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Biomedical subjects

H Jiang

Publications and source records attributed to H Jiang.

At least 451 records · Page 25Linked to original sources

[Regulation of myocardium beta-adrenoreceptor pathway in ventricular remodeling of heart failure patients].

OBJECTIVE: To study the role of myocardium beta-adrenoreceptor pathway in ventricular remodeling of heart failure patients. METHODS: Beta-adrenergic receptor density (Bmax) and the content of cAMP were measured in the papillae of left ventricle and blood lymphocyte of 20 patients with heart failure (CHF) (NYHA classification II to III). Bmax was investigated by 3H-dihydroalpneolol as ligand, cAMP by competitive immunoassay, and left ventricle mass index (LVMI) by echocardiogram. RESULTS: The Bmax and cAMP in failing myocardium were significantly negatively were correlated with LVMI (r = -0.77, P < 0.01 and r = -0.46, P < 0.05 respectively). The Bmax of myocardium and blood lymphocyte in CHF patients with NYHA III (63 +/- 12 fmol/mgpro and 514 +/- 115 fmol/10(7) cell), was significantly lower than that of NYHA II patients (94 +/- 20 fmol/mgpro and 702 +/- 138 fmol/10(7) cell, and that in patients with abnormal LVMI (62 +/- 12 fmol/mgpro and 516 +/- 122 fmol/10(7) cell) decreased more significantly than that in normal LVMI patients. Even in normal LVMI patients (92 +/- 21 fmol/ mgpro and 682 +/- 146 fmol/10(7) cell), the Bmax of blood lymphocyte was already decreased (P < 0.01), when comparing with the controls. The intralymphocyte cAMP content was more significantly decreased than that of the controls (P < 0.05). CONCLUSIONS: The Bmax can reflect the severity of ventricle remodeling and the impairment of myocardium. The regulation of myocardium intracellular messenger transduction is earlier than the pathologic structural change of LV remodeling.

Adult↗

Clinical study of desflurane on low flow anesthesia compared with sevoflurane and enflurane.

OBJECTIVE: To compare the hemodynamic change, course of recovery and adverse reaction in desflurane, sevoflurane and enflurane inhalation under low flow for patients undergoing selective abdominal surgery. METHODS: Following thiopental induction, 42 patients were divided into three groups: the first group received desflurane, the second sevoflurane and the third enflurane. During surgery, one of the agents around 1 minimum alveolar concentration (MAC) was used for maintenance, with fresh gas flow of 0.3-0.5 L/min for either desflurane or enflurane, and (0.8-1.0) L/min for sevoflurane. Heart rate (HR), blood pressure and end-tidal anesthetic concentration were monitored continuously. Time intervals from cutting off anesthetic to patient opening eyes, following commands, stating the time and location and recalling date of birth were all recorded. In addition, postoperative nausea or vomiting was traced. RESULTS: Desflurane caused the least cardiovascular depression. with mean arterial pressure (MAP) maintained significantly better at 10, 30 and 60 minutes of surgery and with HR stabilized right after incision as well. Its emergence was 2 times faster than sevoflurane, and 5-6 times quicker than enflurane. However, nausea or vomiting was found the lowest in patients receiving sevoflurane, though no distinct difference was shown between desflurane and enflurane. Nevertheless, patients under desflurane suffered less. CONCLUSIONS: Desflurane offers significant advantages for clinical anesthesia maintenance over sevoflurane and enflurane. It provides minimal cardiovascular depression, much quicker recovery, yet still causes some nausea during emergence.

Abdomen↗

[Role of nitric oxide in pathogenesis of pregnancy induced hypertension].

OBJECTIVE: To investigate the role of nitric oxide (NO) in pathogenesis of pregnancy induced hypertension (PIH). METHODS: N(G)-nitro-L-arginine-methyl-ester (L-NAME) was used to inhibite the synthesizing of NO in the third trimester of pregnancy rats. Indices including HGB, PLT, HCT, protein uria, serum endothelin (ET), thromboxane B2(TXB2), 6-keto-PGF1 alpha and blood pressure in pregnant rats were measured. The length, weight of body, liver and brain of full-term newborn rats and the weight and pathological changes of placenta were observed. RESULTS: After inhibition of NO synthesis, blood pressure were consistently high. The protein uria, HCT, ET, TXB2/6-keto-PGF1 alpha were significantly higher and PLT was significantly lower than that of control group. The length, weight of body and placenta in neonatal rats were lower than those of the control group (P < 0.01). Severe ischimic lesion, thrombosis of vessels and endothelial proliferation in placenta were observed. CONCLUSION: NO plays an important role in pathogenesis of PIH.

