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Biomedical subjects

C Bai

Publications and source records attributed to C Bai.

At least 37 records · Page 2Linked to original sources
PubMed2000

Mouse Gli1 mutants are viable but have defects in SHH signaling in combination with a Gli2 mutation.

The secreted factor Sonic hedgehog (SHH) is both required for and sufficient to induce multiple developmental processes, including ventralization of the CNS, branching morphogenesis of the lungs and anteroposterior patterning of the limbs. Based on analogy to the Drosophila Hh pathway, the multiple GLI transcription factors in vertebrates are likely to both transduce SHH signaling and repress Shh transcription. In order to discriminate between overlapping versus unique requirements for the three Gli genes in mice, we have produced a Gli1 mutant and analyzed the phenotypes of Gli1/Gli2 and Gli1/3 double mutants. Gli3(xt) mutants have polydactyly and dorsal CNS defects associated with ectopic Shh expression, indicating GLI3 plays a role in repressing Shh. In contrast, Gli2 mutants have five digits, but lack a floorplate, indicating that it is required to transduce SHH signaling in some tissues. Remarkably, mice homozygous for a Gli1(zfd )mutation that deletes the exons encoding the DNA-binding domain are viable and appear normal. Transgenic mice expressing a GLI1 protein lacking the zinc fingers can not induce SHH targets in the dorsal brain, indicating that the Gli1(zfd )allele contains a hypomorphic or null mutation. Interestingly, Gli1(zfd/zfd);Gli2(zfd/+), but not Gli1(zfd/zfd);Gli3(zfd/+) double mutants have a severe phenotype; most Gli1(zfd/zfd);Gli2(zfd/+) mice die soon after birth and all have multiple defects including a variable loss of ventral spinal cord cells and smaller lungs that are similar to, but less extreme than, Gli2(zfd/zfd) mutants. Gli1/Gli2 double homozygous mutants have more extreme CNS and lung defects than Gli1(zfd/zfd);Gli2(zfd/+) mutants, however, in contrast to Shh mutants, ventrolateral neurons develop in the CNS and the limbs have 5 digits with an extra postaxial nubbin. These studies demonstrate that the zinc-finger DNA-binding domain of GLI1 protein is not required for SHH signaling in mouse. Furthermore, Gli1 and Gli2, but not Gli1 and Gli3, have extensive overlapping functions that are likely downstream of SHH signaling.

Abnormalities, Multiple↗
PubMed2000

[A study on the deficiency of anticoagulant proteins in Chinese patients with deep venous thrombosis].

OBJECTIVE: To investigate the incidence of anticoagulant proteins deficiency in Chinese patients with venous thrombosis. METHODS: Eighty-seven patients with otherwise unexplained venous thrombophilia were studied. Both the antigen and antivitity of PC, PS, and antithrombin III (ATIII) were determined using commercial kits (Stago, or IL) activated PC, sensitivity ratio (APC-SR) by Coatest chromogenix, and factor V gene mutation by polymerase chain reaction with restriction fragments long polymorphism (PCR-RFLP). RESULTS: Of all the patients twenty-five were found to be abnormal. These consisted of 3 ATIII deficiencies, 5 PC deficiencies, 10 PS deficiencies, 2 resistance of activated protein C (APC-R), 1 combined ATIII and PC deficiency, 1 combined ATIII and PS deficiency, 1 combined PC and PS deficiency, 1 combined APC-R and PC deficiency and 1 combined APC-R and PS deficiency. The overall prevalence of ATIII, PC and PS deficiencies was 26.4%. The patients with anticoagulant proteins deficiency had earlier onset (35.2 +/- 9.7 vs 42.1 +/- 10.9; P < 0.01) and more recurrent thrombosis (P < 0.05), as well as more pulmonary embolism (44.0% vs 16.1%; P < 0.01) than those of without anticoagulant protein deficiency. CONCLUSION: The overall prevalence of ATIII, PC, and PS deficiency in Chinese venous thrombosis patients was higher than that of Western patients. It suggests that the etiology of thrombophilia may be different between Chinese and Western.

