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Q Gong

Publications and source records attributed to Q Gong.

64 records · Page 4Linked to original sources
PubMed1995

Evidence that pioneer olfactory axons regulate telencephalon cell cycle kinetics to induce the formation of the olfactory bulb.

Early olfactory axons follow a specific pathway to reach the developing telencephalon. We observed that a subpopulation of these axons, the pioneer olfactory axons, penetrate into the ventricular zone of a highly restricted region of the telencephalon at E13 and E14. At E15, this same telencephalic region evaginates to form the olfactory bulb. To investigate the possibility that the pioneer olfactory axons induce the olfactory bulb by influencing precursor cell populations, we compared cell cycle kinetics and differentiation in the olfactory bulb primordium and the adjacent neocortex using cumulative bromdeoxyuridine labeling. The results showed that, 24 hr after the arrival of the first pioneer axons, the duration of the cell cycle is prolonged significantly in the olfactory bulb primordium. In addition, twice as many cells have exited the mitotic cycle in the olfactory bulb primordium versus the adjacent cortex. These findings suggest that pioneer olfactory axons play a role in the induction of the olfactory bulb by selectively modulating cell cycle kinetics in the olfactory bulb primordium. Afferent axons may influence target morphogenesis by modulating target precursor cell proliferation in other developing neural structures.

Animals↗
PubMed1994

Localization and regulation of low affinity nerve growth factor receptor expression in the rat olfactory system during development and regeneration.

Nerve growth factor (NGF), a classic neurotrophic factor, promotes neuronal survival, maintenance, regeneration and differentiation in the peripheral nervous system and parts of the central nervous system. NGF activity is mediated by cell surface bound receptors including the low affinity NGF receptor (LNGFr) which is expressed by some peripheral and central neurons and is present on peripheral nerve Schwann cells during development and regeneration. The olfactory system is a useful model for the study of the role of LNGFr in neuronal development and regeneration. The growth of olfactory axons into the brain begins in the embryo and continues through the first few postnatal weeks. In mature animals there is persistent turnover and generation of olfactory receptor neurons (ORNs) and continuous growth of new axons into the olfactory bulb. These new axons grow along the preexisting olfactory pathway. In the mature olfactory system, LNGFr has been observed in the glomerular layer of the olfactory bulb, the target of ORNs. However, neither the cellular localization nor the developmental expression of LNGFr has been characterized. Here, we tested the hypothesis that LNGFr expression is developmentally regulated in the olfactory nerve and is reinduced following injury to the mature olfactory nerve. LNGFr-immunoreactivity (IR) was first observed in the olfactory mucosa at embryonic day (E)13 and in the olfactory nerve at E14. LNGFr-IR increased in the nerve during embryonic development, began to decrease at around postnatal day (P)5 and was scarcely detectable in normal adults. The staining pattern suggests that LNGFr is located on the olfactory nerve Schwann cells. Streaks of LNGFr-IR were present in the adult olfactory nerve. We reasoned that these streaks might represent transient reexpression of LNGFr associated with normal olfactory neuron turnover and replacement. Consistent with this hypothesis, LNGFr was robustly reexpressed in the adult olfactory nerve following lesion of the olfactory epithelium. Starting late in development (E21) and in the adult, LNGFr-IR was also observed on fibers in deep layers of the olfactory bulb. LNGFr-IR was also observed in neurons of the nucleus of the diagonal band (NDB) in the basal forebrain. NDB is the sole source of cholinergic afferents of the olfactory bulb. Thus, we tested the hypothesis that LNGFr in the deep layers of the olfactory bulb is located on NDB axons by making lesions of NDB. Following the lesion, LNGFr-IR disappeared in the deep layers of the olfactory bulb but remained in the glomerular layer.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholinesterase↗
PubMed1994

Single- and double-label immunocytochemical study of the ovine suprachiasmatic nucleus (SCN): GABAergic and peptidergic relationships.

