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Biomedical subjects

Bo Liu

Publications and source records attributed to Bo Liu.

At least 127 records · Page 7Linked to original sources

A plant-specific kinesin binds to actin microfilaments and interacts with cortical microtubules in cotton fibers.

A novel kinesin, GhKCH1, has been identified from cotton (Gossypium hirsutum) fibers. GhKCH1 has a centrally located kinesin catalytic core, a signature neck peptide of minus end-directed kinesins, and a unique calponin homology (CH) domain at its N terminus. GhKCH1 and other CH domain-containing kinesins (KCHs) belong to a distinct branch of the minus end-directed kinesin subfamily. To date the KCH kinesins have been found only in higher plants. Because the CH domain is often found in actin-binding proteins, we proposed that GhKCH1 might play a role in mediating dynamic interaction between microtubules and actin microfilaments in cotton fibers. In an in vitro actin-binding assay, GhKCH1's N-terminal region including the CH domain interacted directly with actin microfilaments. In cotton fibers, GhKCH1 decorated cortical microtubules in a punctate manner. Occasionally GhKCH1 was found to be associated with transverse-cortical actin microfilaments, but never with axial actin cables in cotton fibers. Localization of GhKCH1 on cortical microtubules was independent of the integrity of actin microfilaments. Thus, GhKCH1 may play a role in organizing the actin network in coordination with the cortical microtubule array. These data also suggest that flowering plants may employ unique KCHs to coordinate actin microfilaments and microtubules during cell growth.

Actin Cytoskeleton↗

Novel isoxazole carboxamides as growth hormone secretagogue receptor (GHS-R) antagonists.

Novel isoxazole carboxamides have been identified as growth hormone secretagogue receptor (GHS-R) antagonists. Substituent modification off the 5-position of the isoxazole ring led to analogues with potent binding affinity and functional antagonism of GHS-R. A potent analogue (32) with high aqueous solubility and good GPCR selectivity was also identified as a potential pharmacological tool for in vivo studies.

Amides↗

Hydrogen loss from nucleobase nitrogens upon electron attachment to isolated DNA and RNA nucleotide anions.

Electron transfer to isolated nucleotide monoanions in collisions with Na vapor induces hydrogen loss from nitrogen of the transient nucleobase anion. The cross section for this process is linearly correlated with the number of N-H hydrogens and is highest for guanine. The process is much faster than microseconds since only dehydrogenated dianions survived for mass spectrometric detection. The lifetime of the adenosine 5(')-monophospate dianions was measured to be 0.2 ms in an electrostatic ion storage ring but also a longer-lived component with a lifetime of at least 10 ms was identified. Implications of dissociation along the N-H coordinate for a nucleotide in DNA are briefly discussed in terms of Watson-Crick base pairs.

Anions↗

Synthesis and properties of tadpole-shaped gold nanoparticles.

In this communication, gold nanoparticles with a tadpole shape were synthesized by a simple aqueous-phase chemical method. The unusual three-dimensional and crystallized structures were demonstrated by TEM, AFM, and HRTEM methods. The SEM and UV-visible absorption measurements and electrophoresis experiments revealed that the tadpoles had novel optical and electrical properties. These attractive structures and properties are expected to find uses in many fields such as electrics, optics, electrochemistry, and biological sensing.

Journal Article↗

Localization of two homologous Arabidopsis kinesin-related proteins in the phragmoplast.

During plant cytokinesis, kinesin-related motor proteins are believed to play critical roles in microtubule organization and vesicle transport in the phragmoplast. Previously, we reported that the motor AtPAKRP1 was associated with the plus end of phragmoplast microtubules in Arabidopsis thaliana [Lee Y-RJ, Liu B (2000) Curr Biol 10:797-800]. In this paper, we report a full-length cDNA from the same organism, which encodes a polypeptide 74% identical to AtPAKRP1. This AtPAKRP1-like protein--AtPAKRP1L--and AtPAKRP1 share similar domain structures along the polypeptides. Peptide antibodies were raised and purified to distinguish the two polypeptides in vitro and in vivo. When monospecific anti-AtPAKRP1 and anti-AtPAKRP1L antibodies were used in immunofluorescence, they both decorated the plus end of phragmoplast microtubules at all stages of phragmoplast development. Their localization patterns were indistinguishable from each other. By using bacterially expressed fusion proteins of motor-less versions of both polypeptides, it was revealed that AtPAKRP1 and AtPAKRP1L were able to interact with themselves and with each other. Using T-DNA insertional mutants, it was also demonstrated that AtPAKRP1 and AtPAKRP1L were not required for each other's localization. Our results therefore indicate that AtPAKRP1 and AtPAKRP1L are both expressed in the same cells, and likely have identical functions in the phragmoplast by forming either homodimers or heterodimers.

