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Biomedical subjects

B He

Publications and source records attributed to B He.

At least 217 records · Page 12Linked to original sources

[The value of CA125 and LDH assays in assisting diagnosis of epithelial ovarian carcinoma].

40 first-treated cases of epithelial ovarian cancer, 13 cases of cervical cancer, 13 cases of corpus cancer and 50 cases of benign tumor were included in this study from Jan. 1991 through May 1992 to evaluate the significance of the blood CA125, LDH, CR and SA levels in assisting diagnosis of epithelical ovarian cancer. The CA125 levels of the 40 canses of ovarian cancer were higher than those of cervical cancer and corpus cancer (P < 0.05); the SS, PLR and AC of CA125 in ovarian cancer were higher than those of LDH, SA and CR (P < 0.05); the SS of CA125 in ovarian cancer was higher than that of LDH isoenzyme (P < 0.05). The results show that CA125 may be the best tumor marker in assisting ovarian cancer; CA125 is more informative than LDH, CR and SA; when CA125 is used incombination with other tumor markers, SS, SP, NPV and PPV can be greatly raised.

Biomarkers, Tumor↗

[Clinical application of spleno-renal shunt].

The results of splenorenal shunt (SRS) in 405 patients were compared with those of simple splenectomy (SS) in 376 cirrhotic patients in the treatment of portal hypertension. The recurrent bleeding rate was 10.12% in SRS group and 21.2% in SS group, respectively (P < 0.001). The mortality of rebleeding was 2.96% in SRS group and 10.6% in SS group, respectively (P < 0.01). Death from hepatic failure developed at 16.5% of SRS patients and at 9.8% of SS patients, respectively (P < 0.01). The rate of postoperative variceal bleeding and mortality in prophylactic SRS group were 4.9% and 6.2%, and 15.1% and 26.4% in prophylactic SS group, respectively (P < 0.01). The authors are in favor of prophylactic SRS and modified side-to-side SRS for its simplicity and good results.

Adult↗

Tumor necrosis factor alpha-308 alleles in multiple sclerosis and optic neuritis.

Tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine, is believed to play an important role in multiple sclerosis (MS) pathogenesis. A bi-allelic polymorphism in the TNF-alpha promoter region (TNF alpha-308), has been reported to influence levels of TNF-alpha production. In the present study, we investigated the TNF alpha-308 polymorphism in 93 patients with MS, 17 patients with optic neuritis (ON) and 95 healthy individuals using an allele-specific PCR technique. Allelic genotype was compared with TNF-alpha mRNA expression levels and HLA class II phenotypes. No significant difference regarding the TNF alpha-308 polymorphism was observed between MS patients and controls. Specifically, the less common allele, TNF2, which is associated with higher expression levels of TNF-alpha, was somewhat less frequent among MS patients. In fact, analysis of 19 patients homozygous for the MS associated HLA-DR-DQ haplotype HLA-Dw2 showed that this haplotype does not carry the TNF2 allele. In addition, in 47 patients, the TNF-alpha alleles did not correlate with expression levels measured as numbers of TNF-alpha expressing cells. Thus, we found no evidence for an important role of TNF alpha-308 polymorphism for genetic susceptibility to MS.

Alleles↗

Phage RNA polymerase vectors that allow efficient gene expression in both prokaryotic and eukaryotic cells.

We have developed expression vectors that direct the synthesis of proteins from a common set of signals in both prokaryotic and eukaryotic cells. To allow transcription from a common promoter the vectors rely upon a phage RNA polymerase (RNAP). To direct initiation of translation to the same start codon the vectors utilize an internal ribosome entry site (IRES) from encephalomyocarditis virus (EMCV) that has been modified to include a prokaryotic ribosome-binding site (RBS) at an appropriate distance upstream from the desired start codon. These vectors provide levels of expression in eukaryotic cells that exceed those of a conventional RNAP-II-based system by 7-fold, and expression in bacterial cells at levels comparable to other phage RNAP-based systems. Inclusion of a lac repressor and a phage promoter/lac operator fusion element allows tight regulation. Cotransfection of eukaryotic cells with the expression vector and a vector that encodes the phage RNAP provides high-level transient expression without the need to construct specialized stable cell lines.

Alkaline Phosphatase↗

Preparation of probe-modified RNA with 5-mercapto-UTP for analysis of protein-RNA interactions.