Animals↗

[The effect of substance P upon middle ear effusion of secretory otitis media and the mode of action].

This experiment aimed to explore the effects of substance P (SP) on secretory otitis media (SOM). Both immunohistochemistry ABC-GDN and image pattern analysis technique were adopted to investigate the relation between SP content of SOM middle ear mucosa and middle ear effusion, and observe the effect of SP receptor antagonist spantide and histamine H2 receptor blocker cimetidin on middle ear effusion. The findings showed: middle ear mucosa SP content tended to increase, and had positive correlation with middle ear effusion, intra-abdominally injecting 1 mg/ml Spantide and 1 mg/ml Cinetidin per day could have middle ear effusion decreased obviously, but the quantities of reduction were more significant. The results suggest that SP plays a role in SOM, might accelerate vasodilation and increase the permeability of cupillary in middle ear mucosa mediated by histamine.

Animals↗

[Effect of intestinal lymph on blood pressure of rat].

The effect of intestinal lymph on blood pressure in rats was observed by the methods of lymph drainage and lymph infusion. The results obtained are as follows: (1) After 150 min of the lymph drained through the cannula of intestinal lymph duct, the blood pressure was significantly lower than that of the sham group (P < 0.05). (2) Equivalent albumin or intralipid infusion was not able to prevent the decrease in blood pressure when the lymph was lost. But in jugular-intestinal lymph duct shunt group, no significant blood pressure decrease could be seen during the drainage procedure for 4 h. (3) The blood pressure of rat with serious hemorrhagic shock could be increased significantly with a little amount of intestinal lymph infusion, and the rats survived longer than those of the control group (P < 0.05-0.01). The above results suggest that the intestinal lymph may play an important role in maintenance of blood pressure, in addition to the known function of lymphatic system by returning tissue fluid to blood and maintaining circulating blood volume.

Animals↗

[Effects of ischemic preconditioning on protection of canine donor lung].

The authors examined the effects of ischemic preconditioning on lung preservation using a canine single left lung transplantation. Twelve adult mongrel dogs underwent left lung allotransplantation. Donor lungs were perfused and flushed with cold Euro-Collins solution (ECS) and stored at 4 degrees C ECS for 2 hours. Six donors were preconditioned by occuluding left lung hilum for 10 minutes and releasing for 15 minutes before flushing (Group PC); other six donors without ischemic preconditioning served as the controls (Group C). Left inferior pulmonary vein blood gas analysis, mean pulmonary artery pressure measurement and donor lung histology examination were made to evaluate the function of transplanted lung after transplantation. Oxygen tension at 2 hrs after reperfusion were significantly better in Group PC than in Group C (431 +/- 130 mmHg vs 246 +/- 66 mmHg, P < 0.05); mean pulmonary artery pressure was much lower in Group PC than in Group C after reperfusion (20.6 +/- 1.3 mmHg vs 36.9 +/- 3.1 mmHg, P < 0.01). Histological findings showed less injury in Group PC. These indicate that ischemic preconditioning combined with cold ECS perfusion is superior to cold ECS perfusion alone in canine lung preservation of 3 hours ischemia with 2 hours reperfusion.

Animals↗

Direct association between the yeast Rad51 and Rad54 recombination proteins.

The RAD54 and RAD51 genes are involved in genetic recombination and double-strand break repair in the yeast Saccharomyces cerevisiae. The Rad51 protein is thought to be a yeast analogue of the Eschericia coli recA gene product and catalyzes strand exchange between homologous single- and double-stranded DNAs in vitro. RAD54 exhibits homologies to several known ATPases and is a member of the SWI2/MOT1 family. We show here that the Rad54 protein interacts with the Rad51 protein in vivo and in vitro and that the NH2-terminal 115 residues of the Rad54 protein are necessary for this interaction. Combined with previously reported results, these data imply that the Rad54 protein is part of a multiprotein yeast recombination complex.

