An association study with Korean alcoholic patients(n=50) and normal controls(n=53) was performed to find the relationship between catechol-O-methyltransferase(COMT) gene polymorphism and alcoholism using polymerase chain reaction-restriction fragment length polymorphism. When we compared the allele and genotype frequencies of Nla III COMT gene polymorphism in alcoholism and normal controls, there was no significant difference between two groups. Our results do not support an association between the Nla III polymorphism of COMT gene and alcoholism.
Alcoholics ; Alcoholism* ; Alleles ; Genotype ; Humans

Isolated fetal ascites may be different from general category of nonimmune hydrops in both prenatal course and prognosis. We experienced one case of isolated fetal ascites of unknown origin treated by in utero ultrasound-directed paracentesis and so present it with brief review of literature.
Ascites* ; Edema ; Paracentesis* ; Prognosis

No abstract available.
Lymphangioma, Cystic* ; Turner Syndrome* ; Ultrasonography*

No abstract available.
Hernia, Inguinal* ; Humans ; Peritoneal Dialysis, Continuous Ambulatory* ; Radionuclide Imaging*

No abstract available.
Humans ; Renal Insufficiency, Chronic* ; Rhabdomyolysis*

OBJECTIVE: Persistent infection of HPV increases the chance of carcinoma in situ of cervix through stages of cervical intraepithelial neoplasia (CIN) 1, 2, and 3, and finally progresses into cervical cancer. We aimed to explore the safety and efficacy of BLS-M07 which is orally administered agent expressing human papillomavirus (HPV) 16 E7 antigen on the surface of Lactobacillus casei in patients with CIN 3. METHODS: Patients with CIN 3 were recruited in our clinical trial. Reid Colposcopic Index (RCI) grading and serum HPV16 E7 specific antibody production were used to evaluate efficacy of BLS-M07. In phase 1, BLS-M07 was administered orally, 5 times a week, on weeks 1, 2, 4, and 8 with dosages of 500 mg, 1,000 mg, and 1,500 mg. In phase 2a, patients were treated with 1,000 mg. The primary endpoints were the safety and the pathologic regression on colposcopic biopsy. RESULTS: Nineteen patients were enrolled in the CIN 3 cohort. In phase 1, no patients experienced dose limiting toxicity. No grade 3 or 4 treatment-related adverse events or deaths were observed. At 16 weeks after treatment, RCI grading was improved and serum HPV16 E7 specific antibody production increased (p<0.05). Six of 8 (75%) patients with CIN 3 were cured in phase 2a. CONCLUSIONS: Oral immunization with BLS-M07 increases production of serum HPV16 E7 specific antibody which induces protective humoral immunity. The safety of this oral vaccine was proved and could be a competitive non-surgical therapeutic agent of CIN 3. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT02195089
Antibody Formation ; Biopsy ; Carcinoma in Situ ; Cervical Intraepithelial Neoplasia ; Cervix Uteri ; Cohort Studies ; Female ; Humans ; Immunity, Humoral ; Immunization ; Lactobacillus casei ; Papillomavirus E7 Proteins ; Papillomavirus Vaccines ; Uterine Cervical Neoplasms

BACKGROUND: Arginine vasopressin (AVP) is widely used as a vasopressor agent. Some recent studies have suggested that AVP may exert an immunomodulatory effect. However, the mechanism about the anti-inflammatory effect of AVP is not well known. We investigated the effect of AVP on the ihibitor of kappa B (IkappaBalpha)/nuclear factor-kappa B (NF-kappaB) pathway in RAW 264.7 cells. METHODS: Cultured RAW 264.7 cells were pretreated with AVP and stimulated with lipopolysaccharide (LPS). To evaluate the effect of AVP on inflammatory cytokines, the concentration of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were assessed by an enzyme-linked immunosorbent assay technique. The expression of IkappaBalpha and nuclear translocation of NF-kappaB p65 were measured by Western blotting, and IkappaB kinase (IKK) activity was analyzed by an in vitro immune complex kinase assay. To confirm the AVP effect on IkappaBalpha/NF-kappaB cascade and via V2 receptor, we added tolvaptan (V2 receptor antagonist) after AVP pretreatment. RESULTS: The increase of IL-6 and TNF-alpha in LPS-stimulated RAW 264.7 cells was suppressed by a treatment with AVP. Pretreatment of AVP inhibited increasing of IKK activity and IkappaBalpha degradation induced by LPS in RAW 264.7 cells. Furthermore, LPS induced and NF-kappaB transcription was inhibited by AVP pretreatment. The observed changes in IKK activity, IkappaBalpha degradation and NF-kappaB transcription by AVP was abolished by tolvaptan treatment. CONCLUSIONS: Our results suggest that AVP showed anti-inflammatory effect on LPS-induced IkappaBalpha/NF-kappaB cascade in mouse macrophages via V2 receptors.
Animals ; Antigen-Antibody Complex ; Arginine Vasopressin ; Blotting, Western ; Cytokines ; Enzyme-Linked Immunosorbent Assay ; I-kappa B Kinase ; Interleukin-6 ; Macrophages ; Mice ; NF-kappa B ; Phosphotransferases ; Receptors, Vasopressin ; Tumor Necrosis Factor-alpha

