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PubMed2001

IgG-mediated histamine release from canine mastocytoma-derived cells.

BACKGROUND: Recent data suggest that normal tissue mast cells can express functional receptors for IgG under certain conditions. However, little is known about IgG receptor expression and functional consequences in mast cell neoplasms. METHODS: In this study, neoplastic mast cells were obtained from a dog with cutaneous mastocytoma (CM-MC) and from a dog with visceral mastocytoma (VI-MC). Both cell populations were characterized morphologically and functionally. RESULTS: Most cells proliferated constantly in suspension without particular supplements. Doubling times of CM-MC and VI-MC were 52.2 and 27.5 h, respectively. Both cell types were sensitive to formalin fixation, did not contain heparin and were tryptase and chymase positive. Electron microscopy showed fine granules with electron-dense content in both cell populations. The total histamine content of CM-MC and VI-MC was 0.25 and 0.10 pg/cell, respectively. Calcium ionophore A23187 and substance P induced dose-dependent histamine release, whereas compound 48/80 had no effect. Most significantly, both cell types, when sensitized with monomeric dog IgG, released histamine upon stimulation by anti-dog IgG. CONCLUSIONS: Dog mastocytoma-derived cells may be useful to study the regulation of neoplastic mast cell growth and differentiation, as well as IgG receptor-mediated activation in neoplastic mast cells. Further research is required to clarify the pathophysiological significance of constitutive expression of IgG receptors in neoplastic (canine) mast cells.

Animals↗

PubMed2004

The primitive streak, the caudal eminence and related structures in staged human embryos.

The caudal region of the trunk was reassessed in 52 serially sectioned human embryos of stages 8-23, 42 of which were controlled by precise graphic reconstructions. The following observations, new for the human, are presented. (1) The neurenteric canal is an important landmark because rostral to it the neural plate of stages 8, 9, and the main part of the notochord develop, whereas caudal to it the neural plate of stages 10-12 and the caudal portion of the notochord are formed. All somites at stages 9-11 and probably also at stage 12 arise rostral to the site of the neurenteric canal. (2) A 'chordoneural hinge' can be detected in stages 10 and 11, where the caudal part of the neural plate gives off cells that probably participate in the production of mesenchyme. (3) When apparent disappearance of the epiblast is used as a criterion, then the primitive streak seems to end during stage 9. (4) The caudal eminence, derived from the primitive streak and covered by ectoderm, forms at stage 10 caudal to the site of the former neurenteric canal and persists as a terminal cap to at least stage 14, although formation of mesenchyme continues in stages 15 to 17 or 18. (5) As the region rostral to the site of the neurenteric canal grows because of the development of somites, the caudal eminence is shifted caudally. (6) The caudal eminence is most active developmentally during stage 13, when most of the required (ca 6 out of 9) pairs of somites appear. (7) The eminence produces the caudal part of the notochord and, after closure of the caudal neuropore, all caudal structures, but it does not produce even a temporary 'tail' in the human. (8) A temporal overlap results between primary and secondary development in the caudal part of the notochord. (9) Primary development begins very early with the formation of the inner cell mass at stage 3, and includes the development of the somites rostral to the neurenteric canal, whereas secondary development, with the exception of the notochord caudally, commences at stage 12. (10) Primary neurulation lasts from stage 8 to stage 12, secondary from stage 12 to stages 17 or 18. (11) Secondary development and secondary neurulation are characterized morphologically by direct formation of structures (notochord, postcloacal gut, neural cord/neural tube) from mesenchyme.

Ectoderm↗

PubMed1988

Development and plasticity of retinal X and Y axon terminations in the cat's lateral geniculate nucleus.