Binding Sites↗

Phospholipase C beta 4 is involved in modulating the visual response in mice.

Expression of G protein-regulated phospholipase C (PLC) beta 4 in the retina, lateral geniculate nucleus, and superior colliculus implies that PLC beta 4 may play a role in the mammalian visual process. A mouse line that lacks PLC beta 4 was generated and the physiological significance of PLC beta 4 in murine visual function was investigated. Behavioral tests using a shuttle box demonstrated that the mice lacking PLC beta 4 were impaired in their visual processing abilities, whereas they showed no deficit in their auditory abilities. In addition, the PLC beta 4-null mice showed 4-fold reduction in the maximal amplitude of the rod a- and b-wave components of their electroretinograms relative to their littermate controls. However, recording from single rod photoreceptors did not reveal any significant differences between the PLC beta 4-null and wild-type littermates, nor were there any apparent differences in retinas examined with light microscopy. While the behavioral and electroretinographic results indicate that PLC beta 4 plays a significant role in mammalian visual signal processing, isolated rod recording shows little or no apparent deficit, suggesting that the effect of PLC beta 4 deficiency on the rod signaling pathway occurs at some stage after the initial phototransduction cascade and may require cell-cell interactions between rods and other retinal cells.

Animals↗

Organization of serpin gene-1 from Manduca sexta. Evolution of a family of alternate exons encoding the reactive site loop.

Manduca sexta serpin gene-1 encodes a family of serpins whose amino acid sequences are identical in their amino-terminal 336 residues but variable in their carboxyl-terminal 39-46 residues, which includes the reactive site loop (Jiang, H., Wang, Y., and Kanost, M. R. (1994) J. Biol. Chem. 269, 55-58). Here, we report the gene's complete nucleotide sequence and exon-intron structure. A unique characteristic of this gene is its exon 9, which is present in 12 alternate forms between exons 8 and 10. Isolation and characterization of cDNA clones containing exons 9C, 9H, and 9I, which were not found previously, indicate that all 12 alternate forms of exon 9 can be utilized to generate 12 different serpins. The splicing pathway apparently allows inclusion of only one exon 9 per molecule of mature serpin-1 mRNA. Analysis of exon-intron border sequences reveals unique features that may be involved in regulation of RNA splicing. The exon 9 region has apparently evolved through rounds of exon duplication and sequence divergence. The exons near the center of the region may have evolved recently, whereas the outermost exons are the most ancient. Exons 9G and 9H were duplicated as a pair from exons 9E and 9F, an event that may have occurred more than once in the history of this gene.

Animals↗

Melatonin levels in idiopathic scoliosis. Diurnal and nocturnal serum melatonin levels in girls with adolescent idiopathic scoliosis.

STUDY DESIGN: Matched pairs of adolescent girls were used to compare serum melatonin levels in adolescent patients and control subjects with idiopathic scoliosis during the day and in the middle of the night. OBJECTIVES: To compare serum melatonin levels in patients with adolescent idiopathic scoliosis and matched control subjects during the day and in the middle of the night. SUMMARY OF BACKGROUND DATA: Recent studies using the chick as the animal model have suggested that the pineal gland and its main product, melatonin, might be involved in the cause of scoliosis. There have been no studies of melatonin levels in patients with adolescent idiopathic scoliosis. METHODS: Blood was collected from seven adolescent girls with idiopathic scoliosis and a group of seven age-matched control subjects. Two samples were collected, one in the middle of the day and one in the middle of the night, to examine the diurnal variation of melatonin production. Serum melatonin levels were measured using a radioimmunoassay technique. RESULTS: No significant differences were found in serum melatonin levels between experimental and control groups either during the day, when melatonin levels were low, or during the night, when melatonin levels were high. CONCLUSIONS: Whereas pinealectomy in young chickens leads to reduced melatonin levels and the development of scoliosis, the results of this study suggest that melatonin levels in mature patients who already have severe scoliosis do not differ from healthy subjects. Whether melatonin levels differ in humans between healthy subjects and patients with scoliosis at the time of onset of the disease remains to be seen.

