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Biomedical subjects

Q L Li

Publications and source records attributed to Q L Li.

At least 19 recordsLinked to original sources
PubMed2006

A two-compartment exposure device for foliar uptake study.

An airtight two-chamber exposure devise was designed for investigating foliar uptake of polycyclic aromatic hydrocarbons (PAHs) by plants. The upper and the bottom chambers of the device were air-tightly separated by an aluminum foil and the plant aerial tissues and roots were exposed in the two chambers, respectively. The device was tested using maize exposed to several PAH species. Positive correlations between air and aerial tissue concentrations of the exposed PAH species were revealed. PAHs spiking in the culture solution had no influence on the leaf concentrations.

Air Pollution↗
PubMed2005

Expressions and regulation of endothelial and inducible nitric oxide synthases in mouse uterus during the estrous cycle and early pregnancy.

Nitric oxide (NO) has been implicated in many cellular processes. We examined the temporal and spatial expressions of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) in mouse uteri during the estrous cycle and early pregnancy, as well as the regulation of eNOS and iNOS by estradiol (E2) and progesterone (P4) in ovariectomized mouse uteri using in situ hybridization and immunohistochemistry. Our results showed that positive eNOS and iNOS signals were localized in the uterine luminal epithelium and glandular epithelium during the estrous cycle. In ovariectomized mice, both E2 and P4 regulated the expression of eNOS and iNOS. During early pregnancy, eNOS and iNOS were detected not only in epithelium, but also in the primary decidual zone surrounding implanting embryos on day 6 of pregnancy, and in the whole decidualized stroma on day 7 of pregnancy. In conclusion, the results demonstrated that two NOS isoforms were localized in mouse uteri in specific temporal and spatial patterns during the estrous cycle and early pregnancy, and ovarian hormones can regulate their expression. Furthermore, the data suggest that the expression of NOS during the peri-implantation period might lead to enhance NO production, which could promote embryo implantation.

Animals↗
PubMed2004

Regulation of matrix metalloproteinases (MMPS) and their inhibitors (TIMPS) during mouse peri-implantation: role of nitric oxide.

Nitric oxide (NO) is believed to play pivotal roles in embryo implantation. The purpose of this study was to investigate the effect of NO on matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs), as well as the mechanism of NO during mouse implantation. Nitric oxide synthase (NOS) inhibitor, L-NAME was administered with or without sodium nitroprusside (SNP), NO donor, into one uterine horn on day 3 of pregnancy, and the contralateral uterine horn served as the control. We collected the uteri on days 5, 6, and 7 of pregnancy and examined the mRNA expression of MMP-2, -9, and TIMP-1, -2, -3, as well as the activities of MMP-2 and -9 by using in situ hybridization and gelatin zymography, respectively. The results showed that, compared with the control, the expression of MMP-2 and -9 mRNAs was decreased in L-NAME-treated uteri during peri-implantation. Treatment of mice with L-NAME had slight effect on the expression of TIMP-1 mRNA on day 5 of pregnancy, and no effect on TIMP-2 mRNA expression during peri-implantation. However, the expression of TIMP-3 mRNA was increased. The gelatin zymography results indicated that the activity of MMP-9 was decreased during peri-implantation, but the activity of MMP-2 did not change significantly in these time points examined. The L-NAME-mediated effect on MMPs and TIMPs were significantly reversed when SNP was co-administered with L-NAME. These data suggest that inhibition of NO production regulates the gene expression of MMP-2, -9, and TIMP-3, together with the activity of MMP-9 during peri-implantation, which may have serious consequence on embryo implantation.

Animals↗
PubMed2001

Up-regulation of splenic prohormone convertases PC1 and PC2 in diabetic rats.

Organisms respond to infection in a complex manner involving bidirectional interactions between the neuroendocrine and immune systems. Many of the bioactive endocrine/immune factors are synthesized in a precursor form and are expected to be activated by prohormone convertases (PCs). Since patients with both type 1 and type 2 diabetes have an increased incidence and severity of infections, we hypothesized that in a condition of hyperglycemia, these processing enzymes would be activated in an immune tissue, the spleen. To test this hypothesis, we treated rats with intraperitoneal streptozotocin (STZ) (50 mg/kg/day) daily for 5 days and measured splenic PC1 and PC2 mRNA by ribonuclease protection assay. We found that PC1 mRNA was increased 6.0+/-0.02-fold (P<0.05) and PC2 mRNA was increased 1.80+/-0.01-fold (P<0.005) in the spleen of rats that received STZ compared to rats that received vehicle. Western blot indicated that the 75-kDa form of PC1 was the only form of PC1 present in the spleen and that this form increased with STZ treatment. Immunohistochemistry revealed that PC1 was found in both the white pulp (T-lymphocytes) and red pulp (monocytes and macrophages) and that its increase in immunoreactivity occurred primarily in the white pulp. PC2 and pro-opiomelanocortin (POMC, a possible splenic substrate for PC1/PC2) immunoreactivity was found predominantly in the red pulp. STZ induced an increase in splenic PC1 and POMC, but not PC2 protein levels. We conclude that in the STZ model of diabetes, splenic PCs are induced, which could lead to an increased activation of many immune-derived hormones. We speculate that this up-regulation of prohormone converting enzymes may be related to the increased infections seen in patients with both type 1 and type 2 diabetes.

