[Improve the quality of glaucoma surgery].
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Filtering Surgery↗
Biomedical subjects
M Li
Publications and source records attributed to M Li.
[Three-dimensional volumetric display--a new application of frequency up-conversion].
This paper discusses the present research situation and the application prospect of 3-D volumetric display technology. The possible usability and science significance of frequency up-conversion in 3-D volumetric display field are also demonstrated systematically. In ZBLAN: Pr, Yb glasses, we primarily demonstrated and achieved a new application of frequency up-conversion three dimensional volumetric display, using the two-frequency up-conversion of the rare earth ions. The efficiency of luminescence of Pr was enhanced much by the energy transfer between Pr and Yb ions.
English Abstract↗
[Simultaneous determination of germanium and molybdenum in mixtures by complexation with 5'-nitrosalicyfluorone and dual-wavelength standard addition spectrophotometry].
In the presence of hexadecyltrimethylammonium bromide and in a medium of 0.3-0.9mol/L sulfuric acid, germanium (IV) and molybdenum (VI) react with 2,6,7-trihydroxy-9 (2'-hydroxy-5'-nitro) phenylfluorone-3, i.e., 5'-nitrosalicyfluorone, to develop red complexes, respectively. The spectra of the two complexes overlap seriously each other, and the additivity of their absorbances is good in the wavelength range of 490-548nm. So a new method for simultaneous spectrophotometric determination of germanium and molybdenum by dual-wavelegth standard addition method has been investigated in detail. The analytical results of five standard mixtures are more accuracy than those obtained by isobestic-point dual-wavelength method. The method has been applied to the analysis of traditional chinese medicine and mineral water with satisfactory results.
Drugs, Chinese Herbal↗
[Indirect sensitized upconversion in Tm3+ and Yb3+ codoped non-crystal pentaphosphate].
We report the blue upconversion luminescence of Tm3+ and Yb3+ codoped non-crystal pentaphosphate pumped by -798nm laser diode. The samples were directly excited to 3F4 level of Tm3+ ion. Two energy transfer processes between Tm3+ and Yb3+ contribute mainly to the population of 1G4 level of Tm3+. Phonon plays an important role in the upconversion process.
English Abstract↗
An evaluation of the Factor V Leiden mutation in a cohort of African-American pregnant women.
The objective of this work was to study the prevalence of the Factor V Leiden mutation in an obstetrical clinic largely comprised of African-American women. A cross-sectional study was performed evaluating a total of 231 consecutive women of African-American origin. Of these patients, 21 were considered at high risk for thrombosis, but none was found to carry the mutation. One patient (0.4 per cent) of the total was heterozygous for the Factor V Leiden mutation. African-American women do not appear to be at an increased risk of being heterozygous or homozygous for the Leiden mutation. This low prevalence may be confounded by ascertainment bias in a population of pregnant women.
Black People↗
Overgrowth syndromes and genomic imprinting: from mouse to man.
Beckwith-Wiedemann syndrome (BWS), a human overgrowth syndrome with a complex genetic basis, is caused by alterations to chromosome 11p15, a region subject to genomic imprinting. These alterations include translocations, duplications, single gene mutations of p57KIP2, and increased expression of insulin-like growth factor 2 (IGF2). A phenotypically related X-linked overgrowth syndrome, Simpson Golabi Behmel syndrome (SGBS), is caused by alterations in glypican-3 (GPC3), a molecule that may interact with the gene products identified to be important in generating the BWS phenotype, that is, IGF2 and p57KIP2. The crucial defect in these overgrowth syndromes is likely to be an imbalance in contributions of growth-promoting genes versus growth-inhibitory genes in critical tissues at specific developmental stages. Murine models have been used to study the effects of targeted deletions of the genes p57KIP2 and GPC3, as well as overexpression of IGF2. At this time, there are still many issues which remain to be explored before we can fully understand the molecular basis of BWS and SGBS.
Animals↗
Use of single dose low-molecular-weight heparin in long hemodialysis.
