No abstract available.

PURPOSE: Peritoneal dialysis (PD) catheter removal is regarded as an important index of patient morbidity. The aim of this study was to evaluate factors influencing catheter loss following peritonitis in PD patients. METHODS: We retrospectively reviewed 917 episodes of peritonitis in 621 new CAPD patients from Jan 2001 to Feb. 2009 in Dongsan Medical center. Episodes requiring PD catheter removal were compared by both univariate and multivariate analyses with those in which PD catheters were preserved. RESULTS: When peritonitis episodes requiring PD catheter removal (n=80) were compared to catheter preserved peritonitis episodes (n=837), the incidence of PD catheter loss increased as the duration on PD preceding the peritonitis were longer (p<0.000). Also, PD catheter removal was more likely to occur after peritonitis episodes with low serum albumin level (p=0.009) and high serum CRP level (p<0.000), those with long duration of PD effluent leukocyte count remaining above 100/mm3 (p<0.000), those with concomitant exit site/tunnel infection (p=0.043), and those with presence of abdominal pathology (p<0.000). The microbiological determinants of PD catheter loss included two or more bacteria cultured (p=0.002) and fungi (p<0.000). In multivariate analysis, the duration of PD effluent leukocyte count remaining above 100/mL and the number of organism cultured were independent risk factors of PD catheter removal in peritonitis episodes. CONCLUSION: Duration of PD effluent leukocyte count remaining above 100/mm3, and the number of organisms cultured were independent risk factors for catheter removal following peritonitis.
Bacteria ; Catheters ; Device Removal ; Fungi ; Humans ; Incidence ; Leukocyte Count ; Multivariate Analysis ; Peritoneal Dialysis ; Peritoneal Dialysis, Continuous Ambulatory ; Peritonitis ; Retrospective Studies ; Risk Factors ; Serum Albumin

BACKGROUND: STDs are major communicable disease group in Korea. This study was carried out to evaluate the current status of sexually transmitted diseases in Seoul. METHODS: We collected the laboratory data of those who visited 11 Public Health Centers in Seoul for venereal disease examination and analyzed abnormal results from Jan 1, 1993 to Dec 31, 1995. The diagnoses of STDs were made by VDRL quantification, TPHA test, Gram's stain, and culture of urine or urethral discharge. RESULTS: There were total of 10,302 patients. There were 7,836 male cases(76.1%) and 2,466 female cases (23.9%). Mean age was 30.6+/-9.7, and the most common age group was 25-34 yearn of age(42.1%). Diagnoses were as follows ; syphilis 2,036 cases(19.8%), gonorrhea 2,249 cases(21.8%), nongonococcal urethritis 4,973 cases(48.3%), vaginitis 954 cases(9.3%), mixed infection of syphilis and gonorrhea 13 cases(0.1% ), mixed infection of syphilis and NGU 50 cases(0.5%), mixed infection of syphilis and vaginitis 27 cases(0.3%). The proportion of PPNG among gonorrhea was as follows ; 43.4% in 1993, 55.1% in 1994, 43.8% in 1995. There were more WBCs on Gram's staining in gonorrhea cases than in NGU cases. CONCLUSIONS: The STD patients seen in 11 Public Health Centers in Seoul were mainly young men. Common diagnoses were as follows ; NGU, gonorrhea, syphilis, vaginitis. The proportion of PPNG increased at first and then decreased.
Coinfection ; Communicable Diseases ; Diagnosis ; Female ; Gonorrhea ; Humans ; Korea ; Male ; Public Health* ; Seoul* ; Sexually Transmitted Diseases* ; Syphilis ; Urethritis ; Vaginitis