Adolescent↗

Benzo(a)pyrene diol epoxide-induced chromosomal aberrations and risk of lung cancer.

Benzo(a)pyrene is considered a classic DNA-damaging carcinogen and is one of a multitude of polycyclic aromatic hydrocarbons commonly found in tobacco smoke and in the ambient environment. In this report, we describe the characteristics of chromosomal aberrations induced in vitro by activated benzo(a)pyrene diol epoxide (BPDE) in lymphocyte cultures of 172 normal individuals ages 19-95 years and present the analysis of a pilot case-control study of 33 lung cancer patients and 96 selected controls without history of cancer and frequency matched on age (50-85 years) to the cases. The BPDE-induced chromosomal aberrations were predominantly single chromatid breaks, with few isochromatid breaks or exchange figures. In the 172 normal subjects, the frequencies of both spontaneous and BPDE-induced chromatid breaks were not correlated with age, sex, ethnicity, or tobacco use. However, the frequency of BPDE-induced chromatid breaks was significantly correlated with the frequency of spontaneous chromatid breaks (r = 0.19, P < 0.05). In addition, Hispanics had significantly higher mean BPDE-induced chromatid breaks than did non-Hispanic whites (P < 0.01). From the case-control analyses, the frequency of BPDE-induced chromosomal aberrations was significantly higher in cases (mean, 0.67 breaks/cell) than in controls (mean, 0.41 breaks/cell; P < 0.0001). An adjusted odds ratio of 6.53 (95% confidence interval, 3.74-11.4) for lung cancer was associated with increased frequency of these chromosomal aberrations. The higher rate of BPDE-induced chromosomal aberrations may be due to inefficient DNA repair. These findings warrant additional molecular epidemiological studies. The BPDE mutagen sensitivity assay will facilitate epidemiological studies of genetic susceptibility to smoking-related cancers.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗

The melanoma differentiation associated gene mda-7 suppresses cancer cell growth.

Cancer is a disease characterized by defects in growth control, and tumor cells often display abnormal patterns of cellular differentiation. The combination of recombinant human fibroblast interferon and the antileukemic agent mezerein corrects these abnormalities in cultured human melanoma cells resulting in irreversible growth arrest and terminal differentiation. Subtraction hybridization identifies a melanoma differentiation associated gene (mda-7) with elevated expression in growth arrested and terminally differentiated human melanoma cells. Colony formation decreases when mda-7 is transfected into human tumor cells of diverse origin and with multiple genetic defects. In contrast, the effects of mda-7 on growth and colony formation in transient transfection assays with normal cells, including human mammary epithelial, human skin fibroblast, and rat embryo fibroblast, is quantitatively less than that found with cancer cells. Tumor cells expressing elevated mda-7 display suppression in monolayer growth and anchorage independence. Infection with a recombinant type 5 adenovirus expressing antisense mda-7 eliminates mda-7 suppression of the in vitro growth and transformed phenotype. The ability of mda-7 to suppress growth in cancer cells not expressing or containing defects in both the retinoblastoma (RB) and p53 genes indicates a lack of involvement of these critical tumor suppressor elements in mediating mda-7-induced growth inhibition. The lack of protein homology of mda-7 with previously described growth suppressing genes and the differential effect of this gene on normal versus cancer cells suggests that mda-7 may represent a new class of cancer growth suppressing genes with antitumor activity.

Animals↗

Binding of thalidomide to alpha1-acid glycoprotein may be involved in its inhibition of tumor necrosis factor alpha production.

In addition to its well known sedative and teratogenic effects, thalidomide also possesses potent immunomodulatory and antiinflammatory activities, being most effective against leprosy and chronic graft-versus-host disease. The immunomodulatory activity of thalidomide has been ascribed to the selective inhibition of tumor necrosis factor alpha from monocytes. The molecular mechanism for the immunomodulatory effect of thalidomide remains unknown. To elucidate this mechanism, we synthesized an active photoaffinity label of thalidomide as a probe to identify the molecular target of the drug. Using the probe, we specifically labeled a pair of proteins of 43-45 kDa with high acidity from bovine thymus extract. Purification of these proteins and partial peptide sequence determination revealed them to be alpha1-acid glycoprotein (AGP). We show that the binding of thalidomide photoaffinity label to authentic human AGP is competed with both thalidomide and the nonradioactive photoaffinity label at concentrations comparable to those required for inhibition of production of tumor necrosis factor alpha from human monocytes, suggesting that AGP may be involved in the immunomodulatory activity of thalidomide.

