The prevalence of latex allergies has been on the increase along with the greater use of rubber products in daily life, medical, dental and occupational settings. Allergic reactions to latex can take two clinical forms of either contact dermatitis or immediate hypersensitivity reactions, which are provoked by the natural latex proteins or chemical additives used in the manufacturing process, respectively. A 25-year-old female, an operating room nurse, complained of recurrent pruritic erythematous wheals on both hands after the wearing of latex rubber gloves. The prick test and the usage Mlit't to the latex gloves were positive, and the RAST was class 3. To the best of our knowledge, is the first case report of contact urticaria from latex rubber gloves in Korean dermatologic literature.
Adult ; Dermatitis, Contact ; Female ; Hand ; Humans ; Hypersensitivity ; Hypersensitivity, Immediate ; Latex Hypersensitivity ; Latex* ; Operating Rooms ; Prevalence ; Rubber ; Urticaria*

No abstract available.
Heart* ; Thoracic Surgery*

BACKGROUND: Ultraviolet light induces sunburn, aging of the skin, disorders of pigment and even promotes skin cancers. Melanin is known to have a protecting role in the skin by blocking ultraviolet light. OBJECTIVE: The purpose of this study was to evaluate UVA blocking effect of epidermal melanin and to compare UVA blocking effect among different anatomical sites. METHODS: From 20 vitiligo patients who had undergone an epidermal graft, we obtained epidermis of normal and vitiliginous skin and measured transmitted UVA energy density. RESULTS: The vitiliginous epidermis, devoid of melanin, blocked lower amount of UVA energy than the normal epidermis. 11.6% of irradiated UVA energy was blocked by epidermal melanin. No significant differences were observed in UVA blocking effect among different anatomical sites in normal and vitiliginous epidermis. CONCLUSION: Epidermal melanin has some UVA blocking effect. No significant differences were found in UVA blocking effect among different anatomical sites despite the differences in the density of melanin pigment among different sites of the body.
Aging ; Epidermis ; Humans ; Melanins* ; Skin ; Skin Neoplasms ; Sunburn ; Transplants ; Ultraviolet Rays ; Vitiligo*

BACKGROUND: The activity of drug metabolizing enzymes and the modulation of their expression by inducers in the skin are the key factors for understanding of pharmacological and toxic effects of topically applied drugs. The role of these enzymes is of major importance, as they may contribute to determine the steady-state levels of biologically active substances. 3-Methylcholanthrene and all-trans- retinoic acid have been known to be inducers of the drug metabolizing enzymes. And all-trans- retinoic acid has many biological actions including anti-cancer effects. OBJECTIVE: The purpose of this study was to evaluate the effect of all-trans-retinoic acid on inducing the expression and modulation of genetic polymorphism of drug metabolizing enzymes as well as to estimate the role of all-trans-retinoic acid in carcinogenesis and drug interactions. METHODS: We analyzed the activities of CYP1A1(Cytochrome P450 1Al), NADPH cytochrome P450-reductase, UGT1 and GST after administration of 3-methylcholanthrene and all-trans-retinoic acid to the Sprague-Dawley male rats. We observed the inducible gene expression of CYP1A1, UGT1, GSTJt by RT-PCR and the genetic polymorphism of CYP1A1, UGT1, GSTK by PCR. RESULTS: 1. The expression of CYP1A1, NADPH cytochrome P450-reductase, UGT1 and GST was induced by 3-methylcholanthrene and all-trans-retinoic acid. That of NADPH cytochrome P450-reductase and UGT1 is pronouncedly enhanced by all-trans- retinoic acid. 2. The effects of 3-methylcholanthrene and all-trans-retinoic acid on inducing the expression of CYP1A1 and UGT1 correlated with an increase of mRNA expression levels of CYP1A1 and UGT1. The modulation of mRNA expression levels of GST was downregulated by all-trans-retinoic acid. 3. The genetic polymorphism of CYP1A1 was induced by 3-methylcholanthrene and all-trans- retinoic acid, and that of GSTM1 was not affected by the inducers. The induction of genetic polymorphism of GST was down regulated by all-trans-retinoic acid. CONCLUSION: 3-Methylcholanthrene and all-trans-retinoic acid modulate the inducible expression and genetic polymorphism of drug metabolizing enzymes differentially. All-trans-retinoic acid can modulate the metabolism of procarcinogen such as 3-methylcholanthrene by inducing drug metabolizing enzymes. Furthermore, the elucidation of the molecular mechanisms underlying the regulation of drug metabolizing enzymes by 3-methylcholanthrene, all-trans-retinoic acid and other drugs could help to understand their respective roles in drug interactions and carcinogenesis.
Animals ; Carcinogenesis ; Cytochrome P-450 CYP1A1 ; Cytochromes ; Drug Interactions ; Gene Expression* ; Humans ; Male ; Metabolism ; Methylcholanthrene ; NADP ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Rats* ; Rats, Sprague-Dawley ; RNA, Messenger ; Skin* ; Tretinoin*

One case of cerebral embolism developed during cessation of supraventricular tachycardia in Wolff-Parkinson-White syndrome is reported with brief review. Twenty five years old, male was admitted to Seoul National University hospital with palpitation. He had numerous episodes of paroxysmal tachycardia for 3 years. He was diagnosed as Wolff-Parkinson-White syndrome at this hospital, ca 6 months prior to admission. Wolff-Parkinson-White syndrome was improved with atropine test at that time. The electrocardiogram on admission revealed Wolff-Parkinson-White synd rome associated with supraventricular tachycardia. He developed cerebral embolism after paroxysmal tachycardia of 22 days.
Atropine ; Electrocardiography ; Humans ; Intracranial Embolism* ; Male ; Seoul ; Tachycardia, Paroxysmal* ; Tachycardia, Supraventricular ; Wolff-Parkinson-White Syndrome*

We found a mistake in our recently published article.

