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Biomedical subjects

Yang Li

Publications and source records attributed to Yang Li.

At least 91 records · Page 5Linked to original sources

Ethanol extract from Artemisia vestita, a traditional Tibetan medicine, exerts anti-sepsis action through down-regulating the MAPK and NF-kappaB pathways.

Artemisia vestita Wall., a traditional Tibetan medicine, has wide clinical application for inflammatory diseases. However, its molecular mechanism of anti-inflammatory effect is poorly understood. In the present study, we investigated the anti-inflammatory activity and underlying mechanism of the ethanol extract from Artemisia vestita (AV-ext) on lipopolysaccharide (LPS)-induced sepsis. Pretreatment with AV-ext significantly decreased the levels of tumor necrosis factor-alpha (TNF-alpha) in serum and liver and lung tissues, and improved the survival of mice with experimental sepsis. AV-ext also remarkably reduced the expression levels of TNF-alpha, interleukin-1beta and cyclooxygenase-2 in LPS-stimulated RAW 264.7 macrophages and dose dependently suppressed the activation of mitogen-activated protein kinases (MAPKs), such as p38, extracellular signal-regulated kinase (ERK1/2) and c-Jun NH2-terminal kinase (JNK). Furthermore, pretreatment with AV-ext dose dependently inhibited the activation of nuclear factor-kappaB (NF-kappaB), as well as the degradation and phosphorylation of inhibitory kappaB (IkappaB) in LPS-activated RAW 264.7 macrophages. These results collectively reveal that AV-ext inhibits TNF-alpha release from macrophages by suppressing MAPK and NF-kappaB signaling pathways and suggest that AV-ext may be beneficial for the treatment of endotoxin shock or sepsis.

Animals↗

[Risk factors and treatment of hemorrhagic cystitis in children after hematopoietic stem cell transplantation].

OBJECTIVE: Hemorrhagic cystitis (HC) is one of the common complications of hematopoietic stem cell transplantation (HSCT), which causes significant pain, prolongs hospitalization, and occasionally results in renal failure and death. This study aimed at investigating the incidence, risk factors, and outcome of HC in children post umbilical cord blood transplantation (UCBT) and peripheral blood stem cell transplantation (PBSCT). METHODS: From October 1998 to June the clinical records of 53 pediatric patients (aged 2-18 years with median age of 7.5 years) in our HCST center who underwent UCBT (n = 37) and PBSCT (n = 16) were retrospectively analyzed. Thirty out of 53 patients were diagnosed as hereditary hemolytic anemia (56.6%), and the others as haematological malignancies (43.4%): of whom 8 had acute lymphoblastic leukemia, 12 acute myeloid leukemia, 2 chronic myeloid leukemia and 1 non-hodgkin lymphoma. Conditioning regimen varied according to disease and clinical status, however based on cyclophosphamide (CTX, 120-200 mg/kg) and busulphan (BU, 12-16 mg/kg) in the cohort. Total body irradiation (TBI) or total lymphoid irradiation was added in 7 patients respectively. The patients were divided into regular treatment group (RTG) with 15 cases who received hyperhydration, alkalinizing, diuresis and Mesna during CTX infusion and prostaglandin E1 (PGE1) group (PEG) with 38 cases who received hyperhydration, alkalinizing, diuresis and Mesna plus prostaglandin E1 (0.03 microg/kg.h). The risk factors of HC were examined by univariate and multivariate analysis. RESULTS: In all, 11 of the 53 transplanted patients developed HC (21%) with a median onset time of day +15 (rage day +2 - +25). HC was classified as early in 4 (36%) and late in 7 (64%), and scored as grade Iin 2 cases (18%), grade II in 4 (36%) and grade III in 5 (46%). There was no significant difference between RTG and PEG in the incidence of HC, however, the incidence was much higher in the group of patients who were > or = 6 years old, positive group of graft-versus-host disease (GVHD) and group of cytomegalovirus (CMV) infection than that in the group of patients who were < 6 years of age (32% vs. 8%, P < 0.05), negative group of GVHD (35% vs. 7%, P < 0.05) and CMV non-infected group (62% vs. 13%, P < 0.05), respectively. Furthermore, by multivariate analysis, > or = 6 years old (OR = 3.53, P < 0.05) and CMV infection (OR = 4.31, P < 0.05) were significant risk factors for HC. Three of 11 patients were treated with bladder irrigation. All patients recovered from HC in a median 12.8 days (range 2-53 days). CONCLUSION: Older age (> or = 6 years) as well as CMV infection were the risk factors of HC. Both hyperhydration and Mesna were effective in preventing HC, while addition of PGE1 could not reduce the incidence of HC. The prognosis of HC in children post HSCT was satisfactory.