The technique of injecting single retinogeniculate fibers with horseradish peroxidase enables the terminal arbors of physiologically identified axons to be fully characterized morphologically. We have used this technique to study the postnatal development of retinal X and Y cell arbors within the cat's lateral geniculate nucleus, and the plasticity of these arbors following a variety of manipulations that perturb normal development. These experiments suggest quite specific sequences and mechanisms for the development of individual X and Y retinogeniculate axons. Retinal X axons appear to innervate the lateral geniculate nucleus before Y axons do, and are probably specified innately to their appropriate target lamina A or A1. By 3-4 weeks postnatally, X axons from each eye develop exuberant terminal arbors within the A laminae that by 12 weeks get pruned to the narrow adult form by later developing Y axon arbors from the same eye. The Y arbors progressively expand to form their characteristic broad terminal zones during this period. The laminar location of Y arbors depends on interactions between axons from the two eyes, and their transverse extent on the presence of normal afferent activity in retinogeniculate fibers.

Animals↗

PubMed1994

Serum propeptides of type I and III procollagens in renal transplant recipients. A comparison of cyclosporine and azathioprine treatment.

Chronic cyclosporine nephrotoxicity is characterized morphologically by cortical interstitial fibrosis. The most important collagens involved in renal fibrosis are collagen types I and III. In order to estimate the synthesis of type III and type I collagens, we analyzed serum levels of the amino-terminal propeptide of type III procollagen (PIIINP) and the carboxy-terminal propeptide of type I procollagen (PICP) in 11 renal transplant recipients receiving cyclosporine (group CY) and a comparable group of 16 renal transplant recipients treated with azathioprine (group AZ). In addition, 27 healthy subjects and 15 patients with chronic renal disease and reduced renal function (group CRD) were examined. The cyclosporine-treated patients had serum PIIINP and PICP similar to the azathioprine-treated patients. Both groups of renal transplant recipients had significantly increased serum PIIINP compared to healthy controls (2p < 0.01) and serum PIIINP levels similar to group CRD in which serum PIIINP was also elevated compared to healthy controls (2p < 0.01). Mean serum PIIINP levels were: group CY 0.81 U/l (n = 11); group AZ 0.98 U/l (n = 16); controls 0.62 U/l (n = 27); and group CRD 1.06 U/l (n = 15). The renal graft recipients--both cyclosporine- and azathioprine-treated patients--had significantly increased PICP serum levels compared to healthy controls, but the patients with chronic renal disease had serum PICP levels which did not differ from that of healthy controls. Mean serum PICP levels were: group CY174 micrograms/l; group AZ151 micrograms/l; controls 106 micrograms/l; and group CRD119 micrograms/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1988

[Therapy of hairy cell leukemia with interferon].

Hairy cell leukemia is a rare lymphoproliferative disorder which is morphologically characterized by circulating lymphatic cells with prominent 'hairy' cytoplasmatic projections. Patients typically present with pancytopenia and splenomegaly. The bone marrow cannot be aspirated because of reticulin fibrosis. Chemotherapy was unable to influence the course of the disease satisfactorily. Therefore, splenectomy was the treatment of choice. The introduction of alpha-interferons into the therapy of hairy cell leukemia was a decisive breakthrough and is exemplary for the use of interferons in the treatment of malignant diseases. However, there are still many questions to be answered. The discussion of clinical implications is achieving growing importance in consequence of the availability of diverse commercial alpha-interferons for treatment of hairy cell leukemia.

Aged↗

PubMed1994

Clinical, histological and ultrastructural characteristics of a spontaneous corneal opacity in Sprague-Dawley rats.

The eyes of 200 rats (Mol:SPRD, Moellegaard Ltd., Skensvet, Denmark), 8 weeks of age and of both sexes, were examined routinely with a photo-slitlamp microscope (Zeiss) and opthalmoscope (Heine) 3-4 times in the course of four different 12-week toxicity studies. The animals were kept under constant lighting conditions at a room temperature of 20 +/- 2 degrees C and 55 +/- 5% humidity on a standard diet. More than 70% of the animals were found to have more or less prominent corneal opacities already at the beginning of the study. These were morphologically characterized as meshwork-like alterations of the deeper corneal epithelium, mostly located in the central and nasal region. The temporal, upper and lower periphery remained always unaffected. Male animals were more frequently and more intensively affected than the females. The occurrence of the opacity was totally independent of the treatment scheme (controls and drug dosages, respectively), showing a slight increase in density in some of the animals of all groups and remaining stable in others. Regression was rarely observed. Light and electron microscopical investigations demonstrated focal degenerations of the basal epithelial cell layer as well as alterations of its basement membrane. The lesion was not associated with inflammation or irritation. Therefore, we considered that a genetically determined metabolic disorder of the basal epithelial cells might have led to the impairment of basement membrane synthesis. Further screenings performed in conjunction with the breeder evidenced that these opacities are probably caused by a spontaneous mutation with a complex, not X-linked genetic background.

