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Hydrogen ion metabolism.

The renal and respiratory systems regulate acid base homeostasis by modifying the bicarbonate buffer pair HCO3- and CO2; other buffer systems adjust to alterations in this pair. The pH change following addition of metabolic acid, or base, is modified initially by the body's buffers. Subsequent respiratory compensation, by retention or excretion of CO2, modifies further this change before renal corrective responses finally occur. A primary respiratory acid base change is modified initially by cellular buffers, with renal compensatory mechanisms adjusting slowly to this change. However correction of the respiratory pH disorder only occurs with correction of the primary disease process. The body's capacity, therefore, to adjust to a matabolic acid base defect, appears greater than that observed with a primary respiratory pH abnormality. Treatment in all acid base disorders focuses initially upon the primary diseases process; thereafter therapeutic manipulation of the HCO3-, CO2 buffer pair, to aid the body's compensatory processes, can be considered.

Acid-Base Imbalance↗

Altered localization of Cav1.2 (L-type) calcium channels in nerve fibers, Schwann cells, odontoblasts, and fibroblasts of tooth pulp after tooth injury.

We have determined the localization of Cav1.2 (L-Type) Ca2+ channels in the cells and nerve fibers in molars of normal or injured rats. We observed high levels of immunostaining of L-type Ca2+ channels in odontoblast cell bodies and their processes, in fibroblast cell bodies and in Schwann cells. Many Cav1.2-containing unmyelinated and myelinated axons were also present in root nerves and proximal branches in coronal pulp, but were usually missing from nerve fibers in dentin. Labeling in the larger fibers was present along the axonal membrane, localized in axonal vesicles, and in nodal regions. After focal tooth injury, there is a marked loss of Cav1.2 channels in injured teeth. Immunostaining of Cav1.2 channels was lost selectively in nerve fibers and local cells of the tooth pulp within 10 min of the lesion, without loss of other Cav channel or pulpal labels. By 60 min, Cav1.2 channels in odontoblasts were detected again but at levels below controls, whereas fibroblasts were labeled well above control levels, similar to upregulation of Cav1.2 channels in astrocytes after injury. By 3 days after the injury, Cav1.2 channels were again detected in nerve fibers and immunostaining of fibroblasts and odontoblasts had returned to control levels. These findings provide new insight into the localization of Cav1.2 channels in dental pulp and sensory fibers, and demonstrate unexpected plasticity of channel distribution in response to nerve injury.

Animals↗

Radial astrocytes and ependymocytes in the spinal cord of the adult toad (Bufo bufo L.). An immunohistochemical and ultrastructural study.

Immunohistochemical and ultrastructural techniques have been used to demonstrate glial fibrillary acidic protein (GFAP) immuno-positive cells in the adult toad spinal cord. Two types of GFAP-immunoreactive cells were observed: ependymocytes and radial astrocytes. GFAP-positive ependymocytes were scarce and contained the immunoreactive product in their processes. They showed intermediate filaments in the basal pole and in their processes when studied with the electron microscope. These immuno-positive ependymocytes represent the tanycytic form of ependymal cells because their processes ended at the subpial zone. The radial astrocytes showed a more intensive immunoreactive product in somata and processes when they were located far away from the ependymal layer. Cell bodies and processes were also associated with blood vessels, but most of the processes ended at the subpial zone forming a continuous subpial glia limitans. The GFAP-positive processes, which form this subpial glia limitans in the toad spinal cord, belong to both tancytic ependymocytes and radial astrocytes, whose somata are located in the grey matter. These findings lead us to suggest that both types of GFAP-immunopositive cells might be the functional equivalents of mammalian astrocytes.

Animals↗

Functional and morphological changes in cultured neurons of rat cerebral cortex induced by long-term application of aluminum.

Aluminum is an environmental neurotoxin and a suspected risk factor for Alzheimer's disease. The neurotoxicity of aluminum on cultured neurons of rat cerebral cortex was investigated using an assay system for synapse formation and immunohistochemistry. The frequency of spontaneous oscillations of intracellular Ca2+, which is correlated to the number of synapses, was decreased after exposure to 100 microM of aluminum chloride for 22 days. Long-term application of aluminum (48 days) caused aggregation of cell bodies and fasciculation of processes. Processes and cell bodies were strongly stained by antibody to tau protein, which is one of the main components of Alzheimer's neurofibrillary tangles. It is suggested that the characteristics of the degeneration of cultured neurons induced by aluminum show some similarities to the pathology observed in brains with Alzheimer's disease.

