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PubMed1995

Aging changes mechanical loading thresholds for bone formation in rats.

The effect of aging on the mechanical loading thresholds for osteogenesis was investigated in rats. We applied mechanical loads varying from 30 to 64 N to the tibiae of 43 19-month-old rats using a four-point bending apparatus. Bone formation rates were measured on the periosteal and endocortical surfaces of the tibial midshaft using double-label histomorphometry. Bone formation rates from the old rats were compared with results from adult (9-month-old) rats that we reported earlier.(4) Bone formation on the periosteal surface of the old rats was predominantly woven-fibered. Periosteal bone formation was observed in a lower percentage of the old rats compared with the younger adult rats for applied loads of 40 N and greater (59% old, 100% adult). However, in the old rats that formed woven bone there were no significant differences in woven bone area (p=0.1) or surface (p=0.24) compared with younger adults. Therefore, the periosteum of old rats had a higher threshold for activation by mechanical loading, but after activation occurred, the cells had the same capacity to form woven bone as younger adult animals. On the endocortical surface, relative bone formation rates in old rats showed a marginal (p=0.06) increase in response to an applied load of 64 N but was not increased at lower loads. The relative bone formation rate in the old rats was over 16-fold less than that reported for the younger adult rats at an applied load of 64 N and the relative bone forming surface in old rats in this study was 5-fold less than it was younger rats under similar loading conditions. In the younger adult rats, a mechanical threshold for lamellar bone formation of 1050 microstrain was calculated for the endocortical bone surface. The old rats required over 1700 microstrain on the endocortical surface before bone formation was increased. The data suggest that both the periosteal and endocortical surfaces of the tibiae of older rats are less responsive to mechanical stimuli.

Adaptation, Physiological↗
PubMed1996

Prostaglandin E2 stimulates osteoclast-like cell formation and bone-resorbing activity via osteoblasts: role of cAMP-dependent protein kinase.

Prostaglandin E2 (PGE2) is an important local regulator in bone. The present study was performed to investigate the effect of PGE2 on osteoclast-like cell formation and bone-resorbing activity of mature osteoclasts in the presence or absence of osteoblasts, PGE2 (10(-8) to 10(-6) M) significantly stimulated osteoclast-like cell formation in osteoblast-containing mouse bone cell cultures, although it did not affect osteoclast-like cell formation from hemopoietic blast cells supported by granulocyte-macrophage colony-stimulating factor in osteoblast-free mouse spleen cell cultures. The conditioned medium from osteoblastic UMR-106 cells pretreated with PGE2 (10(-8) and 10(-6) M) significantly stimulated osteoclast-like cell formation from hemopoietic blast cells. PGE2 also significantly stimulated the bone-resorbing activity of mature osteoclasts in osteoblast-containing mouse bone cell cultures. In contrast, PGE2 significantly inhibited the bone-resorbing activity and osteopontin mRNA expression in isolated rabbit osteoclasts. Rp-cAMPS, a direct protein kinase (PKA) antagonist, significantly inhibited PGE2-stimulated osteoclast-like cell formation and the bone-resorbing activity of mature osteoclasts, although protein kinase C inhibitors, dantrolene (an inhibitor of calcium release from the intracellular calcium pool) and voltage-dependent calcium channel blockers did not affect PGE2-stimulated osteoclast-like cell formation. In conclusion, PGE2 stimulated osteoclast-like cell formation and bone-resorbing activity in mouse bone cell cultures presumably through osteoblasts. The activation of PKA is linked to PGE2-stimulated osteoclast-like cell formation and bone-resorbing activity.

Animals↗
PubMed2003

The phosphorylation state of neuronal processes determines growth cone formation after neuronal injury.