Chromosomal alterations are frequent events in lung cancer progression. Although gains and losses of chromosomal position have been reported, the association between copy number alteration and lung cancer patient survival has not been extensively investigated. In this study, we performed a meta-analysis of public cBioPortal datasets spanning 25 lung cancer studies to identify putative cancer driver genes with copy number alterations associated with overall patient survival. Ten copy-number altered genes enriched in deceased lung cancer patients were identified. Seven of these putative driver genes were located in the 7p11.2 chromosomal location, and two were in the 9p21.3 cytoband. Among these genes, the mitochondrial ribosomal protein S17 (MRPS17) amplification was significantly associated with a lower patient survival rate (P = 1.47e-7). To investigate the functional role of MRPS17, small interfering RNA-mediated knockdown was performed in two non-small cell lung cancer cell lines, A549 and NCI-H460. MRPS17 knockdown significantly reduced cell proliferation, migration, invasion, and anchorage-independent growth in both cell lines. Furthermore, knockdown of MRPS17 decreased the activation of the phosphatidylinositol 3-kinase/protein kinase B signaling pathway, suggesting its role in driving lung cancer progression through this critical oncogenic pathway. Our findings highlight MRPS17 as a potential cancer therapy target and a prognostic biomarker that may improve the survival rates of lung cancer patients. Future studies should explore its inhibition as a therapeutic strategy as well as elucidate its molecular mechanisms in cancer progression.

Chromosomal alterations are frequent events in lung cancer progression. Although gains and losses of chromosomal position have been reported, the association between copy number alteration and lung cancer patient survival has not been extensively investigated. In this study, we performed a meta-analysis of public cBioPortal datasets spanning 25 lung cancer studies to identify putative cancer driver genes with copy number alterations associated with overall patient survival. Ten copy-number altered genes enriched in deceased lung cancer patients were identified. Seven of these putative driver genes were located in the 7p11.2 chromosomal location, and two were in the 9p21.3 cytoband. Among these genes, the mitochondrial ribosomal protein S17 (MRPS17) amplification was significantly associated with a lower patient survival rate (P = 1.47e-7). To investigate the functional role of MRPS17, small interfering RNA-mediated knockdown was performed in two non-small cell lung cancer cell lines, A549 and NCI-H460. MRPS17 knockdown significantly reduced cell proliferation, migration, invasion, and anchorage-independent growth in both cell lines. Furthermore, knockdown of MRPS17 decreased the activation of the phosphatidylinositol 3-kinase/protein kinase B signaling pathway, suggesting its role in driving lung cancer progression through this critical oncogenic pathway. Our findings highlight MRPS17 as a potential cancer therapy target and a prognostic biomarker that may improve the survival rates of lung cancer patients. Future studies should explore its inhibition as a therapeutic strategy as well as elucidate its molecular mechanisms in cancer progression.

Chromosomal alterations are frequent events in lung cancer progression. Although gains and losses of chromosomal position have been reported, the association between copy number alteration and lung cancer patient survival has not been extensively investigated. In this study, we performed a meta-analysis of public cBioPortal datasets spanning 25 lung cancer studies to identify putative cancer driver genes with copy number alterations associated with overall patient survival. Ten copy-number altered genes enriched in deceased lung cancer patients were identified. Seven of these putative driver genes were located in the 7p11.2 chromosomal location, and two were in the 9p21.3 cytoband. Among these genes, the mitochondrial ribosomal protein S17 (MRPS17) amplification was significantly associated with a lower patient survival rate (P = 1.47e-7). To investigate the functional role of MRPS17, small interfering RNA-mediated knockdown was performed in two non-small cell lung cancer cell lines, A549 and NCI-H460. MRPS17 knockdown significantly reduced cell proliferation, migration, invasion, and anchorage-independent growth in both cell lines. Furthermore, knockdown of MRPS17 decreased the activation of the phosphatidylinositol 3-kinase/protein kinase B signaling pathway, suggesting its role in driving lung cancer progression through this critical oncogenic pathway. Our findings highlight MRPS17 as a potential cancer therapy target and a prognostic biomarker that may improve the survival rates of lung cancer patients. Future studies should explore its inhibition as a therapeutic strategy as well as elucidate its molecular mechanisms in cancer progression.

Background: Little is known regarding the effects of continuous positive airway pressure (CPAP) on sleep misperception in obstructive sleep apnea (OSA). Methods: Sleep state perception was measured by subtracting the objective total sleep time from the subjective sleep duration. Sleep underestimation and overestimation were defined as ± 60 minutes sleep perception. Insomnia and depressive symptoms were assessed using questionnaires. Finally, nonparametric statistical analyses were performed. Results: Of the 339 patients with OSA included in the study, 90 (26.5%) and 45 (13.3%) showed sleep underestimation and overestimation, respectively. Overall, a significant underestimation of sleep was noted during CPAP titration comparing to a diagnostic PSG (P < 0.001). OSA patients with insomnia or depressive symptoms did not show any changes in sleep perception between diagnostic and CPAP titration studies, whereas those without insomnia or depressed mood showed significantly underestimated sleep duration during CPAP titration. Patients with OSA and either underestimated or overestimated misperception showed perceptual improvements during CPAP titration regardless of the presence of insomnia or depressive symptoms. However, of 204 patients with normal sleep perception, 138 (67.6%) and 10 (4.9%) had underestimation and overestimation of sleep during CPAP titration. Conclusion CPAP titration may improve sleep perception with moderate to severe OSA who have sleep misperception. However, CPAP titration may result in sleep misperception especially underestimation of sleep in those who have normal sleep perception.