Affinity Labels↗

IFN-alpha beta reconstitutes the deficiency in lipid A-activated AKR macrophages for nitric oxide synthase.

AKR mouse peritoneal macrophages (PM) were previously found to have a defect in their response to lipid A for nitric oxide (NO)-mediated tumor cytotoxicity, which was related to a lower level of C1q synthesis and reconstituted by exogenous IFN-gamma or C1q. We used AKR-PM as a model to further define the role of IFN-alpha beta in modulation of induction of macrophage nitric oxide synthase (NOS) in response to lipid A. Studies have revealed that AKR-PM produced a significantly lower level of IFN-alpha beta than responsive C3H-PM in response to lipid A. AKR-PM failed to increase NOS mRNA synthesis and NO generation when exposed to lipid A, although they had normal levels of TNF-alpha bioactivity and mRNA expression. This partial deficiency of AKR-PM to lipid A stimulation was reconstituted completely by exogenous IFN-alpha beta for both synthesis of NOS mRNA and release of NO. The failure of AKR-PM to produce NOS to lipid A stimulation appears to be related to reduced secretion of IFN-alpha beta and the resultant failure to express TNF-alpha type II receptor (TNF-RII) mRNA, which in turn decreases TNF-alpha binding to its receptor for autocrine induction of NOS. Insufficient synthesis and secretion of endogenous IFN-alpha beta may be the primary reason for AKR-PM refractoriness to induction of NOS in response to lipid A. furthermore, the close correlation between lack of IFN-alpha beta secretion and decreased TNF-RII mRNA synthesis may implicate a critical role for IFN-alpha beta in the upregulation of macrophage TNF-RII receptor expression for autocrine induction of NOS during lipid A stimulation.

Animals↗

Pertussis toxin-sensitive activation of phospholipase C by the C5a and fMet-Leu-Phe receptors.

Signal transduction pathways that mediate C5a and fMet-Leu-Phe (fMLP)-induced pertussis toxin (PTx)-sensitive activation of phospholipase C (PLC) have been investigated using a cotransfection assay system in COS-7 cells. The abilities of the receptors for C5a and fMLP to activate PLC beta2 and PLC beta3 through the Gbetagamma subunits of endogenous Gi proteins in COS-7 cells were tested because both PLC beta2 and PLC beta3 were shown to be activated by the betagamma subunits of G proteins in in vitro reconstitution assays. Neither of the receptors can activate endogenous PLC beta3 or recombinant PLC beta3 in transfected COS-7 cells. However, both receptors can clearly activate PLC beta2 in a PTx-sensitive manner, suggesting that the receptors may interact with endogenous PTx-sensitive G proteins and activate PLC beta2 probably through the Gbetagamma subunits. These findings were further corroborated by the results that PLC beta3 could only be slightly activated by Gbeta1gamma1 or Gbeta1gamma5 in the cotransfection assay, whereas the Gbetagamma subunits strongly activated PLC beta2 under the same conditions. PLC beta3 can be activated by Galphaq, Galpha11, and Galpha16 in the cotransfection assay. In addition, the Ggamma2 and Ggamma3 mutants with substitution of the C-terminal Cys residue by a Ser residue, which can inhibit wild type Gbetagamma-mediated activation of PLC beta2, were able to inhibit C5a or fMLP-mediated activation of PLC beta2. These Ggamma mutants, however, showed little effect on m1-muscarinic receptor-mediated PLC activation, which is mediated by the Gq class of G proteins. These results all confirm that the Gbetagamma subunits are involved in PLC beta2 activation by the two chemoattractant receptors and suggest that in COS-7 cells activation of PLC beta3 by Gbetagamma may not be the primary pathway for the receptors.

Amino Acid Sequence↗

Evidence for endogenous C1q modulates TNF-alpha receptor synthesis and autocrine binding of TNF-alpha associated with lipid A activation of murine macrophages for nitric oxide production.

