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Biomedical subjects

B Li

Publications and source records attributed to B Li.

At least 523 records · Page 29Linked to original sources
PubMed1997

Alpha 1D L-type Ca(2+)-channel currents: inhibition by a beta-adrenergic agonist and pituitary adenylate cyclase-activating polypeptide (PACAP) in rat pinealocytes.

In this study the subunits of the dihydropyridine-sensitive L-type Ca2+ channels (L-channels) expressed in rat pinealocytes were characterized using reverse transcription (RT)-PCR analysis, and the modulation of these channels by adrenergic agonists and by pituitary adenylate cyclase-activating polypeptide (PACAP) was studied using the patch-clamp technique. RT-PCR analysis showed that rat pinealocytes expressed alpha 1D, alpha 2b, beta 2, and beta 4 Ca(2+)-channel subunit mRNAs. Other alpha 1 subunit transcripts were either not expressed or present at very low levels, indicating that the pinealocytes express predominantly alpha 1D L-channels. Electrophysiological studies confirmed that the pineal expressed a single population of L-channels. The L-channel currents were inhibited by two agonists that elevate cyclic AMP: the beta-adrenergic agonist isoproterenol and PACAP. Similar inhibition was observed with a cyclic AMP analogue, 8-bromo-cyclic AMP. The presence of a cyclic AMP antagonist, Rp-adenosine 3',5'-cyclic monophosphorothioate, blocked the inhibition by isoproterenol and PACAP. Norepinephrine, a mixed alpha- and beta-adrenergic agonist, also inhibited the L-channel currents, but the inhibition was smaller. The smaller inhibition by norepinephrine was secondary to the simultaneous activation of alpha- and beta-adrenergic receptors. These results indicate that (a) pinealocytes express predominantly alpha 1D L-channels, and (b) the beta-adrenergic agonist isoproterenol and PACAP inhibit the L-channel currents through elevation of cyclic AMP. However, an alpha-adrenergic-mediated mechanism also appears to be involved in the effect of norepinephrine on the L-channel currents.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1997

Changes in human mucosal gamma delta T cell repertoire and function associated with the disease process in inflammatory bowel disease.

BACKGROUND: Although gamma delta T cells are a major component of the human intestinal mucosa, it is not clear what role they play in mucosal immunity or if they are involved in the disease process of inflammatory bowel disease (IBD). MATERIALS AND METHODS: Flow cytometry and reverse transcriptase-polymerase chain reaction (RT-PCR) assays were used to identify quantitative and qualitative changes in the repertoire of gamma delta T cells present in surgical and/or biopsy samples or normal and inflamed colon from individual patients with ulcerative colitis (UC) or Crohn's disease (CD). Cytokine production and the ability to adhere to and interact with colonic fibroblasts were used to compare the functional properties of gamma delta T cells isolated from the normal and diseased colonic mucosa. RESULTS: Increased numbers of gamma delta T cells localized in areas of inflammation and tissue injury were found in the majority of patients, irrespective of the type of IBD present. This expansion was attributable to an increase in V delta 1+ cells expressing a V delta 1-(D delta 3)-J delta 1-encoded T cell receptor and was seen in patients with severe disease as well as those with newly diagnosed or less severe forms of IBD. Among T cells present in the inflamed mucosa of patients with CD, gamma delta T cells, particularly V delta 1+ cells, were a major source of the proinflammatory cytokine interferon-gamma and could interact with colonic fibroblasts. CONCLUSIONS: Our results demonstrate that the chronic inflammatory immune response characteristic of IBD is associated with distinct changes in the number, distribution, composition, and function of mucosal gamma delta T cells. Through the production of cytokines and physical interaction with other cells, gamma delta T cells can perform an immunoregulatory function and contribute to the pathophysiology of IBDs.

Adult↗
PubMed1997

Dietary arachidonic acid increases eicosanoid production in the presence of equal amounts of dietary eicosapentaenoic acid.