Growth cones are essential for neuronal pathfinding during embryonic development and again after injury, when they aid in neuronal regeneration. This study was aimed at investigating the role of kinases in the earliest events in neuronal regeneration, namely, the formation of new growth cones from injured neuronal processes. Neurites of identified snail neurons grown in vitro were severed, and the formation of growth cones was observed from the ends of such transected processes. Under control conditions, all neurites formed a new growth cone within 45 min of transection. In contrast, growth cone formation in the presence of a general kinase inhibitor, K252a, was significantly inhibited. Moreover, decreasing the phosphorylation state of neurites by activating protein phosphatases with C2-ceramide also reduced growth cone formation. Pharmacological analysis with specific kinase inhibitors suggested that targets of protein kinase C (PKC) and tyrosine kinase (PTK) phosphorylation control growth cone formation. Inhibition of PKC with calphostin C and cerebroside completely blocked growth cone formation, whereas the inhibition of PTK with erbstatin analog significantly reduced growth cone formation. In contrast, inhibitors of protein kinase A, protein kinase G, CaM-kinase II, myosin light-chain kinase, Rho kinase, and PI-3 kinase had little or no effect 45 min after transection. These results suggest that the transformation underlying the formation of a growth cone from an injured (transected) neurite stump is highly sensitive to the phosphorylation state of key target proteins. Therefore, injury-induced signaling events will determine the outcome of neuronal regeneration through their action on kinase and phosphatase activities.

Animals↗
PubMed1992

A real-time analysis of growth cone-target cell interactions during the formation of stable contacts between hippocampal neurons in culture.

Mechanisms of cell-cell recognition and structural changes of growth cones (g.c.) and target membranes during contact formation are poorly understood. To examine these issues, we obtained a high magnification, real-time record of stable contact formation in cultured cells from the hippocampal CA1 area in the newborn rat. We used differential interference contrast (DIC) optics coupled to a video microscope for periods of over 24 h of continuous time-lapse recording. Our goal was to observe the sequential changes exhibited by afferent and target cells as they form a stable contact. Understanding the process of how stable contacts are made is important because such contacts are the first step in synapse formation. Four principal observations emerged from our study: (1) The target cell was receptive to a contact on a specific patch on its surface defined by the presence of lamellae and filopodia. This specific patch (named target site) was invariably present on the target cell surface before the time the growth cone arrived. (2) Stable adhesion between filopodia on the two cells initiated events leading to cell-cell contact formation. Specifically, the remaining filopodia on the growth cone and target cell were redirected toward the adhering filopodia, and the growth cone size decreased dramatically. (3) The axonal process then grew at a significantly accelerated rate (up to 50 times its baseline growth rate). (4) In addition, a number of observations were obtained on axonal turns towards the target cell, induction of target sites, and architectural remodelling of cells after the formation of a new contact. Our findings indicate that in this neuronal system, filopodia are the means used by cells to interact at stages prior to and during contact formation. We speculate that the molecules involved in cell recognition and the machinery that initiates contact formation are embedded in the fine structure of filopodia. Finally, our results provide possible clues as to some of the stages that may be involved in synapse formation in the mammalian central nervous system.

Animals↗
PubMed1997

Salt concentration determines 1,25-dihydroxyvitamin D3 dependency of vitamin D receptor-retinoid X receptor--vitamin D-responsive element complex formation.

The electrophoretic mobility shift assay was used to determine in vitro formation of the vitamin D receptor-retinoid X receptor beta (VDR-RXR beta) heterodimer complex on vitamin D-response elements (VDREs) from rat osteocalcin, mouse osteopontin, rat 25-hydroxyvitamin D3 24-hydroxylase, and human parathyroid hormone (PTH) genes. Baculovirus-expressed rat VDR was used as VDR and the binding reactions were performed at salt concentrations ranging from 50 to 170 mM KCI. Without ligand, optimum complex formation was observed at 50 mM KCI and markedly decreased with increasing KCI for all VDREs. In the presence of 1,25-dihydroxyvitamin D3, optimum complex formation occurred between 110 and 130 mM KCI for positive (enhancer) VDREs. At low salt concentrations (50-70 mM KCI), 1,25-dihydroxyvitamin D3 did not increase complex formation and actually caused a slight decrease. However, above 90 mM KCI, 1,25-dihydroxy-vitamin D3 markedly increased complex formation and at 150-170 mM KCI, a concentration that presumably mimics physiologic nuclear levels, 1,25-dihydroxy-vitamin D3 appeared to be required for complex formation. With the suppressive cis-acting sequence, i.e., PTH-VDRE, optimum detection of VDR complexes in the presence of 1,25-dihydroxyvitamin D3 occurred at a lower salt concentration (90-110 mM KCI). Moreover, no specific complexes were formed at high salt concentrations, even when 1,25-dihydroxyvitamin D3 was added. Thus, when analyzing an effect of ligand on VDR-RXR-VDRE complex formation, it is essential that the reaction be carried out with a range of salt concentrations. Further, 1,25-dihydroxyvitamin D3 appears to be required for formation of the VDR-RXR beta-VDRE complex at salt concentrations approaching physiological.