Adolescent↗

A novel mutation of the VMD2 gene in a Chinese family with best vitelliform macular dystrophy.

INTRODUCTION: In this paper, we report a novel VMD2 gene mutation in a Chinese family with Best vitelliform macular dystrophy. MATERIALS AND METHODS: Ophthalmologic examination and optical coherence tomography (OCT) were performed in 2 members of this family. Mutational screening was performed by single-strand conformation polymorphism (SSCP) and direct sequencing of PCR-amplified DNA fragments, corresponding to the 11 exons of the gene. RESULTS: Sequence analysis identified a previously unreported C to G change, predicting a Phe-113-Leu substitution. Both the proband and his sister harboured this novel mutation. Each had bilateral vitelliform lesions. CONCLUSIONS: A novel mutation in the VMD2 gene (C427G) was found in Chinese patients with Best vitelliform macular dystrophy.

Adult↗

[Cause and treatment of dysuria post trans-urethral resection of prostate].

OBJECTIVE: To evaluate the cause and treatment of dysuria post trans-urethral resection of prostate (TURP). METHODS: The clinical data and the treatment of 22 cases of dysuria post TURP were analyzed retrospectively. RESULTS: All cases including 3 cases of glandular and extraneous material residual, 5 cases of urethrostenosis, 7 cases of bladder neck contracture, and 7 cases of detrusor muscle weakness, were cured after the treatment. CONCLUSION: The main causes of dysuria post TURP were glandular residual, urethrostenosis, bladder neck contracture, and detrusor muscle weakness. Correct preoperative diagnosis and treatment during/post operation are the key to the prevention of dysuria post TURP.

Aged↗

[Correlations of biomolecular markers, such as P53 protein and vascular endothelial growth factor, to radiosensitivity of nasopharyngeal carcinoma].

BACKGROUND & OBJECTIVE: About 20%-40% nasopharyngeal carcinoma (NPC) patients, who are in the same staging group, receiving the same treatment modality and radiotherapy dose, relapse in the irradiated fields within 5 years. This is mainly due to the differences in internal radiosensitivity. This study was to analyze the proliferation, apoptosis, angiogenesis, and lymphogenesis of tumor cells, and to explore the correlation of these factors to radiosensitivity. METHODS: P53 protein, vascular endothelial growth factor (VEGF) protein, survivin protein, VEGF-C protein, Ki67 protein, and microvascular density (MVD) of 60 biopsy samples from radiosensitive group and 60 from radio-resistant group were detected by immunohistochemistry, respectively. Their correlations to clinical characteristics were analyzed. RESULTS: The positive rates of P53, VEGF, survivin, VEGF-C, Ki67 were 65.0%, 57.5%, 60.8%, 42.5%, 57.5%, respectively. The positive rates of P53 and VEGF, and MVD in the radio-sensitive group and in the radio-resistant group were (25.97+/-21.26)%, (18.50+/-19.86)%, 32.65+/-19.61 and (37.85+/-28.67)%, (30.83+/-23.94)%, 41.95+/-16.97, respectively (P<0.05). The positive rates of Survivin, VEGF-C, and Ki67 between the two groups had no statistic difference (P>0.05). The correlations between P53, VEGF, and MVD were obvious. CONCLUSION: P53 protein, VEGF protein and MVD might be biomolecular markers for evaluating the internal radiosensitivity of NPC patients.

Adult↗

[Association of paraoxonase polymorphisms and serum homocysteine thiolactone complex with coronary heart disease].

