[Diagnosis and prognosis of systemic juvenile rheumatoid arthritis].
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Arthritis, Juvenile↗
Biomedical subjects
Min Wei
Publications and source records attributed to Min Wei.
[Surgical correction of orbital and periorbital deformities using lamella and complex osteotomies].
OBJECTIVE: To investigate surgical correction of orbital and periorbital deformities in orbital and periorbital region. METHODS: In order to reconstruct orbital deformities such as orbital hypertelorism, orbital dystopia, radiated orbit, and secondary deformities of traumatic orbit, lamella osteotomies of either orbital rim and wall or complex osteotomies of both adjacent orbital rims and walls using bicoronal or galea aponeurotica incision were employed. The reconstructed complex was placed in new position with rigid fixation. Clinic evaluations were performed before and after operative osteotomies such as cephalometry (measurement of interorbital distance, IOD), exophthalmos (measurement with Hetel exophthalmometer), the angle (between orbital horizontal level and bilateral tragus linkage, A-OT), and the linear distance (between lateral canthus and tragus, LC-T), then the gap differences were analyzed before and after operation. RESULTS: Nearly normal orbital volumes, better contour of orbit and midface, improved eyelids and visions were achieved in total 44 cases. There were 5 cases of supraorbital osteotomy (intracranial routine), 8 cases of medial orbital osteotomy, 3 cases of inferior orbital osteotomy, and 28 cases of both lateral and inferior orbital osteotomy in these series. No complications were found after surgery. The orbital and midfacial appearances were improved significantly. CONCLUSIONS: Lamella and complex osteotomies of orbital rim and wall are proved to be safe and effective to correct most deformities of orbital and periorbital region and various kinds of orbital malposition.
Adolescent↗
[Changes of vasoactive factors in lung tissue of newborn piglets with persistent pulmonary hypertension and effect of magnesium sulphate].
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Angiotensins↗
Cisplatin sensitivity in Hmbg1-/- and Hmbg1+/+ mouse cells.
The study presented here investigates the effect of HMGB1 knockout on the sensitivity of mouse embryonic fibroblasts treated with the anticancer drug cisplatin. We evaluated both the growth inhibition by cisplatin and cisplatin-induced cell death in the Hmgb1(-/-) cells and its wild-type counterpart. No significant differences were observed in the responses of these cells to cisplatin, indicating that HMGB1 does not play a significant role in modulating the cellular responses to cisplatin in this context. Since HMGB1 significantly enhances the cytotoxicity of cisplatin in other cells, these results illustrate the importance of cell type in determining the ability of this and probably other cisplatin-DNA-binding proteins to influence the efficacy of the drug.
Animals↗
Peroxynitrite mediates neurotoxicity of amyloid beta-peptide1-42- and lipopolysaccharide-activated microglia.
The amyloid beta-peptide (Abeta) activates microglia and promotes the generation of cytokines and oxygen species, including nitric oxide (NO) and tumor necrosis factor alpha (TNF-alpha), which can be either neurotoxic or neuroprotective. We show that neuron death in cocultures of rat cortical microglia and neurons activated by lipopolysaccharide (LPS) or Abeta1-42 plus interferon gamma (IFNgamma) is caused by short-lived diffusible molecules and follows the generation of superoxide and/or peroxynitrite as determined by electron paramagnetic spectroscopy. Neurotoxicity induced by LPS or Abeta1-42 plus IFNgamma is blocked by inhibitors of NO synthesis and by the peroxynitrite (ONOO-) decomposition catalysts FeTMPyP [5,10,15,20-tetrakis(n-methyl-4'-pyridyl)porphinato iron (III) chloride] and FeTPPS [5,10,15,20-tetrakis(4-sulfonatophenyl)prophyrinato iron (III) chloride] but not by the TNF-alpha inhibitor pentoxifylline. The specificity of FeTMPyP for ONOO- was confirmed by its ability to block the toxicity of a peroxynitrite donor but not of NO donors or of high levels of superoxide in a yeast mutant lacking superoxide dismutase 1. These results implicate peroxynitrite as a mediator of the toxicity of activated microglia, which may play a major role in Abeta1-42 neurotoxicity and Alzheimer's disease.