This study evaluated the neuropeptide and neurotransmitter content of the ovine suprachiasmatic nucleus (SCN) using both single- and double-label immunocytochemical methods. Single-label immunocytochemistry identified a few lightly labeled gamma aminobutyric acid (GABA) cells within the SCN as well as a dense plexus of fibers staining positive for the GABA biosynthetic enzyme, glutamic acid decarboxylase (GAD). Vasoactive intestinal polypeptide (VIP) fibers exhibited a similar distribution to GAD fibers; VIP cells were found throughout the SCN, as well as in the paraventricular (PVN) and supraoptic nuclei. Both GAD and VIP fibers exited dorsally from the SCN towards the PVN. Neurophysin (NP) and neuropeptide-Y (NPY) fibers were sparsely distributed throughout the SCN. Double-label immunocytochemistry revealed that GAD varicosities were often in close apposition to VIP cells. These results confirm the presence of GABAergic elements within the sheep SCN. Furthermore, they raise the possibility of a GABAergic modulation of VIP neuronal activity within the ovine SCN.

Animals↗
PubMed1994

[Effect of arginine on lymphocyte responses to ConA in burned mice].

It is well accepted that nutritional support improves the immunologic functions in burned patients. Arginine has been demonstrated to have tissue-specific properties which induce beneficial effects upon the immune system. A series of experiments are carried out, in order to evaluate the immune effect of arginine on burned mice. 1. Lymphocytes from both burned and unburned mice are harvested and incubated in various concentrations of arginine solution for 72 hours, and ConA-stimulating lymphocyte transformation is determined after incubation. 2. Burned animals are divided into four groups. Standard diets for nutritional support are formulated. These formulas contain an identical carbohydrate and lipid (61% and 15% of total energy respectively) intake with varied proportions of protein for each group (24%, 23%, 22%, and 20% of total energy, respectively), in addition. 0%, 1%, 2% and 4% of protein energy is supplied by arginine for different groups. Lymphocyte proliferations in responses to ConA stimulation are determined on the 7th postburn day. The data shows that, in vitro study, increasing arginine concentrations enhanced lymphocyte responses to ConA. The arginine needed level for optimal lymphocyte responses is 1.8 mmol/L in burned mice and 0.9 mmol/L in unburned controls. This difference indicates that in burned mice, a higher arginine concentration is required for better lymphocyte responses. On the contrary, further increase of arginine concentration do not give better response. When varied amounts of arginine are given in the diet to the burned mice, the degree of lymphocyte response to ConA is different. The amount of arginine which supplies 2% of total energy is found to be optimal.

Animals↗
PubMed1993

Mitogen-activated Ca++ channels in human B lymphocytes.

Two complementary experimental methods have been used to examine mitogen-induced transmembrane conductances in human B cells using the Daudi cell line as a model for human B cell activation. Spectrofluorometry was used to investigate mitogen-induced changes in [Ca++]i and transmembrane potential. Activation of human B cells with anti-mu antibodies resulted in a biphasic rise in [Ca++]i, the second phase being mediated by the influx of extracellular Ca++. Ca++ influx was inhibited by high [K+]e, suggesting that this influx was transmembrane potential sensitive. Membrane currents of Daudi cells were investigated using voltage clamp techniques. Before mitogenic stimulation, the cells were electrically quiet. Within several minutes of the addition of anti-mu antibodies to the bath solution, inward currents were observed at negative voltages. Whole-cell currents changed instantly with voltage steps and were transmembrane potential sensitive in that at potentials more positive than -40 mV no currents were detectable. A similar conductance was also activated by the introduction of IP3 into the intracellular solution, suggesting that IP3 generation after surface IgM crosslinking is involved in the activation of this conductance. Both anti-mu and IP3 induced currents were blocked by 1 mM La , which is known to block Ca++ channels. These results strongly support the presence of membrane Ca++ channels in human B cells that function in the early stages of activation. Changes in transmembrane potential appear to be important in regulating Ca++ influx. These mechanisms work in concert to regulate the level of [Ca++]i during the early phases of human B cell activation.

B-Lymphocytes↗
PubMed1993

Characterization of the cathepsin B gene and multiple mRNAs in human tissues: evidence for alternative splicing of cathepsin B pre-mRNA.