Low-molecular-weight (LMW) heparin has recently been used for anti-coagulation in maintenance hemodialysis. The LMW heparin was administered as a single bolus in hemodialysis that usually lasted for four hours or less. The regimen for administering LMW heparin in hemodialysis of longer duration (5 hours or more) is not well documented and manufacturers recommend a supplementary dose equivalent to one-quarter of the initial dose to be given at 4 hours after the commencement of hemodialysis. In this study, we explored whether administering a single dose of LMW heparin is feasible in hemodialysis of longer duration. Maintenance five-hour hemodialysis sessions were performed in nine uremic patients with two different heparin regimens: single dose of LMW heparin (nadroparin) 12,500 ICU AXa at the beginning of dialysis or a priming dose of nadroparin 10,000 ICU AXa at the beginning of dialysis followed by a supplementary dose of nadroparin 2,500 ICU AXa at the beginning of the fifth hour of dialysis. Clots in the airtraps or clotting of the dialyser were not observed in hemodialysis with the single dose heparin regimen. The anti-Xa activities at different time intervals during dialysis were above the therapeutic range of 0.5 U/ml except towards the end of the hemodialysis treatment. There was no difference between anti-Xa activities determined in dialysis sessions using two different regimens of LMW heparin at any individual time interval. The anti-thrombotic effect determined by the area under the time response curve for anti-Xa activity was comparable in the two LMW heparin regimens. Hence, our findings suggest a single bolus dose of LMW heparin (nadroparin) at 12,500 ICU AXa provides adequate, safe, and effective anti-coagulation for five-hour hemodialysis. This practice is convenient and avoids the necessity of administering a double dose of LMW heparin.
Adult↗
Decreased benzodiazepine binding with little effect on gamma-aminobutyric acid binding in rat brain after treatment with antisense oligodeoxynucleotide to the gamma-aminobutyric acidA receptor gamma-2 subunit.
Benzodiazepine potentiation of gamma-aminobutyric acid (GABA) neurotransmission is associated with the presence of a gamma-2 subunit in the GABAA receptor. A method was developed to modify the gamma-2 subunit expression in adult rat brain. Unilateral intracerebroventricular (i.c.v.) infusion of a 17-base phosphorothioate-modified antisense oligodeoxynucleotide (ASO) was performed every 12 hr for 3 days. Controls were treated with a sense oligodeoxynucleotide. Parasagittal brain sections were used for quantitative autoradiographic analysis of radioligand binding. ASO treatment caused a 15% to 25% decrease of specific [3H]flunitrazepam binding in most brain areas, with statistically significant decreases in frontal cortex, cerebellar molecular layer, zona reticulata of substantia nigra and CA3 of hippocampus. In contrast, [3H]muscimol binding was not changed. [3H]GABA binding was also unchanged, except for a 10% decrease in cerebellar granule cell layer. The effect on the chloride channel of the GABAA receptor complex was examined by 4'-ethynyl-4-n-[2, 3-3H2]propylbicycloorthobenzoate binding; most brain areas showed small decreases in 4'-ethynyl-4-n-[2, 3-3H2]propylbicycloorthobenzoate binding. However, hippocampal regions showed much larger decreases. Binding of the adenosine A1 receptor antagonist [3H]8-cyclopentyl-1,3-dipropylxanthine was used to examine possible secondary effects of the ASO. There was a decrease in [3H]8-cyclopentyl-1,3-dipropylxanthine binding, but this was much smaller than the change in [3H]flunitrazepam binding, and no area showed a significant effect. Quantitative immunoblotting with a monoclonal antibody that recognizes GABAA receptor beta-2 and beta-3 subunits showed no change in immunoreactivity in cerebellar tissue after ASO treatment. The results indicate a selective effect on benzodiazepine binding to GABAA receptors and a possible change in receptor subunit composition.
Animals↗
Structure of the mouse leukaemia inhibitory factor receptor gene: regulated expression of mRNA encoding a soluble receptor isoform from an alternative 5' untranslated region.
The low-affinity leukaemia inhibitory factor receptor (LIF-R) is a component of cell-surface receptor complexes for the multifunctional cytokines leukaemia inhibitory factor, ciliary neurotrophic factor, oncostatin M and cardiotrophin-1. Both soluble and transmembrane forms of the protein have been described and several LIF-R mRNAs have been reported previously. In order to determine the coding potential of LIF-R mRNAs we have isolated and characterized the mouse LIF-R gene. mRNA encoding soluble LIF-R (sLIF-R) is formed by inclusion of an exon in which polyadenylation signals are provided by a B2 repeat. This exon is located centrally within the LIF-R gene but is excluded from the transmembrane LIF-R mRNA by alternative splicing. The transmembrane receptor is encoded by 19 exons distributed over 38 kb. Two distinct 5' non-coding exons have been identified, indicating the existence of alternative promoters. One of these is G/C rich and possesses a consensus initiator sequence as well as potential Sp1 binding sites. Expression of exon 1 from this promoter occurs in a wide variety of tissues, whereas expression of the alternative 5' untranslated region (exon 1a) is normally restricted to liver, the principal source of sLIF-R. During pregnancy expression of exon 1a becomes detectable also in the uterus. Expression of exon 1a increases dramatically during gestation and is accompanied by a similar quantitative rise in expression of sLIF-R mRNA. These findings establish that expression of LIF-R is under complex transcriptional control and indicate that regulated expression of the soluble cytokine receptor isoform may be due principally to an increase in the activity of a dedicated promoter.
