Perpendicular-electric-field dependence of exciton binding energy studied by continuous-wave photoluminescence.
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Journal Article↗
Biomedical subjects
C Li
Publications and source records attributed to C Li.
Corticotropin-releasing hormone-like axons in the adrenal glands of fetal and postnatal sheep.
The presence of corticotropin-releasing hormone outside of the brain suggests that it may have functional roles besides the stimulation of pituitary adrenocorticotropin. The purpose of the present study was to determine immunohistochemically, the ontogeny of corticotropin-releasing hormone-like immunoreactivity in sheep adrenals from fetal day 100 to adult. Adrenal corticotropin-releasing hormone-like immunoreactivity: 1) was found in all animals examined, 2) existed as clusters of darkly beaded axon-like fibers over medullary cells at the medullary-cortical interface or over islands of medullary cells surrounded by cortex or rays of medullary cells extending into the cortex, 3) showed a definite increase with age, 4) was depleted in newborns < 12 h old, and 5) was found in pre- and postnatal splanchnic nerves. In conclusion, corticotropin-releasing hormone-like immunopositive fibers are present in the ovine adrenal medulla at various stages of development, supporting the concept that corticotropin-releasing hormone in pre- and postnatal sheep may play a direct local part in the regulation of adrenal function.
Adrenal Glands↗
Purified cystic fibrosis transmembrane conductance regulator (CFTR) does not function as an ATP channel.
The gene mutated in cystic fibrosis codes for the cystic fibrosis transmembrane conductance regulator (CFTR). Previously, we provided definitive evidence that CFTR functions as a phosphorylation-regulated chloride channel in our planar lipid bilayer studies of the purified, reconstituted protein. Recent patch-clamp studies have lead to the suggestion that CFTR may also be capable of conducting ATP or inducing this function in neighboring channels. In the present study, we assessed the ATP channel activity of purified CFTR and found that the purified protein does not function as an ATP channel in planar bilayer studies of single channel activity nor in ATP flux measurements in proteoliposomes. Hence, CFTR does not possess intrinsic ATP channel activity and its putative role in cellular ATP transport may be indirect.
Adenosine Triphosphate↗
Mechanisms of transcriptional activation and repression can both involve TFIID.
Regulation of transcription involves the activities of activators and repressors. Recent experiments have provided evidence that the function of both types of regulators can involve interactions with one or more component of the basal transcription machinery. A principal target appears to be TFIID, which consists of the TATA binding protein (TBP) and associated factors (TAFs). Here we describe experiments that provide added support for the idea that interactions affecting TFIID can play important roles in both activation and repression. We show, using transfection assays in Drosophila Schneider cells, that recruitment of TBP to a promoter as a GAL4-TBP fusion protein can provide a substantial activation of transcription. The conserved core of TBP is necessary and sufficient for this effect, which was observed with both TATA-containing and TATA-lacking basal promoters. These findings extend experiments performed in yeast, and strengthen the idea that recruitment of TBP (TFIID) can be an important mechanism of activation. We also provide further support for the idea that TBP can be a target for a transcriptional repressor, the Drosophila Even-skipped protein (Eve). We present evidence that the homeodomain, which is necessary for binding TBP in vitro, can also be required for repression in vivo, independent of its role in DNA binding. On the other hand, deletion of the alanine/proline-rich region that is essential for repression in vivo and TBP binding in vitro does not significantly affect DNA binding by the purified protein. These results strengthen the view that TBP, either directly or indirectly as a component of TFIID, can be a target of both activators and repressors.
Animals↗
Rab3 reversibly recruits rabphilin to synaptic vesicles by a mechanism analogous to raf recruitment by ras.
GTP activates the interaction between the synaptic vesicle proteins rabphilin and rab3. This raises the question of whether rabphilin is a resident vesicle protein that recruits rab3 in a stage-dependent fashion, or if it is instead an effector protein recruited by rab3. We now show that rabphilin, like rab3, dissociates from synaptic vesicles after exocytosis in a manner requiring both Ca2+ and membrane fusion. Rabphilin interacts with GTP-rab3 via a N-terminal domain comprising a novel Zn2+(-)finger motif, and this interaction is essential for rabphilin binding to synaptic vesicles. Thus, in the same way that ras recruits raf to the plasma membrane, rab3 reversibly recruits rabphilin to synaptic vesicles in a stage-dependent manner. These results reveal an unexpected similarity between the molecular mechanisms by which small G protein function in recruiting effector proteins to membranes during membrane traffic and signal transduction.