Adolescent↗
PubMed2000

Surgical treatment of portal hypertension: 45 year experience.

OBJECTIVE: To review the experience in surgery for 912 patients with portal hypertension. METHODS: The 912 patients were divided into three groups: before 1978 (group A), 1978 - 1989 (group B), and 1990 - 1998 (group C). The results were reviewed of portosystemic shunt (PSS), disconnection and disconnection plus PSS for emergency and elective operation at different periods. RESULTS: In the 912 patients of groups A, B, C, the number of PSS, disconnection, and PSS plus disconnection was 345, 13, 0; 84, 209, 0; 63, 204, 63, respectively. The number of emergency operation was 45, 13 and 4 in each group. The operative mortality of shunt in the groups A, B, C was 7.82%, 7.14% and 0, respectively; that of disconnection in the groups A, B, C 15.38%, 6.28% and 4.94%; and that of PSS plus disconnection in group C 3.51%. Encephalopathy occurred in 14.37% of the PSS group, in 5.68% of the disconnection group, and in 5.77% of the disconnection plus PSS group. Rebleeding occurred in 10.78% of the PSS group, in 18.95% of the disconnection group, and in 7.69% of the disconnection plus PSS group. CONCLUSIONS: Operative indications for the cirrhotic patients with portal hypertension depend on their liver function. For those patients with poor liver function, surgery is considered when their liver function is improved. We suggest prophylactic operation is valuable. Other indices from barium meal, color ultrasound, and endoscopy are also considered. The number of emergency operation has been decreasing. Since the 1980s, disconnection operation has been adopted increasingly. In our hospital, the number of patients receiving disconnection has been increasing from the early 1980s and the operation has almost replaced shunt operation in the 1990s. Disconnection combined with splenorenal shunt can lower the portal pressure and maintain the portal flow. Disconnection combined with splenorenal shunt seems to be a better procedure of choice.

Adolescent↗
PubMed2000

[The meridian flowing and ancient Chinese philosophy].

The theories of Yin - Yang and Five - Evolutive phase were extensively applied after pre - Qin and both Han dynasties. In the Song - Ming dynasties, the background of New Confucianism, the achievements of art of Yi(Changes) advocated by the "School of Configuration - Arithmatic" were applied, in which the method of "Adopting of Jia" was almost entirely derived from the above school, mixing the theories of heavenly stems - earthly branches, Five - evolutive phases and Yin - Yang as a whole. An ancient system of Chronological treatment was thus established creatively by integrating clinical experience together. The system is a tight system of grafting medicine and philosophy formed on the basis of successfully utilizing the philosophical framework, thinking proposed by ancient physicians with keen observation and deep ponderation. The system is, by then, an advanced one, which is also an inevitable one.

China↗
PubMed1999

Identification of urotensin II as the endogenous ligand for the orphan G-protein-coupled receptor GPR14.

Urotensin II (UII) is a neuropeptide with potent cardiovascular effects. Its sequence is strongly conserved among different species and has structural similarity to somatostatin. No receptor for UII has been molecularly identified from any species so far. GPR14 was cloned as an orphan G protein-coupled receptor with similarity to members of the somatostatin/opioid receptor family. We have now demonstrated that GPR14 is a high affinity receptor for UII and designate it UII-R1a. HEK293 cells and COS-7 cells transfected with rat GPR14 showed strong, dose-dependent calcium mobilization in response to fish, frog, and human UII. Radioligand binding analysis showed high affinity binding of UII to membrane preparations isolated from HEK293 cells stably expressing rat GPR14. In situ hybridization analysis showed that GPR14 was expressed in motor neurons of the spinal cord, smooth muscle cells of the bladder, and muscle cells of the heart. The identification of the first receptor for UII will allow better understanding of the physiological and pharmacological roles of UII.

Amino Acid Sequence↗
PubMed1999

Role of oxidative stress in nickel chloride-induced cell injury in rat renal cortical slices.