Animals↗
A Schwann cell mitogen accompanying regeneration of motor neurons.
Motor neurons are the only adult mammalian neurons of the central nervous system to regenerate following injury. This ability is dependent on the environment of the peripheral nerve and an intrinsic capacity of motor neurons for regrowth. We report here the identification, using a technique known as messenger RNA differential display, of an extracellular signalling molecule, previously described as the pancreatic secreted protein Reg-2, that is expressed solely in regenerating and developing rat motor and sensory neurons. Axon-stimulated Schwann cell proliferation is necessary for successful regeneration, and we show that Reg-2 is a potent Schwann cell mitogen in vitro. In vivo, Reg-2 protein is transported along regrowing axons and inhibition of Reg-2 signalling significantly retards the regeneration of Reg-2-containing axons. During development, Reg-2 production by motor and sensory neurons is regulated by contact with peripheral targets. Strong candidates for peripheral factors regulating Reg-2 production are cytokines of the LIF/CNTF family, because Reg-2 is not expressed in developing motor or sensory neurons of mice carrying a targeted disruption of the LIF receptor gene, a common component of the receptor complexes for all of the LIF/CNTF family.
Animals↗
Wound healing is accelerated by agonists of adenosine A2 (G alpha s-linked) receptors.
The complete healing of wounds is the final step in a highly regulated response to injury. Although many of the molecular mediators and cellular events of healing are known, their manipulation for the enhancement and acceleration of wound closure has not proven practical as yet. We and others have established that adenosine is a potent regulator of the inflammatory response, which is a component of wound healing. We now report that ligation of the G alpha s-linked adenosine receptors on the cells of an artificial wound dramatically alters the kinetics of wound closure. Excisional wound closure in normal, healthy mice was significantly accelerated by topical application of the specific A2A receptor agonist CGS-21680 (50% closure by day 2 in A2 receptor antagonists. In rats rendered diabetic (streptozotocin-induced diabetes mellitus) wound healing was impaired as compared to nondiabetic rats; CGS-21680 significantly increased the rate of wound healing in both nondiabetic and diabetic rats. Indeed, the rate of wound healing in the CGS-21680-treated diabetic rats was greater than or equal to that observed in untreated normal rats. These results appear to constitute the first evidence that a small molecule, such as an adenosine receptor agonist, accelerates wound healing in both normal animals and in animals with impaired wound healing.
Adenosine↗
Cre-mediated gene deletion in the mammary gland.
To delete genes specifically from mammary tissue using the Cre-lox system, we have established transgenic mice expressing Cre recombinase under control of the WAP gene promoter and the MMTV LTR. Cre activity in these mice was evaluated by three criteria. First, the tissue distribution of Cre mRNA was analyzed. Second, an adenovirus carrying a reporter gene was used to determine expression at the level of single cells. Third, tissue specificity of Cre activity was determined in a mouse strain carrying a reporter gene. In adult MMTV-Cre mice expression of the transgene was confined to striated ductal cells of the salivary gland and mammary epithelial cells in virgin and lactating mice. Expression of WAP-Cre was only detected in alveolar epithelial cells of mammary tissue during lactation. Analysis of transgenic mice carrying both the MMTV-Cre and the reporter transgenes revealed recombination in every tissue. In contrast, recombination mediated by Cre under control of the WAP gene promoter was largely restricted to the mammary gland but occasionally observed in the brain. These results show that transgenic mice with WAP-Cre but not MMTV-Cre can be used as a powerful tool to study gene function in development and tumorigenesis in the mammary gland.
Adenoviridae↗
Expression of beta2-thyroid hormone receptor in euthyroid and hypothyroid rat pituitary gland: an in situ hybridization and immunocytochemical study.