Animals↗
PubMed1995

Formate dehydrogenase activity in cells and outer membrane blebs of Desulfovibrio gigas.

Formate dehydrogenase in Desulfovibrio gigas was measured by following the release of 14CO2 from radiolabeled formate. Experiments with whole cells using sulfate as the electron acceptor revealed optimal formate dehydrogenase activity at pH 7.0 and formate utilization followed saturation kinetics. While formate dehydrogenase was constitutively produced in pyruvate or lactate media, the formate dehydrogenase activity was markedly increased in cells grown with formate as the electron donor. In cell-free experiments with methyl viologen or 2,6 dichlorophenolindophenol, about 1% of the cellular formate dehydrogenase activity was present in blebs from the outer membrane. Electron microscopy revealed that these blebs were closed structures with diameters ranging from 80-800A and were not induced by changes in osmotic pressure or cellular autolysis. Analysis of blebs revealed the presence of lipopolysaccharides and two proteins with molecular masses of 70 and 53 kDa.

Journal Article↗
PubMed2002

Role of c-Fyn in FGF-2-mediated tube-like structure formation by murine brain capillary endothelial cells.

Tube formation of endothelial cells is an important step of angiogenesis. However, little is known about the molecular mechanisms underlying growth factor-mediated tube formation by endothelial cells. FGF-2 stimulates tube formation by a murine brain capillary endothelial cell line, IBE cells, when cultured on collagen gels (differentiation-associated culture condition), whereas cells proliferate and migrate without forming tube on fibronectin-coated surface (proliferation/migration-associated condition). To elucidate FGF-2-mediated signal transduction pathways leading to tube formation by endothelial cells, we focused on the contribution of Src family kinases. Src family kinase inhibitor PP2 attenuated FGF-2-induced tube formation. Stable expression of kinase-inactive c-Src in IBE cells demonstrated no dominant negative effect on FGF-2-induced tube formation. In vitro kinase assay revealed that c-Fyn was activated by FGF-2 only in cells cultured on collagen gels. Three independent cell lines, expressing kinase-inactive c-Fyn, all exhibited attenuation of FGF-2-mediated tube formation. However, FGF-2-mediated proliferation or migration was not clearly perturbed in these cells. These results show the first time that c-Fyn plays a pivotal role in tube formation by endothelial cells.

Animals↗
PubMed1997

Novel microwave technology for cryopreservation of biomaterials by suppression of apparent ice formation.

Ice formation inside or outside cells has been proposed to be a factor causing cryoinjury to cells/tissues during cryopreservation. How to control, reduce, or eliminate the ice formation has been an important research topic in fundamental cryobiology. The objective of this study was to test a hypothesis that the coupled interaction of microwave radiation and cryoprotectant concentration could significantly influence ice formation and enhance potential vitrification in cryopreservation media at a relative slow cooling rate. Test samples consisted of a series of solutions with ethylene glycol (a cryoprotectant) concentration ranging from 3 to 5.5 M. A specific microwave resonant cavity was built and utilized to provide an intense oscillating electric field. Solutions were simultaneously exposed to this electric field and cooled to -196 degrees C by rapid immersion in liquid nitrogen. Control samples were similarly submerged in liquid nitrogen but without the microwave field. The amount of ice formation was determined by analysis of digital images of the samples. The morphology of the solidified samples was observed by cryomicroscopy. It was found that ice formation was greatly influenced by microwave irradiation. For example, ice formation could be reduced by roughly 56% in 3.5 M ethylene glycol solutions. An average reduction of 66% was observed in 4.5 M solutions. Statistical analysis indicated that the main effects of microwave and ethylene glycol concentration as well as the interaction between these two factors significantly (P < 0.01) influenced ice formation amount, confirming the hypothesis. This preliminary study suggests that a combined use of microwave irradiation and cryoprotectant might be a potential approach to control ice formation in cells/tissues during the cooling process and to enhance vitrification of these biomaterials for long-term cryopreservation.