Nickel chloride (NiCl2) induced lactate dehydrogenase (LDH) release and lipid peroxidation (LPO) in rat renal cortical slices in vitro in a concentration- (0-2 mM) and time- (0-4 hr) dependent manner, with initial significant LDH release occurring as early as 1 hr, whereas significant increase in LPO started 3 hr after exposure, suggesting that LPO results from renal cell injury. Both NiCl2-induced LDH release and LPO were prevented significantly by glutathione and dithiothreitol, suggesting that NiCl2-induced renal cell injury is dependent on thiols. However, such injury is not dependent solely on thiols, because (a) these thiols failed to inhibit completely the uptake of Ni2+ by the renal cortex, and (b) diethylmaleate pretreatment failed to increase NiCl2-induced cell injury further. Superoxide dismutase partially reduced the NiCl2-induced LDH release without affecting LPO and glutathione, whereas catalase did not affect such LDH release and LPO. Dimethylthiourea and DMSO completely prevented NiCl2-induced LPO, but only partially reduced LDH release. Deferoxamine prevented NiCl2-induced renal cell injury without affecting LPO and without significantly reducing Ni2+ uptake by the renal cortex, suggesting that nickel chelation is not important in such prevention of injury. NiCl2-induced inhibition of para-aminohippurate uptake was prevented significantly by thiols, deferoxamine, and dimethylthiourea. NiCl2-induced loss of cellular glutathione content was prevented significantly by thiols and deferoxamine, but not by superoxide dismutase and dimethylthiourea. These results suggest that LPO was not related to NiCl2-induced lethal renal cell injury, whereas such injury may be caused by the induction of the Fenton reaction, generating hydroxyl radicals.

Animals↗
PubMed1999

Gadolinium induces domain and pore formation of human erythrocyte membrane: an atomic force microscopic study.

Lanthanide cations bind to human erythrocyte membranes and enhance cell permeability. It was postulated that this effect is due to their likeness with calcium ions, which have been used to induce perforation of cells. However, the nature and mechanism of the perforation are still not clear. In the present work, the change in surface topography of erythrocyte membranes exposed to various gadolinium species was imaged with an atomic force microscope (AFM) in order to get direct evidence of perforation. The images of the whole cell and regions in nanometer scale showed that the normal surface is featured by closely packed nanometer size particles. The AFM images showed that Gd(3+) binding to erythrocytes led to domain structure at low concentration and pore formation at higher concentration. The domain structures that appeared after incubation with 1.0x10(-6)-1.0x10(-5) mol/l Gd(3+) solution for 30 min are featured by the particles aggregated to form ranges and the separations among them enlarged to gorges. With a higher concentration, 2.5x10(-5) mol/l Gd(3+), the further aggregation developed into crater-shaped 'pores'. By washing with EDTA the 'pores' can be resealed but the domain structure remained. The anionic complex of Gd(3+), [Gd(Cit)(2)](3-) of this concentration, can only induce the domain structure formation. The domain and 'pore' structures mediated by Gd(3+) concentrations might be responsible for both enhanced permeability and perforation. The mechanism of Gd-induced domain formation and perforation is discussed on the basis of aggregation of membrane proteins and the coexistence of different phases of membrane lipids resulting from Gd(3+) binding.

Animals↗
PubMed1999

Single molecule physics and chemistry.

New experiments using scanning probe microcopies and advanced optical methods allow us to study molecules as individuals, not just as populations. The findings of these studies not only include the confirmation of results expected from studies of bulk matter, but also give substantially new information concerning the complexity of biomolecules or molecules in a structured environment. The technique lays the groundwork for achieving the control of an individual molecule's motion. Ultimately, this work may lead to such practical applications as miniaturized sensors.

Chemical Phenomena↗
PubMed1999

Toxicity and bioaccumulation of nickel sulfate in Sprague-Dawley rats following 13 weeks of subchronic exposure.