Recently, we have shown an extended distribution pattern of the TR-beta2 isoform in specific sites of rat brain which may be indicative that the localization of this receptor also confers functional specificity. The beta2 thyroid hormone receptor (TR-beta2) is by far the most abundant isoform in the pituitary, although transcripts of TR-alpha and TR-beta1 genes have been reported in developmental and adult rat pituitary gland. Using both in situ hybridization histochemistry (ISH) and immunocytochemistry, we mapped the expression of beta2 thyroid hormone receptor mRNA and protein in euthyroid and hypothyroid adult rat pituitary, particularly in relation to the thyrotrope population. TR-beta2 mRNA localization by ISH showed an anteromedial spatial distribution pattern in euthyroid rat anterior pituitary gland. This localization coincided with the immunostaining pattern for thyrotropes. TR-beta2-immunoreactive cells showed strongly positive signals in the nuclei. Hypothyroidism, induced by propylthiouracil (PTU), abolished the specific localization of TR-beta2 mRNA and upregulated the transcription of TR-beta2 mRNA in vivo and in vitro. Image analysis revealed that the optical density signals within hypothyroid rat pituitary were significantly stronger (2.6-fold) compared with euthyroid counterparts. This correlated strongly with an increased number and staining of TR-beta2 protein positive cells, demonstrating both nuclear and cytoplasmic staining. In response to thyroid hormone deficiency, there was also a marked percentage increase in the thyrotrope population from 10 to 20% of anterior pituitary cells to approximately 80%. In conclusion, these results demonstrate the specific localization of TR-beta2 to the anterior pituitary, especially to the thyrotrope population, and its regulation by thyroid hormone. Hypothyroidism leads to an upregulation of TR-beta2 mRNA and protein in the anterior pituitary, explained not only by an absolute increase in the percentage of thyrotropes but increased expression of TR-beta2 mRNA and protein per cell. These data allude to the TR-beta2 isoform playing a critical role in thyroid hormone-dependent TSH gene expression, although contributions from the other TR isoforms may still remain important.
Animals↗
Transcriptional regulation of OCI-5/Glypican 3: elongation control of confluence-dependent induction.
OCI-5/Glypican 3, a member of the glypican family of proteoglycans, is the defective gene in the Simpson-Golabi-Behmel overgrowth syndrome. OCI-5 expression is developmentally regulated in the intestinal epithelium, and the mechanism of its regulation was studied in the rat intestinal epithelial cell line IEC-18. A large induction of OCI-5 transcript and protein was observed at high cell density. Among other glypican family members, kappa-glypican also exhibited a confluence-dependent induction in select cell types. Nuclear run-on analysis indicated that cell-density regulation of OCI-5 occurs at the level of transcription. The rat and mouse OCI-5 promoters were cloned and found to be highly conserved, located within CpG islands and contain regions of alternating purine and pyrimidine residues. No TATA-box or recognizable INR element was observed. Consensus binding sites for AP-2, SP-1, zeste and NF-1/CTF are conserved across human, mouse and rat promoters. 5' deletion mapping of the rat promoter identified regions which enhance and repress promoter activity, with no apparent confluence-dependence or tissue-specificity. Nuclear run-on analysis probing different regions of the gene suggests that elongation control plays a role in the induction of OCI-5 by confluence.
Animals↗
Growth mechanism of the (110) face of tetragonal lysozyme crystals.
The measured macroscopic growth rates of the (110) face of tetragonal lysozyme show an unexpectedly complex dependence on the supersaturation. In earlier studies it has been shown that an aggregate growth unit could account for experimental growth-rate trends. In particular molecular packing and interactions in the growth of the crystal were favored by completion of the helices along the 4(3) axes. In this study the molecular orientations of the possible growth units and the molecular growth mechanism were identified. This indicated that growth was a two-step process: aggregate growth units corresponding to the 4(3) helix are first formed in the bulk solution by stronger intermolecular bonds and then attached to the crystal face by weaker bonds. A more comprehensive analysis of the measured (110) growth rates was also undertaken. They were compared with the predicted growth rates from several dislocation and two-dimensional nucleation growth models, employing tetramer and octamer growth units in polydisperse solutions and monomer units in monodisperse solutions. The calculations consistently showed that the measured growth rates followed the expected model relations with octamer growth units, in agreement with the predictions from the molecular level analyses.
Journal Article↗
Expression of OCI-5/glypican 3 during intestinal morphogenesis: regulation by cell shape in intestinal epithelial cells.
