Biomedical subjects

Y Yuan

Publications and source records attributed to Y Yuan.

At least 127 records · Page 7Linked to original sources

PubMed1999

Convergence of trigeminal input with visceral and phrenic inputs on primate C1-C2 spinothalamic tract neurons.

Trigeminal, spinal and vagal afferent fibers overlap in C1-C2 segments. We hypothesized that trigeminal input from the superior sagittal sinus (SSS) can excite C1-C2 spinothalamic tract (STT) neurons receiving thoracic visceral or phrenic inputs. Effects of SSS stimulation were evenly divided among cells responding to each nerve stimulus; magnitude of responses to ipsilateral vagal input was greater in neurons excited by SSS input. Somatic fields of 80% of neurons responding to SSS stimulation included face areas innervated by the trigeminal nerve, whereas somatic fields of 89% of neurons unaffected by SSS stimulation were located only on areas innervated by cervical spinal nerves. Results are consistent with the idea that pain referred to trigeminal areas could originate in thoracic organs.

Animals↗

PubMed1999

Establishment of the culture technique of pulmonary vascular pericytes and its identification in rats.

In order to study the cellular origin of muscularization in non-muscular arterioles of the lung, the pulmonary vascular pericytes-culture was established. The terminal lung tissue of the rat was taken out and minced. Then 0.5% of type IV collagenase solution was added for digestion and the microvascular segments were obtained by screening. The targeted cells were cultured by "selective conditioned media". Under phase-contrast microscope, the cultured cells were large in size with ragged margin and numerous pseudopodia, which imparted tubule-like structure. There was no contact inhibition in growing cells, so multiple layers developed. When they were confluent, there were morphologically no "hillock and dale" growth pattern as in smooth muscle cells or "weave-like" pattern as in fibroblasts. The ultrastructure of cultured cells showed numerous digital processes, moderate amount of rough and smooth endoplasmic reticulum, rich Golgi's apparatus, microfilaments, few lysosomes without myofilaments and dense bodies. Immunohistochemical staining revealed that the cultured pericytes had same kind of cellular skeletal protein, alpha-SM-actin, like smooth muscle cells. The cultured cells also exhibited positive reaction to CD34 antigen and S-100 antigen, which were negative in smooth muscle cells and fibroblasts. The cell growth pattern, ultrastructure and immunological phenotype suggested that the cultured cells had characteristics of vascular pericytes. Pericytes are one of the components of microvascular cells, and the establishment of in vitro culture technique of pericytes is of significance for further exploration of the muscularization of non-muscular arterioles in lung and the mechanism of structural remodeling of pulmonary vessels.

Animals↗

PubMed1999

Mifepristone regulation of leukemia inhibitory factor and uterine receptivity in rabbits.

The effects of mifepristone on production of leukemia inhibitory factor (LIF) and uterine receptivity in rabbits was studied. In ovariectomized rabbits, LIF protein was at an undetectable level in control (score = 0), and upregulated by progesterone alone (score = 4). Estrogen had no additive effect, and may even have had a slightly negative effect when the rabbits were treated with both estrogen and progesterone (score = 3). Meanwhile, mifepristone obviously inhibited the stimulation of progesterone on the production of LIF in rabbit uterus (score = 1). The results also showed that LIF protein has a beneficial effect on uterine receptivity and mifepristone prevents this effect. The transfer of embryos to LIF-treated recipients significantly increased pregnancy (70%) and implantation rate (31%) as compared with control (pregnant rate = 50% and implantation rate = 17%). The transfer of embryos to LIF and mifepristone-treated recipients significantly decreased pregnancy (30%) and implantation rate (9%). The results of this study suggest that mifepristone prevented the effects of progesterone on LIF production and the beneficial effect of LIF on uterine receptivity.

Animals↗

PubMed1999

Identification of the immediate-early transcripts of Kaposi's sarcoma-associated herpesvirus.

