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PubMed2007

Inhibition of breast cancer cell growth in vitro and in vivo: effect of restoration of Wwox expression.

PURPOSE: The WWOX gene is down-regulated in breast cancer and loss of Wwox expression correlates with important clinical features of breast cancer. Thus, we have examined the effect of restoration of Wwox expression in breast cancer-derived cells. EXPERIMENTAL DESIGN: Wwox protein expression was restored by the following: (a) infection with a recombinant adenovirus carrying WWOX cDNA (Ad-WWOX) or (b) treatment with the DNA methyltransferase inhibitor, 5-aza-2'-deoxycytidine, to activate the endogenous WWOX gene, in breast cancer-derived cells in vitro and in vivo. RESULTS: Restoration of Wwox expression led to suppression of growth of Wwox-deficient breast cancer-derived cells, through activation of the intrinsic caspase pathway, but did not affect growth of Wwox-sufficient MCF7 cells. Intratumoral Wwox restoration, through Ad-WWOX infection or endogenous Wwox reactivation by 5-aza-2'-deoxycytidine injection, suppressed tumor growth in nude mice by inducing apoptosis. Alteration of global methylation levels was not observed. CONCLUSIONS: The results confirm that overexpression of exogenous Wwox inhibits breast cancer cell growth in vitro and in vivo and, perhaps more importantly, shows that restoration of endogenous Wwox expression, and likely other proteins, by treatment with a de novo methyltransferase inhibitor, also inhibits breast cancer cell growth and reverses breast cancer xenograft growth.

Adenoviridae↗

PubMed2002

T-Bet expression and failure of GATA-3 cross-regulation lead to default production of IFN-gamma by gammadelta T cells.

gammadelta T cells predominantly produce IFN-gamma upon activation. To determine the basis for default production of IFN-gamma by gammadelta T cells, we analyzed the transcription factors T-box expressed in T cells (T-bet) and GATA-3. T-bet, absent in naive cells, was induced upon TCR signaling, with IFN-gamma production. T-bet also regulated IL-4 synthesis, as gammadelta cells isolated from T-bet-deficient mice displayed enhanced IL-4 levels with reduced IFN-gamma production. Notably, T-bet expression after TCR signaling in gammadelta cells was not down-regulated by IL-4, in conjunction with a higher ratio of T-bet:GATA-3 expression than that found in CD4(+) T cells. Indeed, overexpression of GATA-3 failed to inhibit IFN-gamma secretion in gammadelta cells to the degree seen in CD4(+) T cells. These results indicate that T-bet enhances IFN-gamma secretion and suppresses IL-4 secretion in gammadelta cells, and that GATA-3 fails to counterbalance T-bet-mediated IFN-gamma production, accounting for the default synthesis of IFN-gamma by these T lymphocytes.

Animals↗

PubMed2005

Identification of an ectodomain within the LAR protein tyrosine phosphatase receptor that binds homophilically and activates signalling pathways promoting neurite outgrowth.

Elucidation of mechanisms by which receptor protein tyrosine phosphatases (PTPs) regulate neurite outgrowth will require characterization of ligand-receptor interactions and identification of ligand-induced signalling components mediating neurite outgrowth. The first identified ligand of the leucocyte common antigen-related (LAR) receptor PTP consists of a 99-residue ectodomain isoform, termed LARFN5C, which undergoes homophilic binding to LAR and promotes neurite outgrowth. We employed peptide mapping of LARFN5C to identify an active neurite-promoting domain of LAR. A peptide mimetic consisting of 37 residues (L59) and corresponding to the fifth LAR fibronectin type III (FNIII) domain prevented LARFN5C homophilic binding, demonstrated homophilic binding to itself and promoted neurite outgrowth of mouse E16-17 hippocampal neurons and of dorsal root ganglia explants. Response to L59 was partially lost when using neurons derived from LAR-deficient (-/-) mice or neurons treated with LAR siRNA, consistent with homophilic interaction of L59 with LAR. L59 neurite-promoting activity was decreased in the presence of inhibitors of Src, Trk, PLCgamma, PKC, PI3K and MAPK. L59 activated Src (a known substrate of LAR), FAK and TrkB and also activated downstream signalling intermediates including PKC, ERK, AKT and CREB. BDNF augmented the maximal neurite-promoting activity of L59, a finding consistent with the presence of shared and distinct signalling pathways activated by L59 with BDNF and L59 with TrkB. These studies are the first to identify an ectodomain of LAR (located within the fifth FNIII domain) capable of promoting neurite outgrowth and point to novel approaches for promotion of neurite outgrowth.

