抗Di(a)抗體引起新生兒嚴重溶血症的病例

Red cell allo-antibodies directed against the Diego (Di) blood group antigen have rarely been reported to cause a haemolytic reaction against transfusion or haemolytic disease of the newborn. The frequency of the Di(a+) phenotype among the Hong Kong Chinese population is estimated to be 4.4%. We report on a case of severe haemolytic disease of the newborn due to anti-Di(a) antibody--the first local case to the best of our knowledge. Rare but clinically significant antibodies targeting red blood cells have to be considered in the investigation of haemolytic disease of the newborn when common underlying factors have been eliminated.published_or_final_versio

早產嬰兒脾臟破裂

Splenic injuries are very rare in neonates. We report a case of splenic injury in a premature neonate, highlighting the importance of a high-index suspicion in early recognition of this rare but potentially fatal intra-abdominal injury. We also review the literature on possible aetiologies and mechanism of splenic injury, as well as its management. This is the first reported case of a very low-birth-weight neonate with splenic rupture who survived with intact neurology.published_or_final_versio

An Innovative Technique for Evaluating the Integrity and Durability of Wind Turbine Blade Composites - Final Project Report

To build increasingly larger, lightweight, and robust wind turbine blades for improved power output and cost efficiency, durability of the blade, largely resulting from its structural composites selection and aerodynamic shape design, is of paramount concern. The safe/reliable operation of structural components depends critically on the selection of materials that are resistant to damage and failure in the expected service environment. An effective surveillance program is also necessary to monitor the degradation of the materials in the course of service. Composite materials having high specific strength/stiffness are desirable for the construction of wind turbines. However, most high-strength materials tend to exhibit low fracture toughness. That is why the fracture toughness of the composite materials under consideration for the manufacture of the next generation of wind turbines deserves special attention. In order to achieve the above we have proposed to develop an innovative technology, based on spiral notch torsion test (SNTT) methodology, to effectively investigate the material performance of turbine blade composites. SNTT approach was successfully demonstrated and extended to both epoxy and glass fiber composite materials for wind turbine blades during the performance period. In addition to typical Mode I failure mechanism, the mixed-mode failure mechanism induced by the wind turbine service environments and/or the material mismatch of the composite materials was also effectively investigated using SNTT approach. The SNTT results indicate that the proposed protocol not only provides significant advance in understanding the composite failure mechanism, but also can be readily utilized to assist the development of new turbine blade composites

Developing Fatigue Pre-crack Procedure to Evaluate Fracture Toughness of Pipeline Steels Using Spiral Notch Torsion Test

The spiral notch torsion test (SNTT) has been utilized to investigate the crack growth behavior of X52 steel base and welded materials used for hydrogen infrastructures. The X52 steel materials are received from a welded pipe using friction stir welding techniques. Finite element models were established to study the crack growth behavior of steel SNTT steel samples, which were assumed to be isotropic material. A series SNTT models were set up to cover various crack penetration cases, of which the ratios between crack depth to diameter (a/D ratio) ranging from 0.10 to 0.45. The evolution of compliance and energy release rates in the SNTT method have been investigated with different cases, including different geometries and materials. Indices of characteristic compliance and energy release rates have been proposed. Good agreement has been achieved between predictions from different cases in the same trend. These work shed lights on a successful protocol for SNTT application in wide range of structural materials. The further effort needed for compliance function development is to extend the current developed compliance function to the deep crack penetration arena, in the range of 0.55 to 0.85 to effectively determine fracture toughness for extremely tough materials

Bioencapsulation and Colonization Characteristics of Lactococcus lactis subsp. lactis CF4MRS in Artemia franciscana: a Biological Approach for the Control of Edwardsiellosis in Larviculture

Predominance of beneficial bacteria helps to establish a healthy microbiota in fish gastrointestinal system and thus to reduce emerging pathogen. In this study, the colonization efficacy of Lactococcus lactis subsp. lactis CF4MRS in Artemia franciscana and its potential as a probiotic in suppressing Edwardsiella sp. infection were investigated in vivo. The colonization extent of the bioencapsulated L. lactis was established through visualization of gfp gene-transformed L. lactis in A. franciscana. Here, we demonstrate that when A. franciscana is administrated with L. lactis at 108 CFU mL−1 for 8 h, the highest relative percentage of survival (RPS = 50.0) is observed after inoculation with Edwardsiella sp. The total counts of L. lactis entrapped in Artemia were the highest (ranged from 3.2 to 5.1 × 108 CFU mL−1), when 108–109 CFU mL−1 of L. lactis was used as starting inoculum, with the bioencapsulation performed within 8–24 h. Fluorescent microscopy showed gfp-transformed L. lactis colonized the external trunk surfaces, mid-gut and locomotion antennules of the A. franciscana nauplii. These illustrations elucidate the efficiency of colonization of L. lactis in the gastrointestinal tract and on the body surfaces of Artemia. In conclusion, L. lactis subsp. lactis CF4MRS shows a good efficacy of colonization in Artemia and has the potential for biocontrol/probiotic activity against Edwardsiella sp. infection

Gadolinium oxide nanocrystal nonvolatile memory with HfO2/Al2O3 nanostructure tunneling layers

In this study, Gd2O3 nanocrystal (Gd2O3-NC) memories with nanostructure tunneling layers are fabricated to examine their performance. A higher programming speed for Gd2O3-NC memories with nanostructure tunneling layers is obtained when compared with that of memories using a single tunneling layer. A longer data retention (< 15% charge loss after 104 s) is also observed. This is due to the increased physical thickness of the nanostructure tunneling layer. The activation energy of charge loss at different temperatures is estimated. The higher activation energy value (0.13 to 0.17 eV) observed at the initial charge loss stage is attributed to the thermionic emission mechanism, while the lower one (0.07 to 0.08 eV) observed at the later charge loss stage is attributed to the direct tunneling mechanism. Gd2O3-NC memories with nanostructure tunneling layers can be operated without degradation over several operation cycles. Such NC structures could potentially be used in future nonvolatile memory applications