The role of endogenously synthesized complement subcomponent C1q on autocrine binding of tumor necrosis factors (TNF-alpha) and on TNF-alpha receptor (TNF-R) mRNA synthesis by mouse macrophages was investigated. Activation of C3H mouse peritoneal macrophages (C3H-PM phi) by Lipid A induced TNF-alpha and nitric oxide (NO) to kill tumor targets. Such activation also increased macrophage-endogenous C1q synthesis and secretion in a dose-dependent fashion. Antibody for C1q markedly inhibited C3H-PM phi NO production in response to Lipid A, but had no effect on TNF-alpha production. C3H-PM phi treated with C1q or Lipid A displayed increased TNF-R mRNA synthesis and in combination with Lipid A and anti-C1q antibody inhibited TNF-R and nitric oxide synthase (NOS) mRNA synthesis compared with Lipid A only, but had no effect on TNF mRNA synthesis. In vitro treatment of C3H-PM phi with C1q also increased TNF-alpha binding to their surfaces. Taken together, the data indicate that endogenously synthesized C1q is operative in promoting TNF-R mRNA synthesis and resultant autocrine binding of TNF-alpha for induction of NOS in the process of NO-mediated tumor cytotoxicity by Lipid A-activated macrophages.

Adjuvants, Immunologic↗

FTIR studies of recombinant human granulocyte-macrophage colony-stimulating factor in aqueous solutions: secondary structure, disulfide reduction and thermal behavior.

Fourier transform infrared spectroscopy (FTIR) has been used to investigate the secondary structure, disulfide reduction and thermal behavior of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) in aqueous solutions. The contributions of amino-acid side-chain groups to the amide I bands of rhGM-CSF in H2O and in D2O solutions were carefully scrutinized, as 40% of the total 127 amino-acid residues of rhGM-CSF is side-chain absorptive (asparagine, glutamine, etc.). The FTIR results indicated that rhGM-CSF is composed of 46% alpha-helix, 7% beta-sheet, 23% turn and 24% loop/irregular structures which are in good agreement with the X-ray diffractional data. Reduction of rhGM-CSF with dithiothreitol caused apparent unfolding of the native conformation followed by the time-dependent increase of beta-aggregation bands which arose at 1622 and 1693 cm(-1) in H2O, 1613 and 1684 cm(-1) in D2O solutions. The result also showed that tertiary structure can change independently of the secondary structure. Thermal denaturation of rhGM-CSF took place at 55 to 70 degrees C and the denatured protein adopted an irregular structure as revealed by the FTIR spectra. The thermal denaturation did not show the formation of intermolecular beta-aggregates which is typical of most thermal denatured proteins. Moreover, it is partly reversible, indicating a special thermal stability of rhGM-CSF.

Deuterium Oxide↗

Identification of a phospholipase C beta2 region that interacts with Gbeta-gamma.

To delineate the phospholipase C (PLC; EC 3.1.4.3) beta2 sequences involved in interactions with the beta-gamma subunits of G proteins, we prepared a number of mammalian expression plasmids encoding a series of PLC beta2 segments that span the region from the beginning of the X box to the end of the Y box. We found the sequence extending from residue Glu-435 to residue Val-641 inhibited Gbeta-gamma-mediated activation of PLC beta2 in transfected COS-7 cells. This PLC beta2 sequence also inhibited ligand-induced activation of PLC in COS-7 cells cotransfected with cDNAs encoding the complement component C5a receptor and PLC beta2 but not in cells transfected with the alpha1B-adrenergic receptor, suggesting that the PLC beta2 residues (Glu-435 to Val-641) inhibit the Gbeta-gamma-mediated but not the Galpha-mediated effect. The inhibitory effect on Gbeta-gamma-mediated activation of PLC beta2 may be the result of the interaction between Gbeta-gamma and the PLC beta2 fragment. This idea was confirmed by the observation that a fusion protein comprising these residues (Glu-435 to Val-641) of PLC beta2 and glutathione S-transferase (GST) bound to Gbeta-gamma in an in vitro binding assay. The Gbeta-gamma-binding region was further narrowed down to 62 amino acids (residues Leu-580 to Val-641) by testing fusion proteins comprising various PLC beta2 sequences and GST in the in vitro binding assay.

Amino Acid Sequence↗