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At least 433 records · Page 24Linked to original sources
PubMed1999

Quantitative studies of progesterone receptor and nitric oxide synthase colocalization with somatostatin, or neurotensin, or substance P in neurons of the guinea pig ventrolateral hypothalamic nucleus: an immunocytochemical triple-label analysis.

Previous double-label studies have demonstrated that progesterone receptors (PR) may coexist with nitric oxide synthase (NOS) and also with neuroactive peptides such as somatostatin (SOM), neurotensin (NT) and substance P (SP) in neurons of the ventrolateral hypothalamic nucleus (VL) of the guinea pig. In the present study, triple-label immunofluorescence histochemistry was used to determine whether neurons co-expressing both PR and NOS also contain one neuropeptide (SOM, NT or SP) and to quantify these colocalization relationships. Ovariectomized guinea pigs were primed with estradiol to induce PR immunoreactivity and treated with colchicine to visualize immunoreactive (IR) peptidergic neurons. Using three primary antibodies raised in different species and labeled with three different markers, it is possible to recognize which type(s) of immunoreactivity each cell contains on the same sections. We observed that PR, NOS and SOM co-occurred extensively, whereas PR, NOS and NT or PR, NOS and SP were colocalized infrequently in neurons of the VL. Combining our various quantitative observations, we found that SOM immunoreactivity appeared in 33% of the PR/NOS-IR neurons in the caudal aspect of the nucleus and that nearly all neurons containing SOM and NOS contained PR. The occasional localization between PR, NOS and SP seen in the rostral subdivision of the VL represented a very low proportion of the PR/NOS-IR neurons but 48% of NOS/SP-IR neurons. The relatively high proportion of PR/NOS-IR cells expressing SOM in the VL suggests that these neurons are part of a neural circuitry involved in a variety of steroid-dependent functions.

Animals↗
PubMed1991

Evidence for colocalization of glucocorticoid receptor with cytoplasmic microtubules in human gingival fibroblasts, using two different monoclonal anti-GR antibodies, confocal laser scanning microscopy and image analysis.

The cellular distribution of the glucocorticoid receptor (GR) in relation to the microtubule protein tubulin was studied in human gingival fibroblasts, using two different anti-GR antibodies of different Ig-classes, by indirect immunofluorescence immunocytology. Further studies were performed by confocal laser scanning microscopy and digital image analysis. The study focused on fluorochrome separation, optical sectioning, digital subtraction techniques and reconstruction of projections obtained using stacks of recorded transversal sections. The data presented further strengthens the notion of a structural colocalization between GR and cytoplasmic microtubules in human fibroblasts.

Antibodies, Monoclonal↗
PubMed2001

Expression of p53 and human herpesvirus-8 (HHV-8)-encoded latency-associated nuclear antigen with inhibition of apoptosis in HHV-8-associated malignancies.

BACKGROUND: Kaposi sarcoma (KS) and primary effusion lymphoma (PEL) cells express human herpesvirus-8 (HHV-8)-encoded latency-associated nuclear antigen (LANA) (open reading frame [ORF] 73 protein), suggesting that LANA plays an important role in the pathogenesis of HHV-8-associated malignancies. Recently, the binding of LANA to p53 was demonstrated in vitro. In the current study, the authors investigated the association between p53 and LANA expression with apoptosis in HHV-8-associated malignancies in vivo. METHODS: Twenty-six cases of KS, 1 case of HHV-8-associated solid lymphoma, 2 PEL cell lines, and an HHV-8-associated lymphoma engrafted in severe combined immunodeficiency (SCID) mice were examined. Immunohistochemistry using the catalyzed signal amplification system was employed to detect LANA and p53 on paraffin embedded tissues and the immunofluorescence technique was used on cell lines. To detect apoptosis, the TdT-mediated dUTP nick end labeling (TUNEL) method was used. For mutation analysis of p53, exons 5-9 of the p53 gene were amplified by polymerase chain reaction and examined by direct sequencing. RESULTS: Immunohistochemistry revealed that LANA and p53 were expressed in the tumor cells of all these specimens, and apoptotic cells were rarely detected in them using the TUNEL method. Immunofluorescence assay revealed that LANA colocalized with p53 in the nuclei of PEL cells. Sequencing analysis indicated that there was no mutation in the deduced amino acid sequences of p53 in KS tissues. CONCLUSIONS: These data suggest colocalization of p53 and LANA and the inhibition of apoptosis in HHV-8-associated malignancies in vivo, supporting the results found in vitro that p53 inhibition by LANA suppresses cell death, as reported previously. These results also suggest that the p53 pathway is crucial in the pathogenesis of HHV-8-associated malignancies.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