Animals↗

PubMedDate not supplied

Cytologic characteristics of pulmonary papillary adenoma. A case report.

BACKGROUND: Pulmonary papillary adenoma is a benign pulmonary neoplasm. Previously pulmonary papillary adenoma was described in terms of immunohistochemistry and ultrastructure. However, there are no previous reports describing the cytologic characteristics of pulmonary papillary adenoma. CASE: A 50-year-old male was admitted for evaluation of a coin lesion in the left upper lung field. Radiologic images showed a solid, round tumor approximately 25 mm in diameter in the left upper lung. Transbronchial needle aspiration biopsy (TBNA) was performed, and small numbers of atypical cells were collected. Adenocarcinoma was suggested clinically, and left upper segmentectomy was performed. The histologic diagnosis was pulmonary papillary adenoma. Imprint cytology of the cut surface of the tumor showed tumor cells arranged in sheets that contained scant or vesicular cytoplasm. The nuclei were oval or round, without obvious anisokaryosis, and their chromatin was fine, without hyperchromasia. Cytologically, the nuclei of the tumor cells in the imprint specimen (38.70 +/- 8.69 microns 2) were uniform in size and similar to the atypical cells in the TBNA specimen (38.29 +/- 11.56 microns 2) but significantly larger than the nuclei of the bronchial cells (23.61 +/- 5.98 microns 2) (P < .0001). CONCLUSION: The cytologic appearance of pulmonary papillary adenoma was characterized morphologically and morphometrically. The possibility of cytodiagnosis by TBNA was suggested.

Adenoma↗

PubMed2006

Modulation of adipose tissue development by pharmacological inhibition of PAI-1.

OBJECTIVE: The effect of a novel small molecule plasminogen activator inhibitor (PAI-1) inhibitor on adipose tissue physiology was investigated. METHODS AND RESULTS: In human preadipocyte cultures, PAI-039 inhibited both basal and glucose-stimulated increases in active PAI-1 antigen, yet had no effect on PAI-1 mRNA, suggesting a direct inactivation of PAI-1. Differentiation of human preadipocytes to adipocytes was associated with leptin synthesis, which was significantly reduced in the presence of PAI-039, together with an atypical adipocyte morphology characterized by a reduction in the size and number of lipid containing vesicles. In a model of diet-induced obesity, pair-fed C57 Bl/6 mice administered PAI-039 in a high-fat diet exhibited a dose-dependent reduction in body weight, epididymal adipose tissue weight, adipocyte volume, and circulating plasma active PAI-1. Plasma glucose, triglycerides, and leptin were also significantly reduced in drug-treated mice, and concentrations of PAI-039 associated with these physiological effects were near the in vitro IC50 for the inhibition of PAI-1. CONCLUSIONS: Our results indicate that a small molecule inactivator of PAI-1 can neutralize glucose-stimulated increases in PAI-1 in human preadipocyte cultures, reduce adipocyte differentiation, and prevent the development of diet-induced obesity. These data suggest the pharmacological inhibition of PAI-1 could be beneficial in diseases associated with expansion of adipose tissue mass.

Acetates↗

PubMed1994

Development of the atherosclerotic core region. Chemical and ultrastructural analysis of microdissected atherosclerotic lesions from human aorta.