Aluminum↗

Distribution of neurohypophysial peptides in the guinea pig brain. I. An immunocytochemical study of the vasopressin-related glycopeptide.

Using an affinity-purified antibody directed against the vasopressin-related glycopeptide as a marker to distinguish reliably vasopressin-producing from oxytocin-producing cells, we mapped the distribution of vasopressin cell bodies and processes in the brain of adult, untreated guinea pigs. Strongly labelled cell bodies were detected in the area of the paraventricular, supraoptic and suprachiasmatic hypothalamic nuclei. Lightly stained cell bodies were observed in the zona incerta, in the bed nucleus of the stria terminalis, in the medial amygdala and in the brainstem. Immunoreactive axons differed markedly in size and shape. Several pathways other than the hypothalamoneurohypophysial tract could be tentatively identified coursing, toward limbic structures, toward midline thalamic nuclei and toward the mesencephalon and brainstem. In contradistinction to what was observed in the rat in previous studies, no difference in the density of the innervation of the lateral septum was apparent when comparing male and female guinea pigs. A sex difference was, however, detected in the brainstem, where numerous immunoreactive cell bodies and axons were observed in the female but not in the male.

Animals↗

pp60c-src is developmentally regulated in the neural retina.

We have localized normal cellular pp60c-src in the developing chick neural retina by immunocytochemical staining using antisera raised against bacterially expressed pp60v-src, the src gene product of Rous sarcoma virus. pp60c-src was expressed in developing retinal neurons at the onset of differentiation. Expression of pp60c-src persisted in mature neuronal cells that were postmitotic, fully differentiated, and functional. pp60c-src immunoreactivity was localized within processes and cell bodies of ganglion neurons, processes of rods and cones, and in some but not all neurons of the inner nuclear layer. Protein kinase assays and Western transfer analyses identified the immunoreactive protein as pp60c-src, and confirmed that its expression occurs at the time the first neuronal cells in the retina differentiate. We conclude from these studies that pp60c-src is the product of a developmentally regulated gene that is more important in neuronal differentiation or function than cell proliferation.

Animals↗

Lucifer yellow uptake in developing rat retina: selective staining of horizontal cells.

We have examined the uptake of Lucifer yellow CH by developing rat retina. We find that selective dye uptake occurs in retina incubated in vitro in the absence of external Ca2+. The pattern of uptake appears to depend on the developmental stage examined. Although little uptake is seen before postnatal day 5, between days 6 and 9, the dye selectively stains putative horizontal cell bodies and their process. Later, other cell bodies located deeper in the INL begin to show staining until day 21, when the uptake pattern becomes analogous to that seen in adult retina. By nearest neighbor analysis of labeled cell bodies in wholemounts of D-9 retina, we have shown that the labeled cells are distributed in a quasi-regular mosaic in the retina. Upon proteolytic dissociation of labeled retina, individual cells with Lucifer yellow fluorescence could be readily identified in the cell suspensions.

Animals↗

Interaction of L cells and Chlamydia psittaci: entry of the parasite and host responses to its development.

The entry and development of Chlamydia psittaci in the L cell was studied by using purified, infectious parasites at high multiplicity. Entry of the parasite was accomplished by an act of phagocytosis by the host which was independent of an adsorption stage but was temperature-dependent. Kinetic studies of phagocytosis performed with (14)C-amino acid-labeled, purified parasites indicated that the rate of phagocytosis was directly proportional to the multiplicity of inoculation. Electron microscopy of cells infected at high multiplicity with purified infectious C. psittaci showed that phagocytosed chlamydiae were segregated in a host phagocytic vacuole throughout their developmental cycle which consisted of the transition of infecting elementary bodies to reticulate bodies dividing by binary fission, followed by the reemergence of a population of elementary bodies. The process of the transition was examined and a proposed sequence of intermediate bodies is presented. In isopycnic gradients of fractionated, infected L cells, chlamydial phagocytic vacuoles were apparent as a dense band distinct from lysosome and mitochondrion peaks, as indicated by acid phosphatase and cytochrome oxidase activities. Chlamydiae inactivated by heat or neutralized by antiserum were phagocytosed and appeared in lysosomes within 12 hr after infection according to electron microscopy; however, chlamydiae which were continuously inhibited in their development by chloramphenicol were retained intact in the cell for 24 hr without lysosomal response. The possibility of a lysosomal inhibitor on the native parasite is discussed.