Amyloid beta-Peptides↗
Pyruvate site of pyruvate phosphate dikinase: crystal structure of the enzyme-phosphonopyruvate complex, and mutant analysis.
Crystals of pyruvate phosphate dikinase in complex with a substrate analogue inhibitor, phosphonopyruvate (K(i) = 3 microM), have been obtained in the presence of Mg(2+). The structure has been determined and refined at 2.2 A resolution, revealing that the Mg(2+)-bound phosphonopyruvate binds in the alpha/beta-barrel's central channel, at the C-termini of the beta-strands. The mode of binding resembles closely the previously proposed PEP substrate binding mode, inferred by the homology of the structure (but not sequence homology) to pyruvate kinase. Kinetic analysis of site-directed mutants, probing residues involved in inhibitor binding, showed that all mutations resulted in inactivation, confirming the key role that these residues play in catalysis. Comparison between the structure of the PPDK-phosphonopyruvate complex and the structures of two complexes of pyruvate kinase, one with Mg(2+)-bound phospholactate and the other with Mg(2+)-oxalate and ATP, revealed that the two enzymes share some key features that facilitate common modes of substrate binding. There are also important structural differences; most notably, the machinery for acid/base catalysis is different.
Amino Acid Substitution↗
Neostigmine-induced alterations in fast phase of optokinetic responses in myasthenic ocular palsies.
Closed-loop and open-loop optokinetic nystagmus (OKN) eye movements were recorded with an electromagnetic scleral search coil in 16 patients with myasthenic ocular palsies, 8 patients with nonmyasthenic ocular palsies, and 4 normal controls. We calculated the summation of fast-phase amplitude per second (SFPAps), mean of fast-phase amplitude (MFPA) and mean of fast-phase peak velocity (MFPV) of OKN before and after administration of neostigmine. Under open-loop conditions, the myasthenic patients group demonstrated distinct increases in three parameters: SFPAps (P < 0.000001), MFPA (P < 0.001) and MFPV (P < 0.001) following neostigmine injection, and the increase in SFPAps was greater than those of MFPA and MFPV (P < 0.02), while the other two groups showed no significant increases. Under closed-loop condition, only five of the myasthenic patients showed significant changes. These results suggest that the change in SFPAps during open-loop OKN before and after neostigmine administration was a specific measurement that differentiated patients with myasthenic ocular palsies from the other groups.
Adolescent↗
DNA damage repair in bladder urothelium after the Chernobyl accident in Ukraine.
PURPOSE: We determined whether base and nucleotide excision repair is activated in bladder urothelium by chronic persistent low doses of ionizing radiation in male patients with benign prostate hyperplasia and females with chronic cystitis living more than 15 years in Cs contaminated areas after the Chernobyl accident in Ukraine. MATERIALS AND METHODS: Bladder urothelial biopsies from 204 patients were subjected to histological examination and biopsies from 35 were subjected to immunohistochemical study of 8-hydroxy-2'deoxyguanosine, 8-oxoguanine-DNA-glycosylase, apurinic/apyrimidinic endonuclease and xeroderma pigmentosum A endonuclease. RESULTS: Chronic proliferative atypical cystitis with multiple foci of dysplasia and carcinoma in situ were observed in 139 (89%) and in 91 (58%) of 156 group 1 patients from radio contaminated areas, respectively, as well as 10 small transitional cell carcinomas. Chronic cystitis with areas of dysplasia was detected in 9 of 48 patients (19%) in control group 2 from clean (without radio contamination) areas of Ukraine. Greatly elevated levels of 8-hydroxy-2'deoxyguanosine, 8-oxoguanine-DNA-glycosylase, apurinic/apyrimidinic endonuclease and xeroderma pigmentosum A were evident in the urothelium in group 1, accompanied by increased Cs in the urine. CONCLUSIONS: These findings support the hypothesis that significant activation of DNA damage repair (base and nucleotide excision repair) is induced by the oxidative stress generated by long-term low doses of ionizing radiation. The levels of DNA oxidative adducts pointing to mutagenic and carcinogenic potential were in line with the histopathologically diagnosed urothelial lesions.