Lipid deposits in human atherosclerotic fibrous plaques exhibit marked differences in chemistry and ultrastructure from lipid deposits in fatty streaks, leading some investigators to question whether fibrous plaques originate from fatty streaks. To examine lesion transition, we employed lipid microanalysis, electron microscopy, and immunohistochemistry on fatty streaks, fibrolipid lesions (small raised lesions), and fibrous plaques from human aorta. Both fatty streaks and caps of fibrolipid lesions were high in esterified cholesterol content (mean, 62% of total cholesterol) and high in cholesteryl oleate content compared with cholesteryl linoleate content. Fatty streaks and fibrolipid lesion caps also showed similar morphology, characterized mostly by macrophage-derived foam cells in the superficial intima. Core lipids in both small and large raised lesions differed markedly from this pattern. Fibrolipid lesion cores showed mostly vesicular extracellular deposits, sometimes accompanied by cholesterol clefts, while fibrous plaque core deposits were also extracellular but had a variable appearance. Compared with fatty streaks, fibrolipid lesion cores showed significantly increased free/total cholesterol fractions (63%) and decreased fractional contents of cholesteryl oleate. Fibrous plaque cores had variable distributions of free and esterified cholesterol but significantly decreased cholesteryl oleate fractions compared with fatty streaks. The results support the concept of lesion transition, which is marked by deep intimal, extracellular deposition of cholesterol-rich, vesicular lipid deposits in small raised lesions. In the core region of larger raised lesions, both cholesterol-rich and cholesteryl ester-rich lipid deposits appear to form in the extracellular space.

Aorta↗

PubMed1988

In vivo microscopy of the cerebral microcirculation using neonatal allografts in hamsters.

Studies were performed to characterize the morphology and vascular reactivity of the allografted cerebral microcirculation. Cerebral cortical tissue was allografted into the cheek pouch of the hamster so that cerebral parenchymal vessels could be studied. The vascular morphology was characterized by a large number of looping vessels. The ultrastructural examination indicated viable cerebral tissue containing typical vessels, that is, "tight" junctions, not like those of the cheek pouch. Also, the microvasculature was impermeable to 150, 70, and 20 kDa fluorescein isothiocyanate dextrans. Angiotensin II and norepinephrine caused constriction of the cerebral vessels whereas adenosine caused dilation. Isoproterenol did not affect cerebral arterioles; however, it dilated cheek pouch arterioles. Thus, this preparation provides a satisfactory model for studying the living cerebral microcirculation.

Adenosine↗

PubMed1992

Extracellular alkalinity exacerbates injury of cultured cortical neurons.

BACKGROUND AND PURPOSE: We have previously shown that extracellular acidity protects cultured fetal murine neocortical neurons from glutamate toxicity and combined oxygen-glucose deprivation injury, an action at least in part mediated by reduction in N-methyl-D-aspartate receptor activation. We now investigate the effect of extracellular alkalinity on both glutamate neurotoxicity and injury due to combined oxygen-glucose deprivation. METHODS: The effects of extracellular alkalinity during injury induced by exposure of murine neocortical cultures to glutamate (0.5 mM for 5 minutes) or oxygen-glucose deprivation are characterized morphologically and quantitated by efflux of lactate dehydrogenase from both neurons and glia to the bathing medium. Calcium accumulation is measured with calcium-45. RESULTS: Moderate extracellular alkalinity is well tolerated by cortical cells but significantly potentiates both glutamate neuronal toxicity and oxygen-glucose deprivation neuronal injury. In contrast, glial viability in the face of combined oxygen-glucose deprivation is little affected by extracellular alkalinity. Increased accumulation of calcium-45 during oxygen-glucose deprivation in alkalotic medium and blockade of this increase by MK-801 is demonstrated. CONCLUSIONS: These observations suggest that alkaline pH can exacerbate excitotoxic neuronal injury, most likely because of increased N-methyl-D-aspartate receptor activation. Metabolic alkalosis of any etiology may sensitize neurons to ischemic injury and potentiate reperfusion injury.