Animals↗

PubMed2006

Bone morphogenetic protein signaling by hemojuvelin regulates hepcidin expression.

Hepcidin is a key regulator of systemic iron homeostasis. Hepcidin deficiency induces iron overload, whereas hepcidin excess induces anemia. Mutations in the gene encoding hemojuvelin (HFE2, also known as HJV) cause severe iron overload and correlate with low hepcidin levels, suggesting that hemojuvelin positively regulates hepcidin expression. Hemojuvelin is a member of the repulsive guidance molecule (RGM) family, which also includes the bone morphogenetic protein (BMP) coreceptors RGMA and DRAGON (RGMB). Here, we report that hemojuvelin is a BMP coreceptor and that hemojuvelin mutants associated with hemochromatosis have impaired BMP signaling ability. Furthermore, BMP upregulates hepatocyte hepcidin expression, a process enhanced by hemojuvelin and blunted in Hfe2-/- hepatocytes. Our data suggest a mechanism by which HFE2 mutations cause hemochromatosis: hemojuvelin dysfunction decreases BMP signaling, thereby lowering hepcidin expression.

Amino Acid Sequence↗

PubMed1999

Transforming growth factor beta1 enhances platelet aggregation through a non-transcriptional effect on the fibrinogen receptor.

Upon activation, platelets store and release large amounts of the peptide transforming growth factor beta1 (TGFbeta1). The released TGFbeta1 can then act on nearby vascular cells to mediate subsequent vessel repair. In addition, TGFbeta1 may circulate to bone marrow and regulate megakaryocyte activity. It is not known what effect, if any, TGFbeta1 has on platelets. Adult TGFbeta1-deficient mice exhibit thrombocythemia and a mild bleeding disorder that is shown to result from faulty platelet aggregation. TGFbeta1-deficient platelets are shown to contain functional receptors, and preincubation with recombinant TGFbeta1 improves aggregation, demonstrating that TGFbeta1 plays an active role in platelet aggregation. TGFbeta1-deficient platelets fail to retain bound fibrinogen in response to aggregation agonists, but they possess normal levels of the alpha(IIb)/beta(3) fibrinogen receptor. Signaling from agonist receptors is normal because the platelets change shape, produce thromboxane A(2), and present P-selectin in response to stimulation. Consequently, activation and maintenance of alpha(IIb)/beta(3) into a fibrinogen-binding conformation is impaired in the absence of TGFbeta1. 4-Phorbol 12-myristate 13-acetate treatment and protein kinase C activity measurements suggest a defect downstream of protein kinase C in its activation cascade. Because platelets lack nuclei, these data demonstrate for the first time a non-transcriptionally mediated TGFbeta1 signaling pathway that enhances the activation and maintenance of integrin function.

Adenosine Diphosphate↗

PubMed2005

[Effect of compound duzhong jiangu granule on knee joint osteoarthritis: a report of 400 cases].

OBJECTIVE: To study the clinical efficacy and adverse reaction of compound Duzhong Jiangu granule (CDJG) on knee joint osteoarthritis (KJO) of Gan-Shen deficiency with stasis in tendon and muscle syndrome. METHODS: The randomized controlled method was adopted in this study, comparative study was conducted in 400 patients in the treated group treated with CDJG and 200 patients in the control group treated with Zhuanggu Guanjie pill (ZGP). RESULTS: The total effective rate in the treated group was 92% and the curative-markedly effective rate was 47%, which were higher than those in the control group respectively. Moreover, CDJG showed superiority in improving symptoms and with shorter initiating time of action as compared with ZGP. However CDJG had the effect more favourable for patients of mild condition. CONCLUSION: CDJG is a kind of effective and safe medicine for treatment of KJO.