Cardiac arrest (CA) is sudden loss of heart function and abrupt stop in effective blood flow to the body. The patients who initially achieve return of spontaneous circulation (RoSC) after CA have low survival rate. It has been known that multiorgan dysfunctions after RoSC are associated with high morbidity and mortality. Most previous studies have focused on the heart and brain in RoSC after CA. Therefore, the aim of this research was to perform serological, physiological, and histopathology study in the lung and to determine whether or how pulmonary dysfunction is associated with low survival rate after CA. Experimental animals were divided into sham-operated group (n=14 at each point in time), which was not subjected to CA operation, and CA-operated group (n=14 at each point in time), which was subjected to CA. The rats in each group were sacrificed at 6 hours, 12 hours, 24 hours, and 2 days, respectively, after RoSC. Then, pathological changes of the lungs were analyzed by hematoxylin and eosin staining, Western blot and immunohistochemistry for tumor necrosis factor α (TNF-α). The survival rate after CA was decreased with time past. We found that histopathological score and TNF-α immunoreactivity were significantly increased in the lung after CA. These results indicate that inflammation triggered by ischemia-reperfusion damage after CA leads to pulmonary injury/dysfunctions and contributes to low survival rate. In addition, the finding of increase in TNF-α via inflammation in the lung after CA would be able to utilize therapeutic or diagnostic measures in the future.
Animals ; Blotting, Western ; Brain ; Eosine Yellowish-(YS) ; Heart ; Heart Arrest* ; Hematoxylin ; Humans ; Immunohistochemistry ; Inflammation ; Lung* ; Models, Animal* ; Mortality ; Rats* ; Survival Rate ; Tumor Necrosis Factor-alpha*

Background: Hypothermic treatment is known to protect organs against cardiac arrest (CA) and improves survival rate. However, few studies have evaluated the effects of hypothermia on CA-induced liver damages. This study was designed to analyzed the possible protective effects of hypothermia on the liver after asphyxial CA (ACA). Rats were randomly subjected to 5 min of ACA followed by return of spontaneous circulation (ROSC). Body temperature was controlled at 37 ± 0.5 °C (normothermia group) or 33 ± 0.5 °C (hypothermia group) for 4 h after ROSC. Liver tissues were extracted and examined at 6 h, 12 h, 1 day, and 2 days after ROSC. Results: The expression of infiltrated neutrophil marker CD11b and matrix metallopeptidase-9 (MMP9) was investigated via immunohistochemistry. Morphological damage was assessed via hematoxylin and eosin (H & E) staining. Hypothermic treatment improved the survival rate at 6 h, 12 h, 1 day, and 2 days after ACA. Based on immunohistochemical analysis, the expression of CD11b and MMP9 was significantly increased from 6 h after ACA in the normothermia group. However, the expressions of CD11b and MMP9 was significantly decreased in the hypothermia group compared with that of the normothermia group. In addition, in the results of H & E, sinusoidal dilatation and vacuolization were apparent after ACA; however, these ACA-induced structural changes were reduced by the 4 h-long hypothermia. Conclusions In conclusion, hypothermic treatment for 4 h inhibited the increases in CD11b and MMP9 expression and reduced the morphological damages in the liver following ACA in rats. This study suggests that hypothermic treatment after ACA reduces liver damages by regulating the expression of CD11b and MMP9.

Obesity has been known as an independent risk factor for stroke. Effects of high-fat diet (HFD)-induced obesity on neuronal damage in the somatosensory cortex of animal models of cerebral ischemia have not been studied yet. In this study, HFD-induced obesity was used to study the impact of obesity on neuronal damage/loss and microgliosis in the somatosensory cortex of a gerbil model of 5-min transient forebrain ischemia. We used gerbils fed normal diet (ND) and HFD and chronologically examined microgliosis (microglial cell activation) by ionized calcium-binding adapter molecule 1 (Iba-1) immunohistochemistry. In addition, we examined neuronal damage or death by using neuronal nuclear protein (NeuN, a neuronal marker) immunohistochemistry and Fluoro-Jade B (F-J B, a marker for neuronal degeneration) histofluorescence staining. We found that ischemia-induced microgliosis in ND-fed gerbils was increased from 2 days post-ischemia; however, ischemia-mediated microgliosis in HFD-fed gerbils increased from 1 day post-ischemia and more accelerated with time than that in the ND-fed gerbils. Ischemia-induced neuronal death/loss in the somatosensory cortex in the ND-fed gerbils was apparently found at 5 days post-ischemia. However, in the HFD-fed gerbils, neuronal death/loss was shown from 2 days post-ischemia and progressively exacerbated at 5 days post-ischemia. Our findings indicate that HFD can evoke earlier microgliosis and more detrimental neuronal death/loss in the somatosensory cortex after transient ischemia than ND evokes.