8-Hydroxy-2'-Deoxyguanosine↗
Carcinogenicity of dimethylarsinic acid in male F344 rats and genetic alterations in induced urinary bladder tumors.
Arsenic is a well-documented human carcinogen, and contamination with this heavy metal is of global concern, presenting a major issue in environmental health. However, the mechanism by which arsenic induces cancer is unknown, in large part due to the lack of an appropriate animal model. In the present set of experiments, we focused on dimethylarsinic acid (DMA), a major metabolite of arsenic in most mammals including humans. We provide, for the first time, the full data, including detailed pathology, of the carcinogenicity of DMA in male F344 rats in a 2-year bioassay, along with the first assessment of the genetic alteration patterns in the induced rat urinary bladder tumors. Additionally, to test the hypothesis that reactive oxygen species (ROS) may play a role in DMA carcinogenesis, 8-hydroxy-2'-deoxyguanosine (8-OHdG) formation in urinary bladder was examined. In experiment 1, a total of 144 male F344 rats at 10 weeks of age were randomly divided into four groups that received DMA at concentrations of 0, 12.5, 50 and 200 p.p.m. in the drinking water, respectively, for 104 weeks. From weeks 97-104, urinary bladder tumors were observed in 8 of 31 and 12 of 31 rats in groups treated with 50 and 200 p.p.m. DMA, respectively, and the preneoplastic lesion, papillary or nodular hyperplasias (PN hyperplasia), was noted in 12 and 14 rats, respectively. DMA treatment did not cause tumors in other organs and no urinary bladder tumors or preneoplastic lesions were evident in the 0 and 12.5 p.p.m.-treated groups. Urinary levels of arsenicals increased significantly in a dose-responsive manner except for arsenobetaine (AsBe). DMA and trimethylarsine oxide (TMAO) were the major compounds detected in the urine, with small amounts of monomethylarsonic acid (MMA) and tetramethylarsonium (TeMa) also detected. Significantly increased 5-bromo-2'-deoxyuridine (BrdU) labeling indices were observed in the morphologically normal epithelium of the groups treated with 50 and 200 p.p.m. DMA. Mutation analysis showed that DMA-induced rat urinary bladder tumors had a low rate of H-ras mutations (2 of 20, 10%). No alterations of the p53, K-ras or beta-catenin genes were detected. Only one TCC (6%) demonstrated nuclear accumulation of p53 protein by immunohistochemistry. In 16 of 18 (89%) of the TTCs and 3 of 4 (75%) of the papillomas, decreased p27(kip1) expression could be demonstrated. Cyclin D1 overexpression was observed in 26 of 47 (55%) PN hyperplasias, 3 of 4 (75%) papillomas, and 10 of 18 (56%) TCCs. As a molecular marker of oxidative stress, increased COX-2 expression was noted in 17 of 18 (94%) TCCs, 4 of 4 (100%) papillomas, and 39 of 47 (83%) PN hyperplasias. In experiment 2, 8-OHdG formation in urinary bladder was significantly increased after treatment with 200 p.p.m. DMA in the drinking water for 2 weeks compared with the controls. The studies demonstrated DMA to be a carcinogen for the rat urinary bladder and suggested that DMA exposure may be relevant to the carcinogenic risk of inorganic arsenic in humans. Diverse genetic alterations observed in DMA-induced urinary bladder tumors imply that multiple genes are involved in stages of DMA-induced tumor development. Furthermore, generation of ROS is likely to play an important role in the early stages of DMA carcinogenesis.
8-Hydroxy-2'-Deoxyguanosine↗
Lack of a dose-response relationship for carcinogenicity in the rat liver with low doses of 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline or N-nitrosodiethylamine.
For a long period, it has been generally considered that carcinogens, particularly genotoxic ones, have no threshold in exerting their potential for cancer induction. However, the non-threshold theory can be challenged with regard to assessment of cancer risk to humans. Here we show that a food-derived, genotoxic hepatocarcinogen, 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline, forms DNA adducts at low doses, but does not induce glutathione S-transferase placental form (GST-P)-positive foci (considered to be preneoplastic lesions) or 8-hydroxy-2'-deoxyguanosine in rat liver. Moreover a N-nitroso compound, N-nitrosodiethylamine, at low doses was also found not to induce GST-P-positive foci in rat liver. These results imply that there is a no-observed effect level for hepatocarcinogenesis by these genotoxic carcinogens.