Adult male Sprague-Dawley rats were given 0, 0.02, 0.05, and 0.1% nickel sulfate (NiSO4-6H2O) or 0, 44.7, 111.75, and 223.5 mg Ni/L, respectively, in their drinking water for 13 wk. Twenty-four hours following the end of such treatment, all animals survived and no apparent clinical signs of toxicity were noted. The final mean body weights of various nickel sulfate-treated rats were not significantly decreased except for the 0.1% nickel sulfate treated group when compared to those in the control. The absolute and relative organ weights were either increased or decreased or remained unchanged, depending on the organ and the dose of nickel sulfate. Total plasma proteins, plasma albumin and globulins, and plasma glutamic pyruvic transaminase activity were all significantly decreased in 0.1% nickel sulfate-treated rats. Lymphocyte subpopulations (T and B cells) were induced at lower dose levels, but suppressed at the highest (0.1%) dose group. A significant decrease in urine volume and an increase in BUN were observed at the highest dose group. Biochemical analysis of bronchoalveolar lavage fluid and lung tissue showed some lung damage, whereas no damage to the testis or DNA in liver and kidneys were found. No gross or microscopic changes were seen in any of the various tissues examined. The relative order of bioaccumulation of nickel in different organs of rats when treated at 0.1% nickel sulfate (223.5 mg Ni/L) was kidneys > testes > lung = brain > spleen > heart = liver. But with regard to order of toxicity, both immune and pulmonary systems were found to be very sensitive targets, followed by kidney.

Analysis of Variance↗
PubMed1999

Characterization of the human cysteinyl leukotriene CysLT1 receptor.

The cysteinyl leukotrienes-leukotriene C4(LTC4), leukotriene D4(LTD4) and leukotriene E4(LTE4)-are important mediators of human bronchial asthma. Pharmacological studies have determined that cysteinyl leukotrienes activate at least two receptors, designated CysLT1 and CysLT2. The CysLT1-selective antagonists, such as montelukast (Singulair), zafirlukast (Accolate) and pranlukast (Onon), are important in the treatment of asthma. Previous biochemical characterization of CysLT1 antagonists and the CysLT1 receptor has been in membrane preparations from tissues enriched for this receptor. Here we report the molecular and pharmacological characterization of the cloned human CysLT1 receptor. We describe the functional activation (calcium mobilization) of this receptor by LTD4 and LTC4, and competition for radiolabelled LTD4 binding to this receptor by the cysteinyl leukotrienes and three structurally distinct classes of CysLT1-receptor antagonists. We detected CysLT1-receptor messenger RNA in spleen, peripheral blood leukocytes and lung. In normal human lung, expression of the CysLT1-receptor mRNA was confined to smooth muscle cells and tissue macrophages. Finally, we mapped the human CysLT1-receptor gene to the X chromosome.

Amino Acid Sequence↗
PubMed1999

Identification of two hERR2-related novel nuclear receptors utilizing bioinformatics and inverse PCR.

Identification of novel nuclear receptors based on the highly conserved DNA-binding domain (DBD) has previously depended mainly on low stringency hybridization of cDNA libraries and degenerate PCR. Establishment of the expressed sequence tag (EST) database in recent years has provided an alternative approach for the discovery of novel members of gene families. The rate-limiting step is the conversion of ESTs to full-length cDNA. This article describes the identification of two novel nuclear receptors (hERRbeta2 and hERRgamma2) related to human estrogen-receptor-related receptor 2 (hERR2) by mining the EST database and retrieving of full-length cDNA via inverse PCR on subdivided primary cDNA library pools. The deduced protein sequences of hERRbeta2 and hERRgamma2 contain 500 and 458 amino acid (aa) residues respectively. Sequence analysis revealed that hERRbeta2 and hERRgamma2 respectively share 95% and 77% overall aa sequence identity with hERR2. However, the extra C-terminal domain in hERRbeta2 and extra N-terminal domain in hERRgamma2 are not present in the closely related hERR2 or mouse ERR2 (mERR2). Extensive sequence verification revealed that hERR2 previously reported as a human gene is actually a rat gene, whereas hERRbeta2 is the true human ortholog of hERR2 and mERR2. Tissue distribution studies showed that hERRgamma2 was expressed in a broader panel of tissues at a higher level than hERRbeta2. hERRbeta2 was mapped to cytogenetic locus 14q24.3 approximately -14q31, a region containing multiple loci involved in genetic diseases, including Alzheimer and diabetes. hERRgamma2 was mapped to 1q32. Given the high sequence homology between hERRbeta2 and mERR2, the two receptors may have similar biological function in vivo.

