Biomedical subjects

W Dai

Publications and source records attributed to W Dai.

At least 19 recordsLinked to original sources

PubMed2006

Experimental study of the influence of different resonators on thermoacoustic conversion performance of a thermoacoustic-Stirling heat engine.

In this paper, an experimental study of the effect of the resonator shape on the performance of a traveling-wave thermoacoustic engine is presented. Two different resonators were tested in the thermoacoustic-Stirling heat. One resonator is an iso-diameter one, and the other is a tapered one. To have a reasonable comparison reference, we keep the same traveling-wave loop, the same resonant frequency and the same operating pressure. The experiment showed that the resonator shape has significant influence on the global performance of the thermoacoustic-Stirling heat engine. The tapered resonator gives much better performance than the iso-diameter resonator. The tapered resonator system achieved a maximum pressure ratio of about 1.3, a maximum net acoustical power output of about 450 W and a highest thermoacoustic efficiency of about 25%.

Journal Article↗

PubMed2006

Experimental investigation of a thermoacoustic-Stirling refrigerator driven by a thermoacoustic-Stirling heat engine.

In this paper, a thermally-driven thermoacoustic refrigerator system without any moving part is reported. This refrigeration system consists of a thermoacoustic-Stirling heat engine and a thermoacoustic-Stirling refrigerator; that is, the former is the driving source for the latter. Both the subsystems are designed to operate on traveling-wave mode. In the experiment, it was found that the DC-flows had significant negative effect on the heat engine and the refrigerator. To suppress these DC-flows, two flexible membranes were inserted into the two subsystems and worked very well. Then extensive experiments were made to test the influence of different parameters on refrigeration performance of the whole system. The system has so far achieved a no-load temperature of -65 degrees C, a cooling capacity of about 270 W at -20 degrees C and 405 W at 0 degrees C; in fact, the result showed a good prospect of the refrigeration system in room-temperature cooling such as food refrigeration and air-conditioning.

Journal Article↗

PubMed2006

Development of a tri-polar concentric ring electrode for acquiring accurate Laplacian body surface potentials.

Potentials recorded on the body surface from the heart are of a spatial and temporal function. The 12-lead electrocardiogram (ECG) provides a useful means of global temporal assessment; however, it yields limited spatial information due to the smoothing effect caused by the volume conductor. In an attempt to circumvent the smoothing problem, researchers have used the five-point method (FPM) to numerically estimate the analytical solution of the Laplacian with an array of monopolar electrodes. Researchers have also developed a bipolar concentric ring electrode system to estimate the analytical Laplacian, and others have used a quasi-bipolar electrode configuration. In a search to find an electrode configuration with a close approximation to the analytical Laplacian, development of a tri-polar concentric ring electrode based on the nine-point method (NPM) was conducted. A comparison of the NPM, FPM, and discrete form of the quasi-bipolar configuration was performed over a 400 x 400 mesh with 1/400 spacing by computer modeling. Different properties of bipolar, quasi-bipolar and tri-polar concentric ring electrodes were evaluated and compared, and verified with tank experiments. One-way analysis of variance (ANOVA) with post hoc t-test and Bonferroni corrections were performed to compare the performance of the various methods and electrode configurations. It was found that the tri-polar electrode has significantly improved accuracy and local sensitivity. This paper also discusses the development of an active sensor using the tri-polar electrode configuration. A 1-cm active Laplacian tri-polar sensor based on the NPM was tested and deemed feasible for acquiring Laplacian cardiac surface potentials.

Computer Simulation↗

PubMed2006

BubR1 is involved in regulation of DNA damage responses.

