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Biomedical subjects

X F Li

Publications and source records attributed to X F Li.

At least 73 records · Page 4Linked to original sources
PubMed1997

Compartmentalization and cyclic variation of immunoreactivity of renin and angiotensin converting enzyme in human endometrium throughout the menstrual cycle.

Renin and angiotensin converting enzymes (ACE) are responsible for the generation of angiotensin II which regulates blood pressure and fluid/electrolyte homeostasis. The cellular localization and cyclic distribution of renin and ACE in human endometrium are demonstrated in this study. Immunohistochemical studies revealed that both renin and ACE were consistently localized in the endometrial glandular epithelia throughout the menstrual cycle; however, the immunostainings respectively for ACE and renin were weak and moderate in stromal cells of proliferative endometrium and negligible in secretory endometrium. No renin immunostaining was detected around endometrial blood vessels. Although endothelial cells consistently stained for ACE, no renin immunoreactivity was detected in these cells during the menstrual cycle. Western blot analysis using ACE antibody directed against human kidney identified a single protein band with a relative molecular mass of approximately 153 kDa. The intensity of this band showed cyclic variation during the menstrual cycle with the highest ACE expression during the late secretory phase and at menses suggesting that ACE plays a role in the initiation of menstruation. The differences in the cellular distribution patterns of these two enzymes further supports our previous proposition that angiotensin II has different functions at the different stages of the menstrual cycle.

Blotting, Western↗
PubMed1997

Effect of sodium glycyrrhetinate on chemical peritonitis in rats.

AIM: To study the anti-inflammatory mechanisms of sodium glycyrrhetinate (SG). METHODS: Rat chemical peritonitis was used. The protein content and prostaglandin E2 (PGE2) content in exudate were measured by Folin-phenol assay and RIA, respectively. SOD activity in neutrophils (Neu) was determined by pyrogallol-NBT colorimetry. cAMP content in Neu was detected by competitive protein binding assay. RESULTS: In peritonitis caused by histamine, SG 10-20 mg.kg-1 i.m. reduced exudate volume and Neu counts, and 5-20 mg.kg-1 i.m. lowered the protein content in exudate. In peritonitis induced by carrageenan, SG 20 mg.kg-1 i.m. reduced exudate volume, Neu counts, protein content and PGE2 content in exudate, increased SOD activity in Neu, but did not affect beta-glucuronidase release from Neu. In peritonitis induced by arachidonic acid, SG 20 mg.kg-1 i.m. reduced Neu counts, protein content, and PGE2 content in exudate, and attenuated the reduction of cAMP level in Neu. CONCLUSION: SG exerts its anti-inflammatory action by lowering permeability of capillaries in inflammatory site, inhibiting Neu emigration and PGE2 biosynthesis, and scavenging oxygen free radicals.

Animals↗
PubMed1997

Fibroblast growth factor receptor-1 is a critical component for endometrial remodeling: localization and expression of basic fibroblast growth factor and FGF-R1 in human endometrium during the menstrual cycle and decreased FGF-R1 expression in menorrhagia.

Angiogenic growth factors play a critical role in the cyclic growth and vascularization of normal endometrium. Herein, we report the expression and localization of both basic fibroblast growth factor (FGF-2) and its receptor (FGF-R1; flg) in human endometrium and demonstrate the markedly decreased FGF-R1 levels in menorrhagia. In situ hybridization using [35S]-labeled riboprobe demonstrated distinct autoradiographic signals for FGF-2 mRNA in glandular epithelial and stromal cells in endometrium throughout the menstrual cycle, with the strongest hybridization signal in stromal cells of the proliferative endometrium relative to that of the secretory endometrium. Moreover, RNAse protection assay revealed that the mRNA encoding FGF-2 and FGF-R1 was significantly higher in proliferative than in secretory endometrium (p < 0.05, p < 0.01). Immunohistochemistry using anti-flg antibody showed that the intensity of FGF-R1 staining was markedly diminished in the stromal cells of secretory endometrium, which corresponded with the reduced FGF-2 mRNA expression. In contrast, the endometrial glandular epithelial cells showed intense localization of FGF-R1 protein throughout the menstrual cycle, which paralleled FGF-2 mRNA expression. Colocalization of FGF-2 and FGF-R1 in stroma and stimulation of DNA synthesis and phospholipase C activation by FGF-2 in these cells demonstrates that FGF-2 acts in an autocrine manner in endometrial stroma. Western immunoblotting showed that FGF-R1 immunoprotein was markedly reduced or absent in women with menorrhagia throughout the cycle relative to that of normal cycling women, suggesting that FGF-R1 is critical for endometrial "maturation" and regeneration of the normal endometrium following menstruation.