Animals↗
PubMed2001

[Lithotripsy for residual cholelithes by rigid choledochoscopy].

OBJECTIVE: To evaluate a new lithotomy for postoperatively residual cholelithes. METHOD: Using rigid choledochoscopy to extract the residual cholelithes which could hardly be extracted by fibrocholedochoscopy through the T-tube sinus in 31 cases. RESULT: The residual cholelithes were extracted in 30 cases, reoperation was avoided. CONCLUSION: The residual cholelithes can be effectively extracted by the rigid choledochoscopy plus mechanical lithotripsy through T-tube sinus.

Adolescent↗
PubMed2001

Cloning and expression pattern of a novel PEBP2 beta-binding protein (charged amino acid rich leucine zipper-1[Crl-1]) in the mouse.

PEBP2 beta/Cbf beta is the beta subunit of PEBP2/Cbf, which has been demonstrated to have important biological activities in hematopoiesis and osteogenesis. However, PEBP2 beta is ubiquitously expressed, suggesting that PEBP2 has other additionally important physiological activities. In an effort to elucidate other possible functions for PEBP2, we have isolated a novel gene that encodes a PEBP2 beta-interacting protein from a mouse cDNA library. We have called this gene Crl-1 for charged amino acid rich leucine zipper-1 (Crl-1) because it is rich in charged amino acids and contains a putative leucine zipper region. Expression studies in a 17.5 days post-coitum mouse embryo demonstrated Crl-1 expression mainly in the olfactory bulb and cerebral cortex. Post-natally, Crl-1 expression was additionally observed in the cerebellar cortex with strong expression in the hippocampus. These findings show that this novel PEBP2 beta-interacting protein is expressed mainly in subsets of neuronal cells, suggesting that Crl-1 plays some role in the developing mouse brain.

Amino Acid Sequence↗
PubMed2001

Inhibition of thyroid hormone binding to the nuclear receptor by mobilization of free fatty acids.

Through binding to its nuclear receptor (TR), thyroid hormone (T3) activates the expression of the thyroid hormone-responsive genes that are essential for the regulation of energy consumption. Previously, we found that free fatty acids (FFAs) and their CoA esters strongly inhibited the binding of T3 to its nuclear receptor in vitro. In the present study, we have examined the physiological relevance of this inhibitory mechanism. TRs in isolated nuclei and in a solubilized free form were half-maximally inhibited with oleic acid at 120 and 2.8 microM, respectively. The lower sensitivity of the nuclear TR as compared with free TR was attributed to the nuclear envelope and the association of TR with chromatin. Among TRs in chromatin, those in the transcriptionally active chromatin exhibited the highest sensitivities to FFAs and were inhibited half-maximally by oleic acid at 10 microM. While the plasma concentration of FFAs in total was 0.4 to 1 mM, their nuclear concentration was about 5 microM. Thus, the sensitivities of TRs in active chromatin and in solubilized form were at physiological levels with respect to the nuclear FFA concentration. We further examined the effect of FFA mobilization on the T3-binding to TR in animals. Nuclear T3-binding was significantly inhibited when plasma and cellular FFAs were increased by norepinephrine in vivo. The increase in cellular FFAs and the TR-inhibition were well correlated, and much larger in the heart than in the liver and kidney. These results suggest that TR is negatively controlled by increased FFAs in a tissue-dependent manner.

Animals↗
PubMed2001

Regulation of prohormone convertase 1 (PC1) by thyroid hormone.