In the immediate-early phase of reactivation or primary infection, herpesviruses express a small number of genes without requiring prior viral protein synthesis. Immediate-early genes usually encode regulatory proteins critical for the viral life cycle. Kaposi's sarcoma-associated herpesvirus (KSHV) gene transcription in the immediate-early stage of viral reactivation was examined by using a chemical induction combined with a gene expression screening method. RNA transcripts from at least four KSHV genomic loci accumulate when latently infected B-lymphoma cells are induced for reactivation in the presence of an inhibitor of protein synthesis (cycloheximide) and thus represent immediate-early class transcripts. Among them, a 3.6-kb mRNA encodes three putative open reading frames (ORFs), namely, ORF50, K8, and K8.2. ORF50 is a homologue of Rta, a transcription activator encoded by Epstein-Barr virus (EBV). The K8 gene codes for a 237-amino-acid protein with a basic-leucine zipper domain near its C terminus and an acidic domain near its N terminus and which closely resembles the ZEBRA protein of EBV and Jun/Fos family proteins. Other immediate-early mRNAs of KSHV include a 1. 7-kb mRNA encoding ORF45, a 2.0-kb mRNA encoding ORF K4.2, and a 4. 5-kb mRNA. Functional roles of products of these KSHV immediate-early transcripts remain to be studied.

Amino Acid Sequence↗

PubMed1999

Regulation of the mdm2 oncogene by thyroid hormone receptor.

The mdm2 gene is positively regulated by p53 through a p53-responsive DNA element in the first intron of the mdm2 gene. mdm2 binds p53, thereby abrogating the ability of p53 to activate the mdm2 gene, and thus forming an autoregulatory loop of mdm2 gene regulation. Although the mdm2 gene is thought to act as an oncogene by blocking the activity of p53, recent studies indicate that mdm2 can act independently of p53 and block the G1 cell cycle arrest mediated by members of the retinoblastoma gene family and can activate E2F1/DP1 and the cyclin A gene promoter. In addition, factors other than p53 have recently been shown to regulate the mdm2 gene. In this article, we report that thyroid hormone (T3) receptors (T3Rs), but not the closely related members of the nuclear thyroid hormone/retinoid receptor gene family (retinoic acid receptor, vitamin D receptor, peroxisome proliferation activation receptor, or retinoid X receptor), regulate mdm2 through the same intron sequences that are modulated by p53. Chicken ovalbumin upstream promoter transcription factor I, an orphan nuclear receptor which normally acts as a transcriptional repressor, also activates mdm2 through the same intron region of the mdm2 gene. Two T3R-responsive DNA elements were identified and further mapped to sequences within each of the p53 binding sites of the mdm2 intron. A 10-amino-acid sequence in the N-terminal region of T3Ralpha that is important for transactivation and interaction with TFIIB was also found to be important for activation of the mdm2 gene response element. T3 was found to stimulate the endogenous mdm2 gene in GH4C1 cells. These cells are known to express T3Rs, and T3 is known to stimulate replication of these cells via an effect in the G1 phase of the cell cycle. Our findings, which indicate that T3Rs can regulate the mdm2 gene independently of p53, provide an explanation for certain known effects of T3 and T3Rs on cell proliferation. In addition, these findings provide further evidence for p53-independent regulation of mdm2 which could lead to the development of tumors from cells that express low levels of p53 or that express p53 mutants defective in binding to and activating the mdm2 gene.

Animals↗

PubMed1999

Role of phospholipase C, protein kinase C, and calcium in VEGF-induced venular hyperpermeability.