Animals↗
Motor scaling by viewing distance of early visual motion signals during smooth pursuit.
The geometry of gaze stabilization during head translation requires eye movements to scale proportionally to the inverse of target distance. Such a scaling has indeed been demonstrated to exist for the translational vestibuloocular reflex (TVOR), as well as optic flow-selective translational visuomotor reflexes (e.g., ocular following, OFR). The similarities in this scaling by a neural estimate of target distance for both the TVOR and the OFR have been interpreted to suggest that the two reflexes share common premotor processing. Because the neural substrates of OFR are partly shared by those for the generation of pursuit eye movements, we wanted to know if the site of gain modulation for TVOR and OFR is also part of a major pathway for pursuit. Thus, in the present studies, we investigated in rhesus monkeys whether initial eye velocity and acceleration during the open-loop portion of step ramp pursuit scales with target distance. Specifically, with visual motion identical on the retina during tracking at different distances (12, 24, and 60 cm), we compared the first 80 ms of horizontal pursuit. We report that initial eye velocity and acceleration exhibits either no or a very small dependence on vergence angle that is at least an order of magnitude less than the corresponding dependence of the TVOR and OFR. The results suggest that the neural substrates for motor scaling by target distance remain largely distinct from the main pathway for pursuit.
Acceleration↗
Estradiol (E2) enhances neurite outgrowth by repressing glial fibrillary acidic protein expression and reorganizing laminin.
Neuronal remodeling in response to deafferenting lesions in the brain can be enhanced by estradiol (E2). Astrocytes are among the targets of E2 in complex interactions with neurons and may support or inhibit neuronal remodeling. In ovariectomized female rats given entorhinal cortex lesions, E2 replacement inhibited the increase of glial fibrillary acidic protein (GFAP) protein. To model the role of E2 in these complex processes, we used the "wounding-in-a-dish" of astrocyte-neuron cocultures. Low physiological E2 (1 pM) blocks the wound-induced increase of GFAP expression (transcription and protein) and enhances neurite outgrowth. The transcriptional responses to E2 during wounding are mediated by sequences in the 5'-upstream region of the rat GFAP promoter. Concurrently, E2 reorganized astrocytic laminin into extracellular fibrillar arrays, which others have shown support neurite outgrowth. The inhibition of GFAP expression by E2 in this model is consistent with in vivo findings that E2 enhanced recovery from deafferenting cortical lesions by increased neurite outgrowth in association with decreased GFAP expression. More generally, we hypothesize that physiological variations in E2 levels modulate neuronal plasticity through direct effects on GFAP transcription that, in turn, modify GFAP-containing intermediate filaments and reorganize astrocytic laminin.
Animals↗
[Orbital volume measurement of enophthalmos of orbital blowout fractures].
OBJECTIVE: To measure the volumetric changes of enophthalmos of orbital blowout fractures, and to study the relation between the change of the orbital volume and the degree of enophthalmos. METHODS: In 16 patients with enophthalmos of orbital blowout fractures, the measurement of orbital volume was carried out during 3 months to 2 years after injury by using the computed tomography (CT), computer image processing and computer orbital three-dimensional measuring method. The relation between the orbital volume discrepancy and enophthalmos was assessed by using Pearson correlation coefficients. RESULTS: There were significant linear correlation between the increment of the orbital volume and the degree of enophthalmos (r = 0.95, P < 0.001), with each 1.0 cm(3) increment in bony volume causing approximately 0.9 mm of enophthalmos. CONCLUSIONS: Orbital blowout fractures can expand the orbital volume. The measurement of orbital volume may predict the risk and the final degree of the enophthalmos at the late stage, thus it may provide useful information in surgical intervention to estimate the size and volume of the orbital implant for an individual case.
Adolescent↗
Effect of glucocorticoid treatment on insulin like growth factor-I and its binding proteins in children with nephrotic syndrome.