Defective mitotic spindles or an impaired spindle-kinetochore interaction activates the spindle checkpoint. We have previously shown that BubR1 haplo-insufficiency results in enhanced genomic instability and tumorigenesis in mice. Here we report that BubR1 deficiency also leads to a compromised response to DNA damage. Following treatment with doxorubicin, BubR1(+/-) murine fibroblast cells (MEF) were defective in undergoing G(2)/M arrest. Thus, whereas in the presence of DNA damage BubR1(+/+) MEF cells remained arrested in mitosis, BubR1(+/-) MEFs rapidly exited from mitosis and divided. The impaired mitotic arrest of BubR1(+/-) MEFs was associated with low levels of phospho-histone H2AX, p53, and p21 after DNA damage caused by treatment with both doxorubicin and ultraviolet light (UV). The impaired expression of p53 and p21 was also confirmed in human cell lines with BubR1 knockdown via RNA interference. Affinity pull-down coupled with mass spectrometry identified Poly(ADP-ribose) polymerase 1 (PARP-1) as one of the proteins interacting with BubR1. Reciprocal co-immunoprecipitation analysis confirmed the physical interaction between BubR1 and PARP-1. Our further study revealed that the ability of retaining intact PARP-1 or its cleavage product p89 was compromised in BubR1(+/-) MEFs upon treatment with doxorubicin or UV. Given that PARP-1 mediates DNA damage responses and regulates the activity of p53, our studies suggest that there exists a cross-talk between the spindle checkpoint and the DNA damage checkpoint and that BubR1 may play an important role in mediating the cross-talk.

Animals↗

PubMed2006

Preclinical assessment of the feasibility of applying controlled release oral drug delivery to a lead series of atypical antipsychotics.

In this paper, we present a preclinical approach for evaluating the feasibility of applying controlled-release (CR) oral drug delivery to increase the duration of exposure and lower the C(max) of compounds in a lead series of short half-life atypical antipsychotics. Three lead compounds in the series had demonstrated potential pharmacological benefits for the treatment of psychosis, in preclinical studies. However, the compounds showed evidence of insufficient half-lives to enable a once-a-day (QD) product using immediate-release (IR) oral delivery. To evaluate and compare the potential for oral CR delivery to extend the duration of action and thereby enable QD administration, the in vitro solubility and permeability, and the duodenal and colonic absorption of three compounds in the series were measured. Based on the results, one candidate was selected for advancement that showed moderate in vitro solubility, but had the highest in vitro permeability and ratio of colonic to duodenal bioavailability (0.9) in the rat. The results from this study provided evidence that a CR drug delivery system could be used to extend the duration of exposure of the compounds in the series and a scientific basis for selecting one of the three compounds as a candidate.

Administration, Oral↗

PubMed2006

ATM activation and histone H2AX phosphorylation as indicators of DNA damage by DNA topoisomerase I inhibitor topotecan and during apoptosis.

Damage that engenders DNA double-strand breaks (DSBs) activates ataxia telangiectasia mutated (ATM) kinase through its auto- or trans-phosphorylation on Ser1981 and activated ATM is one of the mediators of histone H2AX phosphorylation on Ser139. The present study was designed to explore: (i) whether measurement of ATM activation combined with H2AX phosphorylation provides a more sensitive indicator of DSBs than each of these events alone, and (ii) to reveal possible involvement of ATM activation in H2AX phosphorylation during apoptosis. Activation of ATM and/or H2AX phosphorylation in HL-60 or Jurkat cells treated with topotecan (Tpt) was detected immunocytochemically in relation to cell cycle phase, by multiparameter cytometry. Exposure to Tpt led to concurrent phosphorylation of ATM and H2AX in S-phase cells, whereas G1 cells were unaffected. Immunofluorescence (IF) of the S-phase cells immunostained for ATM-S1981P and gammaH2AX combined was distinctly stronger compared to that of the cells stained for each of these proteins alone. However, because of the relatively high ATM-S1981P IF of G1 cells, the ratio of IF of S to G1 cells, that is, the factor that determines competence of the assay in distinction of cells with DSBs, was 2- to 3-fold lower for ATM-S1981P alone, or for ATM-S1981P and gammaH2AX IF combined, than for gammaH2AX alone. ATM activation concurrent with H2AX phosphorylation, likely triggered by induction of DSBs during DNA fragmentation, occurred during apoptosis. The data suggest that frequency of activated ATM and phosphorylated H2AX molecules, per apoptotic cell, is comparable.

Antineoplastic Agents↗

PubMed2006

Extent of constitutive histone H2AX phosphorylation on Ser-139 varies in cells with different TP53 status.