Bartter syndrome is a renal tubular defect in electrolyte transport characterized by hypokalemia, metabolic alkalosis, hyperreninemia, hyperaldosteronism, normal blood pressure, and other clinical symptoms. As a clinical and genetical heterogeneous disorder, this syndrome can be classified into two clinical variants, antenatal Bartter syndrome and classic Bartter syndrome according to the onset age. Nephrocalcinosis is common in antenatal Bartter syndrome, but is rare in classic Bartter syndrome. It can also be classified into five genetic subtypes by the underlying mutant gene, all of which are expressed in the tubular epithelial cells of the thick ascending limb of the loop of Henle. Patients with Bartter syndrome type 1, 2 and 4 present at a younger age than classic Bartter syndrome type 3. We have experienced a case of Bartter syndrome with nephrocalcinosis in a 42-year-old woman diagnosed by biochemical and radiologic studies. We had successful response with potassium chloride and spironolactone.
Adult* ; Age of Onset ; Alkalosis ; Bartter Syndrome* ; Blood Pressure ; Epithelial Cells ; Extremities ; Female ; Humans ; Hyperaldosteronism ; Hypokalemia ; Loop of Henle ; Nephrocalcinosis* ; Potassium Chloride ; Spironolactone

BACKGROUND: One of the important mechanisms responsible for a tumor escaping the immune response is an absence of the tumor associated antigen (TAA) on the cancer cell surface. To overcome this, combination gene therapy using a herpes simplex thymidine kinase (HSTK) gene, prototype of drug sensitizing gene, was conducted to enhance TAA release by cell destruction, as well as the cytokine genes for immune cell attraction. METHODS: We investigated whether or not transduction with the adenovirus-HSTK (Ad-HSTK) enhanced the sensitivity of Lewis lung carcinoma (LLC) to ganciclovir (GCV) and induced a bystander effect. A Tumor vaccine trial was performed using LLC with ad-HSTK ±ad-GM-CSF±ad-IL-2 to determine if they exhibit some antitumor effect on established lung cancer xenografts. RESULTS: LLC with ad-HSTK revealed a much higher sensitivity to ganciclovir (GCV). LLC transduced with ad-HSTK and/or ad-IL-2, ad-GM-CSF showed a lower in vivo tumorigenicity. In the treatment experiment, vaccination with LLC transduced with ad-HSTK, ad-IL-2, or ad-GM-CSF alone modestly suppressed the growth of an established tumor. Combined transduction with HSTK and GM-CSF induced stronger growth suppression of a established lung cancer, while HSTK and IL-2 combination transduction did not have any antitumor effect on individual transduction. Vaccination with LLC-HSTK-GM-CSF increased the infiltration of dendritic cells in the spleen. CONCLUSION: It was concluded that a tumor vaccine transduced with HSTK and GM-CSF induces strong antitumor immunity by activating the dendritic cells.
Adenoviridae ; Animals ; Bystander Effect ; Carcinoma, Lewis Lung ; Cytokines* ; Dendritic Cells ; Ganciclovir ; Genetic Therapy* ; Granulocyte-Macrophage Colony-Stimulating Factor ; Herpes Simplex* ; Heterografts ; Interleukin-2 ; Lung Neoplasms* ; Lung* ; Phosphotransferases* ; Simplexvirus* ; Spleen ; Thymidine Kinase ; United Nations ; Vaccination

BACKGROUND: Two tumor suppressor genes, p53 and p16, which have different roles in controlling the cell cycle and inducing apoptosis, are frequently inactivated during carcinogenesis including lung cancer. Single tumor suppressor gene therapies using tither with p53 or p16 have been studied extensively. However, there is a paucity of reports regarding a combined gene therapy using these two genes. METHODS: The combined effect of p53 and p16 gene transfer by the adenoviral vector on the growth of lung cancer cell lines and its interactive mechanism was investigated. RESULTS: An isobologram showed that the co-transduction of p53 and p16 exhibited a synergistic growth inhibitory effect on NCI H358 and an additive effect on NCI H23. Cell cycle analysis demonstrated the induction of a synergistic G1/S arrest by a combined p53 and p16 transfer. This synergistic interaction was again confirmed in a soft agar clonogenic assay. CONCLUSION: These observations suggest the potential of a p53 and p16 combination gene therapy as another potent strategy in cancer gene therapy.
Adenoviridae ; Agar ; Apoptosis ; Carcinogenesis ; Cell Cycle ; Cell Line* ; Genes, Neoplasm ; Genes, p16 ; Genes, Tumor Suppressor ; Genetic Therapy ; Lung Neoplasms* ; Lung*