Previously, we demonstrated that dietary n-3 PUFA (1.5%, w/w) effectively inhibited the production of eicosanoids derived from tissue arachidonic acid (AA) (Whelan et al., 1991). More recently, we also reported that dietary AA (1.0%, w/w) significantly augmented platelet and macrophage eicosanoid production in vitro (Whelan et al., 1993). This present study was designed to investigate the antithetic relationship of dietary AA and EPA on eicosanoid production in vivo. Forty-nine CD-1 male mice were randomly divided into four dietary groups. Identical diets were supplemented with ethyl esters (1.5%, w/w) of the following fatty acids: oleic acid (OA), AA, EPA or AA + EPA (A + E). After four weeks on diet, peritoneal cells were stimulated in vivo with opsonized zymosan and analyzed for eicosanoid production (PGE2, 6-keto-PGF1a, TXB2, LTE4, LTB4, LTE5 and LTB5). The pooled eicosanoid production in the AA group was 41% and 300% higher compared to the OA (control) and EPA groups, respectively. Pooled eicosanoid production in the EPA group was 47% that of the OA group. When equivalent amounts of AA and EPA (AA + EPA) were included in the diet, the pooled eicosanoid production was 29% and 274% higher compared to the OA and EPA groups, respectively. These data demonstrate that dietary AA (1) enhances eicosanoid production in vivo and (2) abrogates virtually all of the effects observed with dietary EPA when both are included in the diet. The clinical implications of dietary AA as modulated by increased eicosanoid production could be significant, particularly when n-3 PUFA are used to reduce eicosanoid-mediated events.

Analysis of Variance↗
PubMed1997

[Detection of hepatitis C virus markers in colostrum].

OBJECTIVE: To evaluate the possibility of hepatitis C virus (HCV) transmission through lactation by detection of HCV markers in colostrum. METHODS: Anti-HCV IgG, anti-HCV IgA and anti-HCV IgM antibodies in colostrum and sera were detected by indirect enzyme linked immunosorbent assay (ELISA), and HCV RNA was tested by reverse-transcription polymerase chain reaction simultaneously. RESULTS: Among 35 samples of colostrum from puerperants with anti-HCV IgG-positive sera, anti-HCV IgA, anti-HCV IgG, and anti-HCV IgM were detected in 19, 6 and 1 samples respectively. Fourteen of the 35 sera samples were HCV RNA-positive, and only 2 of colostrum samples showed HCV RNA-positive. A significant difference (P < 0.01) was found between the HCV RNA positive rates of sera and colostrum. CONCLUSIONS: IgA was the predominant anti-HCV antibodies in the colostrum from puerperants with anti-HCV IgG-positive sera. The HCV RNA-positive rate of sera was markedly higher than that of colostrum. It is presumed that puerperants with anti-HCV IgG-positive sera, especially those with both anti-HCV IgA-positive and HCV RNA-positive colostrum, are most likely to transmit HCV through lactation and cause their infants to be infected by HCV.

Adult↗
PubMed1997

Electrophysiological forms of Guillain-Barre syndrome in Beijing suburb.

OBJECTIVE: To recognize different forms of Guillain-Barre syndrome (GBS) in northern China. METHODS: Twenty-one cases were found in two counties of Beijing suburb from January 1993, to December, 1994. Multiple electrophysiological studies including magnetic motor evoked potential, F-wave, motor and sensory conduction velocity, blink reflex and needle electromyography were conducted on nineteen cases of them. Twelve cases accepted electrophysiological follow-up study. RESULTS: Altogether 17 cases showed demyelination features in multiple electrodiagnosis. Ten cases of them were accompanied by different extent of axonal lesion. Only one case showed main or primary axonal lesion. CONCLUSIONS: Demyelination is the main type of pathophysiological lesion of GBS in Beijing suburb. Different extent of axonal lesion can appear in some cases, but primary and main axonal type is rare in this area.

Adolescent↗
PubMed1997

[Changes of BDNF mRNA by molecular hybridization during embryonic spinal cord repairing injury of adult rats].