The prohormone convertases (PCs) PC1 and PC2 are key enzymes capable of processing a variety of prohormones to their bioactive forms. In this study, we demonstrated that 6-n-propyl-2-thiouracil (PTU)-induced hypothyroidism stimulated, whereas triido-L-thyronine (T(3))-induced hyperthyroidism suppressed, PC1 mRNA levels in the rat anterior pituitary. Using 5' deletions of the human PC1 (hPC1) promoter transiently transfected into GH3 (a somatotroph cell line) cells, we found that T(3) negatively regulated hPC1 promoter activity and that this regulation required the region from -82 to +19 bp relative to the transcription start site. Electrophoretic mobility shift assays (EMSAs) using purified thyroid hormone receptor-alpha1 (TR alpha 1) and retinoid X receptor-beta (RXRbeta) proteins and GH3 nuclear extracts demonstrated that the region from -10 to +19 bp of the hPC1 promoter bound TR alpha 1 as both a monomer and a homodimer and bound TR alpha 1/RXR beta as a heterodimer and multimer. EMSAs with oligonucleotides containing point mutations of the putative negative thyroid response elements (TREs) exhibited diminished homodimer and loss of multimer binding. We conclude that there are multiple novel TRE-like sequences in the hPC1 promoter located from -10 to +19 bp.

Alitretinoin↗
PubMed2001

Inhibition of steroidogenesis and induction of apoptosis in rat luteal cells by cell-permeable ceramide in vitro.

The present study was undertaken to investigate the effects of ceramide on progesterone production and apoptosis in rat luteal cells in vitro. Luteal cells were prepared from the ovaries of pregnant mare serum gonadotropin (PMSG) and human chorionic gonadotropin (hCG) primed female Wistar rats and incubated with cell permeable C2-ceramide. The effects of ceramide on progesterone production and apoptosis in luteal cells were assessed by radio immunoassay (RIA) and flow cytometry analysis. In addition, changes in nitric oxide synthase (NOS) activity and nitric oxide (NO) production by luteal cells treated with C2-ceramide were also evaluated. Ceramide was found to reduce hCG-stimulated progesterone production in a dose-dependent manner, whereas it had little effect on basal progesterone content. Spontaneous apoptosis in luteal cells was observed after a 12-hour incubation in vitro and 5 mumol/L of ceramide significantly increased the apoptotic rate (P < 0.05). Enhanced apoptotic peak was seen in the histogram by flow cytometry. Moreover, 50 mumol/L of C2-ceramide significantly increased NOS activity (P < 0.01) and NO production (P < 0.001). It is suggested that ceramide may serve as an important signaling molecule mediating certain ovarian processes, such as luteal regression.

Animals↗
PubMed2001

[Electrochemical behavior of ofloxacin at Pt/GC ion implantation modified electrode and its application].

AIM: To study the electrochemical behavior of ofloxacin at Pt/GC ion implantation modified electrode. METHODS: With Pt/GC ion implantation modified electrode as working electrode, the behavior of ofloxacin was studied by voltammetry in 0.40 mol.L-1 KCl solution. RESULTS: A sensitive reductive peak of ofloxacin was obtained by linear sweep voltammetry. The peak potential was -1.35 V (vs SCE). The peak current was proportional to the concentration of ofloxacin over the range of 1.0 x 10(-6)-3.0 x 10(-5) mol.L-1 with the detection limit of 5.0 x 10(-7) mol.L-1. The behavior of reduction wave was studied and applied to determination of ofloxacin in tablets. CONCLUSION: The reduction process was irreversible. The element composition, atomicity form and depth of distribution at the surface of Pt/GC electrode were determined by Auger electron spectroscopy (AES), X-ray photoelectron spectroscopy (XPS) and scanning electron microscope (SEM). The catalysis behavior and reaction mechanism at Pt/GC modified electrode was also studied.

Carbon↗
PubMed2000

Runx2 is a common target of transforming growth factor beta1 and bone morphogenetic protein 2, and cooperation between Runx2 and Smad5 induces osteoblast-specific gene expression in the pluripotent mesenchymal precursor cell line C2C12.

