Are the beta-adducin C1797T polymorphism and gamma-adducin A386G polymorphism associated with essential hypertension in Yi and Hani populations?
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Calmodulin-Binding Proteins↗
Biomedical subjects
Li He
Publications and source records attributed to Li He.
Crossed polydactyly type I caused by a point mutation in the GLI3 gene in a large Chinese pedigree.
Polydactyly is one of the most common forms of congenital malformation in humans, and is displayed by 119 disorders. Crossed polydactyly (CP) is defined as the coexistence of preaxial and postaxial polydactyly with a difference in the axes of polydactyly between the hands and feet. In an effort to map the gene responsible for CP, we studied a seven-generation Chinese family of 56 individuals, 28 of whom were affected. A thorough search with highly informative polymorphic markers showed no recombination among the affected members with the markers on chromosome 7p15-q11.23, but no linkage with chromosomes 2q31, 7q36, 13q, and 19p. Mutation analysis showed a substitution mutation of 1927C --> T in exon 12 of the GLI3 gene, which is predicted to pretruncate the GLI3 protein. This mutation has variable phenotypes of polydactyly, indicating that other genetic factors also contribute to the diversity of polydactyly phenotypes. Our results increase the phenotypic spectrum caused by GLI3 mutations and are important for the analysis and understanding of the etiology of these limb malformations.
Asian People↗
The relationship between CYP17 -34T/C polymorphism and acne in Chinese subjects revealed by sequencing.
BACKGROUND: Although many arguments have been raised on the role of heredity in the etiology of acne, the relevant genetic elements in the pathogenesis of the disease are not well established. OBJECTIVE: The aim of our study was to evaluate the association between a genetic polymorphism in the promoter region of the CYP17 gene and the development of acne. METHODS: 206 acne patients and 200 controls were included in the study. A polymerase chain reaction (PCR) sequencing technique was used to reveal a CYP17 gene polymorphism in its promoter region. A chi2 test was used for data analysis. RESULTS: CYP17 -34T/C polymorphism was found and the frequency distribution of the C/C homozygotes and C allele in the male patients with severe acne (33.3 and 60.9%, respectively) were statistically significantly different from those of the control samples (18.2 and 46.6%; p < 0.05). No significant difference was observed between the female patients, mild + moderate male patients and their controls, respectively. CONCLUSION: The CYP17 -34C/C homozygote Chinese men are at a significantly increased risk of developing severe acne.
Acne Vulgaris↗
[Effect of dachuanxiongwan on the expression of vascular epithelial growth factor in rats with cerebral ischemia].
OBJECTIVE: To study the effect of Dachuanxiongwan on the expression of vascular epithelial growth factor in the rats after focal cerebral ischemia and reperfusion. METHODS: The ischemia and reperfusion model was established by blocking the middle cerebral artery of the rats with a nylon thread for two hours. Twenty male Sprague-Dawley rats with middle cerebral artery occlusion (MCAO) were randomly divided into two groups. One of the group of rats were administered with DCXW, 4.13 g/kg x d, twice a day for 3 days by gavaging, while other group were given the same volume of saline as a control. Seventy-two hours after reperfusion, the neuropathological function of the rats were evaluated according to Longa. The rats were then sacrificed and the samples of cerebrum were processed and embedded in paraffin and cut into sections. The expression of VEGF was determined by immunocytochemistry. RESULTS: The score of the neuropathological function of the DCXW treated group (1.5 +/- 0.71) was lower than that of the control group (2.3 +/- 0.82, P = 0.032). More VEGF-positive cells were found in the rats treated with DCXW than those in the control group (P = 0.000). CONCLUSION: DCXW upgrades the expression of VEGF and may have a positive effect on the cerebrum following ischemia and reperfusion.
Animals↗
Forty cases of simple obesity treated by acupuncture.
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Acupuncture Therapy↗
[A study on the protective efficacy of magnesium against anoxic damage to cultured neurons of rats].
