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Biomedical subjects

Chia-Yu Chu

Publications and source records attributed to Chia-Yu Chu.

18 recordsLinked to original sources

Staphylococcus colonization in atopic dermatitis treated with fluticasone or tacrolimus with or without antibiotics.

BACKGROUND: The skin of patients with atopic dermatitis (AD) exhibits a striking susceptibility to colonization and infection by Staphylococcus aureus. Treatment with topical anti-inflammatory drugs alone can reduce S. aureus colonization. OBJECTIVES: To compare the clinical severity of AD and the S. aureus colonization rate between AD patients treated with topical glucocorticoids and those treated with tacrolimus and to evaluate the effects of complementary topical antistaphylococcal antibiotic therapy and the development of fusidic acid-resistant S. aureus. METHODS: Sixty AD patients were enrolled in a prospective, parallel, randomized study of an 8-week treatment with topical 0.05% fluticasone propionate or 0.03% tacrolimus, with or without complementary fusidic acid. Disease severity scoring of AD based on SCORing of Atopic Dermatitis (SCORAD), colonization rate and density of S. aureus on the skin, and antibiotic susceptibility of S. aureus isolates were evaluated. RESULTS: The reduction in SCORAD scores correlated with the reduction of S. aureus numbers. Treatment with topical tacrolimus resulted in a comparable reduction in SCORAD scores to fluticasone but a slower eradication of S. aureus. Complementary fusidic acid had no additional benefit compared with fluticasone or tacrolimus alone. Two patients developed fusidic acid-resistant S. aureus after 8 weeks of fusidic acid treatment. CONCLUSION: Tacrolimus is an appropriate alternative treatment for chronic AD. Topical anti-inflammatory therapy alone to improve the allergic skin inflammation of AD can reduce S. aureus colonization of the skin. Topical antibiotics should be reserved for short-term use in obvious secondary bacterial infection.

Adolescent↗

Multiple eruptive dermatofibromas in a patient with dermatomyositis taking prednisolone and methotrexate.

Dermatofibroma (DF) is a common, benign, dermal tumor, often occurring as a single lesion. Multiple eruptive DFs are rare and usually associated with autoimmune diseases, immunosuppressant therapy, or both. We present the case of a 28-year-old woman with dermatomyositis who developed multiple eruptive DFs after undergoing methotrexate and corticosteroid treatment. Immunosuppressants such as methotrexate and corticosteroids might cause multiple eruptive DFs.

Adult↗

Effect of connective tissue growth factor on hypoxia-inducible factor 1alpha degradation and tumor angiogenesis.

BACKGROUND: Connective tissue growth factor (CTGF) inhibits the metastatic activity of human lung cancer cells in a mouse model; however, the mechanism of this modulation is unclear. We investigated the role of angiogenesis in this process. METHODS: CL1-5 and A549 human lung adenocarcinoma cells were stably transfected with vectors containing CTGF or hypoxia-inducible factor (HIF) 1alpha or with vector controls. Transfected cells were injected into nude mice (n = 10 per group), and tumor growth, metastasis, and mouse survival were measured. Excised xenograft tumors and primary human lung adenocarcinomas (n = 24) were subjected to immunohistochemistry with antibodies to the endothelial cell marker CD31 and to CTGF. Expression of HIF-1alpha and vascular endothelial growth factor (VEGF) A was assessed in vitro by using reporter gene assays. Cells were transiently transfected with HIF-1alpha mutant and antisense arrest-defective 1 protein (ARD-1), and HIF-1alpha acetylation was assayed by immunoprecipitation. All statistical tests were two-sided. RESULTS: Xenograft tumors derived from CTGF transfectants grew more slowly than those from control-transfected cells and had reduced expression of HIF-1alpha and VEGF-A, vascularization (as assessed by CD31 expression), and metastasis (all P<.001). Xenograft tumors derived from CTGF-overexpressing cells that were transfected with HIF-1alpha had higher VEGF-A expression than CTGF-overexpressing xenografts. Mice with CTGF/HIF-1alpha xenografts had lower survival than mice carrying CTGF-overexpressing xenografts (CL1-5/Neo, mean = 69.6 days, 95% confidence interval [CI] = 53.9 to 85.3 days versus CL1-5/CTGF, mean = 102.1 days, 95% CI = 92.1 to 112.1 days; P = .001, CL1-5/CTGF, mean = 102.1 days, 95% CI = 92.1 to 112.1 days versus CL1-5/CTGF/HIF-1alpha, mean = 81.7 days, 95% CI = 66.5 to 96.9 days; P = .011, CL1-5/Neo, mean = 69.6 days, 95% CI = 53.9 to 85.3 days versus CL1-5/CTGF/HIF-1alpha, mean = 81.7 days, 95% CI = 66.5 to 96.9 days; P = .122). Tumors of patients with the same disease stage but with high CTGF protein expression had reduced microvessel density compared with tumors with low expression. Transfection with antisense-ARD1 decreased the level of acetylated HIF-1alpha and restored HIF-1alpha and VEGF-A expression in CTGF-overexpressing cells. CONCLUSION: CTGF inhibition of metastasis involves the inhibition of VEGF-A-dependent angiogenesis, possibly by promoting HIF-1alpha protein degradation.