OBJECTIVE: To identify the changes in serum insulin like growth factor-I (IGF-I) and IGF binding proteins (IGFBPs) in children with nephrotic syndrome (NS) and the effect of glucocorticoid on serum IGF-I and IGFBPs. METHODS: We measured serum IGF-I and IGFBPs levels by radioimmune assay and immune radiomagnetic assay in 36 children with NS, consisting of an active stage group (ANS, n = 12), a remission stage group (RE, n = 12), an active stage group with glucocorticoid treatment (GNS, n = 12), and a normal control group (NC, n = 10). RESULTS: 1) Compared to NC, serum levels of IGF-I and IGFBP-3 were decreased (P < 0.01); serum levels of IGFBP-1 and IGFBP-2 were increased (P < 0.01) in the ANS group. 2) Serum levels of IGF-I and IGFBP-3 were higher and IGFBP-1 and IGFBP-2 were lower in the RE Group than in theANS Group (P < 0.01). 3) Compared to the ANS group, serum levels of IGF-I and IGFBP-3 were increased (P < 0.01) and serum levels of IGFBP-1 and IGFBP-2 were decreased (P < 0.01) in the GNS group. 4) A correlation was found between serum levels of IGFBP-3 and albumin in the active stage group (r = 0.76, P < 0.01). There was also a correlation between serum levels of IGF-I and IGFBP-3 and an inverse correlation between the serum level of IGF-I and serum levels of IGFBP-1 and IGFBP-2 in the ANS group. No other correlations were observed. CONCLUSIONS: The serum levels of IGF-I and IGFBPs are altered in children in the active stage of NS, but return to normal in the remission stage. GC treatment may influence serum IGF-I and IGFBPs in children with NS. Changes in IGF-I and IGFBPs levels may play a role in the growth retardation of NS children.
Child↗
[Proliferation and denucleation of K562 cells induced by cytochalasin B].
OBJECTIVE: To observe the effect of cytochalasin B on the denucleation of K562 cells. METHODS: K562 cells were grown in RPMI 1640 medium supplemented with 10% calf serum and 4 microL cytochalasin B (CB). Denucleation was induced in the cultured cells by CB, and the cells were examined by phase contrast microscopy and Giemsa staining respectively. RESULTS: The denucleation of K562 cells induced by CB was clearly observed, and the cell proliferation was obviously inhibited. CONCLUSION: The denucleation efficiency of K562 cells is positively correlated with CB concentrations and the duration of CB treatment. CB at low doses may inhibit the cell proliferation and at high doses causes cell death.
Cell Division↗
Effect of high-lipid diet on glomerular mesangial matrix in adriamycin-induced nephrotic rats.
OBJECTIVE: To determine the effect of hypercholsterolemia induced by a high-lipid diet on glomerulosclerosis. METHODS: Twenty nephrotic syndrome (NS) Wistar rats administrated adriamycin (ADR) with a single intravenous dose of 5 mg/kg body weight, were divided into the standard and high-lipid chow groups. Another 20 weight-matched non-NS rats that received a vehicle alone were grouped as control. Urinary protein excretion and serum cholesterol were assayed; image analysis and techniques of pathology, immunohistochemistry, and molecular biology were used to determine morphological changes in glomeruli and the production of glomerular mesangial matrices in different groups. RESULTS: The serum total cholesterol level was significantly higher in rats with high-lipid chow in both non-NS [(2.2 +/- 0.3) g/L vs. (0.9 +/- 0.1) g/L, P < 0.01] and NS [(9.5 +/- 0.2) g/L vs. (2.3 +/- 0.3) g/L, P < 0.01]. The urinary protein excretion was significantly higher in the high-lipid diet rats than in standard chow rats [(76.2 +/- 24.2) mg/24h vs. (44.8 +/- 13.6) mg/24h, P < 0.05] in NS rats. Although increases in the mesangial matrix and mesangial cells were observed in rats with high-lipid diet in both NS and non-NS group, more obvious pathological changes were found in NS group, such as lipid deposits and foam cell formation in mesangial areas, and progressing to focal and segmental glomerulosclerosis in some glomeruli. The immunohistochemical asay showed that the production of 3 major components (collagen IV, fibronectin, and laminin) was increased in NS group, especially in the rats with high-lipid chow. The increased expression of laminin mRNA was also detected with slot blotting in both NS and non-NS rats with high-lipid chow, and it was more obvious in the rats with NS. CONCLUSION: Our findings indicated that diet-induced hyperlipidemia can lead to over-production of mesangial matrix components, and further aggravate glomerulosclerosis in ADR-induced nephrosis.