We report a modified synthesis for 5-mercapto-UTP (5-SH-UTP) and its use for analysis of protein-RNA interactions utilizing Escherichia coli and T7 RNA polymerases and yeast RNA polymerases I and III. 5-SH-UTP did not affect transcriptional pausing, Rho-independent termination or recognition of the E. coli transcription complex by NusA. RNA containing 5-SH-UMP did not crosslink to polymerase when irradiation was 302 or 337 nm. Transcription complexes containing RNA substituted with 5-SH-UMP were post-transcriptionally modified to attach a photocross-linking group to thiol-tagged nucleotides in the RNA on the surface of the polymerase of free in solution. The pKa for 5-SH-UTP was determined to be 5.6, so modification of the thiol groups in the RNA with p-azidophenacyl bromide could be carried out at pH 7. Addition of the transcription termination factor Rho, a RNA binding protein, to E. coli transcription complexes resulted in RNA crosslinking to Rho and to the beta and beta' subunits of polymerase. Using 5-SH-UTP, one can distinguish RNA binding domains on the surface of RNA polymerases or other RNA binding proteins from those buried within the protein.

Base Sequence↗

Increased bile acid concentration in liver tissue with cholesterol gallstone disease.

Patients with cholesterol gallstone disease have a reduced pool of bile acids. Overly sensitive feedback inhibition of bile acid synthesis has been postulated to explain this size reduction. To test this hypothesis, hepatic bile acid concentration and the activity of cholesterol 7 alpha-hydroxylase, the rate-limiting enzyme for bile acid biosynthesis, were determined in ten patients with cholesterol gallstones and ten patients without gallstones. The bile acids present in liver tissue are the sum of those returning to liver and those newly synthesized in liver. If an overly sensitive feedback inhibition truly existed in our gallstone patients, a decreased concentration of hepatic bile acids would have been expected. However, patients with cholesterol gallstones had significantly higher total (143.3 +/- 25.5 vs 64.5 +/- 10.8 nmol/g liver, P < 0.01), chenodeoxycholic (64.1 +/- 9.9 vs 29.8 +/- 5.4, P < 0.01), deoxycholic (22.8 +/- 10.9 vs 2.0 +/- 0.7, P < 0.05), and ursodeoxycholic acid (6.2 +/- 1.4 vs 1.5 +/- 0.6, P < 0.01) concentrations than patients without gallstones. The activity of cholesterol 7 alpha-hydroxylase did not differ significantly between the two groups. Impaired hepatic transport or secretion of bile acids is strongly suspected in cholesterol gallstone patients. The findings of the present study showed no evidence of overly sensitive feedback inhibition of bile acid synthesis in cholesterol gallstone patients. Bile acid pool size may be affected by the inappropriate increase of hepatic bile acids rather than by overly sensitive feedback inhibition.

Bile↗

Inactivation and unfolding of aminoacylase during denaturation in sodium dodecyl sulfate solutions.

During denaturation by sodium dodecyl sulfate (SDS), aminoacylase shows a rapid decrease in activity with increasing concentration of the detergent to reach complete inactivation at 1.0 mM SDS. The denatured minus native-enzyme difference spectrum showed two negative peaks at 287 and 295 nm. With the increase of concentration of SDS, both negative peaks increased in magnitude to reach maximal values at 5.0 mM SDS. The fluorescence emission intensity of the enzyme decreased, whereas there was no red shift of emission maximum in SDS solutions of increasing concentration. In the SDS concentration regions employed in the present study, no marked changes of secondary structure of the enzyme have been observed by following the changes in far-ultraviolet CD spectra. The inactivation of this enzyme has been followed and compared with the unfolding observed during denaturation in SDS solutions. A marked inactivation is already evident at low SDS concentration before significant conformational changes can be detected by ultraviolet absorbance and fluorescence changes. The inactivation rate constants of free enzyme and substrate-enzyme complex were determined by the kinetics method of the substrate reaction in the presence of inactivator previously described by Tsou [Tsou (1988), Adv. Enzymol. Related Areas Mol. Biol. 61, 381-436]. It was found that substrate protects against inactivation and at the same SDS concentrations, the inactivation rate of the free enzyme is much higher than the unfolding rate. The above results show that the active sites of metal enzyme containing Zn2+ are also situated in a limited and flexible region of the enzyme molecule that is more fragile to denaturants than the protein as a whole.

Amidohydrolases↗

Accumulation of 7 alpha-hydroxycholesterol in liver tissue of patients with cholesterol gallstones.