Amino Acid Sequence↗

Ruthenium-catalyzed transformation of 3-benzyl but-1-ynyl ethers into 1,3-dienes and benzaldehyde via transfer hydrogen.

TpRuPPh(3)(CH(3)CN)(2)PF(6) catalyzed the transformation of various 3-benzyl but-1-ynyl ethers into dienes and benzaldehyde at a catalyst loading of 5 mol %. This process represents an atypical pattern of transfer hydrogenation. This catalytic reaction can be applied to various derivatives of 2-ethynyl tetrahydrofurans and pyrans to cleave their ether rings and gives diene and tethered aldehyde functionalities, respectively.

Journal Article↗

[Microsurgical resection of the recurrent craniopharyngiomas].

OBJECTIVE: To study the effective method of microsurgical resection of the recurrent craniopharyngiomas. METHODS: Microsurgical resection underwent in 40 cases with the recurrent craniopharyngiomas that accounted for 24 men and 16 women with mean age 35.1 year old. Visual deterioration was mainly complained in 25 patents, headache of symptoms in 9 patients, defect of visual field in 2 patients, amenorrhea in 2 patients, hyposexuality in one patient and diabetes insipidus in the one. Average history was 2.9 years. The superior sellar tumors on MR imaging grew in 19 cases, the superior-inferior sellar mass in 9 cases, intra-sellar in 5 cases and the tumors into the third ventricle in 7 cases. The huge calcification tumors were found in 5 cases, cystic tumors in 21 cases, and solid tumors 2 cases. Hydrocephalus presented in 12 cases. Evolution of tumor residuum was revealed in 31 cases after initial surgery and recurrent tumor after completing total removal of the tumor in 9 cases. The pterional approach was employed in 33 cases. The longitudinal fissure to the corpus callus approach in 2 cases was available for resection of the third ventricular tumor through the fornix column and septum pellucidum spaces. RESULTS: In 33 cases with the pterional approaches, total removal of the tumors were completed in 22 cases, subtotal removal of tumors in 9 cases, and partial removal in 2 cases. In 5 cases with subfrontal approach, 4 patients the total removal of tumors obtained in 4 cases and one subtotal removal of tumor in one. Of 2 cases with the longitudinal fissure to the corpus callus approaches, one case was achieved with the total removal of tumor and the other with subtotal removal of tumor. The pituitary stalk was preserved in 8 cases, the pituitary stalk was severed in 9 cases and the pituitary stalk was not identified in 23 cases when surgery. 17 patients experienced diabetes insipidus and 12 patients had the hypothalamic hypofunction after surgery. One death occurred from the hypothalamic hypofunction 35 day after surgery. By follow-up from 3 months to 3 years, 22 patients returned normal life, 11 patients can carry out their self-life, and 6 patients need care. CONCLUSIONS: The desirable removal of recurrent craniopharyngioma could be completed in the majority of patients although the reoperation of the tumors was performed very difficulty owing to the tumor adhesive to the surrounding hypothalamic structures.

Adolescent↗

Formation of C60(2-) dianions in collisions between C60- and Na atoms.

We have observed the formation of C2-60 and C2-70 in collisions between C(-)(60)/C(-)(70) and Na atoms. Cross sections for the electron transfer to the monoanion are determined to be 36+/-9 and 57+/-14 A(2) for C-60 and C-70, respectively. A simple model investigation suggests that the electron is transferred from a Na atom to a low-lying electronic state of the fullerene to form a dianion. The method leads to pico-ampere energetic beams of C60 dianions that can be used for spectroscopy and lifetime studies.