Adult↗
PubMed1996

GABAA and GABAB receptors differentially regulate synaptic transmission in the auditory thalamo-amygdala pathway: an in vivo microiontophoretic study and a model.

Stimulation of the medical geniculate body elicits extracellular single unit responses in the lateral nucleus of the amygdala that are dependent upon glutamatergic neurotransmission [Li et al. (1995) Exp. Brain Res., 105-87-100]. In the present study, we examined the contribution of inhibitory amino acid transmission to these excitatory responses. Antagonists of GABAA or GABAB receptors were delivered microiontophoretically to cells activated by stimulation of the medial geniculate body. Blockade of GABAA receptors with bicuculline resulted in a pronounced increase in evoked short latency unit responses (4-8 ms). In some cases, cells that were not responsive to the stimulation became responsive in the presence of bicuculline. In contrast, delivery of GABAB antagonists, Phaclofen or 2-OH-saclofen, did not affect these short-latency responses. Using paired-pulse stimulation, both short (< 30 ms) and longer (> 50 ms) latency inhibitory processes were revealed. GABAA blockade eliminated the short latency inhibition and GABAB blockade eliminated the longer latency inhibition in most cells. These results suggest that the activation of GABAA and GABAB receptors differentially regulate glutamatergic synaptic transmission in the auditory thalamo-amygdala pathway. Moreover, our findings suggest that at least part of this regulation is via a feedforward mechanism. We tested the sufficiency of feedforward inhibition to account for the data using a simple computational model that incorporates the results presented here.

Amygdala↗
PubMed1996

The postpartum period: the key to maternal mortality.

OBJECTIVES: To assess postpartum care at an international level, we reviewed published literature on postpartum maternal deaths. METHODS: Meta-analysis was used to summarize the literature reviewed. Postpartum deaths in developing countries were compared with those in the United States. RESULTS: In both developing countries and the United States, > 60% of maternal deaths occurred in the postpartum period; 45% of postpartum deaths occurred within 1 day of delivery, > 65% within 1 week, > 80% within 2 weeks. In developing countries, 80% of postpartum deaths caused by obstetric factors occurred within 1 week. CONCLUSIONS: The first 24 h postpartum and the first postpartum week is the high risk of postpartum deaths, and the risk remains significant until the second week after delivery. In developing countries, hemorrhage, pregnancy-induced hypertension complications, and obstetric infection are commonest causes of postpartum deaths. We suggest primary prevention, early detection, and secondary prevention of postpartum deaths.

Developing Countries↗
PubMed1996

Dual role of angiotensin II in the human endometrium.

Angiotensin II (ANG) promotes cell proliferation and angiogenesis as well as being a potent vasoconstrictor. The cellular distribution of renin, ANG and its receptors in the endometrium has yielded useful information about the possible role of the renin-angiotensin system in cyclic menstruation. In the early proliferative phase, intense ANG-like immunostaining was detected in stroma and glandular epithelia, whereas in the late secretory phase, maximal immunoreactivity was localized in the perivascular stromal cells around the endometrial blood vessels. Quantitative receptor autoradiographic studies demonstrated that the human endometrium contains predominantly ANG type 2 receptor (AT2), with a relatively low expression of ANG type 1 receptor (AT1) and a novel non-AT1/non-AT2 ANG recognition site. AT receptors displayed cyclic changes, and the highest renin concentration was detected in the late secretory phase prior to menstruation. After long-term Norplant treatment, an increase in ANG-like immunoreactivity was observed in endometrial stroma and glandular epithelia, while in hyperplastic endometrium, ANG-like immunoreactivity decreased compared with normal cyclic endometria. The pattern of ANG immunostaining in endometria from patients with irregular menstruation was markedly different from that detected in normal endometrium. Normal function of the renin-angiotensin system in endometrium may be necessary for regular cyclic menstruation, and alterations in the distribution of ANG and/or the activity of its receptors are likely to be involved in dysfunctional uterine bleeding.

Angiotensin II↗
PubMed1996

Localisation of placenta growth factor (PIGF) in human term placenta.