Acid Phosphatase↗

Vasopressin gene expression in the normal and Brattleboro rat: a histological analysis in semi-thin sections with biotinylated oligonucleotide probes.

We analyzed expression of the vasopressin (AVP) gene in semi-thin sections in normal and Brattleboro rats by using in situ hybridization and immunohistochemistry. AVP mRNA was detected as follows: vibratome sections of rat hypothalamus were hybridized with a biotinylated oligonucleotide probe, embedded in Araldite, and cut into semi-thin sections which were reacted with streptavidin-alkaline phosphatase and the appropriate substrate. Adjacent serial sections were treated by immunohistochemistry to detect AVP or oxytocin immunoreactivity. In normal rat, AVP mRNA can be detected in magnocellular neurons of the supraoptic and paraventricular nuclei and in parvocellular neurons of the suprachiasmatic nucleus. AVP mRNA was present throughout the cytoplasm of the cell bodies, their processes, and in punctate structures in the vicinity of the AVP cell bodies. Most neurons containing AVP mRNA also contain AVP immunoreactivity, but the staining intensity was not consistently correlated for each reaction. A few neurons contained AVP mRNA without detectable AVP immunoreactivity. In the Brattleboro rat, staining intensity of the reaction was lower than in normal rat and the AVP mRNA was restricted mostly to the periphery of the cytoplasm. In this strain, the neurons containing the AVP mRNA did not contain AVP or oxytocin immunoreactivity. These results demonstrate that neuropeptide mRNA can be detected in semi-thin sections with a biotinylated oligonucleotide probe, and that AVP gene deletion provokes modification of the intracellular localization of the AVP mRNA.

Animals↗

Nuclear medicine--an overview.

A radioactive isotope behaves chemically and biologically like its non-radioactive counterpart. The application of this principle to medical diagnosis has evolved into a whole specialty called nuclear medicine. The development of the rectilinear scanner and gamma camera has extended the study of molecular pathways into an exciting imaging modality while developments in radiopharmaceuticals have made radionuclide imaging of many organ systems widely available. The most significant improvements have occurred in bone, hepatobiliary and cardiac imaging. Today, however, nuclear medicine is evolving into a more dynamic study of physiological processes in the body and how these processes may be affected by disease and medical treatment. Emission tomography with a new generation of both gamma and positron emitters will be integral part of nuclear medicine in the future. The challenge to develop radio-labelled antibodies for immunotherapy and immunodetection remains while many of the older techniques like radioimmunoassay, and even the simple colloid liver scan, will continue to contribute significantly to health care.

Humans↗

Light and electron microscopic localization of GABAA-receptors on cultured cerebellar granule cells and astrocytes using immunohistochemical techniques.

GABAA-receptors were localized in explant cultures of rat cerebellum and in dissociated primary cultures of rat cerebellar granule cells and rat cerebellar astrocytes using the monoclonal antibody bd-17 directed against the beta-subunit of the GABAA/benzodiazepine/chloride channel complex. At the light microscope level specific staining of GABAA-receptors was localized in various types of neurones in explant cultures of rat cerebellum using the indirect peroxidase-antiperoxidase (PAP) technique, whereas no specific staining was found in astrocytes. At the electron microscope level labeling of GABAA-receptors was observed in the plasma membrane of both the cell bodies and processes in dissociated primary cultures of cerebellar granule cells using an indirect preembedding immunogold staining technique which in contrast to the classical PAP technique allows quantitative estimations to be performed. Quantification of the labeling intensity revealed a higher concentration of GABAA-receptors per microns plasma membrane in the cell bodies than in the processes. In discrete areas an extremely high density of the GABAA-receptors was observed. No specific labeling of GABAA-receptors was observed in dissociated primary cultures of cerebellar astrocytes.

Animals↗

Immunocytochemical and ultrastructural studies of Pick's disease.