OBJECTIVE: This is an in vitro study aimed to assess the influence of magnesium on cultured anoxic cortical neurons of rats. METHODS: After being treated with MgSO4 and Mg(2+)-ATP respectively, the cortical neurons of rats were given mixture of 97.5% N2 and 2.5% CO2 continuously to set up the model of anoxic cortical neuron of rats at different time points. The mortality of neurons, the levels of Ca2+ within nerve cells (marked by Fluo-3, detected by laser confocal microscopy), and the levels of lactate dehydrogenase (LDH), K+ and neuron specific enolase (NSE) in the culture fluid were investigated at 1,2,4 hours after the inception of anoxia. RESULTS: MgSO4 and Mg(2+)-ATP reduced the calcium influx of anoxic cortical neuron (P<0.05), lowered the level of LDH, K+, NSE in the culture fluid (P<0.05) and significantly decreased the mortality of neurons (P <0.05). CONCLUSION: The protective efficacy of magnesium against the anoxic damage to cultured cortical neurons of rats is corroborated.
Animals↗
Expression of survivin gene in apoptosis induced by dexamethasone in CEM cells.
OBJECTIVE: The precise mechanism of glucocorticoid-induced apoptosis has not yet been elucidated. Survivin, a member of the inhibitors of apoptosis protein family, correlates with inhibition of apoptosis, proliferation, angiogenesis and multiple drugs resistance. This study aimed to investigate the variation of the survivin gene expression in apoptosis induced by dexamethasone (Dex) in the human T-lineage acute lymphoblastic leukemia (ALL) cell line, CEM-WT cells. METHODS: The logarithmically growing CEM cells cultured in vitro (cell density 2 x10(5)/mL) were exposed to 0.1, 0.5, 1, 5, and 10 microM Dex, then were collected 24, 48 and 72 hrs later. Untreated CEM cells were used as Controls. The cell viability was determined by trypan blue dye exclusion. Apoptosis was evaluated by morphology and flow cytometry. Survivin protein and gene were analyzed by Western Blot and RT-PCR. RESULTS: CEM cells growth was obviously inhibited by 0.1, 0.5, 1, 5, and 10 microM Dex from 48 hrs. The inhibition effect was dose- and time-dependent. CEM cells treated with Dex (> or = 5 microM) exhibited typical apoptotic features. The apoptosis increased after 5 microM Dex treatment in a time-dependent manner, with the apoptosis percentage increasing from 14.9% (12 hrs) to 46.2% (48 hrs). Compared with that of the Control group, the expression of survivin protein was down-regulated, with the expression rate of 54.6%, 45.5%, 15.8% and 9.7% respectively at 12, 24, 48 and 72 hrs after 5 microM Dex treatment. 5 microM Dex treatment also resulted in a decrease of survivin mRNA expression. The survivin mRNA expression was 76.4%, 67.3%, 55.0%, 49.9%, 38.3% and 18.3% of the Control respectively at 6, 12, 24, 48 and 72 hrs after Dex treatment. CONCLUSIONS: Apoptosis induced by Dex in CEM cells is associated with downregulation of the survivin expression.
Apoptosis↗
[Down's syndrome in a child with coexistent congenital leukemia and heart disease].
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Chronic Disease↗
[The effects of antiarrhythmic peptide AAP10 on ventricular arrhythmias in rabbits with healed myocardial infarction].
OBJECTIVE: To evaluate the effects of antiarrhythmic peptide (AAP10) on ventricular arrhythmias in rabbits with healed myocardial infarction (OMI). METHODS: Thirty rabbits were randomly divided into three groups (n = 10 each): Sham group, left thoracotomy was performed without coronary ligation; OMI group and OMI + AAP10 group, the circumflex coronaries were ligated. Three months post operation, the electrophysiological and antiarrhythmic effects of AAP10 were assessed in the arterially perfused rabbit left ventricular wedge preparation. Sham and OMI group were perfused with Tyrode's solution and OMI + AAP10 group was perfused with Tyrode's solution + AAP10 (80 nmol/L). Transmembrane action potentials were recorded simultaneously from endocardium and epicardium together with a transmural ECG by use of 2 separate intracellular floating microelectrodes. The stimulus-response-interval (SRI) of the epicardium and the incidence of ventricular tachycardia (VT) were observed. Whole heart and left ventricular weights, the left ventricular thickness at infarct border zone were measured. RESULTS: Whole heart and left ventricular weights as well as the left ventricular thickness at the infarct border zone significantly increased post infarction. VT was induced in 8 out of 10 rabbits in OMI group and in 2 out of 10 rabbits in OMI + AAP10 group (P < 0.05). SRI was also significantly shortened in OMI + AAP10 group compared to OMI group [SRI-1: (20.59 +/- 0.79) ms vs. (28.71 +/- 0.55) ms; SRI-2: (30.42 +/- 0.74) ms vs. (38.67 +/- 0.49) ms, all P < 0.01]. However, the action potential morphology and duration were similar between OMI and OMI + AAP10 groups. CONCLUSION: The antiarrhythmic peptide (AAP10) can increase gap junctional intercellular conductance without affecting the action potential morphology and duration and decrease the incidence of inducible ventricular tachycardia.
