We recently had a patient(51 year-old man) who was to undergo resection of pheochromocytoma under general ansthesia. The patient was treated with phenoxybenzamine for 10 days preoperatively. Following induction of anesthesia with intravenous thiopental sodium, endotracheal intubation was performed with vecuronium and anesthesia was maintained with isoflurane. Following intubation, tachycardia controlled by intravenous injection of small dose of propranolol. The course of anesthesia was rather stormy reflected by hypertension, arrhythmia and hypotension. But the patient tolerated long anesthesia and operation relatively well with appropriate use of nitroglycerine, lidocaine, etc. Importance of preoperative preparation, sufficient sedation, smooth induction, complete analgesia, and good muscular relaxation, adequate alveolar ventilation and stable cardiovascular control has been discussed. Blood pressure during manipulation of tumor was 150/100 mmHg without arrhythmia, but gradually was controlled to the range of 120/80 mmHg after intravenous infusion of nitroglycerine at the rate of 0.5-5 pg/kg/min. To our surprise, the blood pressure and pulse and pulse rate was controlled very well with nitroglycerine and isoflurane. After removal of tumor, the blood pressure dropped 100/70 mmHg, so, blood pressure was controlled by LV fluid(Hartmans dextrose, normal saline, plasmanate, low molecular weight dextran), packed red blood cell, whole blood, fresh frozen plasma, vasopressor of small amount was used. There was no marked hypertension, hypotension, tachycardia, arrhythmia during anesthesia. Thus, we anticipate that nitroglyecerine with beta-blocker may be good intraoperative antihypertensive regimen for pheochromocytoma.
Analgesia ; Anesthesia ; Arrhythmias, Cardiac ; Blood Pressure ; Erythrocytes ; Glucose ; Heart Rate ; Humans ; Hypertension ; Hypotension ; Infusions, Intravenous ; Injections, Intravenous ; Intubation ; Intubation, Intratracheal ; Isoflurane ; Lidocaine ; Molecular Weight ; Nitroglycerin* ; Phenoxybenzamine ; Pheochromocytoma* ; Plasma ; Propranolol ; Relaxation ; Tachycardia ; Thiopental ; Vecuronium Bromide ; Ventilation

Background: Coffee is one of the most commonly consumed beverages in the world. There is evidence that the consumption of coffee has a strong influence on health outcomes. However, the relationship between coffee consumption and serum uric acid in the Korean population is unclear. In this study, we investigated the relationship between coffee consumption and serum uric acid levels in Korean adults. Methods: This study included 2,966 adults aged ≥19 years who participated in the Korea National Health and Nutrition Examination Survey 2016. The participants were divided into four groups according to the amount of coffee consumed and serum uric acid level. Linear regression analysis was used to analyze the relationship between coffee consumption and serum uric acid level. Results: Serum uric acid level increased with increasing coffee consumption (P<0.001). After adjusting for all confounding factors, serum uric acid level was higher in the groups that consumed coffee daily, at more than four teaspoons, than in the groups that did not consume coffee (P<0.001). Conclusion The findings of this study suggest that coffee consumption has a positive relationship with serum uric acid level.

Taxol, an anticancer drug, blocks cell division by stabilizing microtubules. However, taxol has distinct cell-cycle-independent effects. For example, taxol and bacterial LPS induce strikingly similar responses in murine microglial cells. Here, we report that taxol, like LPS, provides a ""second"" signal for murine microglial cell activation to induce tumoricidal activity. Tumoricidal activity determined by MTT assay appeared that taxol or LPS alone weakly activated microglial cells to kill P815 mastocytoma cells, whereas combinations of taxol or LPS with IFN-r synergized to activate macrophages to lyse tumor cells in a dose dependent manner. Secretion of nitric oxide (NO) correlated with tumor cell killing, and the activated microglial cells failed to kill tumor cell targets in the presence of N'-monomethyl-L-arginine (N'MMA), a competitive inhibitor of NO synthase (NOS). Treatment of the cells with anti-TNF-a neutralizing antibodies clearly blocked taxol plus IFN-r induced tumoricidal activity as well as NO production. Collectively, the data illustrate the potential for taxol to activate microglial cell mediated-antitumor mechanisms in addition to its better characterized role as an anti-mitotic agent.
Antibodies, Neutralizing ; Cell Division ; Homicide ; Macrophages ; Mastocytoma ; Microglia ; Microtubules ; Nitric Oxide Synthase ; Nitric Oxide* ; Paclitaxel*