Journal Article↗

[C(1-2) posterior transarticular screw fixation (Magerl's technique) for patients with incompletely-reduced atlantoaxial dislocation].

OBJECTIVE: To assess the feasibility of performing the C(1-2) transarticular screw fixation (Magerl's technique) for patients whose C(1-2) dislocation could not be reduced completely. METHODS: Nineteen consecutive patients (from 2001 Feb. to 2003 Jan.) underwent bilateral C(1-2) transarticular screw fixation, 8 of which had an incompletely-reduced atlantoaxial dislocation. The patients' clinical outcomes within- and after-operation were evaluated, and the screws position and fixation conditions were studied by postoperative CT. RESULTS: All the patients' symptoms had some improvement, no severe complications, such as injury of nerve or blood vessels, especially the vertebral arteries, were encountered. The screws were placed precisely, and purchased enough bone substance. Firm fixation obtained, no vertebral artery lesion occurred. CONCLUSION: For the patients who have atlantoaxial dislocation that could not be reduced completely, if there is enough bone to contain the screw, performing bilateral transarticular screw fixation (Magerl technique) is still feasible and safe.

Adolescent↗

Therapeutic effects of endoscopic variceal ligation combined with partial splenic embolization for portal hypertension.

AIM: To evaluate the feasibility of a new strategy of endoscopic variceal ligation combined with partial splenic embolization (EVL-PSE) for patients with cirrhosis and portal hypertension. METHODS: From May 1999 to May 2002, 41 cases with cirrhosis and portal hypertension underwent EVL-PSE. Hemodynamics of the main portal vein (MPV), the left gastric vein (LGV) and azygos vein, including maximum velocity, flow rate and vein diameter, were assessed by Doppler ultrasonography. RESULTS: One case died from pulmonary artery embolism. One case complicated with splenic abscess was successfully managed by laparotomy. The esophageal varices and hypersplenism were well controlled after EVL-PSE in other patients. After EVL-PSE, the flow rate and velocity of MPV was significantly reduced (P<0.05), as well as the flow rate of the LGV and azygos vein. During the follow-up, no recurrent bleeding was found. CONCLUSION: Being more convenient and less invasive, EVL-PSE is hopeful to be a proper intervention strategy for portal hypertensive patients with impaired hepatic function or those intolerant to shunting or devascularization surgery.

Adult↗

Diethyl (Z,Z)-3,3'-(ethane-1,2-diyldiimino)dibut-2-enoate.

The title compound, C14H24N2O4, is an intermediate in the synthesis of the corresponding heterocyclic compounds. The molecule lies about a twofold axis and has a 'twist' conformation; it adopts the Z,Z configuration, which is shown to be governed mainly by intramolecular hydrogen bonds.

Journal Article↗

The role of phospholipase C and phosphatidylinositol 3-kinase in vascular smooth muscle cell migration and proliferation.

BACKGROUND: Vascular smooth muscle cell (SMC) proliferation and migration both contribute to the formation of intimal hyperplasia. Phospholipase C (PLC) and phosphatidylinositol 3-kinase (PI3-K) are ubiquitous signaling proteins that mediate multiple cellular events. In this study, we investigate the role of PLC and PI3-K in platelet-derived growth factor (PDGF) and extracellular matrix protein (ECM) induced SMC proliferation and migration. MATERIAL AND METHODS: Proliferation of human saphenous vein SMC was assessed by (3)H-thymidine incorporation. SMC migration was evaluated using a microchemotaxis chamber. U-73122 was used as a general inhibitor for PLC, and D609 and ET-18-OCH3, respectively, were used to block the isotypes of PLC, phosphatidylcholine- (PC-), and phosphatidylinositol- (PI-) specific PLC. PI3-K activity was inhibited using two selective inhibitors, LY-294002 and wortmannin. RESULTS: PDGF and Type 1 collagen (CN-I) stimulated SMC proliferation, whereas PDGF and four distinct extracellular matrix proteins CN-I, Type 4 collagen (CN-IV), fibronectin (FN), and laminin (LN) stimulated SMC migration. Both isotypes of PLC as well as PI3-K were necessary for PDGF- and CN-I-induced proliferation. Signaling for migration, however, was more specific. Of the various signaling proteins studied, only PI-PLC was necessary for PDGF-induced SMC migration. Conversely, PI3-K was the only signaling protein necessary for SMC migration in response to ECM proteins. CONCLUSION: The signaling pathways necessary for PDGF- and CN-I-induced SMC proliferation involve both isotypes of PLC as well as PI3-K. The signaling pathways used by growth factors and ECM to stimulate SMC migration are more selective. Understanding the intracellular signaling pathways required for SMC proliferation and migration may allow the development of tools to selectively block intimal hyperplasia.