OBJECTIVE: To study the changes of (brain-derived neurotrophic factor) BDNF mRNA during embroyonic spinal cord repairing spinal cord injury of adult rats. METHODS: At day 1,3, 5, 7, 10, 15, and 30 after embryonic spinal cord being transplanted into acutely injured spinal cord of adult rats, changes of BDNF mRNA within donor tissue and host tissue were demonstrated qualitatively and quantitatively by in situ hybridization and dot hybridization. RESULTS: Qualitatively, BDNF mRNA was mainly expressed within cytoplasm of motor neurons and a few gliocytes in normal spinal cord. After spinal cord injury, hybridizing products expanded to the mediate and small-sized neurons, also more gliocytes took part in hybridization response. Following transplantation, positively hybridizing neurons and gliocytes increased in number in host tissue, and embryonic spinal cord kept an expressing level similar to that before being transplanted. It was also revealed quantitatively that reacting intensity of the cells in the injured group was strikingly higher than that in the normal group. However, hybridization intensity in the transplanted group was even higher at many intervals than that in the injured group. Besides, the lasting period for hybridization reaction in the transplanted group was also different from that in the injured group. The most intensive reacting phase in the former presented at day 10 and 15, and in the latter at day 7 after operation. CONCLUSIONS: We suggest that transplanted embryonic spinal cord can, besides provision neurol trophines for itself and host spinal cord, evoke synthetic mechanisms of host spinal cord once holding during its embryonic development so as to enhance expression of the neurotrophin. In this way, the host spinal cord may provide neurotrophin for its regeneration and provide an trophic environment for the grafts to develop and differentiate.

Animals↗
PubMed1996

Molecular executors of cell death--differential intrarenal expression of Fas ligand, Fas, granzyme B, and perforin during acute and/or chronic rejection of human renal allografts.

Two distinct cytolytic pathways have been characterized: one in which the interaction between the Fas antigen and its ligand results in apoptosis, and another in which the pore forming protein perforin and the serine protease granzyme B contribute to DNA fragmentation and cell death. We investigated intrarenal expression of these molecular executors of cell death in light of the potential participation of cytolytically active cellular elements in the antiallograft repertory. Reverse transcriptase-polymerase chain reaction was used to identify intrarenal expression of Fas antigen, Fas ligand, granzyme B and perforin in eighty human renal allograft biopsies; mRNA display was correlated with the Banff histological diagnosis of renal allografts. Our studies demonstrate that: (1) intrarenal expression of Fas ligand mRNA and of granzyme B mRNA are correlates of acute but not chronic rejection; (2) Fas ligand mRNA is not detectable in allografts in the absence of rejection; (3) intrarenal coexpression of members of each lytic pathway (Fas ligand and Fas, granzyme B, and perforin) and that of both pathways (e.g., Fas ligand and granzyme B) are correlates of acute rejection; and (4) a direct correlation exists between the histological severity of acute rejection and intrarenal coexpression of mRNA encoding Fas ligand, Fas, granzyme B, and perforin. Our studies identify, for the first time, the differential expression of the two major lytic pathways in acute and chronic allograft rejection and suggest that specific therapy directed at the cytotoxic attack molecules might be efficacious in the prevention and/or treatment of acute rejection.

Acute Disease↗
PubMed1996

High mutation frequencies among Escherichia coli and Salmonella pathogens.

Here it is reported that the incidence of mutators among isolates of pathogenic Escherichia coli and Salmonella enterica is high (over 1 percent). These findings counter the theory, founded on studies with laboratory-attenuated strains, that suggests mutators are rare among bacterial populations. Defects in methyl-directed mismatch repair underlie all mutator phenotypes described here. Of nine independently derived hypermutable strains, seven contained a defective mutS allele. Because these mutant alleles increase the mutation rate and enhance recombination among diverse species, these studies may help explain both the rapid emergence of antibiotic resistance and the penetrance of virulence genes within the prokaryotic community.