OCI-5, the rat homologue of human glypican 3 (GPC3), is believed to be involved in morphogenesis and growth control during development. The finding that GPC3 is mutated in patients with the Simpson-Golabi-Behmel overgrowth syndrome is consistent with this idea. In this report, using RNA in situ hybridization, expression of OCI-5 in the developing intestine is detected in both endoderm- and mesenchyme-derived cells in a phased manner related to age and proximal/distal position. To investigate the mechanism of its regulation during intestinal development, OCI-5 expression was studied in the primitive rat intestinal epithelial cell line IEC-18. The expression of the OCI-5 transcript is increased in IEC-18 cells at confluence, in low calcium media, and during spheroid culture, all conditions which result in the cells acquiring a more rounded cell shape. In contrast, cytoskeletal disruption with colchicine causes cells to flatten and spread and abolishes both the confluence- and the low calcium-dependent induction of OCI-5. Treatment with vanadate, a phosphatase inhibitor, causes cells to acquire a spindle-shaped morphology and prevents OCI-5 induction in all situations. Nuclear run-on analysis demonstrates that the rate of OCI-5 transcription is increased at confluence, in low calcium media, and during spheroid culture of IEC-18, and decreased by treatment of cells with colchicine. Together, these data suggest that OCI-5 expression is regulated in IEC-18 by cell shape. The pattern of expression of OCI-5 in the developing intestine is consistent with it playing a role in epithelial-mesenchymal interactions during intestinal morphogenesis, when cell shape changes are likely to occur.
Animals↗
Differential labeling of dopamine and sigma sites by [3H]nemonapride and [3H]raclopride in postmortem human brains.
The difference between the binding of [3H]nemonapride and [3H]raclopride has been used to quantify dopamine D4 receptors in postmortem schizophrenic brain studies. Recent work, however, has suggested that at least part of the differential between [3H]nemonapride and [3H]raclopride binding may represent sigma rather than D4 receptor sites. We applied the nemonapride-raclopride subtraction method to postmortem, non-schizophrenic human striatum to examine the variation in dopaminergic receptor binding labeled by these ligands. Variation in sigma receptor binding labeled by [3H]nemonapride was studied in frontal cortex, striatum and cerebellum. Specific binding was defined by sulpiride (dopamine receptor ligand), PPAP (sigma receptor ligand) and haloperidol (mixed dopaminergic/sigma agent), respectively. Haloperidol defined a combination of sites, which were approximately the sum of the dopaminergic and sigma components defined by sulpiride and PPAP, respectively. Significant inter-individual variation in the amount of specific binding for dopaminergic and sigma receptor sites was observed. However, no significant nor consistent observation of striatal dopamine D4 receptors or D4-like binding sites was observed in the striatum even though two independent sets of tissues, with different dissections were used. The inconsistencies in some previous postmortem studies appear to be at least partially explained by the inclusion of both sigma and dopaminergic components in [3H]nemonapride binding and the inherent high inter-individual variability of the different components.
Adult↗
Coexistence of two beta subunit isoforms in the same gamma-aminobutyric acid type A receptor.
Three novel subunit-specific antisera to the beta1, beta2, and beta3 subunits of rat gamma-aminobutyric acid type A (GABAA) receptors have been used to study the native receptor in the rat brain. Affinity-purified anti-beta1, anti-beta2, and anti-beta3 antibodies recognized in immunoblots protein bands of 57, 55, and 57 kDa, respectively. Quantitative immunoprecipitation of solubilized GABAA receptors from various rat brain regions showed that the beta2 subunit was the most abundant isoform in cerebellum (in 96% of the GABAA receptors) and cerebral cortex (64%) but that it was the least abundant isoform in hippocampus (44%). The beta3 subunit was found most abundant in hippocampus (64%) followed by cerebral cortex (48%) and cerebellum (33%). The beta1 subunit was present in a very small proportion of the cerebellar GABAA receptors (3%), but it was present in a high proportion of the GABAA receptors from the hippocampus (49%) and cerebral cortex (32%). Quantitative receptor immunoprecipitation or immunopurification followed by immunoblotting experiments have revealed the existence of colocalization of two different beta subunit isoforms in a significant proportion of the brain GABAA receptors. Thus, in the rat cerebral cortex 33% of the GABAA receptors have both beta2 and beta3 subunits, and 19% of the receptors have both beta1 and beta3 subunits. The extent of colocalization of beta subunit isoforms varied among brain regions, being highest in hippocampus and lowest in cerebellum. These and other results taken together suggest that the number of alpha, beta, and gamma subunits (stoichiometry) in the brain GABAA receptor pentamers might not be unique. It might vary depending on receptor type.
Animals↗