Placenta growth factor (PlGF) is a growth factor which belongs to the vascular endothelial growth factor (VEGF) family and is known to bind to the fms-like tyrosine kinase receptor (flt-1). Using Western blot analysis a 50 kDa band was identified in placental protein extract which corresponded to PlGF homodimer. Immunoreactive PlGF was localised to the vasculosyncytial membrane and in the media of large blood vessels of the placental villi, while staining within the mesenchyme was weak and diffuse. There was moderate staining for PlGF in discrete cells in the chorion and no staining in the epithelial layer of the amnion. The maternal decidual cells showed strong staining for PlGF immunoreactive protein. PlGF mRNA was predominantly expressed by the vasculosyncytial membrane of villous trophoblast, whilst there was no apparent expression of PlGF mRNA within the villous mesenchyme. These results suggest that PlGF may be an important paracrine factor for vascular endothelial cells in placental angiogenesis and an autocrine mediator of trophoblast function.

Blotting, Western↗
PubMed1996

Localisation of hepatocyte growth factor and its receptor (c-met) protein and mRNA in human term placenta.

Successful pregnancy depends upon placental growth and development, which follows a specific spatial and temporal sequence. Hepatocyte Growth Factor (HGF) is a potent mitogen, morphogen and motogen to both endothelial and epithelial cell types and is linked to a tyrosine kinase, proto-oncogene, c-met receptor. In 'normal' third trimester placentae (n = 5) full thickness biopsies (obtained at Caesarean section), immunolocalisation and in situ hybridisation studies were performed for HGF and c-met., respectively. HGF immunoreactive protein was present in mesenchymal core, the vaculosyncytial membrane (syncytotrophoblast) and the vascular endothelial cells of villous trophoblast. The HGF mRNA was present particularly strongly in the perivascular stromal cells surrounding the villous vasculature and the amnion/chorionic membranes. Immunoreactive c-met protein was strongly localised to the endothelial cells lining the villous vasculature and the vasculosyncytial membrane. A relatively weak and diffuse hybridisation signal for c-met mRNA was present throughout the villous trophoblast, most pronounced in the vasculosyncytial membrane. These results indicate that HGF may serve as a paracrine mediator to control placental development and growth.

DNA Probes↗
PubMed1996

Expression of angiotensin II and its receptor subtypes in endometrial hyperplasia: a possible role in dysfunctional menstruation.

Dysfunctional uterine bleeding is associated with hyperplastic endometrium, and angiotensin II may affect cyclic menstruation. Cellular distribution of angiotensin II and its receptor subtypes (AT1 and AT2) in hyperplastic endometria from patients who had dysfunctional uterine bleeding with or without progestogen treatment was investigated by immunocytochemistry and quantitative receptor autoradiography. Angiotensin II-like immunoreactivity decreased in the hyperplastic endometrial stroma and glandular epithelia compared with normal cyclic endometria. The pattern of angiotensin II immunostaining on perivascular stromal cells in hyperplastic endometria was markedly different from that detected in the normal endometrium. The angiotensin II-like immunostaining was more intense in the progestogen-treated endometria compared with normal endometria. In the progestogen-treated endometrium from patients who had regular menstrual cycles, the angiotensin II-like immunostaining was localized in the perivascular stromal cell, as seen in the normal cyclic endometrium. Both AT1 and AT2 receptor levels in the hyperplastic and progesterone-treated endometria were significantly lower than the levels detected in normal endometrium. The results suggest that the normal function of angiotensin II in endometrium may be essential for regular cyclic menstruation and that alteration in the distribution of angiotensin II and/or the levels of its receptors are likely to be involved in dysfunctional uterine bleeding associated with hyperplastic endometria.

Angiotensin II↗
PubMed1995

Regulatory mechanisms for production of IFN-gamma and TNF by antitumor T cells or macrophages in the tumor-bearing state.

Spleen cells from BALB/c mice bearing a syngeneic tumor (CSA1 M) 2 to 3 wk after inoculation with CSA1 M cells produced IL-2, IFN-gamma, and TNF upon in vitro cultures. This was previously demonstrated to be a result of collaboration between tumor-primed CD4+ T cells and APCs binding CSA1 M tumor Ags in vivo. The IL-2- and IFN-gamma-producing capacities decreased with the progress of tumor-bearing stages. This was parallel to the levels of IL-2 and IFN-gamma mRNAs expressed by cultured spleen cells. In contrast, comparable levels of TNF mRNA were expressed by all groups of cultured cells. However, large amounts of TNF were secreted by the cells from early but not from late tumor-bearing mice. TNF was produced mainly by the non-T cell fraction upon stimulation with CD4+ T cell-derived IFN-gamma. Therefore, the reduced TNF production by whole spleen cells from late tumor-bearing mice was restored by addition of rIFN-gamma to their cultures. Reciprocally to the progressive decrease in the production of IFN-gamma/TNF, the capacities of tumor-bearing mice to produce TGF-beta and IL-6 increased along with tumor growth. TGF-beta suppressed production of IL-2, IFN-gamma, and TNF, but not of IL-6. Moreover, IFN-gamma/TNF production was negatively regulated by IL-6. Taken together with the fact that the growth of CSA1 M cells is completely inhibited by the combination of TNF and IFN-gamma, these results demonstrate that the tumor-bearing state induces an abnormal cytokine network under which the production of antitumor cytokines is negatively regulated.