In response to DNA damage by genotoxic agents, histone H2AX is phosphorylated on Ser-139. However, during the cell cycle, predominantly in S and G(2)M phase, histone H2AX is also phosphorylated in untreated normal and tumour cells. This constitutive H2AX phosphorylation is markedly reduced by exposure of cells to the reactive oxygen species scavenger N-acetyl-L-cysteine. Therefore, it appears likely that constitutive H2AX phosphorylation reflects the ongoing oxidative DNA damage induced by the reactive oxygen species during progression through the cell cycle. Because the tumour suppressor p53 (tumour protein p53) is known to induce transcription of genes associated with cell response to oxidative stress, we have compared the intensity of constitutive H2AX phosphorylation, and the effect of N-acetyl-L-cysteine on it, in cells with different tumour protein p53 status. These were human lymphoblastoid cell lines derived from WIL2 cells: TK6, a p53 wt line, NH32, a tumour protein p53 knock-out derived from TK6, and WTK1, a WIL2-derived line that expresses a homozygous mutant of tumour protein p53. Also tested were the tumour protein p53-null promyelocytic HL-60 cells. The degree of constitutive H2AX phosphorylation was distinctly lower in NH32, WTK1 and HL-60 compared to TK6 cells in all phases of the cell cycle. Also, the degree of attenuation of constitutive H2AX phosphorylation by N-acetyl-L-cysteine was less pronounced in NH32, WTK1, and HL-60, compared to TK6 cells. However, the level of reactive oxygen species detected by the cells' ability to oxidize carboxyl-dichlorodihydrofluorescein diacetate was not significantly different in the cell lines studied, which would suggest that regardless of tumour protein p53 status, the level of oxidative DNA damage was similar. The observed higher level of constitutive H2AX phosphorylation in cells harbouring wt tumour protein p53 may thus indicate that tumour protein p53 plays a role in facilitating histone H2AX phosphorylation, an important step in the mobilization of the DNA repair machinery at the site of DNA double-strand breaks.

Acetylcysteine↗

PubMed2005

Visual perception of male body attractiveness.

Based on 69 scanned Chinese male subjects and 25 Caucasian male subjects, the present study showed that the volume height index (VHI) is the most important visual cue to male body attractiveness of young Chinese viewers among the many body parameters examined in the study. VHI alone can explain ca. 73% of the variance of male body attractiveness ratings. The effect of VHI can be fitted with two half bell-shaped exponential curves with an optimal VHI at 17.6 l m(-2) and 18.0 l m(-2) for female raters and male raters, respectively. In addition to VHI, other body parameters or ratios can have small, but significant effects on male body attractiveness. Body proportions associated with fitness will enhance male body attractiveness. It was also found that there is an optimal waist-to-hip ratio (WHR) at 0.8 and deviations from this optimal WHR reduce male body attractiveness.

Asian People↗

PubMed2004

Visual perception of female physical attractiveness.

On the basis of visual assessment of figure drawings and front/profile images, past researchers believed that the waist-hip ratio (WHR) and the body mass index (BMI) were two putative cues to female physical attractiveness. However, this view was not tested on three-dimensional (3D) female images. In the present study, 3D images of 31 Caucasian females having varying body weights (BMI ranged from 16 to 35) were shown to 29 male and 25 female viewers, who were asked to rate the physical attractiveness. The results showed that the body volume divided by the square of the height, defined as volume height index (VHI), is the most important and direct visual determinant of female physical attractiveness. In determining the female attractiveness, human observers may first use VHI as a visual cue, which is also a key indicator of health and fertility owing to its strong linear relation to BMI. To fine-tune the judgement, observers may then use body proportions, the most important of which are the ratio of waist height over the chin height (WHC) (a measure of the length of legs over total tallness) and the deviation of WHR from the ideal ratio. It also appears that the effect of the body's physical parameters on the perception of female physical attractiveness conforms to Stevens' power law of psychophysics.

Beauty↗

PubMed2003

Arsenic trioxide-induced mitotic arrest and apoptosis in acute promyelocytic leukemia cells.

