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PubMed2006

Normal distribution of presenilin-1 and nicastrin in skeletal muscle and the differential responses of these proteins after denervation.

Presenilin-1 and nicastrin, two components of gamma-secretase associated with Alzheimer's disease plaques, are present in the synapses of the brain and in various peripheral organs, including skeletal muscle. In the present study, we examined the expression pattern of presenilin-1 and nicastrin in normal and denervated hindlimb muscles of the rat. Using immunohistochemical approaches, we found that presenilin-1 and AChRalpha was co-localized at the neuromuscular junction in the normal skeletal muscles of rats. The immunoreactivities of both presenilin-1 and nicastrin were also observed at the sarcolemma of muscle fibers. We discovered that presenilin-1 mRNA and its protein are upregulated after denervation of the soleus and tibialis anterior muscles. Furthermore, clear co-localization between presenilin-1 and DAPI, but not nicastrin, was noted in several myonuclei in the denervated muscles. We recognized a few fibers possessing both ubiquitin and presenilin-1 protein in the cytosol. The amount of presenilin-1 in the nucleus and membrane fraction was more abundantly expressed in the denervated muscle fibers. In contrast, no significant difference in the nicastrin protein level was observed between normal and denervated muscle fibers. These data suggest that enhanced presenilin-1 protein may play a role in the degeneration and regeneration of skeletal muscle.

Amyloid Precursor Protein Secretases↗
PubMed1978

Normal distribution of acetylation phenotypes in systemic lupus erythematosus.

Previous reports have indicated that idiopathic systemic lupus erythematosus (SLE), like drug-induced lupus, is more frequent in "slow" hepatic acetylators. Using dapsone acetylation rate to determine phenotypes, we found that of the 18 SLE patients studied, 9 were fast acetylators, 8 were slow, and 1 was indeterminate. This result (53% fast) is similar to acetylator phenotypes in our normal controls (50% fast) and in the population at large (52%).

Acetylation↗
PubMed2000

Rat testicular Src: normal distribution and involvement in ethylene glycol monomethyl ether-induced apoptosis.

Kinase activities were previously proposed to be central to germ cell apoptosis induced by ethylene glycol monomethyl ether (EGME) and its active metabolite methoxyacetic acid (MAA). We evaluated the role of tyrosine kinase pp60(c-src) in control and EGME-treated adult rat testis in vivo, as well as in vitro using cultured adult rat seminiferous tubules treated with MAA. In normal testicular tissue, immunoreactivity of Src was mostly detected in Sertoli cell cytoplasm and reached the maximum level around the lumen at spermiation. Src localization was confirmed by immunostaining of cocultures of Sertoli and germ cells and was further confirmed by electron microscopic observation that immunoreactivity was predominant in Sertoli cell cytoplasm as well as occasionally at the Sertoli/germ cell junctions. A single dose of 200 mg/kg EGME induced an increase of Src immunoexpression in both epithelium and interstitium in rat testis. Eight hours after treatment, an intensive immunostaining of Src began to be observed specifically in the cytoplasm of the dying spermatocytes. The apoptotic changes were replicated by exposure of 5 mM MAA in the adult rat seminiferous tubule culture model. Furthermore, spermatocyte degeneration was significantly prevented by cotreatment with 0.1 microM geldanamycin, 10 microM herbimycin A, or 10 microM PP2, which are inhibitors of Src activity. These data collectively suggest that pp60(c-src) mediates Sertoli-germ cell interaction in physiological events, and may play an important role in EGME/MAA-induced germ cell apoptosis.

Animals↗
PubMed1991

Differential immunochemical markers reveal the normal distribution of brain macrophages and microglia in the developing rat brain.

Brain macrophages and microglia play important roles in central nervous system (CNS) development, especially during regressive events in which particular neuronal and glial constituents are eliminated. The purpose of this study is to provide a complete map of brain macrophage and microglia distribution in all regions of the neuraxis from birth to sexual maturity. We have utilized morphology and immunostaining with the specific antibodies OX-42 and ED1 to distinguish between brain macrophages and microglia. Brain macrophages are large, round cells, 10-15 microns in diameter, with few or no cytoplasmic processes; these cells are ED1- and OX-42-immunopositive. Microglia have small cell bodies with numerous, ramified cytoplasmic processes. These cells are OX-42-positive, and ED1-negative. We found a specific pattern of distribution of brain macrophages, targeting specific cortical and subcortical areas transiently, including developing fiber tracts. These cells disappeared completely by the third postnatal week. In contrast, OX-42-positive microglia exhibited a gradual increase in number and were distributed uniformly throughout gray matter and within white matter tracts. These cells remain in the adult CNS, constituting the resident microglia population. We suggest that these two distinct phagocytic cell populations perform unique functions in the developing brain, including remodeling of restricted CNS areas by brain macrophages that is part of a normal morphological process.