Cell Division↗

Stem cell factor and c-kit are expressed by and may affect vascular SMCs through an autocrine pathway.

INTRODUCTION: Stem cell factor (SCF) is a membrane-bound and soluble growth factor that activates the c-kit tyrosine kinase receptor. Given the similarities between c-kit and platelet-derived growth factor (PDGF) receptors, we hypothesized that similar to PDGF, SCF/c-kit signaling may play a role in smooth muscle cell (SMC) function and thus the development of intimal hyperplasia. MATERIALS AND METHODS: Human saphenous vein SMCs were harvested from veins procured at the time of bypass grafting. Carotid arteries from rats that were balloon injured (n = 12) at variable time points were compared to sham-operated controls (n = 3). Expression of SCF and c-kit was measured by immunohistochemistry (IHC) and Western blotting. RESULTS: Western blotting revealed that human SMCs express membrane-bound SCF. In separate experiments, we found that this growth factor undergoes proteolytic cleavage to its soluble form following exposure to matrix metalloproteinase-9 (MMP-9), a ubiquitous MMP released at the time of arterial injury. We next evaluated in human SMCs, expression of the SCF receptor, c-kit. Western blotting of human SMC lysates revealed minor but consistent expression of c-kit. IHC demonstrated c-kit expression to be localized to the media. To determine if c-kit is up-regulated during the development of intimal hyperplasia, we evaluated expression of this receptor in a rat carotid balloon injury model. Quantification of IHC staining on injured vessels revealed that c-kit expression within the media was significantly increased at 3, 7, 14, and 28 days following injury (28.1, 30.8, 16, and 10.4% increase over sham controls, respectively, P < 0.05). Furthermore, c-kit expression was prominent within the neointima and maximal at 7 days (53.4 +/- 7.8% of area c-kit positive). CONCLUSION: Human vascular SMCs express the growth factor SCF and its receptor, c-kit. SCF is released from its membrane-bound form via MMP-9. This finding and the dramatic increase in c-kit expression observed in the rat carotid artery after balloon injury suggests SCF/c-kit signaling may affect SMC function via an autocrine pathway.

Animals↗

Transduction of peptide analogs of the small heat shock-related protein HSP20 inhibits intimal hyperplasia.

BACKGROUND: Human saphenous vein (HSV) is the autologous conduit of choice for peripheral vascular reconstructions. However, vasospasm can lead to early graft failure. The leading cause of delayed graft failure is intimal hyperplasia. OBJECTIVE: To develop a proteomic approach to prevent vein-graft spasm and intimal hyperplasia. METHODS: Biomimetic peptide analogs of the small heat shock-related protein HSP20, containing a protein transduction domain (PTD), a phosphorylated serine, and a sequence of HSP20 surrounding the phosphorylation site (PTD-pHSP20), or a scrambled sequence of the same amino acids surrounding the phosphorylation site (PTD-scHSP20) were synthesized. The peptides were used in muscle bath and organ culture experiments with human saphenous vein (HSV) segments. Cultured smooth muscle cell lines were used to determine the effect of the peptides on proliferation and migration. RESULTS: In HSV rings precontracted with norepinephrine, PTD-pHSP20 but not PTD-scHSP20 led to relaxation. There was no significant difference in smooth muscle cell proliferation in cells treated with PTD-pHSP20 compared with PTD-scHSP20. Treatment with PTD-pHSP20 significantly inhibited cellular migration compared with PTD-scHSP20. Control, untreated, and PTD-scHSP20-treated saphenous veins had significant increases in intimal thickness after culture. This intimal thickening was completely inhibited by treatment with PTD-pHSP20. CONCLUSIONS: Protein transduction of biologically active motifs of HSP20 can affect pathologic and physiologic responses of HSV and represents a novel proteomic-based therapeutic approach. CLINICAL RELEVANCE: We have been a part of the genomics era and are now viewing the emergence of "proteomics." The genome is linear and relatively easy to examine; however the proteome is much more complex and dynamic. In essence, the purpose of gene therapy is to manipulate the genome to produce a particular protein. This manuscript describes a new proteomic approach in which the biologically active part of a protein is directly introduced into vascular cells. Peptides were synthesized which contained a total of 24 amino acids, 11 of which represent a protein transduction domain or "carrier" while the other 13 are the biologically active "cargo." These synthetic peptides prevent spasm (contraction) and intimal hyperplasia in segments of human saphenous vein treated ex vivo. Preclinical development is currently underway to develop these molecules as a proteomic-based vein harvest solution to enhance vein-graft patency.