Arsenic trioxide (As(2)O(3)), an effective drug for the treatment of acute promyelocytic leukemia (APL), can induce apoptosis and partial differentiation in APL cells in vitro and in vivo. However, As(2)O(3) also induces apoptosis in cancer cells other than APL with complex mechanisms, which seem to be cell type dependent. In this study, we report that APL cells (NB4 cell line) are arrested at early mitotic phase before the collapse of mitochondrial transmembrane potential (Deltavarphi(m)) and apoptosis after treatment with pharmacological concentrations (1.0-2.0 micro M) of As(2)O(3). We have also made the following new discoveries: (1) 0.5 micro M As(2)O(3) that fails to induce apoptosis has no effects on cell cycle distribution. (2) With inhibition of As(2)O(3)-induced Deltavarphi(m) collapse and apoptosis, dithiothreitol also effectively inhibits As(2)O(3)-induced mitotic arrest, suggesting that both As(2)O(3)-induced apoptosis and mitotic arrest involve proteins with thiol groups. (3) 1.5 mM caffeine that relieves cells from G(2)/M arrest also inhibits As(2)O(3)-induced Deltavarphi(m) collapse and apoptosis, (4) 1.0 micro M As(2)O(3) increases the expression of both cyclin B(1) and hCDC20 whereas it inhibits Tyr15 phosphorylation of p34(cdc2). In conclusion, our results strongly support that there is a tight link between As(2)O(3)-induced apoptosis and mitotic arrest, the latter being one of common mechanisms for As(2)O(3)-induced apoptosis in cancer cells.

Antineoplastic Agents↗

PubMed2001

Plk3 functionally links DNA damage to cell cycle arrest and apoptosis at least in part via the p53 pathway.

Polo-like kinase 3 (Plk3, previously termed Prk) contributes to regulation of M phase of the cell cycle (Ouyang, B., Pan, H., Lu, L., Li, J., Stambrook, P., Li, B., and Dai, W. (1997) J. Biol. Chem. 272, 28646-28651). Plk3 physically interacts with Cdc25C and phosphorylates this protein phosphatase predominantly on serine 216 (Ouyang, B., Li, W., Pan, H., Meadows, J., Hoffmann, I., and Dai, W. (1999) Oncogene 18, 6029-6036), suggesting that the role of Plk3 in mitosis is mediated, at least in part, through direct regulation of Cdc25C. Here we show that ectopic expression of a kinase-active Plk3 (Plk3-A) induced apoptosis. In response to DNA damage, the kinase activity of Plk3 was rapidly increased in an ATM-dependent manner, whereas that of Plk1 was markedly inhibited. Recombinant Plk3 phosphorylated in vitro a glutathione S-transferase fusion protein containing p53, but not glutathione S-transferase alone. Recombinant Plk1 also phosphorylated p53 but on residues that differed from those targeted by Plk3. Co-immunoprecipitation and pull-down assays demonstrated that Plk3 physically interacted with p53 and that this interaction was enhanced upon DNA damage. In vitro kinase assays followed by immunoblotting showed that serine 20 of p53 was a target of Plk3. Furthermore, expression of a kinase-defective Plk3 mutant (Plk3(K52R)) resulted in significant reduction of p53 phosphorylation on serine 20, which was correlated with a decrease in the expression of p21 and with a concomitant increase in cell proliferation. These results strongly suggest that Plk3 functionally links DNA damage to cell cycle arrest and apoptosis via the p53 pathway.

Apoptosis↗

PubMed2001

Reactive oxygen species-induced phosphorylation of p53 on serine 20 is mediated in part by polo-like kinase-3.

Upon exposure of cells to hydrogen peroxide (H(2)O(2)) phosphorylation of p53 was rapidly induced in human fibroblast GM00637, and this phosphorylation occurred on serine 9, serine 15, serine 20, but not on serine 392. In addition, H(2)O(2)-induced phosphorylation of p53 was followed by induction of p21, suggesting functional activation of p53. Induction of phosphorylation of p53 on multiple serine residues by H(2)O(2) was caffeine-sensitive and blocked in ATM(-/-) cells. Polo-like kinase-3 (Plk3) activity was also activated upon H(2)O(2) treatment, and this activation was ATM-dependent. Recombinant His(6)-Plk3 phosphorylated glutathione S-transferase (GST)-p53 fusion protein but not GST alone. When phoshorylated in vitro by His(6)-Plk3, but not by the kinase-defective mutant His6-Plk3(K52R), GST-p53 was recognized by an antibody specifically to serine 20-phosphorylated p53, indicating that serine 20 is an in vitro target of Plk3. Also serine 20-phosphorylated p53 was coimmunoprecipitated with Plk3 in cells treated with H(2)O(2). Furthermore, although H(2)O(2) strongly induced serine 15 phosphorylation of p53, it failed to induce serine 20 phosphorylation in Plk3-dificient Daudi cells. Ectopic expression of a Plk3 dominant negative mutant, Plk3(K52R), in GM00637 cells suppressed H(2)O(2)-induced serine 20 phosphorylation. Taken together, our studies strongly suggest that the oxidative stress-induced activation of p53 is at least in part mediated by Plk3.