Adenosine Triphosphatases↗
PubMed1996

p202, an interferon-inducible modulator of transcription, inhibits transcriptional activation by the p53 tumor suppressor protein, and a segment from the p53-binding protein 1 that binds to p202 overcomes this inhibition.

p202, an interferon-inducible murine protein, is a member of the "200 family" of proteins and is primarily nuclear. p202 is a modulator of transcription; it binds several transcription factors, including NF-kappaB p50 and p65, AP-1 c-Fos and c-Jun, and E2F1, and inhibits their transcriptional activity. p202 also binds pRb, the retinoblastoma protein, and if overexpressed it retards cell proliferation. Here we report that using the yeast two-hybrid assay we found that p202 bound the murine homolog of the human p53-binding protein 1 (53BP1), a protein shown to interact with the DNA binding domain of the p53 tumor suppressor protein. p202 bound a 98amino acid segment from 53BP1. This binding was inhibited by the replacement in p202 of a histidine (from the M(F/L)HATVA(T/S) sequence that is conserved among all of the 200 family proteins) by phenylalanine. We also report that overexpression of p202 inhibited the p53-dependent expression of reporter genes containing p53-activable segments from the mdm2 and p21 genes, whereas a decrease in the p202 level (in consequence of the expression of 202 antisense RNA) resulted in an increase in the p53-dependent expression of these reporters. Expression of the 53BP1 segment binding to p202 overcame the inhibition by overexpressed p202 of the transcription of reporters mediated by the p53 or the AP-1 transcription factors and of the proliferation of yeast.

Amino Acid Sequence↗
PubMed1996

Disease-specific changes in gammadelta T cell repertoire and function in patients with pulmonary tuberculosis.

Although gammadelta T cells are known to contain the highest frequency of mycobacteria-reactive cells in humans and numerous studies have suggested that they play an important role in the initial immune response to Mycobacterium tuberculosis (Mtb), very few studies have attempted to analyze these cells in patients with active pulmonary tuberculosis. The aim of the present study was therefore to evaluate the consequences of infection on the number and activity of mycobacteria-reactive gammadelta T cells. Three-color flow cytometric analysis of blood and bronchoalveolar lavage gammadelta T cells of patients diagnosed with active pulmonary tuberculosis showed that compared with normal healthy subjects and patients with the unrelated pulmonary granulomatous diseases sarcoidosis and berylliosis the size of the mycobacteria-reactive Vgamma9+/Vdelta2+ gammadelta T cell subset in both the blood and lung was dramatically reduced. In addition, the Vgamma9+/Vdelta2+ cells left intact in patients with tuberculosis were refractory to in vitro stimulation by Mtb Ags, which are potent stimuli for these cells in normal subjects. Our results demonstrate for the first time a strong correlation between the absence or loss of the major Vgamma9+/Vdelta2+ Mtb-reactive subset of gammadelta T cells and manifestations of disease, consistent with the hypothesis that these gammadelta T cells play a role in the protective immune response to Mtb infection.

Adult↗
PubMed1996

Addition of Darwin's third dimension to phyletic trees.

A three-dimensional (3D) approach for visualizing the phyletic relationship of living animals is proposed and developed as an alternative to current two-dimensional (2D) evolutionary trees. The 3D tree enhances visualization and qualitative analysis since it simultaneously provides topological (tree-structure) and spatial information (based upon genetically measured distances). However, the meaning of the third dimension, particularly its relationship to temporal processes, and further quantitative analyses emerge as open questions. Our method consists of two phases. First, a 3D representation of the genetic relationships of a related group of extant animals is produced using an optimization algorithm developed here. Second, linear connections are added to suggest a visual representation of the differing evolutionary trajectories of the organisms involved on the basis of a 2D tree algorithm. The method is applied to a set of distantly related Caenophidian snakes, and the resulting relationships are analysed. The discussions here are meant to stimulate the generation of 3D trees in the goal of complementing standard 2D views and, perhaps ultimately, improving our classification of evolutionary relationships.

Algorithms↗
PubMed1996

Chromatography of hydroxysteroid dehydrogenases.