Animals↗
Evaluation of tributyrin lipid emulsion with affinity to low-density lipoprotein: pharmacokinetics in adult male Wistar rats and cellular activity on Caco-2 and HepG2 cell lines.
The tributyrin lipid emulsion was proved to be able to bind to low-density lipoprotein (LDL) in vitro. The aim of this study was to investigate the pharmacokinetics of the emulsion in vivo and the cellular activity in vitro. The pharmacokinetics of tributyrin and its metabolite, butyrate, was evaluated in male Wistar rats after administration with pure tributyrin or tributyrin emulsion. After oral administration, maximal plasma concentration (C(max)), time to reach maximal plasma concentration (T(max)), and elimination half-life (T(1/2)) of butyrate were 87.6 muM and 25.3 and 63.0 min, respectively, for the pure tributyrin compared with 1344.5 microM and 8.5 and 19.8 min for the 10% (v/v) tributyrin emulsion. C(max) and mean residence time of tributyrin were 2.74 microM and 87.9 min and 4.2 microM and 132.0 min for pure tributyrin and 10% emulsion, respectively. The bioavailabilities of the pure tributyrin versus tributyrin emulsion were 15.3 versus 65.7% and 34.9 versus 64.5% calculated from butyrate and tributyrin, respectively. After the rats were treated with 17alpha-ethynylestradiol (an LDL receptor up-regulator), the distribution volumes calculated from both butyrate and tributyrin were significantly increased after oral administration or infusion of the 10% tributyrin emulsion. The increased distribution volume after coadministration with a LDL receptor up-regulator suggested the increased uptake of tributyrin/butyrate by tissues with increased expression of LDL receptors. The selective uptake of the emulsion by the cellular LDL receptors was further confirmed by testing the cellular viability in the presence of competing LDL. The viable cells can reach 92% of control at IC(50) in Caco-2 and 77% in HepG2 incubated with emulsion in the presence of LDL.
Algorithms↗
Expression of early growth response factor-1 in rats with cerulein-induced acute pancreatitis and its significance.
AIM: To observe the expressions of early growth response factor-1 (Egr-1) and tissue factor (TF) in rats with cerulein-induced acute pancreatitis and to explore its significance. METHODS: A large dose of cerulein was used to create the experimental acute pancreatitis model in rats. The changes of Egr-1 mRNA and protein in rats were observed during 30 min to 4 h after the treatment and immunohistochemical method was used to observe the localized expression of Egr-1 in tissues. In addition to the mRNA expression of Egr-1 target gene, TF was also observed. A blank control group, and a bombesin-administered group were used for comparison. RESULTS: After the stimulation of a large dose of cerulein, the rats showed typical inflammatory changes of acute pancreatitis. Thirty minutes after the stimulation, the mRNA expression of Egr-1 in the pancreatic tissue reached its peak and then declined, while the expression of Egr-1 protein reached its peak 2 h after the stimulation. Histologically, 2 h after the stimulation, almost all pancreatic acinar cells had the expression of Egr-1 protein, which was focused in the nuclei. The mRNA expression of TF occurred 1 h after the stimulation and gradually increased within 4 h. However, a large dose of bombesin only stimulated the pancreatic tissue to produce a little mRNA expression of Egr-1 and no mRNA expression of Egr-1 protein and TF. CONCLUSION: Egr-1 as a pro-inflammatory transcription factor may play an important role in the pathogenesis of acute pancreatitis by modulating the expression of TF.
Acute Disease↗
Association of the C-344T polymorphism of CYP11B2 gene with essential hypertension in Hani and Yi minorities of China.