We previously demonstrated that vascular endothelial growth factor (VEGF)-elicited increase in the permeability of coronary venules was blocked by the nitric oxide (NO) synthase inhibitor NG-monomethyl-L-arginine (L-NMMA). The aim of this study was to delineate in more detail the signaling pathways upstream from NO production in VEGF-induced venular hyperpermeability. The apparent permeability coefficient of albumin (Pa) and endothelial cytosolic Ca2+ concentration ([Ca2+]i) were measured in intact perfused porcine coronary venules using fluorescence microscopy. VEGF (10(-10) M) induced a two- to threefold increase in Pa, which was blocked by a monoclonal antibody directed against the VEGF receptor Flk-1/KDR, the phospholipase C (PLC) antagonist U-73122, or the protein kinase C (PKC) antagonist bisindolylmaleimide (BIM). In 12 venules that displayed the [Ca2+]i response to bradykinin (10(-6) M) and ionomycin (10(-6) M), only 4 vessels responded to VEGF with a transient increase in [Ca2+]i. Furthermore, Western blot analysis of cultured human umbilical vein endothelial cells showed that VEGF increased tyrosine phosphorylation of PLC-gamma and serine phosphorylation of endothelial constitutive NO synthase (ecNOS). The hyperphosphorylation of PLC-gamma was greatly attenuated by the KDR receptor antibody and U-73122, but not by BIM or L-NMMA. In contrast, U-73122 and BIM were able to inhibit VEGF-elicited serine phosphorylation of ecNOS. The results suggest that VEGF induces venular hyperpermeability through a KDR receptor-mediated activation of PLC. In turn, ecNOS is activated by PLC-mediated PKC and/or cytosolic Ca2+ elevation stimulation.

Animals↗

PubMed1999

Comparative effects of methylmercury on parallel-fiber and climbing-fiber responses of rat cerebellar slices.

The environmental neurotoxicant methylmercury (MeHg) causes profound disruption of cerebellar function. Previous studies have shown that acute exposure to MeHg impairs synaptic transmission in both the peripheral and central nervous systems. However, the effects of MeHg on cerebellar synaptic function have never been examined. In the present study, effects of acute exposure to MeHg on synaptic transmission between parallel fibers or climbing fibers and Purkinje cells were compared in 300- to 350-microm cerebellar slices by using extracellular and intracellular microelectrode-recording techniques. Field potentials of parallel-fiber volleys (PFVs) and the associated postsynaptic responses (PSRs) were recorded in the molecular layer by stimulating the parallel fibers in transverse cerebellar slices. The climbing-fiber responses were also recorded in the molecular layer by stimulating white matter in sagittal cerebellar slices. At 20, 100, and 500 microM, MeHg reduced the amplitude of both PFVs and the associated PSRs to complete block, however, it blocked PSRs more rapidly than PFVs. MeHg also decreased the amplitudes of climbing-fiber responses to complete block. For all responses, an initial increase in amplitude preceded MeHg-induced suppression. Intracellular recordings of excitatory postsynaptic potentials of Purkinje cells were compared before and after MeHg. At 100 microM and 20 microM, MeHg blocked the Na+-dependent, fast somatic spikes and Ca++-dependent, slow dendritic spike bursts. MeHg also hyperpolarized and then depolarized Purkinje cell membranes, suppressed current conduction from parallel fibers or climbing fibers to dendrites of Purkinje cells, and blocked synaptically activated local responses. MeHg switched the pattern of repetitive firing of Purkinje cells generated spontaneously or by depolarizing current injection at Purkinje cell soma from predominantly Na+-dependent, fast somatic spikes to predominantly Ca++-dependent, low amplitude, slow dendritic spike bursts. Thus, acute exposure to MeHg causes a complex pattern of effects on cerebellar synaptic transmission, with apparent actions on both neuronal excitability and chemical synaptic transmission.

Action Potentials↗

PubMed1999

[Susceptibility gene location of simple congenital heart defect by transmission disequilibrium test].

OBJECTIVE: To locate the susceptibility gene of human simple congenital heart defect(CHD) and provide a sound basis for further gene cloning. METHODS: Three short tandem repeats(STRs) in regions of chromosome 7p14-15, 17q21 where exist Hox gene family's A, B clusters which regulate the embryonic heart development were chosen. Genotypes of 112 members in 39 CHD families were analyzed by amplifying the STR fragments using fluorescence-PCR technique. Then transmission disequilibrium test(TDT) was used to test the data of genotypes. RESULTS: Statistical chi(2) values of D7S1808, D7S673 and D17S791 were 31.3(P<0.005), 11.12(P<0.05) and 6.65 (P>0.05) respectively. These suggest that the former two are associated with CHD, while the latter is not. CONCLUSION: Human simple CHD is associated with Hox gene A cluster. Hox A gene may be a candidate CHD's susceptive genes. The location of the CHD's susceptive genes is in chromosome 7p14-15.