When C2C12 pluripotent mesenchymal precursor cells are treated with transforming growth factor beta1 (TGF-beta1), terminal differentiation into myotubes is blocked. Treatment with bone morphogenetic protein 2 (BMP-2) not only blocks myogenic differentiation of C2C12 cells but also induces osteoblast differentiation. The molecular mechanisms governing the ability of TGF-beta1 and BMP-2 to both induce ligand-specific responses and inhibit myogenic differentiation are not known. We identified Runx2/PEBP2alphaA/Cbfa1, a global regulator of osteogenesis, as a major TGF-beta1-responsive element binding protein induced by TGF-beta1 and BMP-2 in C2C12 cells. Consistent with the observation that Runx2 can be induced by either TGF-beta1 or BMP-2, the exogenous expression of Runx2 mediated some of the effects of TGF-beta1 and BMP-2 but not osteoblast-specific gene expression. Runx2 mimicked common effects of TGF-beta1 and BMP-2 by inducing expression of matrix gene products (for example, collagen and fibronectin), suppressing MyoD expression, and inhibiting myotube formation of C2C12 cells. For osteoblast differentiation, an additional effector, BMP-specific Smad protein, was required. Our results indicate that Runx2 is a major target gene shared by TGF-beta and BMP signaling pathways and that the coordinated action of Runx2 and BMP-activated Smads leads to the induction of osteoblast-specific gene expression in C2C12 cells.

Animals↗
PubMed2000

Regulation of pancreatic PC1 and PC2 associated with increased glucagon-like peptide 1 in diabetic rats.

The pancreatic processing enzymes, PC1 and PC2, convert proinsulin to insulin and convert proglucagon to glucagon and glucagon-like peptide 1 (GLP-1). We examined the effect of streptozotocin (STZ) treatment on the regulation of these enzymes and the production of insulin, glucagon, and GLP-1 in the rat. Pancreatic PC1 and PC2 mRNA increased >2-fold and >4-fold, respectively, in rats receiving intraperitoneal STZ (50 mg/kg) daily for 5 days. Immunocytochemistry revealed that, although pancreatic islet cells in the STZ-treated rats were sparse and atrophic PC1, PC2, glucagon, and GLP-1 immunoreactivity increased dramatically in the remaining islet cells. Heightened PC1 and PC2 expression was seen in cells expressing glucagon but not in insulin-expressing cells. Furthermore, in STZ-treated rats, bioactive GLP-1(7-36 amide) accumulated in pancreatic extracts and serum 3- and 2.5-fold, respectively, over control animals. This treatment also caused a 2-fold increase in the ratio of amidated forms of GLP-1 immunoreactivity to total glucagon immunoreactivity in the pancreas but did not affect the ratio of proinsulin to insulin. We conclude that hyperglycemic rats have an increased expression of prohormone converting enzymes in islet alpha cells, leading to an increase in amidated GLP-1, which can then exert an insulinotropic effect on the remaining beta cells.

Animals↗
PubMed2000

Interactions between the prohormone convertase 2 promoter and the thyroid hormone receptor.

The majority of prohormones are cleaved at paired basic residues to generate bioactive hormones by prohormone convertases (PCs). As PC1 and PC2, two neuroendocrine-specific PCs, appear to be the key enzymes capable of processing a variety of prohormones, alterations of PC2 and/or PC1 levels will probably have a profound effect on hormonal homeostasis. We investigated the regulation of PC2 messenger RNA (mRNA) by thyroid hormone using GH3 cells to demonstrate that T3 negatively regulated PC2 mRNA levels in a dose- and time-dependent fashion. Functional analysis of progressive 5'-deletions of the human (h) PC2 promoter luciferase constructs in GH3 cells demonstrated that the regulation probably occurs at the transcriptional level, and that putative negative thyroid hormone response elements were located within the region from -44 to + 137 bp relative to the transcriptional start site. Transient transfections in JEG-3 cells and COS-1 cells showed that the suppressive effect of T3 was equally mediated by the thyroid hormone receptor (TR) isoforms TRalpha1 and TRbeta1. Electrophoretic mobility shift assays using purified TRal and retinoid X receptor-beta protein as well as GH3 nuclear extracts showed that regions from +51 to +71 bp and from +118 to +137 bp of the hPC2 promoter bind to TRalpha1 as both a monomer and a homodimer and with TRalpha1/retinoid X receptor-beta as a heterodimer. Finally, the in vivo regulation of pituitary PC2 mRNA by thyroid status was demonstrated in rats. These results demonstrate that T3 negatively regulates PC2 expression at the transcriptional level and that functional negative thyroid hormone response elements exist in the hPC2 promoter. We postulate that the alterations of PC2 activity may mediate some of the pathophysiological consequences of hypo- or hyperthyroidism.

Animals↗
PubMed2000

Changes in soluble interleukin-2 receptor level in serum and Na+-K+-exchanging ATPase activity in semen of infertile men caused by antisperm antibody.