Aged↗

PubMed2006

A characteristic pharmacological action of 'Yang-invigorating' Chinese tonifying herbs: enhancement of myocardial ATP-generation capacity.

In order to investigate the pharmacological basis of 'Yang-invigorating' action, the effect of oral treatment with the methanolic extract of 'Yang-invigorating' herbs on ATP-generation capacity was examined, using heart homogenates prepared from herb-pretreated mice. Tonifying (i.e., health-promoting) herbs of other functional categories were also included for comparison. The results indicated that 'Yang-invigorating' Chinese tonifying herbs could invariably enhance myocardial ATP-generation capacity, with the extent of stimulation varying among the herbs. In contrast, 'Yin-nourishing' herbs either did not stimulate or even decreased myocardial ATP-generation capacity. While 'Qi-invigorating' herbs produced variable effects on myocardial ATP-generation capacity, most of the 'blood-enriching' herbs did not cause any significant changes. The results obtained from studies using myocardial mitochondrial fractions isolated from herb-pretreated mice suggest that 'Yang-invigorating' herbs might speed up ATP generation by increasing mitochondrial electron transport. The ensemble of results has provided evidence for the first time to support the pharmacological basis of 'Yang invigoration' in Chinese medicine.

Adenosine Triphosphate↗

PubMed2000

The Yin-Yang of TCF/beta-catenin signaling.

Wingless/Wnt signaling directs cell-fate choices during embryonic development. In Drosophila, Wingless signaling mediates endoderm induction and the establishment of segment polarity in the developing embryo. The fly Wingless cascade is strikingly similar to the vertebrate Wnt signaling pathway, which controls a number of key developmental decisions such as dorsal-ventral patterning in Xenopus. Factors of the TCF/LEF HMG domain family (Tcfs) have recently been established as the downstream effectors of the Wingless/Wnt signal transduction pathways. Upon Wingless/Wnt signaling, a cascade is initiated that results in the accumulation of cytoplasmic beta-catenin (or its fly homolog, Armadillo). There is also a concomitant translocation of beta-catenin/Armadillo to the nucleus, where it interacts with a specific sequence motif at the N terminus of Tcfs to generate a transcriptionally active complex. This bipartite transcription factor is targeted to the upstream regulatory regions of Tcf target genes including Siamois and Nodal related gene-3 in Xenopus, engrailed and Ultrabithorax in Drosophila via the sequence-specific HMG box, and mediates their transcriptional activation by virtue of transactivation domains contributed by beta-catenin/Armadillo. In the absence of Wingless/Wnt signals, a key negative regulator of the pathway, GSK3 beta, is activated, which mediates the downregulation of cytoplasmic beta-catenin/Armadillo via the ubiquitin-proteasome pathway. In the absence of nuclear beta-catenin, the Tcfs recruit the corepressor protein Groucho to the target gene enhancers and actively repress their transcription. An additional corepressor protein, CREB-binding protein (CBP), may also be involved in this repression of Tcf target gene activity. Several other proteins, including adenomatous polyposis coli (APC), GSK3 beta, and Axin/Conductin, are instrumental in the regulation of beta-catenin/Armadillo. In APC-deficient colon carcinoma cell lines, beta-catenin accumulates and is constitutively complexed with nuclear Tcf-4. A proportion of APC wild-type colon carcinomas and melanomas also contains constitutive nuclear Tcf-4/beta-catenin complexes as a result of dominant mutations in the N terminus of beta-catenin that render it insensitive to downregulation by APC, GSK3 beta, and Axin/Conductin. This results in the unregulated expression of Tcf-4 target genes such as c-myc. Based on the established role for Tcf-4 in maintaining intestinal stem cells it is likely that deregulation of c-myc expression as a result of constitutive Tcf-4/beta-catenin activity promotes uncontrolled intestinal cell proliferation. This would readily explain the formation of intestinal polyps during colon carcinogenesis. Similar mechanisms leading to deregulation of Tcf target gene activity are likely to be involved in melanoma and other forms of cancer.