Cryopreservation↗
PubMed1997

Stimulation of tentacle and bud formation by the neuropeptide head activator in Hydra magnipapillata.

Stimulation of epithelial cell cycling by the neuropeptide head activator was analyzed in Hydra magnipapillata and compared with the action of head activator on bud formation and tentacle formation during head regeneration. The results obtained indicate that head activator treatment stimulates epithelial cell division and induces the formation of more tentacle-specific epithelial cells. The number of additional epithelial cells which undergo mitosis during head activator treatment accounts for the increased number of epithelial cells present in the regenerated tentacles. Therefore, the head activator stimulation of tentacle formation can be explained by the mitogenic action of head activator on tentacle cell precursors. To analyze stimulation of bud formation by head activator, polyps of different developmental age were tested under conditions of long-term treatment, and effects on bud formation were compared with effects on epithelial cell proliferation. Head activator treatment strongly stimulated bud formation, but had no detectable effect on epithelial cell numbers. Bud formation occurs at smaller polyp size as a result of head activator treatment, indicating that head activator significantly interferes with the patterning system in hydra.

Animals↗
PubMed2002

Prevention of gallstone formation in morbidly obese patients undergoing rapid weight loss: results of a randomized controlled pilot study.

INTRODUCTION: An increased risk of gallstone (GS) formation has been linked to obesity and to episodes of rapid and significant weight loss. Previous reports have suggested that bile salt therapy (ursodeoxycholic acid) or prostaglandin inhibition (ibuprofen) may prevent gallstone formation in this high-risk group. The purpose of this study was to investigate GS prevention following bariatric surgery. DESIGN: Randomized double blind controlled trial. METHODS: Sixty patients without gallstones preoperatively (gender, 9 male, 51 female; average preop wt, 349.6 lb; mean age, 38 years) were randomly assigned to receive urso (600 mg/day, n = 20), ibuprofen (600 mg/d, n = 20), or placebo (n = 20). At the time of standard open gastric bypass, intraoperative ultrasonography confirmed the absence of stones or microcalculi, and bile samples were collected via puncture of the gallbladder for bile lipid analysis. Following recovery and resumption of a bariatric diet, study medication was prescribed for the first 6 months postop. Gallbladder emptying and GS formation were assessed using ultrasonograms preop and at 3, 6, 9, and 12 months postop (gallbladder emptying following a high-fat liquid test meal was assessed preop, and at 3 and 6 months postop). RESULTS: Forty-one (68.3%, 8 male, 33 female) of the original 60 patients completed all phases of the study (15 urso, 15 ibuprofen, 11 placebo). The average weight loss was 98.5 +/- 7.2 lb over the 12-month period following bariatric surgery. Twenty-nine (71%) of 41 patients who completed the study developed GS. Of those who formed stones, 12 (41%) developed symptomatic GS and 8/12 (67%) underwent cholecystectomy (4 refused operation). Preoperative gallbladder emptying studies showed no differences in emptying between groups (urso 29%, ibuprofen 32%, and placebo 30%). There was no correlation found between the cholesterol saturation index (CSI mean 205.15, range 67-360) and the incidence of GS. There was a statistical difference (P < 0.01) between the ursodeoxycholic acid group and the ibuprofen group with respect to the incidence of stone formation. There was correlation between weight loss (mean 99 lb, range 21-278 lb) and GS formation, in that patients who lost more weight had a greater tendency to form gallstones. Complete medical compliance was achieved in only 17/60 (28%) of patients originally enrolled. CONCLUSIONS: This pilot study confirms the high incidence of gallstone formation (71% of assessed patients) associated with rapid weight loss in patients undergoing gastric bypass. Despite active enrollment in a supervised prevention trial, the two therapies investigated to reduce gallstone formation were not efficacious, likely because compliance with medical therapy was poor. These findings highlight the significant risk of gallstone formation in this patient cohort even when prevention strategies are utilized.

Adult↗
PubMed2001

Decorin inhibits endothelial migration and tube-like structure formation: role of thrombospondin-1.