AIM: To explore the possible mechanisms of male infertility caused by antisperm antibody (AsAb). METHODS: The soluble interleukin-2 receptor (sIL-2R) level in serum was analyzed by ELISA and Na+-K+-exchanging ATPase activity in semen by phosphorus (Pi) assay. RESULTS: The sIL-2R level in serum was significantly higher and the Na+K+-exchanging ATPase activity in semen significantly lower in AsAb positive infertile men when compared with the controls. CONCLUSION: The AsAb titer varies with the sIL-2R level in serum. A decrease in Na+-K+-exchanging ATPase activity in semen may play a role in male infertility caused by AsAb.

Adult↗
PubMed2000

[The detection and analysis of human papillomavirus in infantile respiratory tract papillomas by PCR/RFLP study].

OBJECTIVE: To study the relationship between human papillomavirus (HPV) and pathological characteristics of the patients with infantile respiratory tract papillomas (IRP). METHOD: Thirteen cases of infantile respiratory tract papillomas tissue were analysed for Papillomavirus by the polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). RESULT: The amplified products of the HPV-L1 region by PCR by using the consensus primers showed that the presence of HPV was 100 percent. Eight cases(61.5 percent) were positive for HPV6 only. Four cases (30.8 percent) were positive for HPV11 only. One case (7.7 percent) showed the presence of HPV18. None were positive for HPV16, 31, 33, 52, 58. CONCLUSION: Infantile respiratory tract papillomas are associated with HPV6, 11, 18 infection, but the subtypes of HPV are not associated with clinical pathological characteristics.

Child, Preschool↗
PubMed1999

Regulation of prohormone convertase 1 (PC1) by gp130-related cytokines.

The processing of pro-opiomelanocortin (POMC) to generate bioactive ACTH in the anterior pituitary is mediated by prohormone convertase 1 (PC1). Leukemia inhibitory factor (LIF) and interleukin 6 (IL-6), two cytokines sharing the common gp130 receptor subunit and functioning through activation of the intracellular JAK/STAT pathway, induce POMC synthesis and ACTH release. We investigated the effects of LIF and IL-6 on PC1 expression and its subsequent processing of POMC. A significant time-dependent up-regulation of both PC1 protein and mRNA by LIF and IL-6 was seen in mouse corticotroph AtT-20 cells. IL-6 or LIF increased the synthesis of ACTH-related products with a concomitant increase in bioactive 5 and 13 kDa ACTH indicating coordinated regulation of substrate and processing enzyme. AtT-20 cells transiently transfected with a human PC1-promoter-luciferase reporter construct and treated with LIF or IL-6 showed significantly increased luciferase activity. Additionally, lipopolysaccharide (LPS) administration to rats resulted in an increase in both pituitary PC1 and POMC mRNA. These findings suggest that the ACTH increase induced by LIF and IL-6 is due to both increased POMC synthesis as well as increased POMC processing by up-regulation of PC1. These two coordinately regulated processing events probably exert central roles in the pathophysiological response to some stresses, such as inflammatory stress.

Animals↗
PubMed1997

Leukemia inhibitory factor (LIF) modulates pro-opiomelanocortin (POMC) gene regulation in stably transfected AtT-20 cells overexpressing LIF.

Leukemia inhibitory factor (LIF) levels are elevated in sepsis and correlate with shock and poor prognosis. We have previously shown that lipopolysaccharide (LPS) administration induces hypothalamic and pituitary LIF expression in vivo, which is associated with the acute rise in circulating adrenocorticotrophic hormone (ACTH) levels. As AtT-20 cells respond to LIF, we established murine LIF (mLIF) stably transfected AtT-20 cell lines to study LIF regulation of pro-opiomelanocortin (POMC) expression and ACTH secretion. Our results show that mLIF transfectants accumulated mLIF (up to 15.6 +/- 3.2 ng/mL after 24 h) as well as increased ACTH secretion (up to 2.4-fold above control cells) in conditioned medium. The magnitude of ACTH induction correlated with mLIF concentrations in different transfectants (r = 0.75-0.88, p < 0.05). Moreover, mLIF transfectants showed a higher sensitivity to CRH stimulation with an increased ACTH production within 8 h (p < 0.05), whereas control cells were responsive to CRH at 24 h. Additionally, mLIF transfectants exhibited a maximum threefold ACTH induction, compared to 1.7-fold in control cells. Furthermore, mLIF transfectants have a blunted dexamethasone-mediated inhibition of ACTH (35% inhibition in control cells vs no inhibition in mLIF-transfected cells at 24 h). These findings support and extend the previous observations of LIF acting at the pituitary level, and indicate that mLIF stably-transfected AtT-20 cells are a useful model for studying mLIF-mediated gene regulation in pituicytes.

Adrenocorticotropic Hormone↗