Central Venous Catheters*

BACKGROUND: Melanin pigment plays a major role in the expression of normal human skin color as well as in the photoprotection against ultraviolet damage. Melanin produced in melanocytes is transferred via dendrites to surrounding keratinocytes, and this anatomical relationship is termed as epidermal melanin unit. The rates of pigment synthesis and transfer by melanocytes appear to be influenced by ultraviolet light, though the precise factors regulating human epidermal pigmentation remain unelucidated. It has been reported that keratinocytes in vitro release factors that could modulate melanocyte behavior. Ultraviolet irradiation was also been known to enhance the release of various kinds of cytokine from keratinocytes in vivo and in vitro. OBJECTIVE: We postulated that keratinocytes rather than melanocytes could play a primary role in UVB-induced pigmentation, and keratinocytes, when irradiated with UVB, release substances that could modulate or stimulate melanin synthesis from melanocytes. The fact that keratinocytes are located efficiently for direct sunlight irradiation at the top of melanocytes, that they release various biological factors known to simulate melanin synthesis from melanocytes and that they constitute the majority of epidermal cells supported this possibility. To investigate this possibility, we evaluated the effect of supernatant from UVB-irradiated cultured keratinocytes on the growth, melanin content, and tyrosinase activity of human melanocytes. METHODS: Human cultured keratinocytes were irradiated with UVB(30, 60, or 120mj/cm2)once, and after 24 hours, supernatant of the keratinocytes were collected and added to a growth medium of melanocytes for 5 days in concentration of 15, 25 or 35%, We observed numeric and morphologic changes as well as melanin content and tyrosinase activity in situ of cultured human melanocytes. RESULTS: 1. When cultured melanocytes were incubated with supernatant of non-irradiated keratinocytes, the number of melanocytes, amount of melanin and tyrosinase activity increased in groups added with 25% or35% concentration of supernatant. 2. The number of melanocytes incubated with 15% or 25% concentrations of supernatant from cultured keratinocytes irradiated with UVB increased in both 30 and 60mj/cm2 of UVB irradiated groups and decreased in 120mJ/cm2of UVB irradiated groups. 3. The melanin content of melanocytes incubated with 15% concentration of supernatant from UVB-irradiated cultured keratinocytes increased in 120mJ/cm2 of UVG irradiated groups. 4. The tyrosinase activity of melanocytes incubated with 15% concentration of supernatant from UVB-irradiated cultured keratinocytes increased in 120mJ/cm2 of UVB irradiated groups and the tyrosinase activity of melanocytes incubated with 25% concentration of supernatant from UVB-irradiated cultured keratinocytes increased with 35% supernatant concentration of supernatant from UVB-irradiated keratinocytes, the tyrosinase activity increased in 30mJ/cm2of UVB irradiated groups. CONCLUSION: The above results suggest that UVB-irradiated kerationcytes release soluble or photoactivated factors which could modulate the growth and melanization of melanocytes, and that keratinocytes play an important or primary role in the regulation of UVB induced pigmentation.
Biological Factors ; Dendrites ; Humans* ; Keratinocytes* ; Melanins* ; Melanocytes* ; Monophenol Monooxygenase* ; Pigmentation ; Skin ; Sunlight ; Ultraviolet Rays