Interactions between endothelial cell receptors and the extracellular matrix (ECM) play a critical, yet poorly understood role in angiogenesis. Based on the anti-adhesive role of decorin, we hypothesized that decorin binding to ECM molecules such as thrombospondin-1 (TSP-1) plays a regulatory role in endothelial tube-like structure (TLS) formation. To test this hypothesis, endothelial cells were plated on TSP-1, decorin, or mixed substrates of TSP-1 plus decorin. TLS formation was induced by applying type I collagen on the confluent endothelial monolayer. Cartilage decorin inhibited the formation of TLSs in a concentration-dependent manner. On substrates of high decorin concentrations (2.5 and 5.0 microg/cm(2)) the reduction in TLSs was due either to a reduction in the number of adhering cells or to decreased cell migration. At low decorin concentrations (0.05 and 0.25 microg/cm(2)) the reduction in TLSs was independent of the number of attached cells. Time-lapse video microscopy revealed that decorin substrates facilitated homotypic aggregation and isolated cord formation at the expense of endothelial migration and TLS formation. Consistent with the reduced migration, endothelial cells formed fewer vinculin-positive focal adhesions and actin-stress fibers on decorin substrates. Endothelial migration and TLS formation were also significantly inhibited by skin decorin and the protein core of cartilage decorin. The inhibition of TLS formation by the protein core of cartilage decorin was potentiated by TSP-1. These findings suggest that decorin alone or in combination with TSP-1 interferes with the activation of endothelial cell receptors by ECM molecules, thus blocking intracellular signals that induce cytoskeletal reorganization, migration, and TLS formation.

Cartilage↗
PubMed1996

Definition of a human herpesvirus-6 betaherpesvirus-specific domain in glycoprotein gH that governs interaction with glycoprotein gL: substitution of human cytomegalovirus glycoproteins permits group-specific complex formation.

Formation of the glycoprotein gH/gL heterooligomer has important implications for understanding the pathology of human herpesvirus-6(HHV-6)-associated disease because this complex is essential for infectivity and fusogenic cell-to-cell spread. Definition of the HHV-6 gH domain involved in protein-protein interactions was addressed by targeting regions defined by conserved cysteines identified by alignment of gH amino acid sequences representative of all herpesvirus subfamilies. Studies using site-directed mutagenesis and transient cellular expression showed that the N-terminus of HHV-6 gH includes a 230-amino-acid domain required for interaction with HHV-6 gL encompassing residues conserved specifically amongst betaherpesviruses. Interestingly, the human cytomegalovirus (HCMV) homologues, UL75 (gH) or UL115 (gL), can substitute for HHV-6 glycoproteins and participate in heterologous complex formation. Furthermore, the region which governs this heterologous gL binding also maps to the N-terminal portion of HHV-6 gH. Although both proteins can functionally substitute for complex formation there are also specific differences. Surprisingly, further deletion of HHV-6 gH to 145-amino-acid-domain residues abolishes complex formation with HHV-6 gL but allows interaction with HCMV gL. This may be related to requirements in HHV-6 for homodimer formation before complex formation between gH and gL. Under nonreducing conditions HHV-6 gH and gL form multimeric complexes consistent with intra- and intermolecular dimer formation stabilised by disulphide bonds whereas for HCMV there is no evidence for dimer formation for gH and multimeric complexes have only been observed between gH and gL. In summary, both HHV-6 and HCMV glycoproteins can interact and the heterologous complex between HHV-6 gH and HCMV gL is possibly more stable. This may result in important biological consequences in vivo during cellular coinfections by facilitating spread of the viruses, with applications to altered cellular tropisms and effects on reactivation from the latently infected cell.

Base Sequence↗
PubMed1989

Lack of effect of opioid peptides, morphine and naloxone on superoxide formation in human neutrophils and HL-60 leukemic cells.