Chromosomes, Human, Pair 7↗

PubMed1999

Effects of electro-acupuncture on somatostatin and pancreatic polypeptide in ischemic cerebrovascular diseases.

The levels of somatostatin (SS) in CSF and blood and pancreatic polypeptide (PP) in plasma were measured by radioimmunoassay in 64 patients with acute ischemic cerebrovascular diseases (ICVD), randomly divided into two groups: group 1 (n = 31, both electro-acupuncture and routine treatments given) and group 2 (n = 33, routine treatment) and 26 non-ICVD patients were used as controls. The points of electro-acupuncture were Quchi (LI 12), Waiguan (SJ 5) and Huantiao (GB 30) and Zusanli (St 36). After a course of treatment, the SS levels in plasma and CSF were significantly increased in the patients of group 1 with good result and their plasma PP level had no significant change. In the patients with poor result, however, the PP level was significantly decreased. The results suggested that electro-acupuncture might play an active role in alleviating the SS metabolic disturbance in CNS of ICVD patients.

Adult↗

PubMed1999

[Measurement and clinical use of recoil pressure of the respiratory system].

Using the principle that the difference of MIP (maximal inspiratory mouth pressure) between RV (residual volume) and FRC (functional residual capacity) equals Prs (recoil pressure of the respiratory system) at RV, we performed the measurement of Prs at RV in 20 normal subjects, 90 patients with COPD (chronic obstructive pulmonary disease) and 15 patients with ILF (interstitial lung fibrosis). We also performed the correlation analysis of Prs at RV and RV/TLC (total lung capacity) %. The results indicated the Prs values at RV (-2.8 +/- 0.5 kPa) in normal subjects measured in this manner was in accord with the values reported by other authors abroad. The Prs in patients with emphysema decreased and it was highly and negatively correlated with RV/TLC% (r = -0.872), but the Prs in patients with ILF was increased. The results suggest that this method for measurement of Prs is simple, reliable, and clinically useful.

Aged↗

PubMed1999

[Expression of cyclin dependent kinase inhibitor p27 during proliferation in vascular smooth muscle cell].

This study was to investigate cell cycle distribution of the vascular smooth muscle cells (VSMCs) and negative regulator of cell proliferation p27 expression caused by platelet derived growth factor BB (PDGF-BB), angiotensin II (Ang II) and arginine vasopressin (AVP). Deprived of fotal calf serum for 48 h, cultured VSMCs in quiescent condition were collected at different times after stimulation of Ang II, AVP and PDGF-BB. Cell cycle distribution and p27 expression were determined with a flow cytometer. The results showed that the protein content of VSMCs was significantly increased (43.6%) by Ang II as a result of hypertrophy, but Ang II did not lead to downregulation of p27. AVP could downregulate p27 slightly. PDGF could inhibit p27 expression significantly and cause VSMCs hyperplasia. These results suggest that the progression of VSMCs through G1 to S phase might be brought out by the inhibition of p27 during proliferation.

Angiotensin II↗

PubMed1999

[Different expressions of cyclins and cyclin dependent kinase inhibitor P27 in vascular smooth muscle cells and cardiac myocytes caused by angiotensin II and PDGF stimulation].

OBJECTIVE: To investigate cell cycle distribution of the vascular smooth muscle cells (VSMC) and cardiac myocytes(CM) and different expressions of cyclins and P27 caused by angiotensin II (Ang II) and platelet derived growth factor BB (PDGF-BB). METHODS: Cultured VSMCs or CMs were collected at 24 h after stimulation of Ang II (10(-6) mol/L) and PDGF-BB (20 ng/ml). Cell cycle distribution, cyclins and P27 expression were determined with flow cytometer. RESULTS: Ang II had no effect on P27 expression in both VSMCs and CMs. It did not cause proliferation of both VSMCs and CMs. Although PDGF-BB could significantly increase cyclins expression in both VSMCs and CMs, it could only significantly inhibit P27 expression in VSMCs (1.8 +/- 1.3 vs 48.1 +/- 5.4, P < 0.01) and cause VSMC proliferation, and had no effect on P27 expression in CMs(39.4 +/- 5.6 vs 44.6 +/- 3.6, P > 0.05). CONCLUSION: The progression of VSMC and CM through G1 to S phase might be brought out by the inhibition of P27 during proliferation.