OBJECTIVE: To investigate the relationship between paraoxonase (PON) polymorphisms and serum homocysteine thiolactone (HTL) and coronary heart diseases. METHOD: In this prospective study, serum complex of HTL levels using ELISA, and the lever of serum Hcy using high pressure liquid chromatography (HPLC), determined the PON1/T(-107)C and PON2/C311S genotypes using PCR-restriction fragment length polymorphisms 203 were measured in patients with angiographic documented coronary heart disease (CAD) and 117 controls. RESULTS: Serum levels of Hcy and the complex of HTL in CAD patients were significantly higher than that in controls (P < 0.05). No significant difference was found in frequencies of PON1/T(-107)C genotypes and alleles (P > 0.05) between CAD patient and controls. The PON2/C311S (SS) genotype was lower in CAD patients than that in controls (P < 0.05), while the frequency of allele was similar between the two groups (P > 0.05). The T allele of PON1/T(-107)C and S alleles of PON2/C311S polymorphism were associated with lower plasma Hcy and HTL complex [Hcy (11.83 +/- 4.76) micromol/L vs (15.32 +/- 10.32) micromol/L, P < 0.05; HTL complex (24.36 +/- 9.30) U/ml vs (32.05 +/- 10.44) U/ml, P < 0.05]. The genetype PON2 and allele C were higher in CAD patients with type 2 diabetes than that in CAD patients without type 2 diabetes and controls (P < 0.005). CONCLUSIONS: The elevation of serum Hcy and the complex of HTL were associated with increased risk of coronary heart disease. The allele PON1/(-107)T and PON2/311S might be protective for the development of atherosclerosis.

Adult↗

[Screening of differentially expressed genes in rats with cardiomyopathy after bone marrow mesenchymal stem cell transplantation].

OBJECTIVE: Earlier studies have confirmed that mesenchymal stem cells (MSCs) can transdifferentiate into myocytes and improve heart function in 2 weeks. But the mechanism is not clear. In this study, the mechanism of improvement of heart function after transplantation of MSCs was examined with suppression subtractive hybridization (SSH). METHODS: MSCs were isolated from thighone and tibia of Wistar rats, purified by adhesion-screening method, and expanded in vitro. Intraperitoneal injection of doxorubicin (at 2.5 mg/kg/time and total doses of 15 mg/kg) established cardiomyopathy models. MSCs were transplanted into cardiomyocytes. The differential genes between tester (rats with cardiomyopathy that were injected with MSCs) and driver (rats with cardiomyopathy that were injected with equivalent volume of culture medium) were screened with suppression subtractive hybridization. RESULTS: After 4 weeks of intraperitoneal injection of doxorubicin, left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) decreased by 26.48% and 40.61%, respectively (P < 0.01), as compared with those of normal group. Cardiomyopathy model was established successfully. And the heart function of the rats with cardiomyopathy was significantly improved after transplantation. Sixteen gene fragments were detected, and 12 of them were up-regulated in testers. They were rattus norvegicus mitochondrial BN/SsNHsdMCW, rattus norvegicus strain mitochondrial F344 X BN F1, rattus norvegicus mitochondrion H(+)-ATP synthase alphase subunit (Atp5al) mRNA, rattus norvegicus BHE/Cdb tRNA-Lys gene, rat mitochondrial H(+)-ATP synthase alpha subunit mRNA, rattus norvegic (wild-caught animal) complete mitochondrial genome, rattus norvegic clone BB.1.4.1 unknown Glu-Pro dipeptide repeat protein mRNA, Arabidopsis thaliana transgenic line C DNA, rat mitochondrial ATP synthase beta subunit mRNA, rattus norvegic mitochondrial genome, rat cardiac troponin T mRNA and rat mRNA for beta-globin. Four gene fragments were down-regulated in testers. They were rat mRNA for sarcomeric mitochondrial creatine kinase, rat mRNA for ribosomal phosphoprotein P2, rat alpha-crystallin B chain mRNA and rattus norvegicus NADH-ubiquinone oxidoreductase Fe-S protein 7 mRNA. CONCLUSION: The expression of the genes relating to mitochondrial synthesizing and contracting proteins synthesizing increased after MSC transplantation. The genes might enhance energy synthesis and promote MSC transdifferentiate into myocytes, and then improve heart function of rats with cardiomyopathy.