[Comparative evaluation of four methods of an endotracheal tube holder. Preliminary results].

OBJECTIVE: To compare four different types of endotracheal tube holders. PATIENTS: Patients admitted to Intensive Care Unit in Thertiary Hospital with 800 patients admitted/year. The minimum sample was 188 to obtain statistically significant differences. During the first 6 months, 68 consecutive patients non selected were randomly assigned to one of four types of tube holders. PARAMETERS: Each 8 hours were evaluated the presence of lesions in skin or mucose membrane, colocation facility and patients commodity. Also security and cost analysis parameters were included. STATISTIC ANALYSIS: SPSS statistical package were used, Kaplan-Meier curve, Kruskal-Wallis test; and making statistical contrasts between the different types of tube holders. We considered significant a p < 0.05. RESULTS AND CONCLUSIONS: The obtained results till this moment showed significant differences in time free of lesions, between Haid holder and the rest of tube holders. Likewise, in the subjective parameters for the nurse and patient evaluations the Haid holder obtained a superior mind in facility of colocation and commodity of patients, consecutive gauze bandage.

Adhesives↗
PubMed2003

Phospholipid transfer protein is present in human atherosclerotic lesions and is expressed by macrophages and foam cells.

Phospholipid transfer protein (PLTP) in plasma promotes phospholipid transfer from triglyceride-rich lipoproteins to HDL and plays a major role in HDL remodeling. Recent in vivo observations also support a key role for PLTP in cholesterol metabolism. Our immunohistochemical analysis of human carotid endarterectomy samples identified immunoreactive PLTP in areas that colocalized with CD68-positive macrophages, suggesting that PLTP could be produced locally by intimal macrophages. Using RT-PCR, Western blot analysis with a monoclonal anti-PLTP antibody, and a PLTP activity assay, we observed PLTP mRNA and protein expression in human macrophages. In adherent peripheral blood human macrophages, this PLTP expression was increased by culture with granulocyte macrophage colony-stimulating factor. Incubation of macrophages with acetylated-LDL induced an increase in PLTP mRNA and protein expression that paralleled cholesterol loading. PLTP expression was observed in elicited mouse peritoneal macrophages and in cultured Raw264.7 cells as well. Thus, this study demonstrates that PLTP is expressed by macrophages, is regulated by cholesterol loading, and is present in atherosclerotic lesions.

Animals↗
PubMed2026

Shared genetic architecture of smoking dependence and Crohn's disease: A cross-trait analysis of GWAS summary statistics.