Angiotensin II↗

PubMed1999

[Mutations of hMLH1 and hMSH2 genes in suspected hereditary nonpolyposis colorectal cancer].

OBJECTIVE: To analyze the molecular characteristics of 29 ICG-HNPCC families and 34 suspected HNPCC families. METHODS: Genomic DNAs were prepared from peripheral blood samples of probands for DNA test. PCR-SSCP and DNA sequencing analysis were employed to screen the germline mutations of hMLH1 and hMSH2 genes. RESULTS: In 29 ICG-HNPCC families, 9 mutations in the hMLH1 gene were detected, while no mutation was found in the hMSH2 gene. The total mutation rate was 31.0% (9/29). In 34 suspected HNPCC families, 8 mutations in the hMLH1 gene and 2 mutations in the hMSH2 gene were detected. The total mutation rate in this group was 29.4% (10/34), including hMLH1 gene 23.5% (8/34) and hMSH2 gene 5.9% (2/34). hMLH1 gene was proven to be the main responsible gene in both ICG-HNPCC and suspected HNPCC families, and no obvious difference was found between the mutation rate in the two kinds of families (P > 0.05). As for the mutation type and location, similar characteristics were also detected. Almost all mutations located in the latter half of both genes, and mutation leading to protein truncation was the commonest type. CONCLUSION: The similarity of mutation rate, mutation type and mutation location between ICG-HNPCC and suspected HNPCC suggested the similarity of molecular basis and genetic background between these two groups, and also strongly indicated our criteria for suspected HNPCC is reasonable, and useful in the clinical diagnosis and management of HNPCC.

Adaptor Proteins, Signal Transducing↗

PubMed1999

[Effect of zinc-intensified milk powder on hematopoiesis in mice].

OBJECTIVE: To observe the effect of Zn-intensified milk powder and zinc on hematopoiesis in mice. METHODS: Kunming mice were randomly divided into four groups (n = 9 each) (control group; milk powder group; equal zinc group; high zinc group) and fed on experimental diet for 24 weeks. RESULTS: 1. In high zinc group: the mice hemoglobin (Hb) declined (P < 0.05) after 12 wk of supplementation and were significantly lower (P < 0.01) than those in control group at 16 wk. At 24 wk, the mice showed lower Hb, red blood cell(RBC), hematocrit (HCT), and mean corpuscular volume (MCV) compared with control group (P < 0.05). Bone marrow aspirates revealed erythroid hyperplasia. Zinc concentrations in serum, liver and kidney were higher (P < 0.01) and copper was lower than that of control group(P < 0.01). 2. At 16 wk, no change occurred in milk powder group and equal zinc group. At 24 wk, parameters changed in milk powder group similar to those in high zinc group, and in equal zinc group liver and kidney copper was lower than that in control group (P < 0.05). CONCLUSION: Ingestion of over-dosed zinc could induce anemia. Generally, intake of Zn-intensified milk powder is safe, but long-term intake of the milk powder may interfere with hematopoiesis.

Animals↗

PubMed1999

[Characteristics and criteria for bronchial responsiveness measurement in cough variant asthma].

OBJECTIVE: To investigate the value of sGaw in the differentiation of CVA from COPD. METHODS: MEFV, airway resistance(Raw) and bronchial responsiveness were measured in 30 cases with CVA, 133 cases with typical bronchial asthma(BA) and 37 cases with COPD. RESULTS: (1) The expiratory-flow parameters (PEF, MMEF, FEV1/FVC) in MEFV curve in remission period of CVA were largely normal, but most patients with CVA (67%) have increased Raw and decreased sGaw, characteristics similar with typical bronchial asthma (BA). (2) If PC35sGaw < 8 g/L was set as the positive limit, 100% of CVA and BA patients showed bronchial hyperresponsiveness(BHR), the average positive MCH concentration being about 1.0 g/L. 5 cases with COPD (13.5%) also showed BHR, but the average MCH concentration was 5.24 g/L. (3) If PC35sGaw < 4 g/L was set as the positive limit for the diagnosis of CVA, the sensitivity was 96.7%, specificity 97.3%, confidence limit 99%. (4) A equation for PC35sGaw was deduced, and its calculation values showed the same results with the ones from diagrammatization. CONCLUSIONS: sGaw is a sensitive index for the measurement of bronchial responsiveness, and it is useful in the differentiation of CVA from COPD. It is suggested that PC35sGaw < 8 g/L be regarded as bronchial hyperresponsiveness, and PC35sGaw < 4 g/L as candidate for CVA.

