Objective To investigate the effects of emulsified isoflurane preconditioning on myocardial NF-κB activity during ischemia-reperfusion(I/R)in rats.Methods Forty-eight healthy male SD rats weighing 230-280 g were randomly divided into 4 groups with 12 animals in each group: sham operation group(group S),I/R group,lipid emulsion + I/R group(group L)and emulsified isoflurane + I/R group(group EI).In group I/R,EI and L,myocardial I/R was produced by occlusion of left coronary anterior descending artery(LAD)for 30 min followed by 120 min reperfusion.In group L,30% lipid emulsion 4 ml·kg-1 ·h-1 was infused intravenously for 30 min before myocardial I/R.In group EI,emulsified isoflurane 4 ml· kg- 1 · h- 1 was infused intravenously for 30 min followed by 15 min washout before myocardial I/R.In group S and I/R,normal saline was given instead.Blood samples were taken from femoral artery at the end of 120 min reperfusion for determination of serum cTnI and IL-6 concentrations and CK-MB activity by ELISA.The rats were then killed and the myocardial tissues were taken for determination of NF-κB activity by Western blot and observation of the ultrastructure by electron microscopy.Results The NF-κB activity,serum cTnI and IL-6 concentrations and CK-MB activity were significantly higher in group I/R,EI and L than in group S(P ＜ 0.05 or 0.01),while lower in group EI than in group I/R(P ＜ 0.05).Microscopic examination showed that emulsified isoflurane significantly attenuated the histopathological changes in group EI.Conclusion Emulsified isoflurane pretreatment can attenuate myocardial I/R injury through decreasing the NF-κB activity and inhibiting inflammatory response in rats.

OBJECTIVETo create transgenic mice expressing hamster- and human-PRNP as a model for understanding the physiological function and pathology of prion protein (PrP), as well as the mechanism of cross-species transmission of transmissible spongiform encephalopathies (TSEs).

METHODSHamster and human-PRNP transgenic mice were established by conventional methods. The copy number of integrated PRNP in various mouse lines was mapped by real-time PCR. PRNP mRNA and protein levels were determined by semi-quantitative RT-PCR, real-time RT-PCR, and western blot analysis. Histological analyses of transgenic mice were performed by hematoxylin and eosin (H & E) staining and immunohistochemical (IHC) methods.

RESULTSIntegrated PRNP copy number in various mouse lines was 53 (Tg-haPrP1), 18 (Tg-huPrP1), 3 (Tg-huPrP2), and 16 (Tg-huPrP5), respectively. Exogenous PrPs were expressed at both the transcriptional and translational level. Histological assays did not detect any abnormalities in brain or other organs.

CONCLUSIONWe have established one hamster-PRNP transgenic mouse line and three human-PRNP transgenic mouse lines. These four transgenic mouse lines provide ideal models for additional research.

Animals ; Blotting, Western ; Cricetinae ; DNA ; genetics ; Disease Models, Animal ; Humans ; Immunohistochemistry ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Organ Specificity ; Plasmids ; Prion Diseases ; genetics ; Prion Proteins ; Prions ; genetics ; Real-Time Polymerase Chain Reaction ; Transcription, Genetic

OBJECTIVETo investigate the clinical, pathological and immunohistochemical features of vulvar intraepithelial neoplasia (VIN).

METHODSAccording to the 2004 modified terminology of International Society for the Study of Vulvovaginal Diseases (ISSVD), the cases were diagnosed as VIN from patients who had performed vulvar biopsy in Beijing Wuzhou Women's Hospital from February 2009 to December 2011, which were reclassified as usual VIN and differentiated VIN. The clinical and pathological studies were conducted respectively. MaxVision immunohistochemical staining was used to detect the expression of Ki-67, p16 and p53 proteins.

RESULTSThere were 20 cases of VIN in 237 patients, and the incidence of VIN was 8.4% in all of contemporary vulvar biopsy. In 17 cases of usual VIN, mean age was 29.6 years, the lesion typically presented with atypical cells involving almost all layers of the epithelium, which was equivalent to the high-grade squamous intraepithelial neoplasia of cervix. Immunohistochemistry for Ki-67 and p16 was strongly positive in usual VIN. High risk human papillomavirus (HPV) detection was also positive. The incidence of differentiated VIN was less than usual VIN, and there were only 3 cases in this study. In differentiated VIN, patients aged over 50 years, with mean of 53.7 years, and the lesion most commonly presented with lichen sclerosis background. There were epithelial thickening and extending, and parakeratosis, and atypia was strictly confined to the basal and parabasal layers of the epithelium where the cells enlarged with abundant eosinophilic cytoplasm, presented with prominent nucleoli, increased cellularity and abnormal keratinization. In differentiated VIN, p53 was strongly positive, Ki-67 and p16 immunohistochemical expression was confined to the basal layer only.