The structure-function study of hydroxysteoid dehydrogenases has stimulated the development of their chromatography, which in turn reveals more mechanisms of these enzymes. Due to the various membrane associations and mild hydrophobic nature of most of the enzymes studied up to now, hydrophobic interaction chromatography has played a crucial role in their purification, using media such as phenyl-Superose or Sepharose-PEG. At the same time, affinity chromatography, especially the dye-containing columns, proves very efficient for these dehydrogenases, as the latter utilizes adenylyl-containing cofactors. Elution by their specific ligand facilitates their purification. In this paper, the use of detergents in the purification of these enzymes is also reviewed. Hydroxysteroid dehydrogenase preparation is further improved by rapid purification which facilitates the elimination of protein microheterogeneity, caused in vitro by oxidation, reduction or partial proteolysis. This process was shown to increase the crystallizability of the enzymes [Lin et al., J. Cryst. Growth, 122 (1992) 242-245; Zhu et al., J. Mol. Biol., 234 (1993) 242-244]. The fast purification permitted a simpler procedure and better combination of various columns than conventional chromatography. This leads to even higher efficiency, yielding homogeneous and highly active preparations.

Animals↗
PubMed1996

Corticofugal feedback improves the timing of retino-geniculate signal transmission.

The temporal accuracy of visually induced spike patterns can be expected to deteriorate with increasing distance from the retina due to synaptic noise and other sources of activity unrelated to the retinal signal. Here we report the opposite effect: the interspike interval distributions of relay cells of cat lateral geniculate nucleus (LGN) are sharper than those of their retinal afferents. A biophysically realistical simulation of the retino-cortical pathway, including excitatory cortico-geniculate feedback, produced a similar effect. Without the feedback the mean firing rate in the LGN dropped and interval peaks broadened by an average of 25%. The same effect was found during reversible experimental inactivation of the visual cortex in cat. This indicates that cortico-geniculate feedback could be employed to improve the temporal accuracy of signal transmission.

Afferent Pathways↗
PubMed1996

Novel analog of atrial natriuretic peptide selective for receptor-A produces increased diuresis and natriuresis in rats.

Atrial natriuretic peptide (ANP) binds to natriuretic peptide receptor-A (NPR-A), a membrane guanylyl cyclase, and to natriuretic peptide receptor-C (NPR-C), which plays a role in peptide clearance. Rat ANP (rANP) mutants that bind rat NPR-A selectively over rat NPR-C were isolated from randomized libraries of rANP-display phage by differential panning. One variant was identified with reduced NPR-C binding; rANP (G16R, A17E, Q18A) [rANP(REA18)]. Synthetic rANP(REA18) was equipotent with rANP in stimulating cGMP production from cloned rat NPR-A (ED50 = 1.8 nM) and was reduced in NPR-C binding by approximately 200-fold. When infused into conscious rats at 0.325 microg/min for 30 min rANP elicited an identical decrease in blood pressure compared with 0.25 microg/min of rANP(REA18), however the natriuretic (P < 0.05) and diuretic (P = 0.07) responses to rANP(REA18) were greater. These data are consistent with a role for NPR-C as a local decoy receptor attenuating NPR-A effects in the kidney, where these receptors are coexpressed. Improved NPR-A specificity could provide more effective natriuretic peptides for treatment of acute renal failure or heart failure.

Amino Acid Sequence↗
PubMed1996

Prk, a cytokine-inducible human protein serine/threonine kinase whose expression appears to be down-regulated in lung carcinomas.