INTRODUCTION: Smoking dependence (SD) and Crohn's disease (CD) are epidemiologically associated, but whether this relationship reflects shared genetic susceptibility remains unclear. METHODS: We conducted a cross-trait genetic analysis of SD and CD using publicly available genome-wide association study (GWAS) summary statistics from European-ancestry populations. Genome-wide genetic correlation was estimated using linkage disequilibrium score regression (LDSC) and high-definition likelihood (HDL). Pleiotropic variants were identified using PLACO and mapped to genomic loci using FUMA. Regional signal sharing was assessed by Bayesian colocalization. Functional analyses included stratified LDSC, Multi-marker Analysis of GenoMic Annotation (MAGMA), GTEx tissue analysis, and Metascape. Expression-linked candidate genes were prioritized using expression quantitative trait locus (eQTL)-based summary-data-based Mendelian randomization (SMR) with heterogeneity in dependent instruments (HEIDI) testing. Genetically informed spatial mapping of cells for complex traits (gsMap) was used for spatial mapping. RESULTS: SD and CD showed positive genetic correlation by LDSC (rg=0.2090, p=0.0008) and HDL (rg=0.3817, p=0.00106). PLACO identified 81 genome-wide significant pleiotropic SNPs, which were mapped by FUMA to three loci at 1p31.3, 5p13.1, and 12q12, represented by rs11209031, rs1395152, and rs17467116, respectively. MAGMA identified 22 FDR-significant genes, four of which remained Bonferroni significant: LRRK2, TNFRSF6B, ZGPAT, and RP4-583P15.15. Cross-trait tissue analysis showed significant enrichment of the shared genetic signal in whole blood and small intestine, while gene-set analysis highlighted inflammatory response (pbon=1.86&#xd7;10-5) and T-helper 17 cell differentiation (pbon=7.37&#xd7;10-4). SMR/HEIDI analysis further prioritized RPS6KB1 as a shared expression-linked candidate. Spatial mapping revealed a prominent signal in the embryonic gastrointestinal tract and gene-specific regional patterns involving LRRK2 and SLC2A13 in the adult mouse brain. CONCLUSIONS: SD and CD showed measurable shared genetic susceptibility, with convergent evidence from pleiotropic loci, immune-inflammatory pathway enrichment, tissue-level associations, and spatial transcriptomic mapping.

Crohn's disease↗
PubMed2025

Integrative proteomic analysis provides novel therapeutic insights for etiological subtypes of diabetes.

AIMS: Type 2 diabetes (T2D) is a highly heterogeneous disease characterised by subtypes with variations in aetiology, disease progression, and risk of complications. However, potential drug targets for these subtypes have not been explored. This study aims to investigate potential drug targets by integrating proteomics. MATERIALS AND METHODS: Summary-level data of circulating proteins were extracted from the UK Biobank and the deCODE Health Study. Genetic associations with five diabetes subtypes were obtained from Swedish All New Diabetics in Scania and Malm&#xf6; Diet and Cancer cohort, including severe autoimmune diabetes (SAID), severe insulin-deficient diabetes (SIDD), severe insulin-resistant diabetes (SIRD), mild obesity-related diabetes (MOD), and mild age-related diabetes (MARD). The associations between circulating proteins and diabetes subtypes were assessed through Mendelian randomisation, followed by multiple sensitivity and colocalization analyses. Additionally, tissue-specific, pathway and functional enrichment analysis, assessment of protein druggability, and the protein-protein interaction (PPI) networks were used to further explore biological mechanisms and therapeutic potential. RESULTS: Genetically predicted levels of 2, 2, 9, 3, and 5 circulating proteins were associated with SIRD, SIDD, MARD, MOD, and SAID, respectively. Colocalization analyses further revealed links between GRN with MARD/SIRD, LILRB5 with SIDD/MARD, CR1 with MARD, TNFSF12 with MOD, and DAPK2 with SAID. Enrichment analysis suggested that these proteins were mainly enriched in blood and adipose tissues and involved in immune and inflammatory related pathways. PPI analysis revealed GRN, TNFSF12, and DAPK2 are associated with known T2D targets. CONCLUSIONS: Our study identified several potential drug targets for different subtypes of diabetes using an integrated genetic approach, yielding new insights for precision medicine of diabetes.

Humans↗
PubMed1989

Analysis of the calcium-modulated proteins, S100 and calmodulin, and their target proteins during C6 glioma cell differentiation.