CONCLUSIONSVIN is a precursor of invasive squamous cell carcinoma of the vulva. The modified terminology of ISSVD classifies VIN as high-grade lesions. Definitive pathological diagnosis of VIN plays an important role in its timely treatment and the prevention of vulvar carcinoma.

Adult ; Carcinoma in Situ ; metabolism ; pathology ; virology ; Cyclin-Dependent Kinase Inhibitor p16 ; metabolism ; Female ; Humans ; Immunohistochemistry ; Ki-67 Antigen ; metabolism ; Middle Aged ; Papillomavirus Infections ; pathology ; Tumor Suppressor Protein p53 ; metabolism ; Vulvar Neoplasms ; metabolism ; pathology ; virology ; Young Adult

Cardio-oncology is a critical field due to the escalating significance of cardiovascular toxicity as a side effect of anti‑ cancer treatments. Cancer therapy-related cardiac dysfunction (CTRCD) is a prevalent condition associated with car‑ diovascular toxicity, necessitating effective strategies for prediction, monitoring, management, and tracking. This comprehensive review examines the definition and risk stratification of CTRCD, explores monitoring approaches during anticancer therapy, and highlights specific cardiovascular toxicities linked to various cancer treatments. These include anthracyclines, HER2-targeted agents, vascular endothelial growth factor inhibitors, immune checkpoint inhibitors, chimeric antigen receptor T-cell therapies, and tumor-infiltrating lymphocytes therapies. Incorporating the Korean data, this review offers insights into the regional nuances in managing CTRCD. Using systematic follow-up incorporating cardiovascular imaging and biomarkers, a better understanding and management of CTRCD can be achieved, optimizing the cardiovascular health of both cancer patients and survivors.

Cardio-oncology is a critical field due to the escalating significance of cardiovascular toxicity as a side effect of anti‑ cancer treatments. Cancer therapy-related cardiac dysfunction (CTRCD) is a prevalent condition associated with car‑ diovascular toxicity, necessitating effective strategies for prediction, monitoring, management, and tracking. This comprehensive review examines the definition and risk stratification of CTRCD, explores monitoring approaches during anticancer therapy, and highlights specific cardiovascular toxicities linked to various cancer treatments. These include anthracyclines, HER2-targeted agents, vascular endothelial growth factor inhibitors, immune checkpoint inhibitors, chimeric antigen receptor T-cell therapies, and tumor-infiltrating lymphocytes therapies. Incorporating the Korean data, this review offers insights into the regional nuances in managing CTRCD. Using systematic follow-up incorporating cardiovascular imaging and biomarkers, a better understanding and management of CTRCD can be achieved, optimizing the cardiovascular health of both cancer patients and survivors.

Cardio-oncology is a critical field due to the escalating significance of cardiovascular toxicity as a side effect of anti‑ cancer treatments. Cancer therapy-related cardiac dysfunction (CTRCD) is a prevalent condition associated with car‑ diovascular toxicity, necessitating effective strategies for prediction, monitoring, management, and tracking. This comprehensive review examines the definition and risk stratification of CTRCD, explores monitoring approaches during anticancer therapy, and highlights specific cardiovascular toxicities linked to various cancer treatments. These include anthracyclines, HER2-targeted agents, vascular endothelial growth factor inhibitors, immune checkpoint inhibitors, chimeric antigen receptor T-cell therapies, and tumor-infiltrating lymphocytes therapies. Incorporating the Korean data, this review offers insights into the regional nuances in managing CTRCD. Using systematic follow-up incorporating cardiovascular imaging and biomarkers, a better understanding and management of CTRCD can be achieved, optimizing the cardiovascular health of both cancer patients and survivors.

Cardio-oncology is a critical field due to the escalating significance of cardiovascular toxicity as a side effect of anti‑ cancer treatments. Cancer therapy-related cardiac dysfunction (CTRCD) is a prevalent condition associated with car‑ diovascular toxicity, necessitating effective strategies for prediction, monitoring, management, and tracking. This comprehensive review examines the definition and risk stratification of CTRCD, explores monitoring approaches during anticancer therapy, and highlights specific cardiovascular toxicities linked to various cancer treatments. These include anthracyclines, HER2-targeted agents, vascular endothelial growth factor inhibitors, immune checkpoint inhibitors, chimeric antigen receptor T-cell therapies, and tumor-infiltrating lymphocytes therapies. Incorporating the Korean data, this review offers insights into the regional nuances in managing CTRCD. Using systematic follow-up incorporating cardiovascular imaging and biomarkers, a better understanding and management of CTRCD can be achieved, optimizing the cardiovascular health of both cancer patients and survivors.