Alkalies↗

PubMed1999

Neuropsychological impairment correlates with hypoperfusion and hypometabolism but not with severity of white matter lesions on MRI in patients with cerebral microangiopathy.

BACKGROUND AND PURPOSE: Cerebral microangiopathy, indicated on MRI by lacunar infarctions (LI) and deep white matter lesions (DWML), is said to lead to vascular dementia. METHODS: Fifty-seven patients with proven cerebral microangiopathy were assessed for changes in regional cerebral blood flow (rCBF) and glucose metabolism (rMRGlu) and compared with 19 age-matched controls. The findings were correlated with results of extensive neuropsychological testing, as well as with MRI findings. A special head holder ensured reproducibility of positioning during rCBF (single-photon emission CT [SPECT]), rMRGlu (positron emission tomography [PET]), and MR imaging. White matter and cortex were quantified with regions of interest defined on MRI and superimposed to corresponding PET/SPECT slices. LI and DWML were graded by number and extent. RESULTS: Even with severe DWML and multiple LI, rCBF and rMRGlu values were not reduced. ANOVAs identified brain atrophy and neuropsychological deficits as the main determinants for reduced rCBF and rMRGlu values in both cortex and white matter. Neuropsychological deficits correlated well with decreased rCBF and rMRGlu, whereas MRI patterns such as LI and DWML did not. Factor analysis revealed no correlation of LI and DWML with rCBF, rMRGlu, atrophy, and neuropsychological deficits, showing instead positive correlations between rCBF, rMRGlu, and neuropsychological performance and negative correlations of the latter 3 with brain atrophy. CONCLUSIONS: From these data, we conclude that LI and DWML are epiphenomena that may morphologically characterize cerebral microangiopathy but do not in themselves indicate cognitive impairment. Dementia or neuropsychological deficits, by contrast, are reflected exclusively by functional imaging parameters (rCBF, rMRGlu) and cerebral atrophy.

Adult↗

PubMed1996

Lead (Pb+2) promotes apoptosis in newborn rat cerebellar neurons: pathological implications.

Despite mandated reduction in environmental lead (Pb++), such exposure still poses a public health hazard for children, with devastating effects on CNS development. To replicate aspects of this neurotoxicity, we used cultured granule cells from newborn rat cerebella to study whether apoptotic or necrotic death is the major consequence of exposure to low micromolar concentrations of Pb++. At a low dose, 1 microM (EC50 approximately equal to 10 microM), Pb++ does not affect glutamate-induced neuronal necrosis but promotes neuronal apoptosis, as characterized morphologically by cell shrinkage and chromatin condensation, biochemically by the typical internucleosomal DNA fragmentation and functionally by dependence on new synthesis of macromolecules (cycloheximide- and actinomycin D-sensitive). The low micromolar doses of Pb++ that promote apoptosis are well within the blood level range reported to impair CNS function in children and to alter synaptogenesis in the neonatal rat brain. Thus these in-vitro results suggest that the highly neurotoxic action of Pb++ in the developing CNS of children might depend on a facilitation of apoptosis. The Pb+2-elicited potentiation of neuronal apoptosis is attenuated by treatment with the voltage-sensitive Ca+2 channel agonist Bay K8644, which suggests the possible use of this agonist for treatment of the neurotoxic effects of Pb++.

Animals↗

PubMed2006

Synthesis of noble metal/carbon nanotube composites in supercritical methanol.

A simple and efficient route has been employed to deposit noble metal nanoparticles (Pt, Ru, Pt-Ru, Rh, Ru-Sn) onto carbon nanotubes (CNTs) in supercritical methanol solution. In this method, the inorganic metallic salts acted as metal precursors, and methanol as solvent as well as reductant for the precursors. The as-prepared nanocomposites were structurally and morphologically characterized by X-ray diffraction spectroscopy, transmission electron microscopy (TEM), scanning electron microscopy, and X-ray photoelectron spectroscopy analyses. It was demonstrated that the CNTs were decorated by crystalline metal nanoparticles with uniform sizes and a narrow particle size distribution. The size and loading content of the nanoparticles on CNTs could be tuned by manipulating reaction parameters. Furthermore, the formation mechanism of the composites was also discussed.