Acetylation↗

Cyclooxygenase-2 overexpression in human basal cell carcinoma cell line increases antiapoptosis, angiogenesis, and tumorigenesis.

Cyclooxygenase-2 (COX-2) is critical for tumor formation, angiogenesis, metastasis, and prognosis. In this study, the role of COX-2 in antiapoptosis, tumorigenesis, and angiogenesis of human basal cell carcinoma (BCC) cells was investigated. Transfection of COX-2 constitutive expression vector into a BCC cell line yielded several overexpressing clones. All transfectants demonstrated remarkable resistance to ultraviolet B-induced apoptosis (confirmed by flow cytometry analysis, morphological change, and DNA fragmentation). Immunoblot analysis revealed marked increases in apoptosis-regulated genes Mcl-1 and Bcl-2. A 10-fold concentrated conditioned medium from COX-2-overexpressing BCC cells exhibited higher angiogenic activity in Matrigel plug and human umbilical vein endothelial cell tube formation assay. Cells exhibited increased levels of vascular endothelial growth factor-A (VEGF-A) mRNA and protein, and secreted VEGF-A and basic fibroblast growth factor (bFGF). COX-2-specific small interfering RNA markedly reduced the secreted species. After 7 weeks of inoculation, the tumor volume of COX-2-overexpressing cells in severe combined immunodeficient mice was significantly greater than that of vector control cells. Immunohistochemical analysis of CD31-positive vessels revealed a two-fold increase in microvessel density in COX-2 tumors, compared to control vector tumors. Our data indicate that Mcl-1 and Bcl-2, as well as VEGF-A and bFGF, are downstream effectors of COX-2-induced antiapoptosis and angiogenesis, respectively.

Animals↗

Concomitant contact allergy to the resins, reactive diluents and hardener of a bisphenol A/F-based epoxy resin in subway construction workers.

An outbreak of suspected contact dermatitis among subway construction workers was suspected to be due to a new bisphenol A/F-based epoxy resin system (ERS). The construction workers used ERSs during the insertion of iron bars into concrete walls. The objective of the study was to determine the components (if any) of the ERS responsible for the contact allergy. Patch testing was performed on 20 of the 22 construction workers who had had contact with the ERS, and to the various subcomponents of component A on 5 of the 7 who reacted to this component. 9 patients (9/22, 40.9%) had clinical symptoms and signs of suspected contact dermatitis at presentation. 7 of these 9, but none of the 11 asymptomatic individuals, were positive to component A, while all were negative to component B. Of the 5 cases receiving further patch testing, all reacted to m-xylylene diamine, 4 to 1,6-hexanediol diglycidyl ether, 3 to epoxy resins of the bisphenol F-type and trimethylolpropane triglycidyl ether 0.25% petrolatum, and only 1 to epoxy resins of the bisphenol A-type. Contact allergy to ERSs may involve hardeners and diluents as well as resins, and patch testing for reaction to all components should be performed.

Adolescent↗

HLA-B*5801 allele as a genetic marker for severe cutaneous adverse reactions caused by allopurinol.

Allopurinol, a commonly prescribed medication for gout and hyperuricemia, is a frequent cause of severe cutaneous adverse reactions (SCAR), which include the drug hypersensitivity syndrome, Stevens-Johnson syndrome, and toxic epidermal necrolysis. The adverse events are unpredictable and carry significant morbidity and mortality. To identify genetic markers for allopurinol-SCAR, we carried out a case-control association study. We enrolled 51 patients with allopurinol-SCAR and 228 control individuals (135 allopurinol-tolerant subjects and 93 healthy subjects from the general population), and genotyped for 823 SNPs in genes related to drug metabolism and immune response. The initial screen revealed strong association between allopurinol-SCAR and SNPs in the MHC region, including BAT3 (encoding HLA-B associated transcript 3), MSH5 (mutS homolog 5), and MICB (MHC class I polypeptide-related sequence B) (P < 10(-7)). We then determined the alleles of HLA loci A, B, C, and DRB1. The HLA-B*5801 allele was present in all (100%) 51 patients with allopurinol-SCAR, but only in 20 (15%) of 135 tolerant patients [odds ratio 580.3 (95% confidence interval, 34.4-9780.9); corrected P value = 4.7 x 10(-24)] and in 19 (20%) of 93 of healthy subjects [393.51 (23.23-6665.26); corrected P value = 8.1 x 10(-18)]. HLA alleles A*3303, Cw*0302, and DRB1*0301 were in linkage disequilibrium and formed an extended haplotype with HLA-B*5801. Our results indicated that allopurinol-SCAR is strongly associated with a genetic predisposition in Han Chinese. In particular, HLA-B*5801 allele is an important genetic risk factor for this life-threatening condition.

Aged↗

Disseminated human papillomavirus type 11 infection in a patient with pemphigus vulgaris: confirmed by DNA analysis.