OBJECTIVE: Decreased adiponectin and increased leptin plasma concentrations are believed to be associated with the occurrence and progression of cancers such as endometrial cancer and breast cancer. The aim of this study was to explore the association of plasma adiponectin and leptin levels with the development and progression of ovarian cancer. METHODS: For patients with ovarian cancer and the control group, adiponectin and leptin levels were measured; anthropometric data were obtained during a chart review. Statistical comparisons between groups were analyzed using the Student's t-test; correlations were confirmed using the Pearson correlation. RESULTS: The mean adiponectin and leptin concentrations in patients with ovarian cancer were lower than those of the control group (8.25 vs. 11.44 µg/mL, respectively; P=0.026) (7.09 vs. 15.4 ng/mL, respectively; P=0.001). However, there was no significant difference in adiponectin and leptin levels between early-stage (I/II) and advanced-stage (III/IV) disease (P=0.078). CONCLUSION: Compared with other gynecological cancers, the level of adiponectin and leptin were decreased in ovarian cancer that may have some diagnostic value; additional study to elucidate the function of these two hormones in the development of ovarian carcinogenesis is necessitated.
Adiponectin* ; Breast Neoplasms ; Carcinogenesis ; Endometrial Neoplasms ; Female ; Humans ; Leptin* ; Ovarian Neoplasms* ; Plasma*

In this study we evaluated the influence of both the thickness of residual enamel and the color of the composite resins applied to lingual surface on the labial surface color. Background plates were made by randomly (A1, A2, A6D, B1, B2, B3, C1, C2, C6D) selected colors of Filtek Supreme (3M ESPE, St. Paul, U.S.A.) composite resin. Crown portion of 9 maxillary central incisors were cut off and embedded with acrylic resin except labial surface. Samples of average thickness of 2.2 mm were obtained after cutting it in a thickness of 2.5 mm from the labial surface and sandpaper polish. The shade of composite resin background was measured using Spectrophotometer (Spectrolino(R) GretagMacbeth, Regensdorf, Switzerland). And CIE L*a*b* value of 2.2 mm thickness tooth samples were measured on the 9 composite resin backgrounds. And then, the cutting side of tooth samples was ground to the extent of 1.9 mm, 1.6 mm, 1.3 mm, 1.0 mm and placed on composite resin backgrounds and measured L*a*b* values with the same method. In all samples, L* value and b* value seemed to have a tendency of decreasing as thickness of tooth sample becomes thinner regardless of background colors (p < 0.05). But, a* value didn't show the significant differences depending on the thickness.
Composite Resins ; Crowns ; Dental Enamel ; Incisor ; Tooth

BACKGROUND: It is thought that hyperuricemia might lower the risk of mortality among hemodialysis patients, unlike in the general population, but the evidence is controversial. The aim of the current study was to evaluate the impact of serum uric acid level on the long-term clinical outcomes of hemodialysis patients in Korea. METHODS: Retrospective analysis was performed on data from the End-Stage Renal Disease Registry of the Korean Society of Nephrology. This included data for 7,333 patients (mean age, 61 ± 14 years; 61% male) who received hemodialysis from January 2001 through April 2015. Initial laboratory data were used in the analysis. RESULTS: The mean serum uric acid level in this study was 7.1 ± 1.7 mg/dL. Body mass index, normalized protein catabolic rate, albumin, and cholesterol were positively correlated with serum uric acid level after controlling for age and sex. After controlling for demographic data, comorbidities, and residual renal function, a higher uric acid level was independently associated with a significantly lower all-cause mortality (hazard ratio [HR], 0.90 per 1 mg/dL increase in uric acid level; 95% confidence interval [CI], 0.83–0.97; P = 0.008), but not cardiovascular mortality (HR, 0.90; 95% CI, 0.80–1.01; P = 0.078). Comparing uric acid levels in the highest and lowest quintiles, the HR for all-cause mortality was 0.65 (95% CI, 0.42–0.99; P = 0.046). CONCLUSION: Hyperuricemia was strongly associated with a lower risk of all-cause mortality, but there seems to be no significant association between serum uric acid level and cardiovascular mortality among Korean hemodialysis patients with end-stage renal disease.
Body Mass Index ; Cholesterol ; Comorbidity ; Humans ; Hyperuricemia ; Kidney Failure, Chronic* ; Korea ; Mortality* ; Nephrology ; Renal Dialysis* ; Retrospective Studies* ; Uric Acid*