Animals↗

A bivalent dissectional analysis of the high-affinity interactions between Cdc42 and the Cdc42/Rac interactive binding domains of signaling kinases in Candida albicans.

The small GTPase Cdc42, a member of the highly conserved Rho family of intracellular GTPases, communicates with downstream signaling proteins via high-affinity interactions with the consensus Cdc42/Rac interactive binding (CRIB) polypeptide sequence. Previous biochemical and structural studies show that the CRIB motif itself is insufficient for high-affinity binding to Cdc42 but requires the sequence segment C-terminal to the CRIB motif for enhanced affinity. In this study, we have investigated the high-affinity (K(d) in units of nanomolar) associations of two highly homologous extended CRIB domains (eCRIBs) from the PAK kinases, Cla4 and Cst20, with Cdc42 from Candida albicans. (1)H-(15)N NMR heteronuclear NOE data of the eCRIB polypeptides in complex with Candida Cdc42 (CaCdc42) indicate that both eCRIB peptides have approximately two binding loci for CaCdc42. When each of the two eCRIB peptides is dissected into two fragments, the N-terminal fragments containing the minimal CRIB motif (mCRIB), mCla4 and mCst20, have relatively high binding affinities with dissociation constants (K(d)) of 4.2 and 0.43 microM, respectively. On the other hand, the C-terminal fragments (cCRIB), cCla4 and cCst20, exhibit significantly lower affinities for their binding to CaCdc42. The cCla4 peptide binds to CaCdc42 with a sub-millimolar K(d) of 275 microM, and the cCst20 peptide shows an even lower binding affinity (K(d) = 1160 microM). Cross-titration experiments with the cognate fragments show that the binding affinity of cCst20 is enhanced approximately 5.5-fold (K(d) = 207 microM) in the presence of saturating amounts of mCst20, and vice versa. No such effect is observed for the binding of cCla4 and mCla4. These results suggest that the Cdc42-CRIB system can be represented by a "dual recognition" model for protein-protein interactions [Kleanthous, C., et al. (1998) Mol. Microbiol. 28, 227-233], following much the same mechanisms of multivalent molecular interactions [Song, J., and Ni, F. (1998) Biochem. Cell Biol. 76, 177-188; Mammen, M., et al. (1998) Angew Chem., Int. Ed. 37, 2754-2794]. The bivalent modeling of linked peptide fragments shows that the binding of eCla4 follows a simple additivity/avidity model, while binding of eCst20 appears to have a more complex mechanism involving cooperative effects. The differential binding mechanisms between closely related eCRIB polypeptides and CaCdc42 provide a new molecular basis for understanding kinase activation and for the design of antifungal agents targeting the large protein interaction interfaces engaged by the fungal GTPase.

Amino Acid Sequence↗

Focal adhesion kinase silencing augments docetaxel-mediated apoptosis in ovarian cancer cells.

OBJECTIVE: Docetaxel causes cell death through induction of apoptosis; however, cell death characteristics for docetaxel have not yet been fully elucidated. We examined the role of focal adhesion kinase (FAK) cleavage in docetaxel-mediated apoptosis. METHODS: FAK degradation after treatment with docetaxel was determined in both taxane-sensitive (HeyA8 and SKOV3) and taxane-resistant (HeyA8-MDR and SKOV3-TR) ovarian cancer cell lines by Western blot analysis. Cell growth was determined with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. FAK-targeting small interfering RNA (siRNA) was used to decrease FAK expression. Apoptosis and caspase activity were determined using commercially available kits. RESULTS: SKOV3 and HeyA8 cell lines were both sensitive to docetaxel (IC50 levels, 1-6.2 nmol/L), whereas the SKOV3-TR and HeyA8-MDR cells were resistant (IC50>or=250 nmol/L for both). Docetaxel induced high rates of apoptosis in SKOV3 and HeyA8 cells (84% and 66% apoptosis, respectively) but minimal apoptosis (5-8%) in SKOV3-TR and HeyA8-MDR cells. Similarly, FAK was cleaved in SKOV3 and HeyA8 cells in response to docetaxel treatment but unchanged in the resistant cells. Caspase-3 and caspase-8 activity also increased significantly in docetaxel-treated SKOV3 and HeyA8 cells but not in the taxane-resistant cells. DEVD-fmk (caspase-3 blocker) was able to block both FAK cleavage and apoptosis mediated by docetaxel in SKOV3 and HeyA8 cells. FAK siRNA transfection resulted in 70% to 90% decrease in FAK levels in all cell lines within 72 hours. FAK silencing augmented docetaxel-mediated growth inhibition (5- to 8-fold increase) and apoptosis in both of the taxane-sensitive and taxane-resistant cell lines. CONCLUSIONS: Docetaxel induces FAK cleavage, mediated through activation of caspase-3, in taxane-sensitive ovarian cancer cells but not in taxane-resistant cells. The absence of FAK degradation may contribute to cell survival in taxane-resistant cells. FAK silencing promotes the in vitro efficacy of docetaxel in both taxane-sensitive and taxane-resistant cell lines and may serve as a novel therapeutic approach.