Animals↗
PubMed1994

Cholecystokinin gene expression in rat amygdaloid neurons: normal distribution and effect of morphine tolerance.

Previous studies have shown that repeated opioid administration induces a tolerance to opioid, presumably due in part to an opioid-mediated compensatory increase in brain cholecystokinin (CCK) synthesis and/or release. In this study, in situ hybridization histochemistry was used to examine the effect of morphine tolerance on CCK gene expression in the amygdala of rat brains, by using a 35S-labeled synthetic oligonucleotide probe. CCK mRNA-positive neurons in normal rats were seen throughout the amygdaloid complex, with the most heavily labeled neurons in lateral, basal, and cortical nuclei, followed by the medial nucleus. Only a few labeled neurons were found in central and intercalated nuclei. The development of morphine tolerance in the rat was associated with increased hybridization signals for CCK mRNA in each subnucleus of the amygdala. Increases were seen in the numbers of positively labeled neurons and/or the numbers of hybridization grains per positively labeled neuron. Furthermore, differential patterns of increase in CCK mRNA in morphine tolerant rats occurred in different subnuclei of the amygdala, with the highest magnitude of increase in the cortical nucleus, followed in order by the medial, central, basal, intercalated and lateral nuclei. The present study demonstrated that repeated administration of morphine increased CCK gene expression in the amygdaloid complex, and suggested that the development of the tolerance to morphine analgesia is due, in part, to an increase in CCK activity in the amygdaloid complex. These findings substantiate the hypothesis that long-term administration of opioid may induce a compensatory increase in CCK synthesis and/or release, which then results in a progressive antagonism of opioid analgesia.

Amygdala↗
PubMed1991

[Comparison between the aged and children of the normal distribution of pharyngeal and intestinal hemolytic streptococci].

A marked difference between the aged and children has been observed in the group distribution of hemolytic streptococci isolated from various clinical specimens. Group B strains from the urine and sputum, and group G from the sputum, pus and exudate have been predominant in the aged, whereas group A strains from the throat swab have dominated in children. The present study was undertaken to clarify the background for such a marked difference by investigating the normal state of pharyngeal and intestinal carriage of hemolytic streptococci both in the aged and children. 1. As to the pharyngeal carriage, quite a contrast was observed between the aged and children. In the former, the rate of carries was low and the predominant groups among the streptococcus isolates were B (Streptococcus agalactiae) and G (identified as Streptococcus equisimilis), while in the latter, the rate was high and group A (Streptococcus pyogenes) strains comprised approximately 75% of the isolates, most of them being from the throat swab. 2. Both the aged and children showed a similar state of streptococcus carriage in the intestine. The rate of carriers was low and the predominant group among the isolates was B in both populations. Although group G strains were occasionally isolated, group A strains were isolated neither in the aged nor in children. These results explain well the difference between the aged and children in the group distribution of the clinical isolates of hemolytic streptococci.

Age Factors↗
PubMed1993

Normal distribution of tumor necrosis factor-alpha messenger ribonucleic acid and protein in the uteri, placentas, and embryos of osteopetrotic (op/op) mice lacking colony-stimulating factor-1.