There are controversial reports in the literature concerning the effects of opioids on superoxide (O2-) formation in phagocytes, these agents being either inhibitory or stimulatory. We re-examined this issue and compared the effects of the chemotactic peptide, N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMet-Leu-Phe), phorbol myristate acetate (PMA), ATP, platelet activating factor (PAF), cytochalasin B (CB) and prostaglandin E1 (PGE1) with those of various opioids on O2- formation in human neutrophils and HL-60 leukemic cells under defined experimental conditions. In the presence of CB, fMet-Leu-Phe and PAF concentration-dependently activated O2- formation in neutrophils with EC50 values of 20 nM and 100 nM, respectively. In the absence of CB, fMet-Leu-Phe and PAF were much less effective. PAF synergistically enhanced O2- formation induced by fMet-Leu-Phe. ATP at a concentration of 100 microM and the opioids, methionine enkephalin, beta-endorphin, dynorphin, [D-Ala2, N-Me-Phe4, Gly5-ol]-enkephalin, [D-Ala2-D-Leu5]-enkephalin and morphine at concentrations between 10 pM to 1 microM did not activate O2- formation. ATP but not beta-endorphin potentiated fMet-Leu-Phe-induced O2- formation. O2- formation induced by a maximally stimulatory concentration of PMA (100 ng/ml) was enhanced by fMet-Leu-Phe but was unaffected by methionine enkephalin or PGE1. PMA at a non-stimulatory concentration (2 ng/ml) potentiated the effect of fMet-Leu-Phe but did not induce responsiveness to PAF, ATP or beta-endorphin. PGE1 strongly inhibited fMet-Leu-Phe-induced O2- formation, whereas morphine, methionine enkephalin and the opioid antagonist, naloxone, were without effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1991

Tissue adhesives inhibit experimental new bone formation.

The effect of the cyanoacrylate tissue adhesive Histoacryl on new bone formation was studied in rats. Experimental heterotopic new bone formation was induced by implanting pieces of demineralized allogeneic bone matrix (DABM) in the abdominal wall of 10 growing Sprague-Dawley rats. This produces cartilage formation within and around the implants after 10 days, followed by enchondral ossification and the formation of an ossicle with remodelling bone and bone marrow after three weeks. Prior to implantation, the DABM-implants were treated with increasing amounts of the tissue adhesive n-Butyl-2-cyanoacrylate-monomer (Histoacryl). New bone formation was quantified at three weeks by assay of the ash content of the implants as a measure of net bone formation, by 45calcium uptake prior to sacrifice, and by histology. Treatment of DABM with the cyanoacrylate caused an intense inflammatory process with a foreign body reaction, and abolished bone induction and new bone formation. Tissue adhesives should be used with caution in fracture surgery since they inhibit new bone formation, cause a foreign body reaction, and may impede fracture healing.

Animals↗
PubMed1993

Effect of 24R,25-dihydroxyvitamin D3 on the formation and function of osteoclastic cells.

Previous reports demonstrated that the administration of large doses of 24R,25-dihydroxyvitamin D3 [24R,25(OH)2D3] to animals with normal vitamin D supply causes an increase in bone volume with reduced bone resorption and decreased osteoclast number. The present study was undertaken to clarify if 24R,25(OH)2D3 has any inhibitor effect on the formation and function of osteoclasts. The effect of 24R,25(OH)2D3 on the formation of osteoclastic cells was examined by measuring the number of tartrate-resistant acid phosphatase-positive multinucleated cells (MNCs) formed from hemopoietic progenitor cells obtained from spleens of 5-fluorouracil-treated mice. Treatment with 1,25(OH)2D3 or parathyroid hormone fragment 1-34 [PTH(1-34)] stimulated osteoclast-like MNC formation in a dose-dependent manner. Addition of 24R,25(OH)2D3 alone showed a weak stimulatory effect on MNC formation at 10(-6) M, which appeared to be due to its binding to 1,25(OH)2D3 receptors. In contrast, when 24R,25(OH)2D3 was added together with 1,25(OH)2D3 or PTH(1-34), it inhibited osteoclast-like MNC formation stimulated by these hormones. A significant inhibition of MNC formation was observed with 10(-7) M 24R,25(OH)2D3, and the stimulatory effect of 1,25(OH)2D3 or PTH(1-34) was almost completely eliminated with 10(-6) M 24R,25(OH)2D3. Neither 24S,25(OH)2D3 nor 25(OH)D3 exhibited a similar inhibitory effect. The effect of 24R,25(OH)2D3 on the resorptive function of osteoclasts was examined by measuring the formation of resorption pits by mouse bone cells on dentine slices. Treatment with 24R,25(OH)2D3 also inhibited the resorption pit formation stimulated by 1,25(OH)2D3 or PTH(1-34) with similar dose response.(ABSTRACT TRUNCATED AT 250 WORDS)

24,25-Dihydroxyvitamin D 3↗
PubMed1991

Effects of dietary calcium, magnesium and phosphorus on the formation of struvite stones in the urinary tract of rats.