Background: Hypothermic treatment is known to protect organs against cardiac arrest (CA) and improves survival rate. However, few studies have evaluated the effects of hypothermia on CA-induced liver damages. This study was designed to analyzed the possible protective effects of hypothermia on the liver after asphyxial CA (ACA). Rats were randomly subjected to 5 min of ACA followed by return of spontaneous circulation (ROSC). Body temperature was controlled at 37 ± 0.5 °C (normothermia group) or 33 ± 0.5 °C (hypothermia group) for 4 h after ROSC. Liver tissues were extracted and examined at 6 h, 12 h, 1 day, and 2 days after ROSC. Results: The expression of infiltrated neutrophil marker CD11b and matrix metallopeptidase-9 (MMP9) was investigated via immunohistochemistry. Morphological damage was assessed via hematoxylin and eosin (H & E) staining. Hypothermic treatment improved the survival rate at 6 h, 12 h, 1 day, and 2 days after ACA. Based on immunohistochemical analysis, the expression of CD11b and MMP9 was significantly increased from 6 h after ACA in the normothermia group. However, the expressions of CD11b and MMP9 was significantly decreased in the hypothermia group compared with that of the normothermia group. In addition, in the results of H & E, sinusoidal dilatation and vacuolization were apparent after ACA; however, these ACA-induced structural changes were reduced by the 4 h-long hypothermia. Conclusions In conclusion, hypothermic treatment for 4 h inhibited the increases in CD11b and MMP9 expression and reduced the morphological damages in the liver following ACA in rats. This study suggests that hypothermic treatment after ACA reduces liver damages by regulating the expression of CD11b and MMP9.

Background: Aging is one of major causes triggering neurophysiological changes in many brain substructures, including the hippocampus, which has a major role in learning and memory. Thioredoxin (Trx) is a class of small redox proteins. Among the Trx family, Trx2 plays an important role in the regulation of mitochondrial membrane potential and is controlled by TrxR2. Hitherto, age-dependent alterations in Trx2 and TrxR2 in aged hippocampi have been poorly investigated. Therefore, the aim of this study was to examine changes in Trx2 and TrxR2 in mouse and rat hippocampi by age and to compare their differences between mice and rats. Results: Trx2 and TrxR2 levels using Western blots in mice were the highest at young age and gradually reduced with time, showing that no significant differences in the levels were found between the two subfields. In rats, however, their expression levels were the lowest at young age and gradually increased with time. Nevertheless, there were no differences in cellular distribution and morphology in their hippocampi when it was observed by cresyl violet staining. In addition, both Trx2 and TrxR2 immunoreactivities in the CA1-3 fields were mainly shown in pyramidal cells (principal cells), showing that their immunoreactivities were altered like changes in their protein levels. Conclusions Our current findings suggest that Trx2 and TrxR2 expressions in the brain may be different according to brain regions, age and species. Therefore, further studies are needed to examine the reasons of the differences of Trx2 and TrxR2 expressions in the hippocampus between mice and rats.

Background: Aging is one of major causes triggering neurophysiological changes in many brain substructures, including the hippocampus, which has a major role in learning and memory. Thioredoxin (Trx) is a class of small redox proteins. Among the Trx family, Trx2 plays an important role in the regulation of mitochondrial membrane potential and is controlled by TrxR2. Hitherto, age-dependent alterations in Trx2 and TrxR2 in aged hippocampi have been poorly investigated. Therefore, the aim of this study was to examine changes in Trx2 and TrxR2 in mouse and rat hippocampi by age and to compare their differences between mice and rats. Results: Trx2 and TrxR2 levels using Western blots in mice were the highest at young age and gradually reduced with time, showing that no significant differences in the levels were found between the two subfields. In rats, however, their expression levels were the lowest at young age and gradually increased with time. Nevertheless, there were no differences in cellular distribution and morphology in their hippocampi when it was observed by cresyl violet staining. In addition, both Trx2 and TrxR2 immunoreactivities in the CA1-3 fields were mainly shown in pyramidal cells (principal cells), showing that their immunoreactivities were altered like changes in their protein levels. Conclusions Our current findings suggest that Trx2 and TrxR2 expressions in the brain may be different according to brain regions, age and species. Therefore, further studies are needed to examine the reasons of the differences of Trx2 and TrxR2 expressions in the hippocampus between mice and rats.