Cell Cycle Proteins↗

PubMed2001

New ferrocenyl chiral auxiliary substituents for amines: applications to syntheses of mossambine and vinblastine.

(+)-(R)-1,2-(alpha-(R)-Mesyloxy-beta-dimethyltetramethylene)-ferrocene was synthesized and used as a chiral auxiliary for N-alkylation of methyl 1,2,3,4,5,6-hexahydroazepino[4,5-b] indole-5-xi-carboxylates. Condensation with aldehydes then provided tetracyclic products in a diastereomeric ratio of at least 97:3. Gentle cleavage in acetic acid removed the chiral auxiliary to give the corresponding secondary amines in >99% ee. Thus, key intermediates leading to mossambine and vinblastine could be synthesized with high enantioselectivity. The enantioselectivity greatly exceeds that found with other chiral N-auxiliaries developed in our studies.

Amines↗

PubMed2001

Intron/exon organization and polymorphisms of the PLK3/PRK gene in human lung carcinoma cell lines.

PLK3/PRK, a conserved polo family protein serine/threonine kinase, plays a significant role at the onset of mitosis and mitotic progression. Recently, PLK3/PRK has been shown to induce apoptosis when overexpressed in cell lines and is also implicated in cell proliferation and tumor development. Forty lung tumor cell lines were used for single-strand confirmation polymorphism (SSCP) analysis and DNA sequencing to examine the mutational status of PLK3/PRK. No missense or nonsense mutations were revealed in the lung carcinoma cell lines examined. However, three polymorphisms were identified as: a G to A at position 720, an A to G at 1053, and a G to C at 1275. Intron/exon boundaries were determined by amplification of genomic DNA with PLK3/PRK exon-specific primers. The amplification products with increased size relative to the cDNA were sequenced. Fifteen exons throughout the open reading frame were characterized. None of the introns were exceptionally large, typically ranging from 100-300 basepairs in length. These results suggest that although PLK3/PRK expression is downregulated in a majority of lung carcinoma samples, mutational inactivation of the coding sequence of the PLK3/PRK gene appears to be a rare event in lung cancer.

Carcinoma↗

PubMed2001

Comparative study on the immunogenicity between Hsp70 DNA vaccine and Hsp65 DNA vaccine in human Mycobacterium tuberculosis.

The BALB/c mice were immunized with Hsp70 DNA and Hsp65 DNA vaccines in human Mycobacterium tuberculosis. Eight weeks after immunization, the eyeballs were removed, blood and spleen taken, and intraperitoneal macrophages were harvested. The lymphocytic stimulating index (SI) was used to measure the cellular proliferating ability and NO release to measure the phagocytic activity of the macrophages. With ELISA kit, the levels of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) in serum and the splenic lymphocytic cultured supernatant were detected. The results showed that after the mice were immunized with 100 micrograms/mouse of Hsp70 DNA vaccine intramuscularly, the splenic lymphocytic proliferating ability in the mice was significantly increased as compared with that in the control group, vector group and Hsp65 DNA vaccine group (P < 0.01); The contents of NO in the intraperitoneal macrophages of the mice were significantly lower than in the control group and Hsp65 DNA vaccine group (P < 0.01); The levels of serum IL-2 in the mice were significantly higher than in the control group, but there was no statistical difference between Hsp65 DNA group and vector group (P > 0.05); The contents of serum IFN-gamma in the mice were significantly higher than in the control group, but significantly lower than in the Hsp65 DNA vaccine group (P < 0.05). It was indicated that immunization with Hsp70 DNA vaccine could obviously enhance the immune response, but its intensity seemed inferior to Hsp65 DNA vaccine. The anti-infection mechanisms and clinical use in the future of the vaccines of Hsp70 DNA and Hsp65 DNA are worth further studying.

Animals↗

PubMed2001

The protective effect of hepatocyte growth-promoting factor (pHGF) against hydrogen peroxide-induced acute lung injury in rats.