Adaptor Proteins, Signal Transducing↗
Murine laminin B1 gene regulation during the retinoic acid- and dibutyryl cyclic AMP-induced differentiation of embryonic F9 teratocarcinoma stem cells.
Retinoic acid (RA) and cyclic AMP analogs cause the differentiation of F9 embryonic teratocarcinoma stem cells into parietal endoderm, an epithelial cell of the early mouse embryo. Laminin B1 is induced in this differentiation process, but is not transcriptionally activated until 24-48 h after RA addition and is not maximally induced until approximately 72 h. Cyclic AMP analogs enhance this transcriptional activation. Although several DNase I hypersensitive sites (DHSS) were observed in the LAMB1 5 -flanking DNA, one of the sites, DHSS2, was detected only after 72 h of RA treatment. Transient transfections have demonstrated that the DHSS2 region functions as a "late-acting RA-inducible enhancer," and motifs in this enhancer contain the homeobox protein-binding site TTATTAACA. Greater binding is observed at these sites by electrophoretic mobility shift assay when cells are cultured with RA and cyclic AMP analogs versus RA alone, and no binding is seen in extracts from RA-treated F9 RAR gamma-/- cells which lack RAR gamma mRNA and protein. Laminin B1 mRNA is not induced by RA in the RAR gamma-/- cells (Boylan, J. F., Lohnes, D., Taneja, R., Chambon, P., and Gudas, L. J. (1993) Proc. Natl. Acad. Sci. U. S. A. 90, 9601-9605). Our data show that these DNA regulatory elements contribute to the transcriptional activation of the LAMB1 gene during the later stages of the differentiation process.
Animals↗
Myelin from MAG-deficient mice is a strong inhibitor of neurite outgrowth.
Myelin-associated glycoprotein (MAG) has potent neurite outgrowth inhibitory activity in vitro. To assess the importance of MAG in the neurite outgrowth inhibitory activity in CNS myelin, we used an in vitro bioassay to characterize neurite growth on CNS myelin derived from mice carrying a null mutation of the MAG gene. Myelin proteins from MAG-deficient mice inhibited neurite outgrowth to a similar degree to the wild-type CNS myelin. These results suggest that CNS myelin molecules other than MAG exert strong inhibitory effects on the growth of neurites.
Animals↗
Tissue-specific expression of rat neutral endopeptidase mRNAs.
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Animals↗
Dynamic changes in the locus control region of erythroid progenitor cells demonstrated by polymerase chain reaction.
The locus control region (LCR) far upstream of the human beta-like globin genes is defined by the preferential chromatin accessibility/DNase I hypersensitivity of four constituent DNA sites HS4, 3, 2, and 1. In an attempt to understand the mechanism of LCR function during early stages of erythropoiesis, a new polymerase chain reaction (PCR) method has been developed to examine the chromatin structure/DNase I hypersensitivity of the LCR in progenitor cells logistically available in limited cell numbers. In erythroid progenitors as well as in multipotent cells with erythroid potential, hypersensitive sites HS4, 3, 2, and 1 were present and the chromatin structure of the LCR was accessible. Moreover, the chromatin structure of the LCR underwent dynamic changes during erythropoiesis. In early erythroid progenitors, the HS2 site was more accessible than the HS3 site. In more mature erythroid progenitors, HS2 became less accessible than HS3 and the other sites. The results indicate that the transcriptional program of the globin genes is encoded, at least in part, in the chromatin accessibility of the LCR. This globin program was apparently initiated in multipotent cells and maintained in erythroid progenitors. Furthermore, the program could be modulated in response to cellular changes accompanying differentiation of the progenitor cells.
Adult↗
In vivo measurements of ion transport in long-living CF mice.
The Cftr (Cystic Fibrosis Transmembrane Conductance Regulator) gene codes for an epithelial chloride (C1) channel essential for fluid secretion into the respiratory and gastrointestinal tract and from exocrine glands. Mice lacking CFTR function due to a disruption of Cftr exon 10 or exon 1 (Cftr (m1UNC/m1UNC) or Cftr(m1HSC/m1HFC) mice, respectively) generally suffer from severe gastrointestinal disease resulting in death shortly after birth or at the time of weaning. However, a subgroup of the Cftr(m1HSC/m1HSC) mice have been characterized which exhibit relatively mild intestinal pathology resulting in a noncompromised lifespan compared to the more severely affected Cftr(m1UNC/m1UNC) mice. We compared the ion transport capacity of the intestinal mucosa of the mildly and severely affected CF mice using the in vivo technique of rectal potential difference (PD) measurement and found that the net calcium-activated chloride conductance toward the lumen was much greater in the rectum of mildly affected mice than in the severely affected mice. Hence, the milder phenotype may be related to the expression of a factor which enhances the net calcium-activated chloride conductance into the lumen of the intestinal tract.