Animals↗

PubMed2024

The Protective Role of DDIT4 in Helicobacter pylori-induced Gastric Metaplasia Through Metabolic Regulation of Ferroptosis.

BACKGROUND & AIMS: Helicobacter pylori (H pylori) infection is a significant factor leading to gastric atrophy, metaplasia and cancer development. Here, we investigated the role of the stress response gene DDIT4 in the pathogenesis of H pylori infection. METHODS: Cell lines, transgenic mice, and human tissue samples were implemented. Proteomics were performed on Ddit4+/+ and Ddit4-/- mice infected with H pylori strain PMSS1. C57BL/6 mice were administered with tamoxifen to induce gastric metaplasia. Stomach tissues were analyzed for histopathologic features, reactive oxygen species, Fe2+, lipid peroxidation, expression of DDIT4, and ferroptosis-related proteins. RESULTS: DDIT4 expression was upregulated at 6 hours but significantly decreased at 24 hours in response to H pylori infection in gastric epithelial cells. Gastric DDIT4 were downregulated in INS-GAS mice at 4 months post H pylori infection. Notably, H pylori infection led to more severe gastric metaplasia lesion in Ddit4-knockout mice. The proteomic profiling revealed an increase in ferroptosis in the gastric tissues of infected Ddit4-deficient mice, compared with infected wild-type mice. Mechanistically, knockout of DDIT4 promoted H pylori-induced ferroptosis through the accumulation of lipid peroxides and ROS levels, and alterations in proteins such as GPX4, ALOX15, and HMOX1. Overexpression of DDIT4 counteracted H pylori-induced stem cell marker CD44V9 through modulation of ferroptosis. Similarly, in another mouse model of gastric metaplasia treated with tamoxifen, as well as in human GIM tissues, we observed the loss of DDIT4 and induction of ferroptosis. CONCLUSIONS: Our results indicate that DDIT4 serves as a protective factor against H pylori-induced gastric metaplasia by metabolic resistance to ferroptosis.

Ferroptosis↗

PubMed2006

Neurodevelopmental outcome of severe neonatal hemolytic hyperbilirubinemia.

We recruited 128 neonates with hyperbilirubinemia over a 5-year period (1995-2000) to study the short- and long-term effects of hemolytic hyperbilirubinemia on the auditory brainstem pathway and neurodevelopmental status. These children were divided into two groups: (1) a hemolytic group (n = 29; ABO incompatibility [n = 19], Rh incompatibility [n = 1], glucose-6-phosphate dehydrogenase deficiency [n = 8] and both ABO incompatibility and glucose-6-phosphate dehydrogenase deficiency [n = 1]) and (2) a nonhemolytic group (n = 99). All received phototherapy. Exchange transfusions were performed for four (13.8%) in the hemolytic group and three (3%) in the nonhemolytic group. The brainstem auditory evoked potential was recorded at a mean age of 3.2 months in the hemolytic group and 3.1 months in the nonhemolytic group. Serial brainstem auditory evoked potential assessments were performed until 2 years of age (3 in the hemolytic group and 18 in the nonhemolytic group). All had regular physical, neurologic, visual, and auditory evaluation until 3 years of age. The rate of exchange transfusion was significantly higher in the hemolytic group than in the nonhemolytic group (P < .05). Brainstem auditory evoked potential abnormalities at the initial assessment occurred in three (10.4%) in the hemolytic group (all related to ABO incompatibility) and nine (9.1%) in the nonhemolytic group. At 2 years, the brainstem auditory evoked potential returned to normal except in three cases with a slightly increased hearing threshold (one [3.5%] in the hemolytic group at 60 dB nHL and two [2%] in the nonhemolytic group at 50 dB nHL]). There were no significant differences in the rate of brainstem auditory evoked potential abnormalities at the initial or subsequent assessments between both groups. All except five cases had a normal neurodevelopmental outcome at 3 years (three [two with ABO incompatibility and one with glucose-6-phosphate dehydrogenase deficiency] in the hemolytic group [10.4%] and two [2%] in the nonhemolytic group). All had mild motor delay and hypotonia, which returned to normal at 3 years. The rate of abnormal neurodevelopmental outcome was higher in the hemolytic group than in the nonhemolytic group, although with no significant difference between both groups (P = .08). All five cases in both groups with abnormal neurodevelopment had a normal brainstem auditory evoked potential at the initial assessment. There was no relationship between the abnormal initial brainstem auditory evoked potential and the final neurodevelopmental outcome. The toxic effect of hyperbilirubinemia on the auditory brainstem pathway and neurodevelopmental status in our cohort was transient. The prognosis of neonatal hemolytic hyperbilirubinemia in our Chinese cohort is excellent, possibly owing to an aggressive early-intervention approach.