Antineoplastic Agents, Phytogenic↗

[Proteomic analysis of prostate cancer using surface enhanced laser desorption/ionization mass spectrometry].

OBJECTIVE: To identify the serum biomarkers of prostate cancer by using protein chip and bioinformatics. METHODS: Eighty three prostate cancer (PCA) patients and ninety five healthy people from mass screen in Changchun were detected by surface-enhanced laser desorption/ionization mass spectrometry (SELDI-MS). The data of spectra were analyzed by bioinformatics tools-Biomarker Wizard and Biomarker Pattern. RESULTS: Compared with the spectra of healthy people, there were 18 potential markers detected in the spectra of the PCA patients, the protein expression was high in 4 of which and low in the 10 of which. The softwares Biomarkerwizard and Biomarker Pattern automatically, under given conditions, selected 8 biomarker proteins to be used to establish a five layer decision tree differentiate to diagnose PCA and differentiate PCA from healthy people with a specificity of 92.632% and a sensitivity of 96.386%. CONCLUSION: New serum biomarkers of PCA have been identified, and this SELDI mass spectrometry coupled with decision tree classification algorithm will provide a highly accurate and innovative approach for the early diagnosis of PCA.

Aged↗

Synthesis of single-crystalline CoP nanowires by a one-pot metal-organic route.

A simple one-pot method has been used to prepare uniform single-crystalline CoP nanowires with a high aspect ratio by the thermal-decomposition reaction of cobalt(II) acetylacetone with long-chain alkylphosphonic acid in the presence of hexadecylamine (HDA) and trioctylphosphine oxide (TOPO) at high temperature. The crystal morphology of the resulting nanowires can be influenced by the ratio of HDA and TOPO.

Journal Article↗

Catalpol prevents the loss of CA1 hippocampal neurons and reduces working errors in gerbils after ischemia-reperfusion injury.

Catalpol, an iridoid glycoside, contained richly in the roots of Rehmannia glutinosa, was found for the first time to be of neuroprotection in gerbils subjected to transient global cerebral ischemia. Catalpol (1 mg/kg ip) used immediately after reperfusion and repeatedly at 12, 24, 48 and 72 h significantly rescued neurons in hippocampal CA1 subfield and reduced working errors during behavioral testing. The neuroprotective efficacy of catalpol became more evident when the doses of catalpol were increased to 5 and 10mg/kg. In addition, it was exciting that the significant neuroprotection by catalpol was also evident when catalpol was applied up to 3 h after ischemia. But the neuroprotective efficacy of catalpol became weak when catalpol was given at 6h after ischemia. Of great encouragement was the finding that the neuroprotection of catalpol could be seen not only in a short post-ischemic period (12 days) but also in a long period (35 days). All these indicated that catalpol was truly neuroprotective rather than simply delayed the onset of neuronal damage and might be of therapeutic value for the treatment of global cerebral ischemia.

Analysis of Variance↗

Regulation of Kv7 (KCNQ) K+ channel open probability by phosphatidylinositol 4,5-bisphosphate.