In order to map mouse tumor necrosis factor-alpha (TNF) gene expression in detail and to determine whether transcription or translation of the TNF gene is regulated by uterine colony stimulating factor-1 (CSF-1), preimplantation embryos, oviducts, uteri, and uteroplacental units were studied in various strains of mice. These included homozygous osteopetrotic (op/op) female mice, which completely lack CSF-1, and heterozygous (+/op) females, which have normal levels of CSF-1. TNF mRNA was identified in all samples except preimplantation embryos by use of Northern blot hybridization or reverse transcriptase polymerase chain reaction. In situ hybridization and immunocytochemical experiments showed that the TNF gene was expressed in mouse oviduct and uterine epithelial cells, decidual cells, macrophage-like cells, placental trophoblast, and embryos. Despite an absence of CSF-1, TNF gene expression in the uteri, placentas, and embryos of op/op mothers did not differ in any major respect from expression in +/op or other strains of mice. The results of this study therefore indicate that the TNF gene is transcribed and translated in an ordered sequence through mouse gestation, and that maternal CSF-1 is not essential to expression of this cytokine gene. Collectively, these findings are consistent with a major role for TNF in mouse reproduction and development and with a potential compensatory function for this potent polypeptide factor in CSF-1 deficiency.

Animals↗
PubMed1996

NK1.1+ T cells from IL-7-deficient mice have a normal distribution and selection but exhibit impaired cytokine production.

Particular subsets of T cells expressing the NK1.1 antigen have been proposed to play an immune regulatory role by their fast and strong production of cytokines, in particular IL-4. We sought to determine factors driving the functional differentiation of NK1.1+ T cells. Since NK1.1+ T cells are exquisitely sensitive to IL-7 stimulation, we analyzed the development, selection and IL-4 production of NK1.1+ T cells in IL-7-deficient mice (IL-7-/-m mice). Besides a sharp reduction of all T cell subsets, NK1.1+ T cells develop at normal relative frequencies in IL-7-/- mice. They also undergo a normal selection process, as revealed by the biased V beta TCR repertoire identical to the one in IL-7+/+ mice. However, NK1.1+ T cells from IL-7-/- mice were found to be impaired in IL-4 and IFN-gamma production in in vitro and in vivo models. In addition, IL-7 was able to restore IL-4 production by NK1.1+ thymocytes from IL-7-/- mice. Finally, IL-7 but not IL-2 or IL-4 was able to maintain and increase IL-4 production by NK1.1+ thymocytes from normal mice. These data suggest that the functional maturation of NK1.1+ T cells requires a cytokine-driven differentiation process, in which IL-7 plays a major role.

Animals↗
PubMed2001

Aberrant pyramidal tract in the medial lemniscus of the human brainstem: normal distribution and pathological changes.

We examined the consistency of the so-called aberrant pyramidal tract (APT) in 150 consecutive autopsied human brains using the modified Bielschowsky stain for axons. We were able to identify the APT in all brains except for one with holoprosencephaly. The APT left the pyramidal tract within the crus cerebri and passed in the medial lemniscus of the pons through the upper medulla oblongata. In 13 of the 63 brains with cerebrovascular diseases, wallerian degeneration was found in the APT on the ipsilateral side of the cerebral lesions. Further, the APT showed depletion of small-sized fibers in 2 of the 5 brains with multiple-system atrophy. These findings confirmed that the APT is a normal descending fiber tract and a part of the pyramidal tract.

Adult↗
PubMed2003

Autoradiographic analysis of rat brain kinin B1 and B2 receptors: normal distribution and alterations induced by epilepsy.

Kindling-induced seizures constitute an experimental model of human temporal lobe epilepsy that is associated with changes in the expression of several inflammatory proteins and/or their receptors in distinct brain regions. In the present study, alterations of kinin receptors in the brain of amygdaloid-kindled rats were assessed by means of in vitro autoradiography, using (125)I-labeled 3-4 hydroxyphenyl-propionyl-desArg(9)-D-Arg degrees -[Hyp(3), Thi(5), D-Tic(7), Oic(8)]-bradykinin (B(1) receptors) and (125)I-labeled 3-4 hydroxyphenyl-propionyl-D-Arg degrees -[Hyp(3), Thi(5), D-Tic(7), Oic(8)]-bradykinin (B(2) receptors) as ligands. Results demonstrate that B(2) receptors are widely distributed throughout the brain of control rats. The highest densities were observed in lateral septal nucleus, median preoptic nucleus, dentate gyrus, amygdala, spinal trigeminal nucleus, mediovestibular nucleus, inferior cerebellar peduncles, and in most of cortical regions (0.81-1.4 fmol/mg tissue). In contrast, very low densities of B(1) receptors were detected in all analyzed areas from control rats (0.18-0.26 fmol/mg tissue). When assessed in kindled rats, specific binding sites for B(2) receptors were significantly decreased (41 to 76%) in various brain areas. Conversely, B(1) receptor binding sites were markedly increased in kindled rats, especially in hippocampus (CA2 congruent with CA1 congruent with CA3), Amy and entorhinal, peririnal/piriform, and occipital cortices (152-258%). Data show for the first time that kindling-induced epilepsy results in a significant decline of B(2) receptor binding sites, accompanied by a striking increase of B(1) receptor labeling in the rat brain. An altered balance between B(1) and B(2) receptor populations may play a pivotal role in the onset and/or maintenance of epilepsy.