Chromatography, Supercritical Fluid↗

PubMed2003

Double cone dystrophy and RPE degeneration in the retina of the zebrafish gnn mutant.

PURPOSE: To characterize morphologic alterations in the retina of the visual mutant zebrafish gantenbein (gnn) and to examine whether these alterations correlate with those present in human hereditary eye diseases. METHODS: The gnn mutant was isolated by behavioral and macroscopic screening. Retinas of gnn zebrafish larvae were examined at different developmental stages from 2 to 9 days postfertilization (dpf) by standard histologic staining techniques and by immunocytochemistry. Ultrastructural alterations were examined by electron microscopy. The genetic map position of the induced mutation was identified by mapping with two candidate primer pairs on single larvae. RESULTS: The gnn mutant exhibited shortened outer photoreceptor segments and altered RPE morphology. In the photoreceptor layer of the mutant, the total number of lectin-labeled cones was reduced in all developmental stages from 2 to 7 dpf, whereas the amount of rhodopsin-positive cells remained at the wild-type (WT) level. Labeling with zebrafish opsin antibodies revealed dystrophic red cones at 5 dpf, whereas the morphology of all other cone types was largely unaffected. Electron microscopy unveiled electron-dense deposits between the discs of the double cone outer segments. In addition, the onset of progressive RPE degeneration was observed at this stage of development. At later stages, all cone types and the RPE became degenerative. The morphology of distinct second-order neurons remained largely unaffected by the mutation. The gnn mutation was located approximately 4.3 cM from the simple sequence length polymorphism (SSLP) marker Z15453 on linkage group 16. CONCLUSIONS: In gnn mutant zebrafish, cones, and especially red cones, are dystrophic in early retinal development. Subsequent to this cone dystrophy, the RPE becomes dysfunctional and starts to degenerate in later stages of development. Thus, the early developmental morphology of gnn exhibits similarities to cone dystrophies most commonly seen in age-related macular degeneration (AMD) among humans, whereas the later stages of degeneration in gnn resemble RPE alterations in retinitis pigmentosa (RP) in humans. The gnn zebrafish mutant may therefore be a useful model for examining the possible interplay and connection between cone dystrophy and RPE degeneration.

Animals↗

PubMed2004

Melanopsin is expressed in PACAP-containing retinal ganglion cells of the human retinohypothalamic tract.

PURPOSE: The putative circadian photoreceptor melanopsin is found in rodents in a subpopulation of intrinsic light-sensitive retinal ganglion cells (RGCs) constituting the retinohypothalamic tract (RHT). The study was conducted to determine whether melanopsin is expressed in the human retina and costored with the neuropeptide pituitary adenylate cyclase activating polypeptide (PACAP), a marker for the RHT, projecting to the suprachiasmatic nucleus (SCN). Furthermore, whether melanopsin expression is conserved in retinas of blind patients with severe retinal degeneration was investigated. METHODS: In situ hybridization and immunohistochemistry was used to demonstrate melanopsin synthesis in human eyes of 17 donors and two postmortem hypothalami containing the SCN. The coexistence of melanopsin and PACAP in elements of the retinohypothalamic tract was studied by dual-labeling immunocytochemistry. RESULTS: Melanopsin expression was found in a subpopulation of RGCs located in the ganglion cell layer and displaced in the inner nuclear cell layer. Melanopsin-containing cells comprised approximately 0. 8% of all RGCs, with a distinct morphology characterized by two to four dendritic processes constituting a panretinal network. Melanopsin immunoreactivity was primary present at perikaryal boundaries and neuronal processes and to some extent also in the cytoplasm. PACAP and melanopsin were colocalized in the RGCs and PACAP-containing nerve fibers, seemingly innervating the retinorecipient part of the SCN. Melanopsin-expressing RGCs were conserved in retinas of blind patients with severe degeneration of the outer and/or inner layers. CONCLUSIONS: Given the expression of melanopsin in PACAP-containing RGCs of the human RHT, this photoreceptor is a likely first base in the chain of events leading to photoentrainment of both normal and blind people.