Animals↗
Formation of and coalescence from the inclusion complex of a biodegradable block copolymer and alpha-cyclodextrin. 2: A novel way to regulate the biodegradation behavior of biodegradable block copolymers.
A biodegradable block copolymer (PCL-b-PLLA, M(n) = 1.72 x 10(4), M(w)/M(n) = 1.37) of poly(epsilon-caprolactone) (PCL) and poly(L-lactide) (PLLA) with very low crystallinity was obtained by forming the inclusion complex between alpha-cyclodextrin molecules and PCL-b-PLLA followed by coalescence of the guest polymer chains. Films of the as-synthesized and coalesced copolymer samples, PCL and PLLA homopolymers of approximately the same chain lengths as the corresponding blocks of PCL-b-PLLA, and a physical blend of PCL/PLLA homopolymers with the same molar composition as PCL-b-PLLA were prepared by melt-compression molding between Teflon plates. Subsequently, the in vitro biodegradation behavior of these films was studied in phosphate buffer solution containing lipase from Rhizopus arrhizus, by means of ultraviolet spectra, attenuated total reflectance FTIR spectra, differential scanning calorimetry, wide-angle X-ray diffraction measurements, and weight loss analysis. PCL segments were found to degrade much faster than PLLA segments, both in the pure state and in copolymer or blend samples. Consistent with our expectation, suppression of the phase separation, as well as a decrease of crystallinity, in the coalesced copolymer sample led to a much faster enzymatic degradation than that of either as-synthesized copolymer or the PCL/PLLA physical blend sample, especially during the early stages of biodegradation. Thus the biodegradation behavior of biodegradable block copolymers, which is of decisive importance in drug delivery and controlled release systems, may be regulated by the novel and convenient means recently reported by us.(1)
Biocompatible Materials↗
Melting and crystallization behaviors of biodegradable polymers enzymatically coalesced from their cyclodextrin inclusion complexes.
Inclusion complexed (IC) and coalesced biodegradable poly(epsilon-caprolactone) (PCL), poly(L-lactic acid) (PLLA), and their diblock copolymer (PCL-b-PLLA) were achieved by forming ICs between host alpha-cyclodextrin(alpha-CD) and guest PCL, PLLA, and PCL-b-PLLA, followed by removing the alpha-CD host with an amylase enzyme. FTIR spectra of the coalesced polymers reveal that the host alpha-CD can be completely removed, without polymer degradation, by treatment with an amylase enzyme. The melting and crystallization behavior of these CD-IC treated polymers, which are crystallizable, biodegradable, and bioabsorbable, are investigated by differential scanning calorimetry (DSC) and polarized optical microscopy. Results show that coalescence increased the crystallinities of the homopolymers but decreased that of the diblock copolymer. The Avrami exponent (n), derived from both isothermal and nonisothermal crystallization models for homo-PCL and -PLLA and the PCL and PLLA blocks in the diblock copolymer samples coalesced from their ICs, is close to 4, indicating homogeneous crystallization, whereas crystallization of the blocks in the as-synthesized diblock copolymer yields an Avrami exponent around 3, indicating heterogeneous crystallization. All of these results demonstrate that the PCL and PLLA homopolymers and blocks in the IC-coalesced samples are more readily and homogeneously crystallized than those in the as-synthesized samples or their physical blend, even though the level of crystallinity in the IC-coalesced diblock copolymer is significantly lower. Moreover, unlike the as-synthesized diblock copolymer, the crystallization of PCL and PLLA blocks in the IC-coalesced diblock copolymer are not influenced by their covalent connection.
Biodegradation, Environmental↗