Amino Acid Sequence↗
PubMed1999

DNA-Protein crosslinks induced by nickel compounds in isolated rat renal cortical cells and its antagonism by specific amino acids and magnesium ion.

Suspensions of isolated renal cortical cells in modified Krebs-Henseleit buffer (pH 7.4) were incubated with nickel chloride, nickel acetate, nickel sulfate, and nickel subsulfide (0-2 mM) at 37 degreesC for 2 h. A significant increase (63%) in DNA-protein crosslinks was observed at 2 mM nickel sulfate, whereas nickel subsulfide induced a significant increase in such crosslinks beginning at 0.5 mM concentration and a maximum increase of 200% of the control value reached at 2 mM concentration. No significant reduction in viability of renal cortical cells (as measured by trypan blue exclusion) was observed due to these nickel compounds at any concentration used. In the second series of experiments, coincubation of nickel subsulfide (2 mM) with l-histidine (8 or 16 mM), l-cysteine (4 or 8 mM), or l-aspartic acid (8 or 24 mM) significantly reduced the DNA-protein crosslinks induced by 2 mM nickel subsulfide. Similarly Mg2+ (24 mM), but not Ca2+ (24 mM), was able to antagonize nickel subsulfide-induced increase in DNA-protein crosslinks. High extracellular levels of Mg2+ and these amino acids significantly decreased the accumulation of Ni2+ from nickel subsulfide in renal cortical cells. Furthermore, these amino acids at high concentrations significantly inhibited the binding of Ni2+ from nickel subsulfide to deproteinized DNA from renal cortical cells, whereas such inhibition due to Mg2+ was close to significant (0.1 > p > 0.05). In vitro exposures of renal cortical cells to nickel subsulfide (0-2 mM) increased the formation of reactive oxygen species in concentration-dependent manner. Furthermore, coincubation of 2 mM nickel subsulfide with either catalase, dimethylthiourea, mannitol, or vitamin C at 37 degreesC for 2 h resulted in a significant decrease of nickel subsulfide-induced formation of DNA-protein crosslinks, suggesting that nickel subsulfide-induced DNA-protein crosslink formation in isolated rat renal cortical cells is caused by the formation of reactive oxygen species. The potent protective effects of these specific amino acids and Mg2+ against nickel subsulfide-induced DNA-protein crosslink formation in isolated renal cortical cells are due to reduction of cellular uptake of Ni2+ and inhibition of the binding of Ni2+ to deproteinized DNA.

Amino Acids↗
PubMed1999

Influence of 5-bromodeoxycytosine substitution on triplex DNA stability and conformation.

Three triple-helical hairpin DNAs with substitution of 5-bromocytosine for cytosine in different strands have been investigated by molecular mechanics and Raman spectroscopy. The stability of the three substituted triplexes were compared with the corresponding unsubstituted triplex DNA by the molecular mechanics method. Base stacking interactions and strand--strand interactions of each triplex were analyzed in detail. Sugar conformations in these triplexes have been determined by both vibrational spectroscopy and molecular dynamics simulation. The hairpin triplexes with substitution occurring in strand I or both in strands I and III have the main sugar conformation of C3'-endo, while the triplex with substitution occurring in strand III is the combination of C3'-endo and C2'-endo sugar conformation. Theoretical results are basically in agreement with experiments.

Base Sequence↗
PubMed1999

Purification and stabilization of a monomeric isocitrate dehydrogenase from Corynebacterium glutamicum.