Voltage-gated Kv7 (KCNQ) channels underlie important K+ currents, including the neuronal M current, and are thought to be sensitive to membrane phosphatidylinositol 4,5-bisphosphate (PIP2) and PIP2 depletion to underlie muscarinic receptor inhibition. We studied regulation of Kv7.2-7.4 channels by PIP2 in Chinese hamster ovary (CHO) cells using single-channel and whole-cell patch clamp and biochemical analysis. Maximal open probabilities (Po) of Kv7.2-Kv7.4 homomultimers and of Kv7.2/7.3 heteromultimers were found to be strongly dependent on the [diC8-PIP2] applied to inside-out patches, with differential apparent affinities that correlate with their maximal Po in on-cell mode. Unitary conductance was not affected by PIP2. Raising tonic [PIP2] by coexpression of phosphatidylinositol (4)5-kinase increased the maximal Po of both Kv7.2 and Kv7.2/7.3 channels studied in on-cell patches and increased whole-cell Kv7.2, but not Kv7.3, current amplitudes. In cells coexpressed with muscarinic M1 receptors, bath application of muscarinic agonist reduced the maximal Po of Kv7.2/7.3 channels isolated in on-cell patches. Coexpression of a PIP2 sequestering construct moderately reduced whole-cell Kv7.2/7.3 currents, and coexpression of a construct containing a PIP2 phosphatase nearly abolished them. Finally, biochemical analysis of anionic phospholipids in CHO cells stably expressing M1 receptors shows that PIP2 and PIP are nearly depleted 1 min after muscarinic stimulation, with an unexpected rebound after 10 min. These results strongly support the direct regulation of Kv7 channels by PIP2 and its depletion as the mechanism of muscarinic suppression of M channels. Divergent apparent affinities of Kv7.2-7.4 channels for PIP2 may underlie their highly differential maximal Po observed in cell-attached patches.

Animals↗

Kinetics and template nucleation of self-assembled hydroxyapatite nanocrystallites by chondroitin sulfate.

Biomineralization is an important process, which is often assisted by biomolecules. In this paper, the effect of chondroitin sulfate on the crystallization of hydroxyapatite was examined quantitatively based on a generic heterogeneous nucleation model. It is found that chondroitin sulfate can suppress the supersaturation-driven interfacial structure mismatch between the hydroxyapatite crystal and the substrate and promote the formation of ordered hydroxyapatite nanocrystallite assemblies. The nucleation mechanism of self-aligned hydroxyapatite nanocrystallites was examined from the viewpoints of kinetics and interfacial structure and properties, which contributes to an understanding of the fundamentals of biomineralization of self-assembled structures. The results obtained from this study will provide a basic principle to design and fabricate highly orderly organic-inorganic hybrid materials.

Biocompatible Materials↗

Acute and chronic effects of relaxin on vasoactivity, myogenic reactivity and compliance of the rat mesenteric arterial and venous vasculature.

We investigated the effect of relaxin on vasodilation, myogenic reactivity, and compliance of small mesenteric arteries and veins. In acute experiments, small (second order) mesenteric arteries and veins from female rats were mounted in a pressure myograph, perfused intraluminally with relaxin, and exposed to incremental increases in intraluminal pressure (20-120 mm Hg for arteries, 2-12 mm Hg for veins). We expressed myogenic reactivity as the ratio of active to passive diameter at each pressure step. In chronic experiments, relaxin was administered to rats (4 microg/h) for 3 days prior to isolating the vessels and measuring myogenic reactivity. Arteries were more sensitive than were veins to the acute vasodilatory activity of relaxin (EC50: arteries=1.32+/-0.18x10(-8) M; veins=3.19+/-0.88x10(-8) M, P<0.05). Acute relaxin reduced myogenic reactivity of mesenteric arteries, but not veins. Chronic pretreatment with relaxin did alter the pressure/diameter relationship in Ca(2+)-containing medium, but this was due to increased passive compliance (control: 2.96+/-0.14 microm mm Hg(-1), n=5; relaxin: 3.72+/-0.16 microm mm Hg(-1), n=5) rather than to reduced myogenic reactivity. Chronic relaxin did not alter myogenic reactivity or compliance (control: 43.8+/-1.4 microm mm Hg(-1), n=5; relaxin: 46.1+/-2.3 microm mm Hg(-1), n=5) of veins. Thus, although relaxin reduces total peripheral resistance, it does not affect splanchnic venous capacitance or tone. In the face of elevated plasma relaxin levels, such as during pregnancy, cardiac preload may thus be maintained, concurrent with a reduction in cardiac afterload and blood pressure. We caution that, if an experimental treatment alters compliance, myogenic reactivity must be expressed as the ratio of active:passive diameter.