Patients with cholesterol gallstones have a reduced pool of bile acids. This study was undertaken to clarify the mechanism by which bile acid biosynthesis does not increase to supranormal levels to cause a reexpansion of the pool. We investigated the first two steps of the bile acid biosynthesis pathway by assaying the activities of cholesterol 7 alpha-hydroxylase, the rate-limiting enzyme in this pathway, and 3 beta-hydroxy-delta 5-C27-steroid dehydrogenase/isomerase, and by measuring the concentrations of 7 alpha-hydroxycholesterol and 7 alpha-hydroxy-4-cholesten-3-one in liver specimens from ten patients with cholesterol gallstones and ten gallstone-free controls. In the patients with gallstones, cholesterol 7 alpha-hydroxylase activity, 3 beta-hydroxy-delta 5-C27-steroid dehydrogenase/isomerase activity, and hepatic 7 alpha-hydroxy-4-cholesten-3-one concentration did not significantly different from levels in controls, but hepatic 7 alpha-hydroxycholesterol concentration was more than twofold that of controls (12.9 +/- 2.6 vs 5.3 +/- 1.2 nmol/g liver, P < 0.01). The concentration of 7 alpha-hydroxycholesterol positively correlated with the ratio of cholesterol 7 alpha-hydroxylase activity to 3 beta-hydroxy-delta 5-C27-steroid dehydrogenase/isomerase activity (r = 0.93; P < 0.005) in the gallstone-free controls. In contrast, this correlation disappeared in the patients with gallstones. These results suggest a derangement of the normal 7 alpha-hydroxycholesterol metabolism in the patients with gallstones. The reason for the accumulation of 7 alpha-hydroxycholesterol remains unclear; however, it is possible that, in patients with cholesterol gallstone, the accumulated 7 alpha-hydroxycholesterol causes inappropriate suppression of cholesterol 7 alpha-hydroxylase activity by product inhibition.

3-Hydroxysteroid Dehydrogenases↗

B cell responses to acetylcholine receptor in rats orally tolerized against experimental autoimmune myasthenia gravis.

Oral administration of acetylcholine receptor (AChR) to Lewis rats prior to myasthenogenic immunization with AChR and complete Freund's adjuvant (CFA) results in the prevention of experimental autoimmune myasthenia gravis (EAMG), and decreased serum levels of anti-AChR antibodies. Using an ELISPOT assay, we have now determined numbers of cells in the popliteal, inguinal and mesenteric lymph nodes, spleen and thymus secreting anti-AChR IgG antibodies. Except for mesenteric lymph nodes, a marked diminution of such cells was detected in these lymphoid organs in rats orally tolerized with AChR compared to buffer-fed or vehicle-fed control rats with EAMG. Of note is that, after AChR feeding, the B cell response to AChR in thymus was diminished to the same low level as in CFA-injected, buffer-fed control rats. The relative affinity of serum anti-AChR IgG antibodies measured by KSCN-ELISA was lower in the orally tolerized rats compared to buffer-fed or vehicle-fed rats. The observations showed that oral administration of AChR, besides preventing clinical EAMG, also counteracts the development of AChR-specific B cells, especially those with high affinity antibody production, in most lymphoid organs.

Administration, Oral↗

Transforming growth factor-beta 1 suppresses autoantigen-induced expression of pro-inflammatory cytokines but not of interleukin-10 in multiple sclerosis and myasthenia gravis.

Multiple sclerosis (MS) is associated with high levels of circulating T lymphocytes that respond to the myelin antigens myelin basic protein (MBP) and proteolipid protein (PLP) by producing various cytokines including interferon-gamma (IFN-gamma) that makes MS worse and transforming growth factor-beta (TGF-beta), an endogenously produced immunosuppressant that might act beneficially. To further define the role of TGF-beta in MS, we examined the effects of recombinant TGF-beta 1 (rTGF-beta 1) on autoantigen-mediated regulation of cytokines in MS and myasthenia gravis (MG). Blood mononuclear cells (MNC) were cultivated with or without rTGF-beta 1, and with or without autoantigen or the recall antigen PPD. MNC expressing cytokine mRNA were detected after in situ hybridization with radiolabeled cDNA oligonucleotide probes. Femtogram concentrations of rTGF-beta 1 suppressed MBP-, PLP- and PPD-induced upregulation of IFN-gamma, IL-4, IL-6, tumor necrosis factor-alpha (TNF-alpha), TNF-beta and perforin in MS, and acetylcholine receptor (AChR)-induced augmentation of these pro-inflammatory cytokines in MG, but had no effects on autoantigen- or PPD-induced expression of IL-10 or TGF-beta itself. rTGF-beta 1 also suppressed numbers of myelin antigen-reactive IFN-gamma- and IL-4-secreting cells in MS and AChR-reactive IFN-gamma and IL-4 secreting cells in MG. The selective suppressive effects of TGF-beta 1 on autoantigen-induced upregulation of pro-inflammatory cytokines makes TGF-beta 1 attractive as a treatment alternative in MS and MG.