Amiloride↗
Plasmodium chabaudi chabaudi: differential susceptibility of gene-targeted mice deficient in IL-10 to an erythrocytic-stage infection.
Female and male mice deficient in IL-10 production by targeted disruption of the IL-10 gene were infected with Plasmodium chabaudi chabaudi (AS) blood-stage parasites. Both male and female mutant mice exhibited more severe signs of disease than did +/+ or heterozygous control mice. Female defective mice also displayed an increased mortality; 56% of mice died within 20 days of infection. Mortality did not appear to be due to a fulminating parasitemia as death occurred at different levels of parasitemia in the individual mice. The acute infection was accompanied by an enhanced Th1 IFN-gamma response. This response was retained in the chronic phase of infection of both male and female mutant mice, whereas in controls the responding CD4+ T cells were predominantly Th2 cells secreting IL-4. The data suggest that IL-10 regulates the inflammatory response to the parasite and that in its absence the combined effects of malaria toxins and the sustained or enhanced IFN-gamma response lead to increased pathology. In the case of female mice absence of IL-10 is sufficient to induce a lethal endotoxin-like reaction.
Anemia↗
Transcranial magnetic stimulation downregulates beta-adrenoreceptors in rat cortex.
Recently, a method for transcranial magnetic stimulation (TMS) of the brain has been developed. Thus, it is possible to explore neurochemical and behavioral effects of TMS in rats. Repeated TMS (9 days) reduced beta-adrenergic receptor binding in cortex, as does electroconvulsive shock (ECS) and other antidepressant treatments. Thus TMS appears to be a potential antidepressive treatment.
Adrenergic beta-Agonists↗
A newly developed PCR assay of H. pylori in gastric biopsy, saliva, and feces. Evidence of high prevalence of H. pylori in saliva supports oral transmission.
We have recently developed a new PCR assay for the detection of H. pylori. In this study, the polymerase chain reaction (PCR) assay was used to detect H. pylori in 88 gastric biopsy, 85 saliva, and 71 fecal specimens from 88 patients. H. pylori infection was confirmed in 71 of 88 patients by culture and/or histological stain of gastric biopsies. Serum IgG antibody to H. pylori was also measured and resulted in 97% sensitivity and 94% specificity. H. pylori DNA was detected by the PCR assay in gastric biopsy specimens from all 71 patients (100% sensitivity) with proven gastric H. pylori infection but not from 17 noninfected patients (100% specificity). In saliva specimens, H. pylori DNA was identified in 57 of the 68 patients (84%) with proven gastric H. pylori infection and in three of the 17 patients without gastric H. pylori infection. However, the PCR assay was only able to detect H. pylori DNA in the feces from 15 of 61 patients (25%) with proven gastric H. pylori infection and one of the 10 patients without gastric H. pylori infection. The results show that the PCR assay is reliable for detecting the presence of H. pylori in gastric biopsy and saliva specimens. The data indicate that H. pylori exists in a higher prevalence in saliva than feces and that the fecal-oral route may be an important means of transmission of this infection in developing countries but not as significant as previously suspected in the developed countries. It is likely that the oral-oral route is more prominent.
Antibodies, Bacterial↗
Human acute myeloid leukemias may be etiologically associated with new human retroviral infection.
The etiology of human acute myeloid leukemias (AML) remains uncertain. In order to examine the possibility of retroviral etiology in AML, we determined retroviral antigens related to HTLV-I in leukemic cell samples from 32 AML cases and peripheral blood mononuclear cells (PBMNCs) from 20 healthy donors by D-IGSS with high sensitivity and specificity, reverse transcriptase (RT) activity by a simple and sensitive non-radioisotopic RT assay, and retroviral particles by electron microscopy. The HTLV-I-related antigens were detected in 50.0% (16/32) of fresh leukemic cell samples and 87.5% (28/32) of cultured leukemic cell samples. The HTLV-I-related antigen-positive cells in fresh and cultured leukemic samples were 10.2% and 52.8%, respectively. Both frequency and level of HTLV-I-related antigens in cultured samples were much higher than in fresh samples. In contrast, no HTLV-I-related antigens were found in normal hematopoietic cells from 20 healthy donors. Further study results show that RT activity was detected not only in HTLV-I-related antigen-positive samples, but was also well correlated with the level of HTLV-I-related antigens in these samples, and preferred Mn+2 to Mg+2 as a cation. Moreover, typical retroviral particles were localized in most cultured HTLV-I-related antigen-positive samples by immunoelectron microscope. These data suggest that human acute myeloid leukemias may be etiologically associated with new human retroviral infection.