No abstract available.
Autoantibodies* ; DNA*

BACKGROUND: Leptin gene is known to be related to obesity in human and animals and complete genetic defect of the gene in ob/ob mouse has been identified. Therefore, ob/ob mouse is widely used as an animal model for the study of etiology and therapy of obesity. The main biological function of leptin was thought to involve in the regulation of food intake and weight gain, however, the regulatory mechanisms by which leptin functions in the weight reduction and lowering the blood glucose level are uncertain. In the present study, retroviral-mediated leptin gene transduction into ob/ob mouse was attempted for the correction of biochemical parameters of obesity. METHODS: Leptin cDNA was inserted into pLXSN retroviral vector (pLXSN-lep) and recombinant leptin expressing retrovirus particles (3 X10 CFU/mL) were produced in psi2 ecotropic packaging cells and subsequent transfection into PA317 amphotropic packaging cells. The leptin expressing recombinant viruses (LER) were transduced into NIH3T3 mouse fibroblasts and insertion of leptin cDNA into chromosomal DNA of PA317 and MH3T3 mouse fibroblasts was confirmed by Southern blot hybridizations. Leptin mRNA and its protein expressed in the cells were identified by Northern blot hybridization and Western blot immunodetection method, respectively. LER were injected I. P. into ob/ob mice, and body weight, food intake, serum leptin level and blood glucose level were measured. RESULTS: Expression of leptin was identified in PA317 and NIH3T3 mouse fibroblasts transduced with LER. Leptin content in sera of mice transfused with LER was drastically increased after 1 week and decreased to the almost basal level at 3 weeks after the transfusion. The body weight as well as food intake of ob/ob mouse transduced by LER decreased for the first 3 weeks and slightly increased thereafter. The reduction of both body weight and food intake in ob/ob mice transduced with LER was observed with the concomitant increase of serum leptin level, indicating that retroviral-mediated transduction of leptin gene in ob/ob mouse in vivo produced a biologically active leptin protein and released it into blood circulation. CONCLUSION: A transient expression of leptin cDNA in ob/ob mice by a retroviral-mediated transduction was performed and further studies are required for long term expression of the gene in vivo.
Animals ; Blood Circulation ; Blood Glucose ; Blotting, Northern ; Blotting, Southern ; Blotting, Western ; Body Weight ; DNA ; DNA, Complementary ; Eating ; Fibroblasts ; Humans ; Leptin* ; Mice ; Mice, Obese* ; Models, Animal ; Obesity ; Product Packaging ; Retroviridae ; RNA, Messenger ; Transfection ; Weight Gain ; Weight Loss ; Zidovudine*

Phospholipase C (PLC) plays a pivotal role in transmembrane signal transduction pathway for cellular proliferation differentiation and growth. Thus far, there have been few reports in which PLC activity was investigated in human malignant neoplastic tissues. In the present study, we evaluated PLC activity in 23 human gastric cancer tissues and normal mucosal tissues to investigate whether alteration of PLC activity is associated with gastric cancer. The amount of [14C] diacylglycerol, one of the earliest products of inositol phospholipid hydrolysis by PLC, was measured by thin layer chromatography. Also, expression of PLC-gamma1, which is one of the most important PLC isozymes,was examined by immunohistochemistry using specific monoclonal antibody directed against PLC-gamma1. The results are summarized as follows. PLC activity in all 23 gastric cancer tissues (1.35+/-1.04 units/mg of protein) was significantly higher than normal mucosal tissues (0.28+/-0.21 units/mg of protein) (P<0.001). PLC activity in gastric cancer tissues was not correlated with histologic grade (P>0.05). PLC-gamma1 immunoreactivity was detected in all of 23 cases studied. The intensity and extent of PLC-gamma1 immunoreactivity was not correlated with PLC enzyme activity, although stronger intensity was demonstrated in malignant cells in comparison to normal gland epithelial cells. The present study provides the first evidence of significant elevation of PLC activity in human stomach cancer tissues. Our results strongly suggest that PLC might be involved in tumorigenesis and/or progression(uncontrolled continuous cycling of cells) of human gastric cancer. Further studies are needed to elucidate the role of elevated PLC activity in cancer tissues.
Humans ; Cell Transformation, Neoplastic ; Stomach Neoplasms