Cells, Cultured↗

Intracellular calcium transients are necessary for platelet-derived growth factor but not extracellular matrix protein-induced vascular smooth muscle cell migration.

PURPOSE: Vascular smooth muscle cell (SMC) migration is a critical component of the hyperplastic response that leads to recurrent stenosis after interventions to treat arterial occlusive disease. We investigated the relationship between intracellular calcium ([Ca(2+)](i)) and migration of vascular SMCs in response to platelet-derived growth factor (PDGF) and extracellular matrix (ECM) proteins. METHODS: Human saphenous vein SMCs were used for all experiments. SMC migration in response to agonists was measured with a microchemotaxis assay. A standard fluorimetric assay was used to assess changes in [Ca(2+)](i) in response to the various combinations of growth factors and ECM proteins. RESULTS: The calcium ionophore A23187 produced a rapid rise in [Ca(2+)](i) and a corresponding 60% increase in SMC migration, whereas chelation of [Ca(2+)](i) with BAPTA (1,2-bis [aminophenoxy] ethane-N,N,N',N'-tetraacetic acid) produced a fivefold decrease in PDGF-induced chemotaxis, suggesting that [Ca(2+)](i) is both sufficient and necessary for SMC migration. Stimulation of SMCs with PDGF produced an early peak followed by a late plateau in [Ca(2+)](i). To establish a relationship between temporal fluctuations in [Ca(2+)](i) and SMC migration, SMCs were pretreated with caffeine and ryanadine, which eliminated the initial peak but not the late plateau in [Ca(2+)](i), and had no effect on chemotaxis in response to PDGF. Incubation of SMCs with nickel chloride eliminated the late plateau, but had no effect on the initial peak in [Ca(2+)](i), and reduced PDGF-stimulated migration by fivefold. We then evaluated the role of calcium in SMC migration induced by ECM proteins such as laminin, fibronectin, and collagen types I and IV. All four matrix proteins stimulated SMC migration, but none produced an elevation in [Ca(2+)](i). Moreover, preincubation of SMCs with caffeine and ryanadine or nickel chloride had no effect on ECM protein-induced chemotaxis. CONCLUSION: [Ca(2+)](i) transients are necessary for PDGF but not ECM protein-induced SMC chemotaxis. Moreover, the ability of PDGF to stimulate vascular SMC migration appears dependent on influx of extracellular calcium through membrane channels. CLINICAL RELEVANCE: Recurrent stenosis after angioplasty or surgical bypass remains a significant challenge in treating vascular occlusive disease. In addition to growth factors, extracellular matrix (ECM) proteins may be potent agonists of this process. In this study we show that the influx of extracellular calcium is an important mechanism for platelet-derived growth factor-induced smooth muscle cell migration but not ECM-induced migration. Of note, in clinical trials calcium channel blockers failed to inhibit recurrent stenosis. Our data provide mechanistic insight to help explain this negative outcome in that therapies designed to inhibit restenosis depend on the effects of both growth factors and ECM proteins.

Calcimycin↗