Acute Disease↗
Genotypic and phenotypic characterization of two newly established renal cell carcinoma cell lines.
Two new cell lines from human renal cell carcinoma are reported. Primary cell cultures from 75 consecutive cases of nephrectomy and metastatic surgery due to different stages of RCC during 4 years were studied. Two cell cultures could be propagated for more than 50 passages in vitro. HN4 was derived from a grade III clear cell carcinoma. HN51 originated from a metastatic brain lesion of a clear cell carcinoma grade III. Karyotype analysis of HN4 revealed triploidy with a clonal aberration, der(10)t(3;10)(q13;p12). HN51 also had a triploid pattern with different marker chromosomes but without any clonal aberration. Loss of heterozygosity studies revealed no loss of heterozygosity on 3p or other chromosomal markers in HN4 but LOH was found on one 3p marker and one 14q marker in addition to all 17 p and q markers in HN51. In vitro light microscopy showed distinctly different morphology in the two cell lines although they both had a typical epithelial growth pattern. Doubling times in vitro were low but slightly higher for HN51. Repeated tumorigenenic experiments in athymic mice only gave rise to subcutaneous tumors with HN51. On characterization by 2-dimensional gel electrophoresis, the two cell lines exhibited different polypeptide patterns with higher expression of proliferating cell nuclear antigen in HN51 and higher expression of glutathione-S-transferase in HN4 constituting the most prominent differences.
Aged↗
Disposition of poloxamer 407 in rats following a single intraperitoneal injection assessed using a simplified colorimetric assay.
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Animals↗
Expression of cytokeratins in Warthin's tumour (adenolymphoma) of parotid glands: specific detection of individual cytokeratin types by monoclonal antibodies.
This study evaluated the distribution of cytokeratins detected by monoclonal antibodies directed against individual keratin proteins in normal human salivary glands and epithelial tumour cells of Warthin's tumour arising in parotid glands to determine a more precise mapping of their cellular distribution. The normal salivary ducts showed the presence of cytokeratin 7, 8, 18 and 19 in the intercalated, striated and excretory ducts, the primary keratins of stratified and simple epithelia with a profile very similar to the non-cornified epithelium of the oral mucosa. The basally located cells of salivary gland ducts other than myoepithelial cells were reactive for keratins 7 and 19 suggesting a close similarity in profile of keratin in the basal cells of the oral epithelium. In Warthin's tumour, keratins 7, 8, 18 and 19 were consistently detected in the epithelial cells of the tumour, a profile with a tendency to mimic the same in normal ductal epithelium. The distribution, however, was diverse and a heterogeneity was observed in the basal and luminal cells of Warthin's tumour which differed even in different areas of the same tumour specimen.
Adenolymphoma↗
Age-dependent spatial memory deficits in transgenic mice expressing the human mid-sized neurofilament gene: I.
Previous studies have revealed that the transgenic mouse line expressing the human neurofilament-mid-sized (NF-M) gene evidences age-dependent and cell-specific pathological neurofibrillary accumulation in the central nerve system. In the current study, we investigated the learning and memory processes of NF-M transgenic mice at 3 and 8 months of age in a modified Morris water maze using a series of tasks including those primarily related to reference memory (i.e., spatial learning, reversal learning and probe trials) and to working memory (i.e., matching to sample tasks with or without delays). At 3 months of age, NF-M transgenic mice were indistinguishable from age- and litter-matched non-transgenic wild-type controls on any of the tests of reference and working memory. At 8 months of age, however, the NF-M transgenic mice exhibited significantly poorer performance than the age- and litter-matched wild-type control mice on both reference and working memory tasks. Immunohistological study of the brains of the 8-month-old NF-M transgenic mice revealed spherical and tangle-like neurofilamentous accumulation in their cerebral cortices. These results suggest that NF-M transgenic mice express both age-related histopathological changes and age-dependent learning and memory deficits. Whether NF-M transgenic mice exhibit even more severe behavioral impairments when they become aged is currently under study.
Aging↗