TRAPPC4-ERK2 Interaction Activates ERK1/2, Modulates Its Nuclear Localization and Regulates Proliferation and Apoptosis of Colorectal Cancer Cells

The trafficking protein particle complex 4 (TRAPPC4) is implicated in vesicle-mediated transport, but its association with disease has rarely been reported. We explored its potential interaction with ERK2, part of the ERK1/2 complex in the Extracellular Signal-regulated Kinase/ Mitogen-activated Protein Kinase (ERK-MAPK) pathway, by a yeast two-hybrid screen and confirmed by co-immunoprecipitation (Co-IP) and glutathione S-transferase (GST) pull-down. Further investigation found that when TRAPPC4 was depleted, activated ERK1/2 specifically decreased in the nucleus, which was accompanied with cell growth suppression and apoptosis in colorectal cancer (CRC) cells. Overexpression of TRAPPC4 promoted cell viability and caused activated ERK1/2 to increase overall, but especially in the nucleus. TRAPPC4 was expressed more highly in the nucleus of CRC cells than in normal colonic epithelium or adenoma which corresponded with nuclear staining of pERK1/2. We demonstrate here that TRAPPC4 may regulate cell proliferation and apoptosis in CRC by interaction with ERK2 and subsequently phosphorylating ERK1/2 as well as modulating the subcellular location of pERK1/2 to activate the relevant signaling pathway

Constitutively Nuclear FOXO3a Localization Predicts Poor Survival and Promotes Akt Phosphorylation in Breast Cancer

Background: The PI3K-Akt signal pathway plays a key role in tumorigenesis and the development of drug-resistance. Cytotoxic chemotherapy resistance is linked to limited therapeutic options and poor prognosis. Methodology/Principal Findings: Examination of FOXO3a and phosphorylated-Akt (P-Akt) expression in breast cancer tissue microarrays showed nuclear FOXO3a was associated with lymph node positivity (p = 0.052), poor prognosis (p = 0.014), and P-Akt expression in invasive ductal carcinoma. Using tamoxifen and doxorubicin-sensitive and -resistant breast cancer cell lines as models, we found that doxorubicin- but not tamoxifen-resistance is associated with nuclear accumulation of FOXO3a, consistent with the finding that sustained nuclear FOXO3a is associated with poor prognosis. We also established that doxorubicin treatment induces proliferation arrest and FOXO3a nuclear relocation in sensitive breast cancer cells. Induction of FOXO3a activity in doxorubicin-sensitive MCF-7 cells was sufficient to promote Akt phosphorylation and arrest cell proliferation. Conversely, knockdown of endogenous FOXO3a expression reduced PI3K/Akt activity. Using MDA-MB-231 cells, in which FOXO3a activity can be induced by 4-hydroxytamoxifen, we showed that FOXO3a induction up-regulates PI3K-Akt activity and enhanced doxorubicin resistance. However FOXO3a induction has little effect on cell proliferation, indicating that FOXO3a or its downstream activity is deregulated in the cytotoxic drug resistant breast cancer cells. Thus, our results suggest that sustained FOXO3a activation can enhance hyperactivation of the PI3K/Akt pathway. Conclusions/Significance: Together these data suggest that lymph node metastasis and poor survival in invasive ductal breast carcinoma are linked to an uncoupling of the Akt-FOXO3a signaling axis. In these breast cancers activated Akt fails to inactivate and re-localize FOXO3a to the cytoplasm, and nuclear-targeted FOXO3a does not induce cell death or cell cycle arrest. As such, sustained nuclear FOXO3a expression in breast cancer may culminate in cancer progression and the development of an aggressive phenotype similar to that observed in cytotoxic chemotherapy resistant breast cancer cell models. © 2010 Chen et al.published_or_final_versio

Unregulated miR-96 Induces Cell Proliferation in Human Breast Cancer by Downregulating Transcriptional Factor FOXO3a

FOXO transcription factors are key tumor suppressors in mammalian cells. Until now, suppression of FOXOs in cancer cells was thought to be mainly due to activation of multiple onco-kinases by a phosphorylation-ubiquitylation-mediated cascade. Therefore, it was speculated that inhibition of FOXO proteins would naturally occur through a multiple step post-translational process. However, whether cancer cells may downregulate FOXO protein via an alternative regulatory mechanism is unclear. In the current study, we report that expression of miR-96 was markedly upregulated in breast cancer cells and breast cancer tissues compared with normal breast epithelial cells (NBEC) and normal breast tissues. Ectopic expression of miR-96 induced the proliferation and anchorage-independent growth of breast cancer cells, while inhibition of miR-96 reduced this effect. Furthermore, upregulation of miR-96 in breast cancer cells resulted in modulation of their entry into the G1/S transitional phase, which was caused by downregulation of cyclin-dependent kinase (CDK) inhibitors, p27Kip1 and p21Cip1, and upregulation of the cell-cycle regulator cyclin D1. Moreover, we demonstrated that miR-96 downregulated FOXO3a expression by directly targeting the FOXO3a 3′-untranslated region. Taken together, our results suggest that miR-96 may play an important role in promoting proliferation of human breast cancer cells and present a novel mechanism of miRNA-mediated direct suppression of FOXO3a expression in cancer cells