Animals↗
PubMed1995

NMDA and non-NMDA receptors contribute to synaptic transmission between the medial geniculate body and the lateral nucleus of the amygdala.

We examined whether the NMDA class of excitatory amino acid receptors contribute to synaptic transmission in the pathway connecting the medial geniculate body (MGB) with the lateral nucleus of the amygdala (LA) using extracellular single unit recordings and microiontophoresis. Cells were identified in LA on the basis of responsivity to electrical stimulation of the MGB. For each cell, a level of current was found for the iontophoretic ejection of the NMDA antagonist AP5 that blocked responses elicited by iontophoresis of NMDA, but had no effect on responses elicited by AMPA. Iontophoresis of AP5 with this level of current blocked the excitatory response elicited by MGB stimulation in most cells tested. Microinfusion of AP5 (25, 50, or 100 microM) also blocked the responses. Additional studies tested individual cells with both AP5 and the AMPA antagonist CNQX and showed that blockade of either NMDA or AMPA receptors interferes with synaptic transmission. Finally, iontophoretic ejection of either AP5 or CNQX blocked short-latency (< 25 ms) responses elicited in LA by peripheral auditory stimulation. Together, these results suggest that the synaptic evocation of action potentials in the thalamo-amygdala pathway depends on both NMDA and non-NMDA receptors. We hypothesize that non-NMDA receptors are most likely required to depolarize the cell sufficiently to remove the blockade of NMDA channels by magnesium and NMDA receptors are required to further depolarize the membrane to the level required for action potential generation.

Acoustic Stimulation↗
PubMed1995

Localization of the angiotensin II and its receptor subtype expression in human endometrium and identification of a novel high-affinity angiotensin II binding site.

Angiotensin (ANG) II is not only a potent vasoconstrictor but may also be involved in the regeneration of new blood vessels. In proliferative endometrium, ANG II-like immunoreactivity was detected in glandular epithelium and stroma with negligible staining around the vascular endothelium. In contrast, in secretory endometrium intense immunostaining was seen in the perivascular stromal cells around the endometrial spiral arterioles with negligible staining of the other cell types. Quantitative receptor autoradiography using the nonselective radioligand [125I]-ANG II and subtype selective competing compounds showed that endometrium contained predominantly AT2 receptors, with relatively low expression of AT1 receptors and a novel non-AT1/non-AT2 angiotensin II recognition site that was insensitive to AT1 or AT2 selective ligands. Levels of specific [125I]-ANG II receptor binding displayed cyclic changes during the menstrual cycle, reaching a maximum in early secretory endometrium and then decreasing in mid to late secretory endometrium to levels seen in early to mid proliferative endometrium. In situ hybridization showed AT1 receptor mRNA expression in the glands and in the endometrial blood vessels. The cyclic changes in ANG II-like immunoreactivity together with expression of both the known and the novel AT receptor subtypes imply that this octopeptide may play a dual role both in the control of the uterine vascular bed and also in the regeneration of the endometrium after endometrial shedding, acting as an angiogenic and mitogenic mediator.

Adult↗
PubMed1995

Localisation of bradykinin-like immunoreactivity and modulation of bradykinin-evoked phospholipase D activity by 17 beta-oestradiol in human endometrium.

Bradykinin may act as a promoter of endometrial regeneration. Bradykinin-like immunoreactivity was detected immunocytochemically in the glandular epithelium and stroma of human endometrium. The staining was localized around the stroma and especially in the cells undergoing mitosis. Relatively weak staining was seen in the stromal cells of secretory endometrium, which was predominantly localised around the basal vacuoles of endometrial glands. During the late secretory phase, the intensity of staining was diminished throughout the endometrium: the glandular epithelium showed weak staining and stroma appeared negative. As phosphatidate, the product of phospholipase D pathway, may mediate cell proliferation, the effect of 17 beta-oestradiol on bradykinin-evoked phospholipase D activity assayed as accumulation of [3H]phosphatidylbutanol ([3H]PtdBut) was examined in [3H]myristic acid-labelled primary cultures of human endometrial stromal cells. Bradykinin induced a rapid accumulation of [3H]PtdBut in a time-dependent manner, indicating phospholipase D activation. Pretreatment of stromal cells with 17 beta-oestradiol enhanced the bradykinin-evoked phospholipase D activity. These results suggest that bradykinin-like immunoreactivity is strongly associated with proliferative stromal cells undergoing mitosis, a process that may be mediated by phospholipase D activation as the magnitude of this enzyme's activation in vitro appears to be regulated by 17 beta-oestradiol.