Cerebral cortical changes in 10 cases with Pick's disease were studied immunocytochemically and ultrastructurally. All cases contained Pick's argentophilic bodies and ballooned neurons. The antibodies against phosphorylated tau proteins that intensely stained all Pick bodies recognized numerous neuronal processes around Pick body-bearing cells and focal portions in the perikarya of ballooned neurons. Monoclonal and polyclonal anti-ubiquitin antibodies stained not only some Pick bodies with variable intensity, but also the perikarya of all ballooned neurons. Ultrastructurally, Pick bodies consisted of accumulation of randomly oriented, approximately 15-nm straight filaments and paired twisted profiles with a minimal diameter of 13 nm, maximal diameter of 26 nm, and twist periodicity of 120 nm. These Pick body-type filaments were also observed in the perikarya of ballooned neurons and neuronal processes around Pick body-bearing cells. Our studies demonstrate, for the first time, the characteristic pathological feature of neuropil in Pick's disease. Pick body-bearing cells and ballooned neurons show unique immunocytochemical and ultrastructural properties that may be a clue to the pathogenesis of Pick's disease.

Aged↗

[Comparison between clinical Cobb angles and measurements performed on vertebral bodies, pedicle centroids and spinous processes].

GOAL: Evaluate the relations between the clinical Cobb angle measured on radiographic images and the computerized Cobb angles measured on curves passing through: 1) the vertebral body centroids, 2) the pedicle centroids and 3) the spinous process tips, in the frontal plane, the sagittal plane and the plane of maximum curvature. MATERIAL AND METHODS: A bi-planar radiographic technique was used to reconstruct in 3D the spine geometry for 39 adolescent girls having double-curved idiopathic scoliosis. The Cobb angles were measured clinically on the radiographs and were computed on the 3 curves. RESULTS: Every relation was found significant and their determination coefficient (R2) was between 0.38 and 0.98. Linear relations were established between clinical and computerized angles. Angles measured on the curve passing through the pedicle centroid correlated best with clinical indices. CONCLUSIONS: The computerized measurements of Cobb angles from 3D models can be used with confidence and are interchangeable, provided the appropriate conversion factor is used.

Adolescent↗

Protein-rich cytoplasmic bodies of substantia nigra and locus ceruleus. A comparative study in parkinsonian and normal brain.

A histochemical study of substantia nigra and locus ceruleus from postmortem brains showed the presence of small spherical cytoplasmic bodies stained selectively by the anionic phosphotungstic acid-hematoxylin (PTAH) stain at a pH of 2.5. The metachromatic reaction to PTAH indicates that these protein bodies contain a protein rich in free basic amino groups. The protein bodies are localized within the neuronal perikaryon as well as in their dendritic processes. These bodies abundantly present in the substantia nigra and locus ceruleus of normal brains were noticeably reduced or absent in parkinsonian brains. Lewy bodies when present show that their core gives the same metachromatic reaction to PTAH as do the protein bodies. These findings suggest that an abnormality of protein synthesis in the substantia nigra and locus ceruleus of parkinsonian brains may be related to the absence of protein bodies and the formation of Lewy bodies and play a role in pathogenesis of the parkinsonian state.

Aged↗

Basal laminae and Meissner corpuscle regeneration.

Murine Meissner corpuscles (mouse digital corpuscles), located in pad skin at the toe tip, consist of lamellar cells with long cellular processes (lamellae) surrounding axon terminals in an onion-skin fashion. Lamellar cell bodies and processes were provided with a basal lamina. The present study was made to examine whether these lamellar cell basal laminae have any specific role in the differentiation of regenerating axons and Schwann cells into specialized axon terminals and lamellar cells, respectively. Pad skin at the toe tip was treated 3-5 X by freezing and thawing. By this treatment, cellular constituents of the corpuscles die and disintegrate into cell debris, leaving in situ basal laminae of the lamellar cells in stacked hollow loops, reminiscent of the original configuration of lamellae. Schwann cells and axons of the ordinary nerve fibers in the pad skin were similarly damaged, and basal laminae of the Schwann cells remained as basal lamina tubes. Three days after treatment, regenerating axons were seen extending through the basal lamina tubes of Schwann cells deep in the toe pad skin. However, no regenerating axons were found in the vicinity of the old corpuscles. Five days after treatment, regenerating axons, some of which were accompanied by migrating Schwann cells and others which were still naked, were noted at the subepidermal region, and began to enter the hollow basal lamina loops of the old corpuscles. Eight-15 days after treatment, regenerating axons which entered the basal lamina loops successively gave rise to branches, and at the same time, accompanying Schwann cells emanated cellular processes through well-preserved basal lamina loops. Fifteen-25 days after treatment, regenerating axons seemed to be morphologically specialized as axon terminals, and accompanying Schwann cells differentiated into definite lamellar cells which surrounded the axon terminals in the same manner as in the normal murine Meissner corpuscles. Although the incidence of good regeneration of the corpuscle was relatively low, these findings suggested that basal laminae of lamellar cells might have some specific properties which could be responsible for the differentiation as well as maintenance of lamellar cells and axon terminals in the Meissner corpuscles.