PURPOSE: AP DNA endonuclease (APE), an enzyme responsible for the repair of damaged DNAs, is essential for the maintenance of genetic information of cells. Deficiency of APE in certain hereditary skin tumor and senescent cells has been implicated but the regulation of APE activity as well as the expression of APE gene in response to DNA damage has not been well documented. Genotoxic agents including ultimate carcinogens that can damage DNA were treated to cultured normal and transformed human cells and adaptive response of APE gene expression to these treatments was measured in order to evaluate the role of APE in chemical carcinogenesis. MATERIALS AND METHODS: Hydroxyl radical ('OH) generated from H2O2 (60 uM) through Fenton reaction, each 100 uM of N-nitrosomethylurea (NMU), 3-methyl-4-monomethyl- aminoazobenzene (3'-MeMAB) and N-acetoxy-2-acetaminofluorene (AAAF) were treated to umbilical cord blood cells (UCBC), HepG2 cells and HL-60 cells. APEX mRNA and APEX protein contents expressed in these cells exposed to each of these agents were measured by Northern blot hybridization and Western blot immunodetection analysis. The changes of APE activity in cells exposed to these genetoxic agents were measured. RESULTS: Treatment of H2O2 (60 uM) to UCBC, HepG2, and HL-60 cells increased APE activity significantly and pretreatment of a catalytic agent for OH, FeSO4 (60 pM) to the cells prior to H2O2 exposure did not further increase the APE activity in cells. Adaptive response to H2O2 in HL-60 cells increased in proportion to the concentration of H2O2 up to 60 pM. However, further increase in H2O2 concentration had no effect on the enzyme activity. Treatment of NMU (100 pM), 3-MeMAB (100 pM) and AAAF (100 pM) to these cells brought about a slight increase in the APE activity. APEX mRNA expression in UCBC and HepG2 cells exposed to H2O2, NMU, 3-MeMAB was markedly increased in APEX mRNA expression. APEX mRNA expression was also increased in HL-60 cells exposed to H2O2 (60 pM) and 3-MeMAB (100 uM) but NMU (100 pM) exposure to the cells resulted in a slight increase of it (Fig. 2). APEX protein expression was increased in all UCBC, HepG2 and HL-60 cells exposed to these genotoxic agents (Fig. 3). CONCLUSION: These results implicate that exposure of genotoxic agents to the cultured cells may cause DNA damage and lead to adaptive increase in APE activity as well as APE gene expression. It is probable that APE gene is transcriptionally regulated in response to the exposure of H2O2 or 3-MeMAB in cultured human cells as a consequence of activation of DNA repair system for the adaptation to the crisis.
Blotting, Northern ; Blotting, Western ; Carcinogenesis ; Carcinogens ; Cells, Cultured ; Deoxyribonuclease I* ; DNA Damage ; DNA Repair ; DNA* ; Fetal Blood ; Gene Expression ; Hep G2 Cells ; HL-60 Cells ; Hominidae ; Humans ; Hydroxyl Radical ; RNA, Messenger ; Skin

To investigate the incidence of hypoxemia which was defined as arterial blood oxygen saturation (SaO2) of 90% or less following general endotracheal anesthesia, 112 adult patients were randomly allocated to one of 8 groups aceording to oxygen administration or not. SaO2 was continually measured during postanesthetic period using a pulse oximeter (Nellcor, N-100 C, USA). The incidence of hypoxemia was lower in oxygen administration groups (5%) than in no administration groups (14%) in the recovery room. The mean discharge time of oxygen administration groups in the recovery room (37.9 min) was significantly shorter than that of no administration groups (45.6 min) (P=0.003). There were two cases of hypoxemia during transfer of patients from the operating room to the recovery room. The incidence of hypoxemia in oxygen administration groups (9%) was lower than no oxygen administration groups (71%) during 5 minutes after endotracheal extubation. It was coneluded that the incidence of hypoxemia can be reduced by administrating oxygen during postanesthetic period. Therefore, it is recommended that oxygen should be administered to all postoperative patients for prevention of hypoxemia following general endotracheal anesthesia.
Adult ; Airway Extubation ; Anesthesia* ; Anoxia ; Humans ; Incidence ; Operating Rooms ; Oxygen* ; Recovery Room

OBJECTIVE: To investigate whether there is a significant effect of growth hormone(GH) treatment with diet and exercise over the diet and exercise alone in obese non-insulin dependent diabetes mellitus(NIDDM). METHOD: Twenty obese NIDDM adults were studied. We measured the body weight, body composition and exercise capacity before and after 12 weeks of treatment program. The subjects were assigned in a double-blind manner either to the diet, aerobic exercise with placebo treatment group(group A) or to the diet, aerobic exercise with GH treatment group(group B) for twenty-week period. Two groups were compared for the demographic data. RESULTS: After 12-weeks of treatment program, each group showed a significant weight loss (group A: 8.54+/-2.29 kg vs group B: 7.14+/-2.99 kg) than before the treatment, however there was no significant weight loss between two groups. After 12-weeks, the fat fraction of body weight loss was significantly higher in group B than group A(0.80+/-0.40%kg versus 0.55+/-0.30%kg). After 12-weeks, the maximal oxygen consumption was similarly increased in both groups(23.75% in the group A versus 29.2% in the group B). After 12-weeks, the peak torque was similarly increased in both groups(9.7% in the group A versus 17.3% in the group B). After 12-weeks, the endurance was similarly increased in both groups(10.1% in the group A versus 8.1% in the group B). CONCLUSION: Both group A and B showed a significant weight loss and resulted in a comparable gain in the muscle strength, endurance, and maximal oxygen consumption. The addition of GH in a low dose to a the calorie-restricted diet and aerobic exercise resulted in a significant fat loss especially around the visceral area.
Adult ; Body Composition ; Body Weight ; Diabetes Mellitus, Type 2 ; Diet* ; Exercise ; Growth Hormone* ; Humans ; Muscle Strength ; Obesity ; Oxygen Consumption ; Torque ; Weight Loss