BACKGROUND: Aldosterone synthase (CYP11B2) is a key enzyme in the biosynthesis of aldosterone. Recently, a C-344T polymorphism in the promoter region of the CYP11B2 gene has been reported to be in association with high blood pressure. We investigated the association between this polymorphism and essential hypertension in Hani (n=305 individuals) and Yi (n=233 individuals) minorities of China. METHODS: CYP11B2 genotyping with polymerase chain reaction-restriction fragment length polymorphism was performed in 267 normotensive subjects and 271 essential hypertensive subjects. At the same time, the T(-344)C polymorphism detection in 33 subjects was also performed by sequencing. RESULT: The frequency of CYP11B2 C-344T genotype in normotensive controls and essential hypertensive cohort in Hani population were TT: 0.729 vs. 0.610; CT + CC: 0.271 vs. 0.390, respectively. The frequency of CYP11B2 C-344T genotype in normotensive controls and essential hypertensive cohort in Yi population were TT: 0.612 vs. 0.475; CT + CC: 0.388 vs. 0.525, respectively. The frequency of CC + CT genotype in the essential hypertensive group was significantly higher than that in the normotensive controls in both Hani and Yi populations (P<0.05). CONCLUSION: The -344C allele of the CYP11B2 may play a role in genetic predisposition to developing essential hypertension in Hani and Yi minorities of China.
Adult↗
NIBP, a novel NIK and IKK(beta)-binding protein that enhances NF-(kappa)B activation.
The transcription factor NF-kappaB plays an important role in both physiological and pathological events in the central nervous system. Nevertheless, the mechanisms of NF-kappaB-mediated regulation of gene expression, and the signaling molecules participating in the NF-kappaB pathway in the central nervous system are, to date, poorly understood. To identify such molecules, we conducted a yeast two-hybrid screen of a human brain cDNA library using NIK as bait. As a result, we identified a novel NIK and IKK(beta) binding protein designated NIBP that is mainly expressed in brain, muscle, heart, and kidney. Interestingly, low levels of expression were detected in immune tissues such as spleen, thymus, and peripheral blood leukocytes, where NF-kappaB is known to modulate immune function. We demonstrated by immunohistochemistry that NIBP expression in the brain is localized to neurons. NIBP physically interacts with NIK, IKK(beta), but not IKK(alpha) or IKK(gamma). NIBP overexpression potentiates tumor necrosis factor-alpha-induced NF-kappaB activation through increased phosphorylation of the IKK complex and its downstream I(kappa)B(alpha) and p65 substrates. Finally, knockdown of NIBP expression by small interfering RNA reduces tumor necrosis factor-alpha-induced NF-kappaB activation, prevents nerve growth factor-induced neuronal differentiation, and decreases Bcl-xL gene expression in PC12 cells. Our data demonstrate that NIBP, by interacting with NIK and IKK(beta), is a new enhancer of the cytokine-induced NF-(kappa)B signaling pathway. Because of its neuronal expression, we propose that NIBP may be a potential target for modulating the NF-(kappa)B signaling cascade in neuronal pathologies dependent upon abnormal activation of this pathway.
Animals↗
An opiate cocktail that reduces morphine tolerance and dependence.
Morphine is an exceptionally effective analgesic whose utility is compromised by the development of tolerance and dependence to the drug. Morphine analgesia and dependence are mediated by its activity at the mu opioid peptide (MOP) receptor [1]. The MOP receptor is activated not only by morphine, but also by other opiate drugs such as methadone and endogenous opioids such as endorphins. Morphine, however, is a unique opioid agonist ligand because it fails to induce endocytic trafficking of the MOP receptor [2], whereas the endogenous ligands and methadone do facilitate endocytosis [3]. Using the unique pharmacology of the MOP receptor and its proposed existence as an oligomeric structure [4], we designed a pharmacological cocktail that facilitates endocytosis of the MOP receptor in response to morphine. This cocktail consists of morphine and a small dose of methadone. Importantly, this cocktail, while retaining full analgesic potency, does not promote morphine dependence. We further demonstrate that dependence is reduced, at least in part, because endocytosis of the MOP receptor in response to morphine prevents the upregulation of N-methyl-D-aspartate (NMDA) receptors.
Analysis of Variance↗
Fusion proteins comprising annexin V and Kunitz protease inhibitors are highly potent thrombogenic site-directed anticoagulants.