Animals↗
PubMed1988

Opioid peptide gene expression in rat trigeminal nucleus caudalis neurons: normal distribution and effects of trigeminal deafferentation.

Preproenkephalin (preproenkephalin A) and preprodynorphin (preproenkephalin B) are the opioid peptide genes expressed in neurons of the nucleus caudalis of the trigeminal nuclear complex. We have used recently developed techniques for quantitative in situ hybridization to identify the neurons in laminae I and II of the nucleus caudalis that display the mRNA products of each of these genes. The specificity of these hybridization patterns is supported by several biochemical features, and by qualitative and quantitative parallels with previous immunohistochemical results. In animals killed 4 days after unilateral lesions of the trigeminal ganglion, neuronal expression of both preproenkephalin and preprodynorphin is altered in the nucleus caudalis. Decreases in preproenkephalin mRNA are due to a decline in the number of neurons that appear to express this gene. Conversely, preprodynorphin mRNA increases by adding a significant population of expressing neurons. These deafferentation-induced changes in gene expression may provide clues to the role of primary afferent information in modulating the functions of nucleus caudalis neurons containing opioid peptides.

Acid Phosphatase↗
PubMed2004

A latent normal distribution model for analysing ordinal responses with applications in meta-analysis.

We consider the comparison of two treatments (or a treatment and a control/placebo) with responses that are classified into ordinal categories. By operating on the assumption that the responses are manifestations of some underlying continuous variables and that the definitions of the categories for the treatment group and the placebo group are the same in the same clinical test centre, we develop a model to examine the possible treatment effects. These treatment effects can be identified as location effect or dispersion effect. The method can be generalized to analyse clinical test results coming from different centres, where each centre may have its own standard in classifying responses. The method is technically undemanding and can be implemented in a very simple and straightforward way by using easily accessible software that can be downloaded at no cost. Real data sets are analysed for illustration.

Alzheimer Disease↗
PubMed1986

The lymphatic route. 1) Albumin and hyaluronidase modify the normal distribution of interferon in lymph and plasma.

When human recombinant interferon-alpha 2 diluted in saline was injected s.c. into rabbits, the total amount recovered in thoracic lymph was less than 0.4%. Recoveries increased from 2- to 8-fold if interferon was injected in 4% albumin or with hyaluronidase, respectively. Albumin added to interferon acts as an interstitial fluid expander, thus favoring interferon absorption through lymphatics rather than blood capillaries. This strategy may increase the therapeutic index of interferon.

Animals↗
PubMed1987

Acetylcholine in the interpeduncular nucleus of the rat: normal distribution and effects of deafferentation.

We studied the cholinergic projection to the interpeduncular nucleus (IPN) by examining localization of choline acetyltransferase (ChAT) in the habenula, fasciculus retroflexus (FR) and among the subnuclei of the IPN of the rat, using and antibody raised against ChAT. ChAT-containing neurons were present in the ventral portion of the medial habenula, ChAT-stained axons were present in the FR and ChAT-stained axons and terminals were present in the rostral, central and intermediate subnuclei of the IPN. No ChAT staining was seen in the lateral or dorsal subnuclei. The pattern of ChAT localization was thus complementary to the pattern of the habenular substance P projection to the IPN. Lesions of the FR eliminated all ChAT from the IPN while lesions of the stria medullaris produced a modest decrease. Unilateral FR lesions indicated that the FR projection to the central and rostral subnuclei is largely bilateral and symmetrical and that to the intermediate subnuclei is largely ipsilateral. We found no evidence of lesion-induced plasticity, i.e. replacement of ChAT immunoreactivity, by surviving FR axons in these adult brains.

Acetylcholine↗