The Brunner's gland adenoma is characterized by a nodular proliferation of histologically normal Brunner's gland, accompanied by ducts and scattered stromal elements. First descrived by Salvioli in 1876, the tumor is relatively rare, with 119 cases reported by 1977, The most common benign tumor of the small bowel is the adenoma, 25% of which occur in the duodenum. They make up 30% to 50% of all hyperplastic polyps of the duodenum. Most frequently these tumors are discovered in patients in the fourth to sixed decades of life, though the age in reported caes ranges from l 1 days to 80 years. The benign tumors of the duodenum 30% to 50% contain elements of Brunner's gland and 10.6% of them are adenomas of Brunner's gland. We report a case of Brunner's gland adenoma treated by endoscopic polypectomy in 63 year-old woman, and reviewed the literatues of adenoma of the Brunne'r gland.
Adenoma* ; Duodenum ; Female ; Gastrointestinal Hemorrhage ; Humans ; Middle Aged ; Polyps

Apoptosis is a distinct mechanism of cell death involved in many physiological and pathological processes. Various stimuli, including phagocytosis of bacteria, can induce apoptosis. As the cells proceed through apoptosis, functional activities decline in accord with phenotypic changes. However, decline in functional activities does not mean instantaneous shut-down of all functions, which is rather the characteristic of necrosis. Phagocytosis and oxidative burst are two of the major tasks of mloid cells for engulfment and killing of microbes. It was reported that the myeloid cells which phagocytosed bacteria underwent apoptosis, rendering resolution of acute inflammation. On the contrary, it was known that phagocytosis of latex beads did induce apoptosis. However, we found phagocytosis of latex beads within the apoptotic cell fraction. Thus we investigated whether phagocytosis of latex beads induced apoptosis or apoptotic cells phagocytosed the beads. We used human promyelocytic cell line HL-60 cultured for 4 days in RPMI1640 supplemented with 10% fetal bovine serum and 1 uM all-trans retinoic acid for phagocytic assay. Phagocytic activity was analyzed by flow cytometry after shaking incubation of HL- 60 cells (5 x 10 cells/ml) with fluorochrome-cougated latex beads for 1 hour at 37C followed by elimination of the un-phagocytosed beads by centrifugation on the density of fetal bovine serum. Apoptotic cells were identified as subdiploid fraction by staining the cells with DNA-dye. To investigate whether phagocytosis of latex beads leads to apoptosis or apoptotic cells phagocytose the beads, the cells wbich had phagocytosed the beads were sequentially analyzed before and after 1, 3, 6, 12 and 24 hours of incubation. On the other hand, the apoptotic cell fraction was sorted to be analyzed for phagocytic activity. The sorted cells were also analyzed by chemiluminescence assay for capability of oxidative burst by stimulation with PMA (5 mM). The results showed little increase in the apoptotic fraction among phagocytic cells during incubation up to 24 hours. Rather the sorted apoptotic cells did phagocytose latex beads. But the sorted cells did not show any capability of oxidative burst. Taken these results into consideration, the apoptotic cells seemed to be on the way of dying process in which oxidative burst was lost while phagocytic activity remained. Thus it was suggested that the primitive function of phagocytosis remained longer in the cells proceeding through apoptosis, while oxidative bunt, requiring mitochondrial function, was lost earlier.
Apoptosis ; Bacteria ; Cell Death ; Cell Line ; Centrifugation ; Flow Cytometry ; Hand ; Homicide ; Humans ; Inflammation ; Luminescence ; Microspheres ; Myeloid Cells ; Necrosis ; Pathologic Processes ; Phagocytes ; Phagocytosis ; Respiratory Burst ; Tretinoin