Asian People↗

PubMed2001

[Posterior stabilized knee arthroplasty: 5-year follow up].

OBJECTIVE: To evaluate the middle-term results of posterior stabilized knee arthroplasty (PSKA). METHODS: From July 1995 to July 2000, 19 knees of 18 patients were replaced with posterior stabilized prosthesis (Insall-Burstein II). Among the patients, 2 were male, and 16 female. Their average age was 62.5 years (44-78 years). One patient was operated on bilaterally. Preoperative diagnosis revealed osteoarthritis in 16 knees, and rheumatoid arthritis in 3 knees. Four knees demonstrated severe bone deficiency during surgery. Before operation, 15 of the rest knees were varusly deformed, 4 were valgusly deformed, and 8 had flexion contracture. Two patients underwent surgery previously. 17 patients (18 knees) were followed-up for 41-60 months, each of them was evaluated with the Special Surgery Knee Scoring System. RESULTS: Average preoperative scores increased from 62 preoperatively to 89 postoperatively. The range of motion was significantly improved from 91 degrees preoperatively to 115 degrees postoperatively. Eleven knees were rated as excellent, 5 good, 1 fair, and 1 poor. The excellent and good rate was 88.9%. CONCLUSIONS: With its design features, PSKA can effectively improve the range of motion and maximum flexion angle without compromising posterior stability. PSKA is suitable for both primary and revision total knee arthroplasty but caution should be taken for patellar complications.

Adult↗

PubMed2002

Signalling pathways induced by protease-activated receptors and integrins in T cells.

Recent characterization of the thrombin receptor indicates that it plays a role in T-cell signalling pathways. However, little is known regarding the signalling events following stimulation of additional members of the protease-activated receptor (PAR) family, i.e. PAR2 and PAR3. Most of the postligand cascades are largely unknown. Here, we illustrate that in Jurkat T-leukaemic cells, activation of PAR1, PAR2 and PAR3 induce tyrosine phosphorylation of Vav1. This response was impaired in Jurkat T cells deficient in p56lck (JCaM1.6). Activation of PARs also led to an increase in tyrosine phosphorylation of ZAP-70 and SLP-76, two key proteins in T-cell receptor (TCR) signalling. We also demonstrated that p56lck is meaningful for integrin signalling. Thus, JCaM1.6 cells exhibited a marked reduction in their adherence to fibronectin-coated plates, as compared to the level of adherence of Jurkat T cells. While the phosphorylation of Vav1 in T cells is augmented following adhesion, no additional increase was noted following treatment of the adhered cells with PARs. Altogether, we have identified key components in the postligand-signalling cascade of PARs and integrins. Furthermore, we have identified Lck as a critical and possibly upstream component of PAR-induced Vav1 phosphorylation, as well as integrin activation, in Jurkat T cells.