We have analyzed the levels, subcellular distribution, and target proteins of two calcium-modulated proteins, S100 and calmodulin, in differentiated and undifferentiated rat C6 glioma cells. Undifferentiated and differentiated C6 cells express primarily the S100 beta polypeptide, and the S100 beta levels are four-fold higher in differentiated compared to undifferentiated cells. Double fluorescent labeling studies of undifferentiated cells demonstrated that S100 beta staining localized to a small region of the perinuclear cytoplasm and colocalized with the microtubule organizing center and Golgi apparatus. Analysis of differentiated C6 cells demonstrated that S100 beta distribution and S100 beta-binding protein profile changed significantly upon differentiation. In addition, the brain-specific isozyme of one S100-binding protein, fructose-1,6-bisphosphate aldolase C, can be detected in differentiated but not undifferentiated C6 cells. While changes in the subcellular distribution of calmodulin were not observed during differentiation, calmodulin levels and calmodulin-binding protein profiles did change. Altogether these data suggest that S100 beta and calmodulin regulate different processes in glial cells and that the regulation of the expression, subcellular distribution, and target proteins of S100 beta and calmodulin during differentiation is a complex process which involves multiple mechanisms.

Animals↗
PubMed2001

Testing life-history pleiotropy in Caenorhabditis elegans.

Much life-history theory assumes that alleles segregating in natural populations pleiotropically affect life-history traits. This assumption, while plausible, has rarely been tested directly. Here we investigate the genetic relationship between two traits often suggested to be connected by pleiotropy: maternal body size and fertility. We carry out a quantitative trait locus (QTL) analysis on two isolates of the free-living nematode Caenorhabditis elegans, and identify two body size and three fertility QTLs. We find that one of the fertility QTLs colocalizes with the two body size QTLs on Chromosome IV. Further analysis, however, shows that these QTLs are genetically separable. Thus, none of the five body size or fertility QTLs identified here shows detectable pleiotropy for the assayed traits. The evolutionary origin of these QTLs, possible candidate loci, and the significance for life-history evolution are discussed.

Animals↗
PubMed1997

Vascular endothelial growth factor and fibroblast growth factor 5 are colocalized in vascular and avascular epiretinal membranes.

PURPOSE: To determine by immunocytochemical analysis of epiretinal membranes whether vascular endothelial growth factor and the fibroblast growth factor FGF-5 are present in patients with proliferative diabetic retinopathy or proliferative vitreoretinopathy. METHODS: Human surgical specimens of epiretinal membranes were obtained from 11 eyes with proliferative diabetic retinopathy and five eyes with proliferative vitreoretinopathy. Sections were immunostained with an affinity-purified antibody against an internal sequence of human FGF-5 and with a commercially available affinity-purified antibody corresponding to the first 20 residues of human vascular endothelial growth factor. Slides were visualized using avidin-biotin-peroxidase complex. Control studies were performed with nonimmune immunoglobulin G and preabsorbed vascular endothelial growth factor and FGF-5 antibody, respectively. RESULTS: Immunoreactive FGF-5 is present in most cells, including endothelial cells of vascular and avascular epiretinal membranes, but seems to be absent from the extracellular matrix. A similar staining pattern was observed for vascular endothelial growth factor. CONCLUSIONS: Vascular endothelial growth factor and FGF-5 are remarkably colocalized in both vascular and avascular epiretinal membranes arising from proliferative diabetic retinopathy and proliferative vitreoretinopathy, respectively. This result questions the concept that the presence of a single angiogenic factor determines the vascular status of an epiretinal proliferation.

Diabetic Retinopathy↗
PubMed2000

Quantitative fluorescence cytometric analysis of Bcl-2 levels in tumor cells exhibiting a wide range of inherent Bcl-2 protein expression: correlation with Western blot analysis.