We have cloned and characterized multiple messages for cathepsin B that differ in their 5' and 3' untranslated regions (UTRs) from human kidney and the hepatoma cell line HepG2. A comparison of these messages with the cloned human cathepsin B gene reveals that they arise by alternative splicing of a single gene. Processing at a cryptic intron donor site in exon 11 and splicing to exon 12 produces a 4.0-kb message with an alternate 3' UTR in addition to the 2.3-kb message described previously by Chan et al. (1986). Variable removal of exon 2 produces cathepsin B mRNAs which differ by 88 nucleotides in their 5'-UTRs. The ratio of the 2.3-kb to 4.0-kb transcript is about 2:1 in most of the tissues examined, but the ratio of mRNAs with variant 5' UTRs differs widely. Cathepsin B mRNAs lacking exon 2 are predominant in human tumors. In addition, human breast and colon carcinomas and a human melanoma contain a cathepsin B transcript that is also missing exon 3 encoding the signal peptide and 7 residues of the activation propeptide. An in vitro transcription/translation assay was used to demonstrate that this message could be translated from an internal methionine codon (residue 52), producing a 32-kD product lacking the signal peptide and more than half the propeptide. The transcription/translation assay also demonstrated that the variant messages differ in their rates of translation. The relative rates are about 8:2:1 for mRNA lacking exons 2 and 3 compared to mRNA lacking exon 2 and mRNA containing the full-length 5' end, respectively. These results suggest that the expression of cathepsin B in human tissues may be regulated in part at the level of mRNA processing.

Alternative Splicing↗
PubMed1993

Enhancer-dependent transcription of the epsilon-globin promoter requires promoter-bound GATA-1 and enhancer-bound AP-1/NF-E2.

We analyzed epsilon-globin transcription in erythroid cells and in erythroid extracts to determine the requirements for enhancer-dependent expression of this gene. Mutations that abolished GATA-1 binding at a single position in the promoter prevented interaction with enhancers, whereas elimination of a second more distal promoter GATA-1 site had no effect. Deletion or mutation of the GATA-1 sites in either the human beta-globin locus control region DNase-hypersensitive site II enhancer or the chicken beta A/epsilon-globin enhancer did not diminish the ability of the enhancers to interact with the promoter. In contrast, mutation of the AP-1/NF-E2 sites in these enhancers resulted in elimination of enhancement. In vitro transcription of these constructs was promoter dependent and was not sensitive to abolition of GATA-1 binding in the promoter, consistent with the role of GATA-1 solely as a mediator of the enhancer effect. Thus, GATA-1 regulates the response of the epsilon-globin gene to enhancers through a specific site in the promoter and requires enhancer AP-1/NF-E2 binding to transduce the enhancer effect on transcription.

Base Sequence↗
PubMed1991

[Change of T lymphocyte subsets in peripherial blood of children with malnutrition and zinc deficiency].

Sixty children with malnutrition were investigated in this study. The results showed a reduction of serum zinc in moderate and severe cases compared with the mild and normal groups. OKT3+, OKT4+ and OKT8+ cells in peripheral blood of mild malnutrition were significantly decreased in contrast to normal control. The reductive degree of OKT8+ and OKT4+ cells correlated with the severity of malnutrition. OKT8+, OKT4+ and OKT4+/OKT8+ ratio of moderate and severe malnutrition with infection were much lower than those without infection. Our findings suggested that main effective and regulative cells of cell-mediated immunity were impaired. OKT3+ and OKT4+ cells might be used as a sensitive index for early assessment of the immune function in malnutrition children.

CD4-CD8 Ratio↗
PubMed1990

[Evaluation of T cell subsets in myasthenia gravis by anti-T cell monoclonal antibodies].

In this paper, T lymphocyte subsets were measured in the peripheral blood of 46 patients with myasthenia gravis (MG) and 86 healthy controls, by using a modified microcytotoxicity assay and OKT monoclonal antibodies. The results showed that the OKT+3, OKT+4, OKT+8 cells of the patients with MG decreased significantly as compared with those of the controls (57.71% versus 66.42%; 34.50% versus 41.65%; 21.23% versus 27.19% respectively, P less than 0.01), and the OKT4/OKT8 ratio increased significantly (2.19 versus 1.64, P less than 0.05). Furthermore, the patients with the ocular type had less OKT+8 cells than those with the general type (14.19% versus 23.47%, P less than 0.05 and had a high OKT4/OKT8 ratio (3.27 versus 1.57, P less than 0.01). No correlating changes of T cell subsets with clinical conditions in that age, sex, and severity showed, and also that there was no difference between the patients whether prednisone was used or not (P greater than 0.05).

Adolescent↗