Adult↗

Suppression of experimental autoimmune myasthenia gravis and experimental allergic encephalomyelitis by oral administration of acetylcholine receptor and myelin basic protein: double tolerance.

Oral administration of acetylcholine receptor (AChR) or myelin basic protein (MBP) to Lewis rat prior to immunization with AChr or MBP and complete Freund's adjuvant (CFA) has previously been shown to prevent or delay the onset of experimental autoimmune myasthenia gravis (EAMG) or experimental allergic encephalomyelitis (EAE), which represent animal models of myasthenia gravis and multiple sclerosis, respectively. Here we show that Lewis rats immunized with AChr+MBP+CFA developed both signs of muscular weakness seen in EAMG and paresis characteristic for EAE. This disease was associated with high levels of anti-AChR and anti-MBP antibody secreting cells and of AChR- and MBP-reactive INF-gamma secreting Th1-like cells in lymph nodes. The diseased rats also showed upregulation of AChR- and MBP-induced mRNA expression of IFN-gamma in lymph node cells. Oral tolerization with AChR and MBP in combination prior to immunization with AChR+MBP+CFA alleviated clinical disease as well as AChR- and MBP-specific B cell node cells. The results implicate that oral tolerization simultaneously to more than one autoimmune disease-related autoantigen is feasible, and that suppression of autoantigen-induced IFN-gamma and augmentation of TGF-beta are pivotal in tolerance induction.

Administration, Oral↗

Secondary structure of holo- and apo-aminoacylase from prediction, circular dichroism, and FT-Raman spectroscopy.

The secondary structures of native (Holo-) and Zn(2+)-free (Apo-) aminoacylase were examined by circular dichroism (CD) and Fourier transform Raman (FT-Raman) spectroscopic techniques and prediction methods. Quantitative analysis of the conformationally sensitive amide I band indicates that Holo- and Apo-enzyme contain 19.3 and 17.2% helical structure, respectively. Far-UV CD spectra of Holo- and Apo-enzyme show that they contain 20.1 and 17.6% alpha-helix, respectively. Secondary structure prediction of aminoacylase indicates that it contains approximately 20.9% alpha-helical structure including 10 alpha-helix segments. The results show that after removal of Zn2+ in aminoacylase, the extent of ordered structure was decreased markedly. The conformation at or near the active site of aminoacylase may contain more ordered structure and the presence of Zn2+ may help to maintain the catalytically active conformation at the active site.

Amidohydrolases↗

An equivalent body surface charge model representing three-dimensional bioelectrical activity.

A new surface-source model has been developed to account for the bioelectrical potential on the body surface. A single-layer surface-charge model on the body surface has been developed to equivalently represent bioelectrical sources inside the body. The boundary conditions on the body surface are discussed in relation to the surface-charge in a half-space conductive medium. The equivalent body surface-charge is shown to be proportional to the normal component of the electric field on the body surface just outside the body. The spatial resolution of the equivalent surface-charge distribution appears intermediate between those of the body surface potential distribution and the body surface Laplacian distribution. An analytic relationship between the equivalent surface-charge and the surface Laplacian of the potential was found for a half-space conductive medium. The effects of finite spatial sampling and noise on the reconstruction of the equivalent surface-charge were evaluated by computer simulations. It was found through computer simulations that the reconstruction of the equivalent body surface-charge from the body surface Laplacian distribution is very stable against noise and finite spatial sampling. The present results suggest that the equivalent body surface-charge model may provide an additional insight to our understanding of bioelectric phenomena.

Body Surface Potential Mapping↗

Computational flow optimization of rotary blood pump components.

In an effort to improve and automate the fluid dynamic design of rotary blood pumps, a coupled computational fluid dynamics (CFD) shape optimization methodology has been developed and implemented. This program couples a finite element flow simulation with a gradient-based optimization routine to modify automatically the shape of an initial candidate blood path, according to a variety of desired fluid dynamic criteria, including shear stress, vorticity/circulation, and viscous dissipation. Preliminary results have led to both intuitive and nonintuitive transformations of the initial blood flow paths for both internal and external flows. This application of computer design optimization offers the ability to explore a much broader design space much more efficiently than would be possible with traditional parametric methods. It is believed that this computer tool can assist developers of rotary blood pumps in designing blood-wetted components that minimize thrombosis and hemolysis while simultaneously providing maximum flow performance.

Biomechanical Phenomena↗

Cytokine mRNA profiles in mononuclear cells in acute aseptic meningoencephalitis.