We have cloned and characterized a putative protein serine/threonine kinase termed prk through a combination of polymerase chain reaction and conventional cDNA library screening approaches. There are apparently two distinct domains within prk protein deduced from its nucleotide sequences. The amino-terminal portion has the feature of the catalytic domain of a serine/threonine kinase and shows strong homology to mouse fnk and other polo family kinases including mouse snk, human and murine plk, Drosophila polo, and yeast Cdc5. The carboxyl-terminal portion, presumably the regulatory domain, shares extensive homology to mouse fnk. Northern blotting analyses reveal that prk expression is restricted to a very limited number of tissues with placenta, ovaries, and lung containing detectable amounts of prk mRNA. prk mRNA expression is also detected at a low level in the megakaryocytic cell line Dami, MO7e, and three brain glioma cell lines. In addition, refeeding of serum-deprived MO7e, Dami, and K562 cells of hematopoietic origin and GMOO637D of lung fibroblasts rapidly activates prk mRNA expression with its peak induction around 2 h after serum addition. prk gene activation by the serum requires no new protein synthesis. The recombinant cytokines such as interleukin-3 and thrombopoietin also activate prk mRNA expression in MO7e cells. Furthermore, a survey of RNAs isolated from the tumor and the uninvolved tissues from 18 lung cancer patients reveals that prk mRNA expression is significantly down-regulated in tumor tissues. Southern blotting analysis indicates that the prk gene is present in a single copy in the genome of tumors and normal cells. Taken together, these results suggest that prk expression may be restricted to proliferating cells and involved in the regulation of cell cycle progression. The molecular cloning of prk cDNA will facilitate the study of its biological role as well as its potential role in tumorigenesis.

Amino Acid Sequence↗
PubMed1996

Overexpression of insulin-like growth factor-1 in the heart is coupled with myocyte proliferation in transgenic mice.

Transgenic mice were generated in which the cDNA for the human insulin-like growth factor 1B (IGF-1B) was placed under the control of a rat alpha-myosin heavy chain promoter. In mice heterozygous for the transgene, IGF-1B mRNA was not detectable in the fetal heart at the end of gestation, was present in modest levels at 1 day after birth, and increased progressively with postnatal maturation, reaching a peak at 75 days. Myocytes isolated from transgenic mice secreted 1.15 +/- 0.25 ng of IGF-1 per 10(6) cells per 24 hr versus 0.27 +/- 0.10 ng in myocytes from homozygous wild-type littermates. The plasma level of IGF-1 increased 84% in transgenic mice. Heart weight was comparable in wild-type littermates and transgenic mice up to 45 days of age, but a 42%, 45%, 62%, and 51% increase was found at 75, 135, 210, and 300 days, respectively, after birth. At 45, 75, and 210 days, the number of myocytes in the heart was 21%, 31%, and 55% higher, respectively, in transgenic animals. In contrast, myocyte cell volume was comparable in transgenic and control mice at all ages. In conclusion, overexpression of IGF-1 in myocytes leads to cardiomegaly mediated by an increased number of cells in the heart.

Animals↗
PubMed1996

Programmed myocyte cell death affects the viable myocardium after infarction in rats.

To determine whether apoptotic and necrotic myocyte cell death occur acutely and chronically after infarction, the formation of DNA strand breaks and the localization of myosin monoclonal antibody labeling were analyzed in the surviving myocardium from 20 min to 1 month. DNA strand breaks in myocyte nuclei were detected as early as 3 h following coronary artery occlusion and were still present at 1 month. This cellular process was characterized biochemically by internucleosomal DNA fragmentation which produced DNA laddering on agarose gel electrophoresis. Quantitatively, 155 myocyte nuclei per 10(6) cells exhibited DNA strand breaks in the portion adjacent to the infarcted tissue at 3-12 h. This parameter increased to 704 at 1-2 days and subsequently decreased to 364 at 7 days, 188 at 14 days, and 204 at 1 month. In the remote myocardium, the number of myocyte nuclei with DNA strand breaks was 84 per 10(6) at 3-12 h and remained essentially constant up to 1 month. Programmed myocyte cell death was accompanied by a decrease in the expression of bcl-2 and an increase in the expression of bax. The changes in the expression of these genes were present at 1 and 7 days after coronary artery occlusion. In conclusion, the mechanical load produced by myocardial infarction and ventricular failure may affect the regulation of bcl-2 and bax in the viable myocytes, triggering programmed cell death and the remodeling of the ventricular wall.

Animals↗