After feeding various diets we studied the effects of dietary calcium, magnesium and phosphorus on the formation of struvite stones in rats with urinary tract infections, and also studied the effects of the administration of vitamin D3 and aluminium gel on stone formation. A low-magnesium diet decreased urinary magnesium and prevented stone formation, but a medium-calcium diet did not significantly decrease stone weight. A high-calcium diet decreased urinary phosphorus and inhibited stone formation. A high-calcium and high-phosphorus diet decreased urinary excretion of magnesium and inhibited stone formation. Although the administration of vitamin D3 did not inhibit stone formation, aluminium gel decreased the urinary level of phosphorus and prevented stone formation. A marked decrease in urinary magnesium and/or phosphorus may prevent struvite stone formation in rats with urinary tract infections.

Aluminum↗
PubMed1995

Clinical course and cystine stone formation during tiopronin treatment.

The formation of stones in patients with cystinuria can be counteracted by reducing the urinary concentration of cystine and by increasing its solubility. Thirty-one patients with homozygous cystinuria and treated with tiopronin (2-mercaptopropionylglycine) were followed for between 0.4 and 12 years (median 8.8). With the aim of avoiding cystine concentrations above 1200 mumol/l, the daily dose varied between 500 and 3000 mg (median 1500). The therapeutic effect was evaluated from the clinical symptoms and repeated radiographic examinations. The rate of stone formation during the treatment period was reduced by 60% in comparison with the pretreatment period (P < 0.001). The frequency of active stone removal was reduced by 72% (P < 0.05). The formation of new stones was associated with a higher cystine concentration than was the case during periods when stone formation and stone growth were excluded (P < 0.05). The probability of new stone formation increased with increasing concentrations of cystine up to 1100 mumol/l, but stone formation was not accentuated above 1200 mumol/l. There was no significant relationship between the 24 h excretion of cystine and stone formation. It is concluded that the formation of cystine stones can be efficiently counteracted during treatment with tiopronin, guided by analysis of the concentration of urinary cystine.

Adolescent↗
PubMed1988

In vitro inhibition of leukotriene B4 formation by exogeneous 5-lipoxygenase inhibitors is associated with enhanced generation of 15-hydroxy-eicosatetraenoic acid (15-HETE) by human neutrophils.

Leukotrienes, products of the 5-lipoxygenase pathway of arachidonic acid metabolism, have been suggested to play a pathogenic role in psoriasis, because of their ability to induce skin inflammation and to stimulate epidermal proliferation. The 15-lipoxygenase product 15-hydroxy-eicosatetraenoic acid (15-HETE) has no proinflammatory capacity. In contrast, it can inhibit the activity of the 5-lipoxygenase. The purpose of the present study was to study the effect of 5-lipoxygenase inhibitors on the formation of 15-HETE by human neutrophils in vitro. Purified neutrophils were incubated with A 23187 (5 microM) and arachidonic acid (25 microM) with and without different inhibitors of 5-lipoxygenase activity (RS 43179, benoxaprofen, NDGA, and CP 66248). Methods for identifying eicosanoids included RP-HPLC and radioimmunoassay. Formation of leukotriene B4 was inhibited in a dose-dependent way, which was strongly correlated with a concomitant increase in the formation of 15-HETE (r = 0.97, p less than 0.01). The cyclooxygenase inhibitor indomethacin did not change 15-HETE formation. The stimulation of 15-HETE formation was not associated with cell damage as assessed by LDH release. Furthermore, identical incubations of T lymphocytes, characterized by a low 5-lipoxygenase activity, did not result in increased 15-HETE formation. These results show that inhibition of 5-lipoxygenase activity can lead to increased formation of 15-HETE. Because 15-HETE inhibits formation of 5-LO products, it may amplify the effect of 5-lipoxygenase inhibitors.

Arachidonate Lipoxygenases↗