Autoradiography↗

PubMed2003

Effects of baicalin on the gene expression of surfactant protein A (SP-A) in lung adenocarcinoma cell line H441.

Pulmonary surfactant, a complex lipoprotein, is secreted by alveolar type II cells. It lies at the alveolar air-fluid interface and prevents alveolar collapse by reducing surface tension. The high incidence of respiratory distress syndrome (RDS) in premature infants results principally from a deficiency of pulmonary surfactant. Surfactant protein A (SP-A) is the most abundant surfactant protein and reduces surface tension at the alveolar air-liquid interface in lung cells. In this study, RT-PCR and Western blot analyses of SP-A were performed to evaluate the biological activity of baicalin, a Chinese medicine prescribed extensively for preventing miscarriage. In in vitro experiments, lung adenocarcinoma cell line H441 was cultured with baicalin in varying concentrations and for varying lengths of time. The results show that the expression of SP-A gene was positively affected by baicalin in dose-dependent and time-course manners. The maximal expression of the SP-A gene, 1.7-fold greater than control, is induced at 150 nM of baicalin treated for 48 h.

Blotting, Western↗

PubMed2001

DNA damage by the enediyne C-1027 results in the inhibition of DNA replication by loss of replication protein A function and activation of DNA-dependent protein kinase.

Treatment of cells with the enediyne C-1027 is highly efficient at inducing single- and double-strand DNA breaks. This agent is highly cytotoxic when used at picomolar levels over a period of days. For this study, C-1027 has been used at higher levels for a much shorter time period to look at early cellular responses to DNA strand breaks. Extracts from cells treated with C-1027 for as little as 2 h are deficient in SV40 DNA replication activity. Treatment with low levels of C-1027 (1-3 nM) does not result in the presence of a replication inhibitor in cell extracts, but they are deficient in replication protein A (RPA) function. Extracts from cells treated with high levels of C-1027 (10 nM) do show the presence of a trans-acting inhibitor of DNA replication. The deficiency in RPA in extracts from cells treated with low levels of C-1027 can be fully complemented by the addition of exogenous RPA, and may be due to a C-1027-induced decrease in the extractability of RPA. This decrease in the extractability of RPA correlates with the appearance of many extraction-resistant intranuclear RPA foci. The trans-acting inhibitor of DNA replication induced by treatment of cells with high levels of C-1027 (10 nM) is DNA-dependent protein kinase (DNA-PK). DNA-PK is activated by the presence of DNA fragments induced by C-1027 treatment, and can be abrogated by removal of the DNA fragments. Although it is activated by DNA damage and phosphorylates RPA, DNA-PK is not required for either RPA focalization or loss of RPA replication activity.

Aminoglycosides↗

PubMed2001

Preservation of ancient and fertile lithospheric mantle beneath the southwestern United States.

Stable continental regions, free from tectonic activity, are generally found only within ancient cratons-the centres of continents which formed in the Archaean era, 4.0-2.5 Gyr ago. But in the Cordilleran mountain belt of western North America some younger (middle Proterozoic) regions have remained stable, whereas some older (late Archaean) regions have been tectonically disturbed, suggesting that age alone does not determine lithospheric strength and crustal stability. Here we report rhenium-osmium isotope and mineral compositions of peridotite xenoliths from two regions of the Cordilleran mountain belt. We found that the younger, undeformed Colorado plateau is underlain by lithospheric mantle that is 'depleted' (deficient in minerals extracted by partial melting of the rock), whereas the older (Archaean), yet deformed, southern Basin and Range province is underlain by 'fertile' lithospheric mantle (not depleted by melt extraction). We suggest that the apparent relationship between composition and lithospheric strength, inferred from different degrees of crustal deformation, occurs because depleted mantle is intrinsically less dense than fertile mantle (due to iron having been lost when melt was extracted from the rock). This allows the depleted mantle to form a thicker thermal boundary layer between the deep convecting mantle and the crust, thus reducing tectonic activity at the surface. The inference that not all Archaean crust developed a strong and thick thermal boundary layer leads to the possibility that such ancient crust may have been overlooked because of its intensive reworking or lost from the geological record owing to preferential recycling.