BACKGROUND: A protocol to measure a wide range of Bcl-2 protein expression using quantitative fluorescence cytometry (QFCM) in different cell types was developed for use with flow cytometry. Bcl-2 measurements obtained by flow cytometry were correlated with Western blot Bcl-2 measurements to confirm specificity of the Bcl-2-FITC staining. This protocol was applied to measure absolute levels of Bcl-2 protein in different tumor cell lines including Bcl-2-transfected breast carcinoma cell lines and in peripheral blood lymphocytes (PBL). METHODS: HL-60, K562, DOHH2, Jurkat, MDA435/LCC6, MCF7 cell lines, and PBL derived from normal donors were fixed, permeabilized, stained with anti-Bcl-2-FITC antibody and evaluated by QFCM. In parallel, the same cells were evaluated for Bcl-2 protein expression by Western blot analysis. Mitochondrial localization of anti-Bcl-2-FITC antibody inside cells was confirmed using fluorescence imaging microscopy. RESULTS: Bcl-2 expression in different cell types could be accurately quantified based on antibody-binding capacity (ABC) ranging from 12.6 x 10(3) antibody-binding sites in HL-60 cells to 1.64 x 10(6) antibody-binding sites in a Bcl-2-transfected MDA435/LCC6 clone. The data from flow cytometry analysis correlated well with Western analysis (R(2) = 0.78). Bcl-2-FITC staining colocalized with dyes specific for mitochondria. CONCLUSIONS: The Bcl-2 staining protocol described here was shown to be specific, sensitive, and it was able to provide higher resolution as well as more reproducible quantitation of Bcl-2 protein content in cells when compared with Western blot methods. Quantitation of Bcl-2 content in cells by QFCM may be useful for monitoring Bcl-2 expression in cells undergoing various treatments in vitro and in vivo.

Blotting, Western↗
PubMed2005

Nucleocytoplasmic distribution of opioid growth factor and its receptor in tongue epithelium.

The subcellular distributions of the opioid growth factor (OGF), [Met(5)]-enkephalin, and opioid growth factor receptor (OGFr) in the epithelium of the rat tongue were determined in order to reveal structure-function relationships. Laser scanning confocal microscopic analysis showed that both OGF and OGFr were colocalized in the paranuclear cytoplasm and in the nuclei of keratinocytes in the stratum basale. Using immunoelectron microscopy and postembedding techniques, double labeling experiments disclosed that complexes of OGF-OGFr were colocalized on the outer nuclear envelope, in the paranuclear cytoplasm, perpendicular to the nuclear envelope in a putative nuclear pore complex, and in the nucleus adjacent to heterochromatin. Anti-OGF IgG alone was detected in the cytoplasm, and anti-OGFr IgG alone was associated with the outer nuclear envelope. Study of chronic treatment with the opioid antagonist, naltrexone (NTX), which blocks opioid-receptor binding, revealed the presence of OGFr immunoreactivity alone in the cytoplasm and the nucleus; some OGF-OGFr complexes were also observed. Colocalization of OGFr and karyopherin (importin) beta was recorded in the cytoplasm and nucleus. These results in tongue epithelium are the first to suggest that OGFr resides on the outer nuclear envelope, where OGF interacts with OGFr; that the OGF-OGFr complex translocates between cytoplasm and nucleus at the nuclear pore; and that the nuclear localization signal of OGFr interacts with karyopherin beta for nuclear transport. These novel data also indicate that signal transduction for cell proliferation appears to involve an OGF-OGFr complex that interfaces with chromatin in the nucleus. Moreover, the unique finding that OGFr was found in the cytoplasm and nucleus in NTX-treated specimens may suggest that NTX-OGFr complexes have the same pathway as OGF-OGFr.

Animals↗
PubMed2002

Coinduction of nitric oxide synthase and arginine metabolic enzymes in endotoxin-induced uveitis rats.