Animals↗

Effect of infection with rubella virus on the development of rat cerebellar cells in culture.

Immunogold-silver staining of mixed rat cerebellar neuron/glial cell cultures, using Ranscht monoclonal antibody, resulted in labelling of neuronal processes and oligodendrocytes. This antibody was originally believed to react with galactocerebroside alone, and it was concluded that labelling by it resulted from the presence of myelin [2]. Electron microscopic examination of the cultures did not reveal myelination. Infection of such cultures with rubella virus resulted in a cytopathic effect. This effect was initially characterized as a disaggregation of neuronal processes, and the disruption of a layer of membranous material covering both cell bodies and processes. The virus causes disruption of cultures of pure glial cells, but there is no evidence of virus multiplication or cytopathic effect in pure neuron cultures. The cytopathic effect in mixed neuron/glial cell cultures is concluded to be glial cell mediated.

Animals↗

The turnover of body water as an indicator of health.

Water homeostasis is essential for healthy living. Body water turnover, meaning the replacement of body water that is lost in a given period of time, has been examined in a number of previous studies, and a review of their results has yielded the following findings. Children up to 15 years of age show higher body water turnover than adults, although it is not clear how the aging process influences body water. Among people of similar age, the rate of body water turnover seems to be higher in those who exercise than in those who are sedentary. Therefore we hypothesized that healthy individuals have a higher body water turnover than unhealthy individuals whose metabolic balance, as indicated by water turnover, has broken down, and that a prolonged condition of excessively slow body water turnover may be associated with a lower level of metabolism. If so, body water turnover can be an indicator of human health. However, there is a paucity of information regarding water turnover rates in individuals with various physical characteristics. This study indicates the need for further investigation of body water turnover levels associated with significant changes in physiological condition and metabolic state.

Adult↗

Geriatric nutrition.

The aging process alters body composition so that nutritional status changes as we get older. The aging process shows interindividual variability in its rate of development. Determinants of the rates of aging of systems and tissues are largely genetic. Premature aging of cells and tissues is due to genetic factors and to long-term exposure to physical or chemical environments that cause irreversible tissue damage. Whereas maximal lifespan is fixed for us all, individuals vary in life expectancy both because of variability in the risk of genetic disease which shortens life and because of variable capability for avoidance of those factors in our environment which cause early aging. Early aging as well as geriatric disease foreshorten life, but both can be prevented to some extent by diet or by diet and exercise. Diseases that can be nutritionally prevented, giving us a greater chance of achieving our genetically determined lifespans, include nutritional deficiency states and chronic diet-related diseases such as non-insulin-dependent diabetes, hypertension, coronary artery disease, and cancer. Disabilities resulting from these diseases and from degenerative arthritis are also subject to modulation by diet. The nutritional requirements of the elderly are mostly similar to those of younger people. Elderly usually need fewer calories and similar nutrient intakes compared with those of younger people. Elderly with higher needs for specific nutrients include homebound or institutionalized people who lack sunlight exposure and therefore require more vitamin D. Nutritional requirements to promote longer life expectancy and freedom from disabilities that result from chronic disease include restriction of food energy and fat. Nutritional assessment of the elderly is aimed at identifying not only the presence of deficiency states but also states of nutrient excess and chronic diet-related diseases. There are certain problems in carrying out nutritional assessment in the elderly, but techniques are now available which make valid assessment possible even in the oldest old. Those who live longest have less genetic risk of premature aging, but as a result of native intelligence, education, coping skills, and higher socioeconomic status, they also have a greater likelihood of eating a diet that best meets their long-term nutritional needs. Those most at risk for developing malnutrition as they get older are those who lack food access because of poverty, because of disability resulting from chronic geriatric disease, or because of a combination of these factors. Malnutrition is found in elderly in our society who live in their own homes if they are indigent, isolated, and homebound because of disability.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