Cytokines are important modulators of inflammation and immune responses. Using in situ hybridization with radiolabelled cDNA oligonucleotide probes, we studied the expression of mRNA encoding the cytokines gamma interferon (IFN-gamma), interleukin 4 (IL-4), IL-6, IL-10, transforming growth factor beta (TGF-beta), tumor necrosis factor alpha (TNF-alpha), lymphotoxin, and perforin in mononuclear cells (MNC) from blood and cerebrospinal fluid (CSF) of patients with acute aseptic meningoencephalitis (AM) and from blood of healthy controls. Patients in the acute phase of AM had elevated numbers of IFN-gamma mRNA-expressing cells in the blood compared with that of controls and higher numbers of IFN-gamma mRNA-expressing cells in their CSF compared with that of convalescent-phase patients, which is in accordance with the antiviral effects of this cytokine. Upregulation of IL-4, IL-6, and IL-10 was found in convalescent-phase patients, which is consistent with the longstanding B-cell response found in AM. TGF-beta and perforin were upregulated in both stages of AM, while the numbers of blood and CSF MNC expressing cytokine mRNA of the TNF family (TNF-alpha and lymphotoxin) did not differ between patients with AM and controls. An even higher elevation in CSF was noticed for MNC expressing most of the cytokines, particularly IL-4 and TGF-beta, reflecting the autonomy of the immune response in the CSF. The definition of cytokine profiles in AM, a self-limiting and benign disease, provides a foundation for future comparisons with other infectious and inflammatory nervous system diseases.

Acute Disease↗

Body surface Laplacian electrocardiographic mapping--a review.

It is of great importance and significance to be able to noninvasively map spatially distributed cardiac electrical activity from body surface electrical recordings. The standard electrocardiographic monitoring techniques provide little spatial information regarding cardiac electrical activity. Recently, a new approach-body surface Laplacian electrocardiographic mapping-has been aggressively pursued to provide high-resolution spatial mapping of cardiac electrical activity. The fundamental innovation is the measurement of the Laplacian electrocardiogram distribution over the body surface. The body surface Laplacian electrocardiographic maps have been shown to provide enhanced ability to map multiple spatially separate cardiac bioelectric sources. This article reviews the theoretical and experimental aspects of this emerging mapping technique. First of all, the paper briefly reviews the historical development of body surface mapping and inverse solutions for mapping the distributed cardiac electrical activity. Then the paper reviews the theoretical basis of body surface Laplacian mapping and the biophysical interpretation of body surface Laplacian signals, as well as technical consideration of the Laplacian recording and instrumentation. Investigations of body surface Laplacian maps in computer models and a physical tank model, as well as physiological studies are also reviewed.

Animals↗

[Naloxone suppresses ischemic arrhythmias via potentiating baroreflex].

AIM: To study the relationship between the anti-arrhythmia action of naloxone (Nal) and its effect on baroreflex sensitivity (BRS). METHODS: Acute myocardial infarction was produced by ligating coronary artery in Sprague-Dawley rats. Ventricular extrasystole (VE), tachycardia (VT), and fibrillation (VF) were recorded on ECG. The slopes of linear regression (b) from systolic blood pressure and cardiac cycle after intravenous injection (i.v.) of phenylephrine 2 micrograms was taken as the BRS. The area of infarct was estimated after TTC staining. RESULTS: Nal 0.5 mg i.v., intracisternal injection (i.c.) of Nal 0.1 mg, and i.c. beta-endorphin (beta-End) antiserum 10 microL suppressed the ischemic arrhythmias, arrhythmia score was 1.8 +/- 1.1 (Nal i.v.) vs 3.8 +/- 2.1 (Saline i.v.); 1.7 +/- 1.5 (Nal i.c.) vs 4.0 +/- 2.6 (Artificial CSF i.c.) and 1.7 +/- 1.6 (beta-End antiserum i.c.) vs 4.1 +/- 2.0 (Serum i.c.) (P < 0.05) and potentiated the BRS, BRS was 4.2 +/- 1.8 (Nal i.v.) vs 2.9 +/- 0.8 (saline i.v.); 4.5 +/- 1.7 (Nal i.c.) vs 2.8 +/- 0.7 (Artificial CSF i.c.) and 4.4 +/- 1.1 (beta-End antiserum i.c.) vs 3.0 +/- 0.9 (Serum i.c.) (P < 0.05). BRS showed negative relations to the arrhythmia scores with r of -0.69 for i.v Nal, -0.72 for i.c. Nal, and -0.67 for i.c. beta-End antiserum (P < 0.05). CONCLUSION: Nal suppressed ischemic arrhythmias via antagonization of beta-endorphin and potentiation of BRS.

Animals↗