The regulation of expression of the arginine-recycling enzymes and arginase isoforms in association with inducible nitric oxide synthase (iNOS) in the eye of endotoxin-induced uveitis (EIU) rats is investigated. An animal model of EIU was created in Wistar rats by intravitreal injection of lipopolysaccharide (LPS). mRNAs for argininosuccinate synthase (AS) and arginase I as well as for iNOS, measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR), were induced in the eye of EIU rats. iNOS mRNA increased markedly 3 hr after injection, reached a maximum at 6-12 hr, and then decreased at 24 hr. AS mRNA remained little change at 3 hr and increased maximally at 6 hr (by about 3.3-fold), whereas arginase I mRNA increased later and reached a maximum at 12 hr (by about 4.2-fold). iNOS, AS, and arginase I proteins were also induced. AL and arginase II mRNAs remained little changed. In immunohistochemical analysis, iNOS, AS and arginase I were almost colocalized in infiltrated inflammatory cells in the vitreous, iris, ciliary body and inner layers of the retina. In conclusion, AS and arginase I are coinduced with iNOS in infiltrated inflammatory cells in the eyes of EIU rats, and may regulate NO production by changing intracellular concentration of arginine.

Animals↗
PubMed1996

Cloning, comparative mapping, and RNA expression of the mouse homologues of the Saccharomyces cerevisiae nucleotide excision repair gene RAD23.

The Saccharomyces cerevisiae RAD23 gene is involved in nucleotide excision repair (NER). Two human homologs of RAD23, HHR23A and HHR23B (HGMW-approved symbols RAD23A and RAD23B), were previously isolated. The HHR23B protein is complexed with the protein defective in the cancer-prone repair syndrome xeroderma pigmentosum, complementation group C, and is specifically involved in the global genome NER subpathway. The cloning of both mouse homologs (designated MHR23A and MHR23B) and detailed sequence comparison permitted the deduction of the following overall structure for all RAD23 homologs: an ubiquitin-like N-terminus followed by a strongly conserved 50-amino-acid domain that is repeated at the C-terminus. We also found this domain as a specific C-terminal extension of one of the ubiquitin-conjugating enzymes, providing a second link with the ubiquitin pathway. By means of in situ hybridization, MHR23A was assigned to mouse chromosome 8C3 and MHR23B to 4B3. Because of the close chromosomal proximity of human XPC and HHR23B, the mouse XPC chromosomal location was determined (6D). Physical disconnection of the genes in mouse argues against a functional significance of the colocalization of these genes in human. Northern blot analysis revealed constitutive expression of both MHR23 genes in all tissues examined. Elevated RNA expression of both MHR23 genes was observed in testis. Although the RAD23 equivalents are well conserved during evolution, the mammalian genes did not express the UV-inducible phenotype of their yeast counterpart. This may point to a fundamental difference between the UV responses of yeast and human. No stage-specific mRNA expression during the cell cycle was observed for the mammalian RAD23 homologs.

Amino Acid Sequence↗
PubMed2001

Ultrahigh-resolution colocalization of spectrally separable point-like fluorescent probes.

An ultrahigh-resolution colocalization method based on the simultaneous acquisition and analysis of spectrally separated images of the excitation point-spread function of point-like fluorescent probes is reviewed. It is shown that molecular distances can be measured with accuracy better than 10 nm using conventional far-field optics. A detailed account of the methodology, theoretical considerations, signal processing, and data fitting algorithms is given.

Fluorescent Dyes↗
PubMed2026

Genetic interconnections between personality-related phenotypes and psychiatric disorders.