Adult↗
PubMed1995

Colocalisation of vascular endothelial growth factor and its Flt-1 receptor in human placenta.

Vascular endothelial growth factor (VEGF) is an angiogenic protein which acts on both endothelial and trophoblast cells. In first trimester placenta, VEGF immunoreactive protein was detected in cytotrophoblast shell suggesting a role in the regulation of cytotrophoblast growth and differentiation as they also expressed VEGF receptor (flt-1) protein. VEGF and flt-1 immunoreactive proteins were expressed in Hofbauer cells within the villous mesenchyme, macrophages and in maternal decidual cells while weak VEGF immunoreactive protein was seen in syncytiotrophoblast surrounding the placental villi in first and second trimester placentae. At term, there was relatively weak VEGF and flt-1 immunostaining in the syncytiotrophoblast while intense VEGF immunostaining was seen in the Hofbauer and maternal decidual cells. Extravillous trophoblast showed immunostaining for flt-1 but no staining for VEGF. Both amnion and chorion expressed strong VEGF immunoreactivity throughout gestation. Smooth muscle cells surrounding the vein and arteries of the umbilical cord showed weak VEGF immunoreactivity while no immunoreactivity was localised in endothelial cells. VEGF stimulated parathyroid hormone-related protein (PTHrP) release (mean (+/- SD): basal, 0.96 +/- 0.03; 10 ng/ml VEGF165, 2.07 +/- 0.18 and 20 ng/ml VEGF165, 2.43 +/- 0.18 pmol/l/well of PTHrP1-86) in condition medium from immortalised first trimester trophoblast cell line. These results suggest that VEGF in addition to acting as an autocrine mitogen for trophoblast proliferation may also function as a paracrine mediator of vascular tone by releasing vasorelaxants from trophoblasts.

Cell Differentiation↗
PubMed1994

Immunolocalisation of vascular endothelial growth factor in human endometrium.

Angiogenesis is an essential component of endometrial regeneration after menses in preparation for implantation. Vascular endothelial growth factor (VEGF) is a secreted angiogenic peptide with mitogenic activity specific for endothelial and trophoblast cells. VEGF-immunoreactivity was detected in glandular epithelium throughout the menstrual cycle by immunohistochemistry, but, showed cyclic variation in the stroma and the blood vessels. During the early proliferative phase, strong staining was seen in the glandular epithelial cells while staining in the stroma was confined to a subpopulation of stromal cells and endometrial blood vessels appeared negative. In contrast, very intense staining of the endometrial stromal cells was seen in the mid proliferative endometrium possibly due to increased synthesis of VEGF by oestrogen. In the late proliferative endometrium, staining was seen in the endothelial cells and the perivascular stromal cells around the endometrial blood vessels. The greatest degree of immunostaining of stromal cells was observed in the mid to late proliferative endometrium. Throughout the secretory phase no staining was seen around the endometrial blood vessels and staining of endometrial stromal cells was confined to early secretory endometrium. In the late secretory endometrium only the glands were positive to VEGF antibody. The observed increase in the immunostaining of stroma suggests increased production of VEGF from early to mid and late proliferative endometrium which parallels the increase in the oestradiol levels in the proliferative phase of the menstrual cycle. It is proposed that VEGF may serve as a paracrine mediator of the effects of ovarian steroids on endometrial vascular development.

Adult↗
PubMed1994

[Leukemia associated with bimkolane].

Psoriatic patients and mice treated with bimolane were observed. The frequency of chromosomes aberration and micro-nuclear cells presence in the treated group (11 cases) was significantly higher than that in the control group (11 cases, P < 0.005; < 0.001). Study of lymphocytic subsets showed that value of CD4/CD8 in the peripheral blood of the treated group was lower than that of the control group (P < 0.05). The level of serum IgM in the treated group was also lower (P < 0.05). There were 10 mice suffering from leukemia (7 mice with acute promyelocytic leukemia) in a treated group of 40 mice of an inbred line of 615 mice, while there was no leukemia in a control group of 20 mice of the same species. The morbidity of leukemia in the treated mice was higher than that of controls (P < 0.05).

Adolescent↗