteration in gene expression and histological injury, in conjunction with the relative simplicity of this model, offer a new approach in the study of such timely biological and clinically relevant phenomena as differential gene expression in response to hemodynamic forces, processes involved in vascular remodeling, mechanisms of injury in venous bypass grafts, and mechanisms of dysfunction of AV fistulae used in hemodialysis.