BACKGROUND: Personality-related phenotypes are genetically correlated with psychiatric disorders, but whether these relationships reflect shared genetic loci and differ across individual phenotypes remains unclear. We investigated their shared genetic architecture at the level of specific phenotype-disorder pairs. METHODS: We analyzed genome-wide association study summary statistics for 13 personality-related phenotypes and eight psychiatric disorders in populations of European ancestry. Genetic correlations were evaluated separately for 104 phenotype-disorder pairs using linkage disequilibrium score regression and high-definition likelihood. For pairs supported by both methods, MTAG and CPASSOC were applied separately to identify pleiotropic signals, followed by linkage disequilibrium clumping, Bayesian colocalization, gene prioritization, functional enrichment and bidirectional two-sample Mendelian randomization analyses. No composite personality or psychiatric-disorder phenotype was constructed. RESULTS: Among the 104 evaluated pairs, 77 showed significant positive genetic correlations in both analyses. Joint screening of MTAG and CPASSOC results identified pleiotropic signals in 61 pairs, comprising 1088 independent lead SNV-pair associations and 776 unique SNVs. Bayesian colocalization supported 351 signals across 42 pairs and 284 unique lead SNVs. MAGMA identified 1293 unique genes, of which 379 were prioritized by PoPS and 151 were further supported by SMR. These genes were enriched in brain tissues and biological processes involving nervous system development, synaptic organization and intercellular connectivity. Inverse-variance weighted Mendelian randomization identified 41 forward and 32 reverse associations after false-discovery-rate correction, including 21 pairs with bidirectional evidence. CONCLUSION: These item-resolved analyses identify widespread but heterogeneous genetic sharing between personality-related phenotypes and psychiatric disorders. The findings provide a pair-specific map of shared loci and prioritized genes, while the Mendelian randomization results should be interpreted cautiously because of residual heterogeneity and potential horizontal pleiotropy. Further validation in diverse populations and functional studies is required.

Colocalization↗
PubMed2005

JNK activation contributes to DP5 induction and apoptosis following traumatic spinal cord injury.

Growing evidence suggests that cells undergo apoptosis after spinal cord injury (SCI). However, little is known about the early events that trigger apoptosis in the contused cord. The BH3-only subfamily of pro-apoptotic regulators (e.g., bim, bad, and dp5) is recognized as initiators of the apoptotic cascade, and is subject to stringent control, both at the transcriptional and post-translational level. In the current study, we studied upstream events regulating trauma-induced apoptosis in the spinal cord. Within 1 h after SCI in rats, DP5 was induced, while Bim and Bad levels remained unchanged. In parallel, SCI also activated the stress-induced c-Jun N-terminal kinase (JNK), leading to the phosphorylation of c-Jun, with a similar temporal profile. Immunohistochemical analysis revealed that p-JNK and DP5 colocalized to neurons and oligodendrocytes undergoing apoptosis in the injured cord, but were absent in uninjured spinal cord. Furthermore, inhibition of JNK activity with in vivo delivery of SP600125 or a jnk1 antisense oligodeoxynucleotide (ODN) attenuated DP5 induction and caspase-3 activation. These results suggest that JNK activation contributes to trauma-induced DP5 expression and subsequent apoptosis in SCI.

Animals↗
PubMed2005

Mating activates estrogen receptor-containing neurons in the female monkey brain.

In contrast to some other species, the numbers of activated neurons in the brains of male and female macaques are high in both mated and unmated animals. Dual labeling with the 1D5 anti-estrogen receptor antibody and the c-fos [4] [corrected] polyclonal anti-c-fos antibody was used in 19 female cynomolgus monkeys to examine whether mating selectively increases the activation of neurons containing estrogen receptors (ER). Mated females, and social controls exposed to males without mating, were euthanized about 75 min after the start of the test, exactly 60 min after the first ejaculation (mated females, N=7) and 75 min after the start of exposure to a male (social controls, N=4). A second control group of unmated females (N=8) remained in their individual cages until euthanasia. Neuronal nuclei containing Fos immunoreactivity (Fos-ir) alone, ER-immunoreactivity (ER-ir) alone, or both Fos-ir and ER-ir, were counted in 8 brain regions, but 2 of these regions contained too few ER-ir neurons to permit analysis. The proportion of ER-ir neurons colocalizing Fos-ir was significantly higher in the preoptic area (P=0.027) and ventromedial hypothalamus (P=0.04) of mated than of control females, suggesting the selective activation of ER-containing neurons by mating in these two brain regions known to be important in the control of female mating. The proportion of Fos-ir neurons not containing ER-ir was significantly lower in the cortical amygdala (P=0.045) of mated than in control females, suggesting a selective deactivation of neurons not containing ER-ir.

Animals↗