Depending on the type of epithelium infected, human papillomaviruses (HPVs) are often subclassified as "cutaneous" or "mucosal" types of HPV. HPV type 11 is a mucosal type of virus and infects the genital tract or larynx. Disseminated HPV-11 infection involving multiple body sites in cases of pemphigus vulgaris (PV) has not been reported. We report here an unusual case of severe pemphigus vulgaris associated with disseminated HPV-11 infection on the arms, hands, axillae, chest, abdomen, and both thighs from the genital area, confirmed by the same DNA sequence.

Adult↗

1,2-Ethanedithiol-induced erythema multiforme-like contact dermatitis.

Contact dermatitis simulating erythema multiforme can be caused by many allergens. The chemical agent 1,2-ethanedithiol, which serves as a protective group in chemical synthesis, has hitherto only been implicated as an irritant. We report on a 22-year-old female chemistry student who developed widespread erythema multiforme-like lesions after local contact with 1,2-ethanedithiol. Many target lesions were observed bilaterally on her hands, forearms, arms, and on her forehead. One such lesion was histologically compatible with erythema multiforme. The patient had a positive patch test to 1,2-ethanedithiol, whereas none of 30 healthy subjects showed a positive reaction. However, eight of the 30 controls (26.7%) developed irritant reactions to 1,2-ethanedithiol. Cautious handling of the compound is a prudent precaution.

Adrenal Cortex Hormones↗

Interleukin-6 induced basic fibroblast growth factor-dependent angiogenesis in basal cell carcinoma cell line via JAK/STAT3 and PI3-kinase/Akt pathways.

We have previously demonstrated a xenograft of interleukin-6 (IL-6) overexpressing basal cell carcinoma (BCC) cell line induced tumors with high vasculature in nude mice. Here we asked whether IL-6 could induce angiogenic activity in BCC cell line. Tenfold concentrated conditioned medium (CM) from IL-6 overexpressing BCC cells exhibited higher angiogenic activities in chorioallantoic membrane and Matrigel plug assays, when compared with CM from vector control or parental BCC cells. The level of basic fibroblast growth factor 2 (bFGF) mRNA and secreted bFGF increased in IL-6 overexpressing BCC cells as shown by RT-PCR and ELISA, respectively. Concordantly, recombinant IL-6 treatment caused the elevation of bFGF mRNA and protein levels in parental BCC cells in a time-dependent manner. Neutralizing bFGF function by anti-bFGF antibody significantly inhibited CM-induced human umbilical vein endothelial cells (HUVEC) tube formation and Matrigel plug formation. Meanwhile, cyclooxygenase 2 (COX-2)-specific siRNA markedly abolish HUVEC tube formation. These data indicated both bFGF and COX-2 play an essential role for IL-6-induced angiogenesis in BCC cell line. Treatment with AG490 (Janus tyrosine kinase [JAK] inhibitor) and LY294002 (PI3-Kinase inhibitor) inhibited IL-6-mediated upregulation of bFGF mRNA and protein secretion. Consistently, transfection with dominant negative mutants of signal transducer and activator of transcription 3 (STAT3) and acutely transforming retrovirus AKT8 in rodent T cell lymphoma (Akt) effectively abolished IL-6-mediated expression of bFGF mRNA and protein. Our data suggest that under in vitro experimental condition, bFGF and COX-2 are downstream effectors of IL-6-induced angiogenic activity in BCC cell. The IL-6-mediated bFGF upregulation is through activation of JAK/STAT3 and PI3-Kinase/Akt pathways.

Antibodies↗

Transformation between Kaposiform hemangioendothelioma and tufted angioma.

Kaposiform hemangioendothelioma and tufted angioma are viewed as two separate disease entities in the current classification of vascular tumors. However, the concurrence of features of both vascular tumors in the same specimen of some patients raises the question whether these tumors exist on a continuum. Herein, we report a dynamic transformation between both tumors within a single patient, which suggests they are two variants of the same vascular tumor.

Adult↗

HLA-Cw6 specificity and polymorphic residues are associated with susceptibility among Chinese psoriatics in Taiwan.

Previous serotyping in Chinese patients has failed to confirm an association between HLA-Cw6 and psoriasis. As serotyping has proved to be less valuable in the determination of HLA-C, genotyping of HLA-C in 68 Taiwanese psoriasis vulgaris (PSV) patients was performed using polymerase chain reaction/sequence-specific oligonucleotide probe hybridization (PCR-SSOPH) of HLA-Cw genes. Compared to 213 non-PSV control subjects, HLA-Cw6 was significantly associated with PSV (16.18% of PSV patients vs 5.16% of controls; odds ratio 3.53, Pc</=10(-4)). The amino acid residues on the heavy chain of the HLA-Cw antigens from exon one to exon five were also analyzed. Asp 9, Ser 24, Ala 73, Asp 90, Trp 97, Trp 156 and Asn 77/Lys 80 were found to be positively associated with PSV ( Pc</=0.0044, 0.0008, 0.0026, 0.0014, 0.039, 0.0020 and 0.0000, respectively).

Adolescent↗