Aged↗

PubMed1973

Response of the distal tubule and cortical collecting duct to vasopressin in the rat.

Renal micropuncture observations in the rat suggest that the entire "distal tubule" (defined by the micropuncturist as that portion of the renal tubule extending between the macula densa and its first junction with another (renal tubule) may be responsive to vasopressin. However, this portion of the renal tubule contains two segments that are morphologically dissimilar. The "early" distal tubule is lined by epithelium characteristic of the distal convoluted tubule, while the "late" distal tubule is lined by epithelium characteristic of the cortical collecting duct. Thus, the present study was initiated to identify the most proximal site of action of vasopressin in the distal renal tubule. A water diuresis was established in rats with hereditary hypothalamic diabetes insipidus. In one-half of the animals the diuresis was interupted by an i.v. infusion of exogenous vasopressin. Morphological preservation of the kidneys was initiated after induction of vasopressin-induced antidiuresis or during maximum water diuresis. Cell swelling and dilatation of intercellular spaces, morphological findings indicative of vasopressin responsiveness, were observed in the cortical collecting duct including the late segment of the distal tubule, a segment that has also been described by morphologists as the initial collecting tubule. Morphological evidence of vasopressin-responsiveness was not observed in the early distal tubule (distal convoluted tubule). Additional morphological studies in Wistar, Long-Evans, and Sprague-Dawley rats demonstrated a marked difference in the random availability of distal convoluted tubules versus initial collecting tubules potentially available for micropuncture just beneath the renal capsule. The results suggest that hypotonic tubular fluid entering the early distal tubule (distal convoluted tubule) remains hypotonic to plasma until it enters the late distal tubule (initial collecting tubule) and that vasopressin-induced osmotic equilibration is a function of the latter segment alone. The findings emphasize the importance of morphological characterization of those segments of the renal tubule that are subjected to physiological investigation.

Animals↗

PubMed1978

Protein degradation in normal and beige (Chediak-Higashi) mice,.

The beige mouse, C57BL/6 (bg/bg), is an animal model for the Chediak-Higashi syndrome in man, a disease characterized morphologically by giant lysosomes in most cell types. Half-lives for the turnover of [(14)C]bicarbonate-labeled total soluble liver protein were determined in normal and beige mice. No significant differences were observed between the normal and mutant strain for both rapidly and slowly turning-over classes of proteins. Glucagon treatment during the time-course of protein degradation had similar effects on both normal and mutant strains and led to the conclusion that the rate of turnover of endogenous intracellular protein in the beige mouse liver does not differ from normal. The rates of uptake and degradation of an exogenous protein were determined in normal and beige mice by intravenously injecting (125)I-bovine serum albumin and following, in peripheral blood, the loss with time of phosphotungstic acid-insoluble bovine serum albumin and the parallel appearance of phosphotungstic acid-soluble (degraded) material. No significant differences were observed between beige and normal mice in the uptake by liver lysosomes of (125)I-bovine serum albumin (t((1/2)) = 3.9 and 2.8 h, respectively). However, it was found that lysosomes from livers of beige mice released phosphotungstic acid-soluble radioactivity at a rate significantly slower than normal (t((1/2)) = 6.8 and 3.1 h, respectively). This defect in beige mice could be corrected by chronic administration of carbamyl choline (t((1/2)) = 3.5 h), a cholinergic agonist which raises intracellular cyclic GMP levels. However, no significant differences between normal and beige mice were observed either in the ability of soluble extracts of liver and kidney to bind [(3)H]cyclic GMP in vitro or in the basal levels of cyclic AMP in both tissues. The relevance of these observations to the presumed biochemical defect underlying the Chediak-Higashi syndrome is discussed.

Animals↗