Analysis of Variance↗

New biodegradable amphiphilic block copolymers of epsilon-caprolactone and delta-valerolactone catalyzed by novel aluminum metal complexes. II. Micellization and solution to gel transition.

In our previous study [J. Yang, L. Jia, L. Yin, J. Yu, Z. Shi, Q. Fang, A. Cao, Macromol. Biosci. 2004, 4, 1092.], new biodegradable copolymers of diblock methoxy poly(ethylene glycol)-block-poly(epsilon-caprolactone) and methoxy poly(ethylene glycol)-block-poly(delta-valerolactone), and triblock poly(epsilon-caprolactone)-block-poly(ethylene glycol)-block-poly(epsilon-caprolactone) and poly(delta-valerolactone)-block-poly(ethylene glycol)-block-poly(delta-valero-lactone) bearing narrow molecular weight distributions and well-defined block architectures were reported to be prepared with our original aluminum metal complex templates. This work will continue to report new investigations on their water solubility, and reversible thermal responsive micellization and solution to gel transition in distilled water. Among the new synthesized copolymers (P1-P23), seven diblock or triblock samples (P3, P6, P7, P11, P12, P19, and P21) with higher hydrophilic building block populations were revealed to be water soluble under ambient temperature. By means of UV spectrophotometer attached with a thermostat, important parameters as critical micellization mass concentrations (CMCs) and critical micellization temperatures (CMTs) were characterized for these new amphiphile dilute aqueous solution with the aid of an lipophilic organic dye probe of 1,6-diphenyl-1,3,5-hexatriene (DPH). Furthermore, the critical gelation temperatures (CGTs) were simultaneously investigated for these water-soluble block copolymers via a tube tilting method. It was found that the CMC, CMT, and CGT were strongly affected by the population and nature of the hydrophobic building blocks, and a higher hydrophobicity of the new amphiphilic block copolymer finally led to lower CMC and CMT, and higher CGT. In addition, the salts of KBr and NaCl were found to play as a salt-out effect on the solution to gel transition for the diblock P6 and triblock P11, exhibiting an interesting tunable gelation temperature close to 35-42 degrees C. These results will pave new possibility for the synthesized block structural amphiphiles as potential biomaterials to be applied in vivo.

Alum Compounds↗

Novel mutations in the CYP4V2 gene associated with Bietti crystalline corneoretinal dystrophy.

PURPOSE: Bietti crystalline corneoretinal dystrophy (BCD) is an autosomal recessive disorder of retinal degeneration characterized by small glittering crystals in the corneal limbus, posterior pole of the eye, and circulating lymphocytes. Recently mutations in a new gene CYP4V2, encoding a protein belonging to a novel member of the cytochrome P450 family, have been identified as the cause of BCD. To further characterize the role of CYP4V2 in BCD, mutation screening has been undertaken in a cohort of affected patients with BCD from China. METHODS: Eight unrelated families, including 14 patients and 18 unaffected relatives, and 10 sporadic patients were examined clinically. Fifty normal Chinese individuals served as control subjects. Genomic DNA was extracted from venous blood of all participants. The coding region (including the intron-exon boundary) of CYP4V2 was amplified by polymerase chain reaction (PCR). The PCR products were analyzed using direct sequencing and single strand conformation polymorphism (SSCP). RESULTS: Fundus examination revealed clinical features of BCD with many small, yellowish-sparkling crystals at the posterior pole of the fundus. Sequencing of CYP4V2 identified nine (5 missense, 1 nonsense, 2 deletion, and 1 point A-->G transversion in the splice acceptor site) mutations in 8 families and 9 independent patients. Five of these mutations are novel. CONCLUSIONS: Our finding expands the spectrum of CYP4V2 mutations causing BCD, and further confirms the role of CYP4V2 in the pathogenesis of BCD.

Corneal Dystrophies, Hereditary↗