The anionic phospholipid, phosphatidyl-L-serine (PS), is sequestered in the inner layer of the plasma membrane in normal cells. Upon injury, activation, and apoptosis, PS becomes exposed on the surfaces of cells and sheds microparticles, which are procoagulant. Coagulation is initiated by formation of a tissue factor/factor VIIa complex on PS-exposed membranes and propagated through the assembly of intrinsic tenase (factor VIIIa/factor IXa), prothrombinase (factor Va/factor Xa), and factor XIa complexes on PS-exposed activated platelets. We constructed a novel series of recombinant anticoagulant fusion proteins by linking annexin V (ANV), a PS-binding protein, to the Kunitz-type protease inhibitor (KPI) domain of tick anticoagulant protein, an aprotinin mutant (6L15), amyloid beta-protein precursor, or tissue factor pathway inhibitor. The resulting ANV-KPI fusion proteins were 6- to 86-fold more active than recombinant tissue factor pathway inhibitor and tick anticoagulant protein in an in vitro tissue factor-initiated clotting assay. The in vivo antithrombotic activities of the most active constructs were 3- to 10-fold higher than that of ANV in a mouse arterial thrombosis model. ANV-KPI fusion proteins represent a new class of anticoagulants that specifically target the anionic membrane-associated coagulation enzyme complexes present at sites of thrombogenesis and are potentially useful as antithrombotic agents.
Amyloid beta-Peptides↗
Expression of CD28 and CTLA4 on T cells in bone morrow of immune-mediated aplastic anemia mice.
To investigate the expression and significance of CD28 and CTLA4 on T cells in bone marrow of aplastic anemia (AA) mice, in vitro bone marrow mononuclear cells (BMMNCs) were activated through being incubated with PHA (15 microg/mL). The expression of CD28 and CTLA4 on T cells incubated with or without PHA was detected by two-color flow cytometry. The expression of CD28 and CTLA4 was significantly increased after PHA stimulation. In the AA mice, the expression of CD28 with or without PHA stimulation was both higher than that in the normal mice (both P < 0.01), but the expression of CTLA4 with or without PHA stimulation showed no significant difference in comparison to that in the normal mice (both P > 0.05). In the AA mice, there were more activation and activated potential of T cells than the normal, and the abnormal expression of CD28 and CTLA4 may participate in immunological disorder mediated by T cells.
Anemia, Aplastic↗
[Studies on the flavonoid constituents in herb of Eremosparton songoricum].
OBJECTIVE: To study the chemical constituents from Eremosparton songoricum. METHOD: The compounds were isolated with silica gel column chromatography and the structures of these compounds were elucidated by means of spectral analysis. RESULT: The seven compounds were identified as: 5,7,4'-trihydroxyflavone (apigenin) (I), 5-hydroxy-7,4'-dimethoxyflavone (II), 5,7-dihydroxy-3',4'-dimethoxyflavone (III), 5,7-dihydroxy-4'-methoxyflavone (acacetin) (IV), 5,7,4'-trihydroxy-3'-methoxyflavone (chrysoeriol) (V), 5,6,3',4'-tetrahydroxy-7-methoxyflavone (pedalitin) (VI) and 5,4'-dihydroxy-7,3'-dimethoxyflavone-4'-O-D-glucoside (flavogadorinin) (VII). CONCLUSION: These constituents were obtained from E. songoricum for the first time.
Apigenin↗
[Effects of ligustrazine on expression of VCAM-1/VLA-4 in syngenic bone marrow transplantation of mice].
To explore the effect of ligustrazine on the expression of adherent molecule VCAM-1/VLA-4 of bone marrow cells in syngenic bone marrow transplantation (BMT) mice, the mice were divided into 3 groups: normal group (which received no treatment), BMT control group and ligustrazine-treated groups. BMT mouse models were established. The BMT control group and the ligustrazine-treated group were orally administered 0.2 ml saline per mouse and 2 mg ligustrazine per mouse, respectively, twice a day. On the day 7, 14, 21, 28 after BMT, mice were respectively killed. Bone marrow nucleated cells were detected, and then the expression of VCAM-1/VLA-4 was assayed by immunohistochemistry, RT-PCR and flow cytometry analysis, respectively. The results showed that in ligustrazine-treated group, the accounts of bone marrow nucleated cells on the day 7, 14, 21, 28 after BMT were all higher than that in BMT control group. The expression level in the ligustrazine-treated group was significantly higher than that in the BMT control group (P < 0.05 or P < 0.01). It is concluded that ligustrazine can enhance VCAM-1/VLA-4 expression in bone marrow after syngenic bone marrow transplantation in mice, which may be related to the mechanisms underlying the ligustrazine accelerating hematopoietic reconstitution in allogenic bone marrow transplantation.
Animals↗