Adult↗

PubMed1999

[Mutation of human mismatch repair genes in hereditary nonpolyposis colorectal cancer (HNPCC) families].

OBJECTIVE: To investigate germline mutations of mismatch repair genes hMLH1 and hMSH2 in 29 HNPCC families. METHODS: Mutations were detected by PCR-SSCP analysis, and confirmed by DNA sequencing. RESULTS: (1) In 29 families, the overall mutation rate of these two genes was 31.0% (9/29). Mutation detected in all of the 9 families was located in the hMLH1 gene, indicating that the hMLH1 gene was the main responsible gene in these families. An obvious difference was observed when compared to the mutation rate in the control group (P < 0.01); (2) All of the 10 family members who developed colorectal cancer (CRC) harbored the same mutation as detected in their proband, indicating a strong association between gene mutation and development of CRC. In 29 healthy family members, 5 asymptomatic carriers of mutation were found who were considered as the high-risk populations of CRC. CONCLUSION: A certain number of HNPCC families can be benefited from the genetic screening for mutation of the mismatch repair genes.

Adaptor Proteins, Signal Transducing↗

PubMed1999

[Evaluation of CT in the diagnosis of esthesioneuroblastoma].

OBJECTIVE: To assess the role of CT in the diagnosis, staging and post-treatment follow-up of esthesioneuroblastoma. METHODS: Thirteen cases of pathologically comfirmed esthesioneuroblastoma were analysed retrospectively. RESULTS: On preoperative check up, according to Kadish staging, no case was in stage A, 4 cases were in stage B, 7 in stage C. Tumor scans showed soft tissue density. In 3 cases, calcification was found inside of the tumor. In the 4 cases on scan and enhanced CT, the tumors were heterogeneously enhanced in 3. On enhanced CT, the tumor density was obviously higher than that of the surrounding soft tissue in 6 cases. Postoperative follow-up CT revealed tumor recurrence within 3 months to 2 years in 4 cases. Tumor invasion involved nasal cavity and ethmoid sinus(13 cases), maxillary sinus (12 cases), sphenoid sinus(10 cases), frontal sinus (2 cases), orbit (7 cases). Intracranial invasion occurred in 3 cases, and lymph node metastases in 4 cases. CONCLUSION: CT is valuable in pre-operative staging and monitoring recurrence of esthesioneuroblastoma. Although esthesioneuroblastoma has characteristic CT features on enhancement and multiple invasions to neighboring structures, reliable diagnosis is dependent on pathological confirmation.

Adolescent↗

PubMed1999

[The effect of sandostatin on sphincter of Oddi in acute severe pancreatitis in dogs].

OBJECTIVE: To study the pressure change of sphincter of Oddi (SO) in acute severe pancreatitis (ASP) and the effect of sandostatin on it. METHODS: Fifteen dogs were used and allocated into 2 groups: ASP untreated group and sandostatin group. The ASP model was prepared by retrograde ductal injection of a mixture of 5% taurocholic acid and autologous bile. SO manometic parameters including basal pressure (BP) and phasic contraction amplitude (PCA) were measured at each time spot before and after the preparation of ASP and after the administration of sandostatin. RESULTS: BP was obviously increased after ASP preparation and sandostatin could significantly decrease the BP of SO in ASP group but not PCA. CONCLUSION: Dysmotility of SO might play an important role in the severity and progression of ASP. Sandostatin may have beneficial effects in the treatment of ASP by decreasing BP of SO.

Acute Disease↗