Journal Article↗

PubMed2005

Genomic instability in laminopathy-based premature aging.

Premature aging syndromes often result from mutations in nuclear proteins involved in the maintenance of genomic integrity. Lamin A is a major component of the nuclear lamina and nuclear skeleton. Truncation in lamin A causes Hutchinson-Gilford progerial syndrome (HGPS), a severe form of early-onset premature aging. Lack of functional Zmpste24, a metalloproteinase responsible for the maturation of prelamin A, also results in progeroid phenotypes in mice and humans. We found that Zmpste24-deficient mouse embryonic fibroblasts (MEFs) show increased DNA damage and chromosome aberrations and are more sensitive to DNA-damaging agents. Bone marrow cells isolated from Zmpste24-/- mice show increased aneuploidy and the mice are more sensitive to DNA-damaging agents. Recruitment of p53 binding protein 1 (53BP1) and Rad51 to sites of DNA lesion is impaired in Zmpste24-/- MEFs and in HGPS fibroblasts, resulting in delayed checkpoint response and defective DNA repair. Wild-type MEFs ectopically expressing unprocessible prelamin A show similar defects in checkpoint response and DNA repair. Our results indicate that unprocessed prelamin A and truncated lamin A act dominant negatively to perturb DNA damage response and repair, resulting in genomic instability which might contribute to laminopathy-based premature aging.

Aging, Premature↗

PubMed2006

An overview of veterinary medical education in China: current status, deficiencies, and strategy for improvement.

Especially in developing countries, the profession of veterinary medicine is closely tied with agriculture and government economic development, the national structure of education, and national public health. Currently, the Chinese veterinary medical educational system and accreditation standards are distinctly different from those of some more developed countries, such as the United States, Japan, or the countries of the European Union. Chinese veterinary education is still closely based on traditional Chinese education approaches and standards, which has led to some deficiencies in the Chinese system. With the development of a stronger economy in China and the growing trend toward globalization, and particularly since China joined the World Trade Organization (WTO), some important questions about China's system of veterinary education are being raised: How can veterinary science develop more rapidly in China? How can it meet the needs of the growing Chinese society? How can China bring its veterinary medical practice more in line with that of other, more advanced countries? This article describes some of the realities of veterinary medical education in China, discusses several existing problems, and puts forward some ideas for possible reforms. It is hoped that by this means those outside China may gain insight into our veterinary education program and that this, in turn, will lead to helpful input from international educators and other professionals to help improve our programs.

China↗

PubMedDate not supplied

Phenylalanine hydroxylase deficiency: intelligence of patients after early dietary treatment.

Neonatal screening for hyperphenylalaninemia (HPA) has been performed in Taiwan for more than 20 years. In this paper, we studied 21 cases of HPA caused by phenylalanine hydroxylase (PAH) deficiency. These patients were detected by a single newborn screening center over ten-years, and the incidence was one in 63,690. According to the initial plasma phenylalanine levels, four of the 21 patients belonged to classical phenylketonuria (PKU), seven were mild PKU, and ten were mild HPA. They commenced diet control at the age of 47 +/- 22 (17-106) days. Fourteen patients completed IQ tests, three of the 14 patients having classical PKU, five having mild PKU, and six having mild HPA. Their average IQ scores were within normal ranges (full-scale IQ 98 +/- 14, verbal IQ 92 +/- 8, and performance IQ 104 +/- 19), but patients with classical PKU tended to have lower IQ scores than other patients. Since classical PKU is rare in Taiwan, further studies including detailed neuropsychological tests will be required to evaluate the effect of treatment in this group of patients.

Age Factors↗