Monomeric isocitrate dehydrogenase was expressed in Corynebacterium glutamicum cells harboring pEK-icdES1, a plasmid carrying the gene for the enzyme. Two- to three-fold higher expression levels of the recombinant enzyme were observed in such cells when grown in fermentors, compared to those grown in shaker incubators. The enzyme was purified to homogeneity by ammonium sulfate fractionation, Sephadex G-150 gel filtration, FPLC Mono Q anion-exchange chromatography, and affinity gel chromatography. Approximately 4 mg of 98% pure recombinant enzyme was obtained per liter of bacterial culture. Our results also include optimum buffer conditions for purification and storage of the enzyme.

Chromatography, Affinity↗
PubMed1999

Crystallization and preliminary X-ray diffraction studies of monomeric isocitrate dehydrogenase from Corynebacterium glutamicum.

A monomeric isocitrate dehydrogenase has been crystallized for the first time. This enzyme catalyzes the conversion of isocitrate to oxalosuccinate and subsequently to alpha-ketoglutarate and CO(2); the coenzyme NADP(+) is reduced to NADPH during the reaction. Polyethylene glycol 2000 monomethyl ether was used to crystallize the enzyme in space group C2 with unit-cell parameters a = 137.1, b = 54.6, c = 126.4 A, beta = 108.2 degrees. The very small crystal (0. 05 x 0.20 x 0.05 mm) diffracted to 3.5 A d spacing using synchrotron radiation.

Bacterial Proteins↗
PubMed1999

A projector/backprojector with slice-to-slice blurring for efficient three-dimensional scatter modeling.

Scatter correction is an important factor in single photon emission computed tomography (SPECT). Many scatter correction techniques, such as multiple-window subtraction and intrinsic modeling with iterative algorithms, have been under study for many years. Previously, we developed an efficient slice-to-slice blurring technique to model attenuation and system geometric response in a projector/backprojector pair, which was used in an ML-EM algorithm to reconstruct SPECT data. This paper proposes a projector/backprojector that models the three-dimensional (3-D) first-order scatter in SPECT, also using an efficient slice-to-slice blurring technique. The scatter response is estimated from a known nonuniform attenuation distribution map. It is assumed that the probability of detection of a first-order scattered photon from a photon that is emitted in a given source voxel and scattered in a given scatter voxel is proportional to the attenuation coefficient value at that voxel. Monte Carlo simulations of point sources and an MCAT torso phantom were used to verify the accuracy of the proposed projector/backprojector model. An experimental Jaszczak torso/cardiac phantom SPECT study was also performed. For a 64 x 64 x 64 image volume, it took 8.7 s to perform each iteration per slice on a Sun ULTRA Enterprise 3000 (167 MHz, 1 Gbyte RAM) computer, when modeling 3-D scatter, attenuation, and system geometric response functions. The main advantage of the proposed method is its easy implementation and the possibility of performing reconstruction in clinically acceptable time.

Computer Simulation↗
PubMed1999

Activation and fragmentation of Bacillus thuringiensis delta-endotoxin by high concentrations of proteolytic enzymes.

Commercial enzymes and insect gut juice at various concentrations were used to digest Bacillus thuringiensis subsp. sotto Cry1Aa protoxin and examine the fragmentation pattern and effect on insecticidal activity. Trypsin at both high (5 mg/mL) and low (0.05 mg/mL) concentrations converted protoxin to toxin with no difference in insecticidal activity against Bombyx mori larvae. In both cases, the toxin protein had an apparent M(r) of 58.4 kDa (SDS-PAGE). Active toxin of identical M(r) was also produced with low concentrations of Pronase and subtilisin, but at high concentration, it was degraded into two protease-resistant fragments of apparent M(r) 31.8 and 29.6 kDa, and exhibited no insecticidal activity. Sequencing data established the primary cleavage site to be in domain II, the receptor-binding region of the toxin, in an exposed loop between two beta-sheet strands. Fragmentation was not observed, however, when the digests were analyzed by native protein techniques, but rather the toxin molecule appeared to be intact. The amount of activated toxin produced by Choristoneura fumiferana gut juice was markedly reduced when the gut-juice concentration was increased from 1 to 50% and correlated with a loss in insecticidal activity. However, no lower M(r) protease-resistant fragments were evident in the SDS-PAGE of these digests.

Amino Acid Sequence↗