To examine the protective effect of hepatocyte growth-promoting factor (pHGF) in hydrogen peroxide (H(2)O(2))-induced acute lung injury in rats, we observed the pathological changes in lung tissue by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and by light and electron microscopy. We also measured the serum levels of lipid peroxide (LPO). At 6 to 24 h after H(2)O(2) injection, the level of LPO was significantly higher in the H(2)O(2) group than in the H(2)O(2) + pHGF-treated group. This finding indicated that pHGF protected against cell membrane damage in H2O2-induced acute lung injury. Positive TUNEL signals were found in capillary endothelial cells, alveolar epithelial cells, and inflammatory cells. In the H(2)O(2) + pHGF-treated group, TUNEL-positive signals were reduced compared with those in the H(2)O(2) group. This finding indicated that pHGF acts to suppress apoptosis. In the H(2)O(2) group, severe pulmonary edema was seen 3 h after H(2)O(2) injection, and at 24 h, severe atelectasis was seen. In the H(2)O(2) + pHGF-treated group, pulmonary edema was scarcely seen and severe atelectasis was not found. This finding indicated that pHGF acts to suppress both severe pulmonary edema and atelectasis. In the H(2)O(2) group, the formation of subendothelial blebs and disruption of endothelial cells was observed. Edema and disruption were seen in type I epithelial cells. In type II lung epithelial cells, mitochondria were swollen and microvilli had disappeared. In the H(2)O(2) + pHGF-treated group, the formation of subendothelial blebs was seen, but no severe subendothelial blebs were observed. Disruption of capillary endothelial cells and type I epithelial cells was not evident, nor was there damage to type II lung epithelial cells. These findings indicated that pHGF protects the progression of H(2)O(2)-induced acute lung injury, and showed that pHGF acts to stabilize the cell membrane in capillary endothelial cells and lung epithelial cells.

Animals↗

PubMed2001

The role of strand 1 of the C beta-sheet in the structure and function of alpha(1)-antitrypsin.

Serpins inhibit cognate serine proteases involved in a number of important processes including blood coagulation and inflammation. Consequently, loss of serpin function or stability results in a number of disease states. Many of the naturally occurring mutations leading to disease are located within strand 1 of the C beta-sheet of the serpin. To ascertain the structural and functional importance of each residue in this strand, which constitutes the so-called distal hinge of the reactive center loop of the serpin, an alanine scanning study was carried out on recombinant alpha(1)-antitrypsin Pittsburgh mutant (P1 = Arg). Mutation of the P10' position had no effect on its inhibitory properties towards thrombin. Mutations to residues P7' and P9' caused these serpins to have an increased tendency to act as substrates rather than inhibitors, while mutations at P6' and P8' positions caused the serpin to behave almost entirely as a substrate. Mutations at the P6' and P8' residues of the C beta-sheet, which are buried in the hydrophobic core in the native structure, caused the serpin to become highly unstable and polymerize much more readily. Thus, P6' and P8' mutants of alpha(1)-antitrypsin had melting temperatures 14 degrees lower than wild-type alpha(1)-antitrypsin. These results indicate the importance of maintaining the anchoring of the distal hinge to both the inhibitory mechanism and stability of serpins, the inhibitory mechanism being particularly sensitive to any perturbations in this region. The results of this study allow more informed analysis of the effects of mutations found at these positions in disease-associated serpin variants.

Antithrombins↗

PubMed2001

Patterning the optic neuroepithelium by FGF signaling and Ras activation.

During vertebrate embryogenesis, the neuroectoderm differentiates into neural tissues and also into non-neural tissues such as the choroid plexus in the brain and the retinal pigment epithelium in the eye. The molecular mechanisms that pattern neural and non-neural tissues within the neuroectoderm remain unknown. We report that FGF9 is normally expressed in the distal region of the optic vesicle that is destined to become the neural retina, suggesting a role in neural patterning in the optic neuroepithelium. Ectopic expression of FGF9 in the proximal region of the optic vesicle extends neural differentiation into the presumptive retinal pigment epithelium, resulting in a duplicate neural retina in transgenic mice. Ectopic expression of constitutively active Ras is also sufficient to convert the retinal pigment epithelium to neural retina, suggesting that Ras-mediated signaling may be involved in neural differentiation in the immature optic vesicle. The original and the duplicate neural retinae differentiate and laminate with mirror-image polarity in the absence of an RPE, suggesting that the program of neuronal differentiation in the retina is autonomously regulated. In mouse embryos lacking FGF9, the retinal pigment epithelium extends into the presumptive neural retina, indicating a role of FGF9 in defining the boundary of the neural retina.

Animals↗