PURPOSE: The purpose of this study is to compare the frequency with which pseudole-sions around the gallbladder (GB) fossa are revealed by multiphasic CT, by CT during arterial portography (CTAP), and by CT during hepatic arteriography (CTHA) and to determine their radiological characteristics. MATERIALS AND METHODS:Multiphasic CT, CTAP, and CTHA examinations of 81 patients without pathology of the GB and around the GB fossa were evaluated for pseudolesion around the GB fossa. The definition of pseudolesion was as follows: 1) hyperattenuation during the arterial phase and isoattenuation during the delayed phase of multipha-sic CT, or perfusion defect on CTAP and hyperattenuation on CTHA; 2) no Lipiodol tagging on Lipiodol CT; 3) all findings observed adjacent to the gallbladder fossa; and 4) no interval change on follow-up CTAP and CTHA. We compared the frequency of pseudolesions around the GB fossa, as seen on multiphasic CT, CTAP, and CTHA, and determined their size, location, and shape, as revealed by CTHA. RESULTS: The frequency of pseudolesion was 2.5% (2/81) on multiphasic CT, while on CTAP or CTHA, the frequency was 53.1% (43/81), and 58 pseudolesions were identi-fied. Of 58 pseudolesions, 56 were revealed by CTAP and 57 by CTHA. Forty-nine of 58 pseudolesions were larger and all pseudolesions showed more contrast to parenchyma on CTHA than on CTAP. The location of pseudolesions was segment V(32 of 58), IV (25 of 58), and VI (1 of 58), and their size ranged from 5 to 30 (mean, 17.5)mm. Pseudolesions were wedge-shaped (48 of 58), oval (6 of 58), bandlike (3 of 58), or round (1 of 58). CONCLUSION: CTAP and CTHA frequently revealed pseudolesion around the GB fossa. The radiological characteristics of these modalities help differentiate pseudolesions from true tumoral hepatic lesions.
Angiography ; Ethiodized Oil ; Follow-Up Studies ; Gallbladder* ; Humans ; Pathology ; Perfusion ; Portography

OBJECTIVE: The purpose of this investigation was to establish the prenatal diagnosis for identifying the risk for epidermolytic palmoplantar keratoderma(EPPK) of a fetus by sequence analysis of fetal genomic DNA from chorionic villi. METHODS: Chorionic villus sampling under transvaginal sonography at 12 weeks of gestation from a woman at risk for a child in a EPPK-affected family was perfomed. Polymerase chain reaction amplification of specific allele (PASA) assay was carried out for the detection of mutation(R162W in keratin 9 [K9] gene) previously identified in this family. Direct DNA sequencing analysis of K9 gene was accomplished to confirm the mutation. RESULTS: We had found the point mutation, R162W of K9 gene, in affected family members and confirmed by PASA assay. Affected family members were shown to have PCR products reactive with both the mutant and wildtype specific primers. Because we could not find any expected products after PASA assay with the primers la(+)/KSmt(-) of the fetal DNA, we predicted that the fetus did not inherited the mutant allele and that the fetus could be unaffected. After PASA assay, we analyzed DNA sequences of two family members to confirm the mutation. A C-to-T substitution at bp 545 was detected in the father, instead the fetus did not have any mutant band at that base pair. CONCLUSION: The PASA assay and direct DNA sequencing analysis of K9 gene through chorionic villi sampling and extraction of genomic DNA had validity to early prenatal diagnosis whether fetus was affected in EPPK or not.
Alleles ; Base Pairing ; Base Sequence ; Child ; Chorionic Villi ; Chorionic Villi Sampling ; DNA* ; Fathers ; Female ; Fetus ; Humans ; Keratin-9 ; Keratoderma, Palmoplantar, Epidermolytic* ; Point Mutation ; Polymerase Chain Reaction ; Pregnancy ; Prenatal Diagnosis* ; Sequence Analysis ; Sequence Analysis, DNA

No abstract available.
Veins*

30 patients were randomly divided into three groups : halothane in oxygen(N=10) ; enflurane in oxygen(N= 10) ; Thalamonal plus nitrous oxide in oxygen(N= 10). Standardized bleeding time was measured using Ivy method before and at leaat 40 min after the induction of anesthesia. Arterial pressure was maintained at+/- 200 of control values and tem-perature was kept at 35~37 degrees C. The bleeding time was prolonged by 58% in the halothane group (P<0.001). There was essentially no change in bleeding time in the groups receiving enflurane and nitrous oxide-Thalamonal group, although there was considerable variability within each group, which did not seem to be related to differences in sex, age, type of surgery, concentration of agent used or surgical procedure. In conclusion, our resultg suggest that halothane may be contraindicated in situations where optimal hemostasis is critical.
Anesthesia ; Arterial Pressure ; Bleeding Time* ; Enflurane* ; Halothane* ; Hemorrhage* ; Hemostasis ; Humans ; Nitrous Oxide

The interruption of hepatic blood flow has been adopted as a method of bleeding control in hepatectomy and liver transplantation. But this occlusion of hepatic inflow may result in significant hepatic injury by various kinds of oxygen radicals produced as a result of hepatic ischemia and following reperfusion. Arterial ketone body ratio(AKBR) is adequatc and convenient parameter by which both acute and prolonged changes of the hepatic function can be estimated. Pharmacological modulation of hepatic injury during warm ischemia and early reperfusion has shown some benefical effects. The authors conducted an experiment to evaluate the inhibitory effect of glutathione and prostaglandin E on hepatic injury due to acute hepatic ischemia and reperfusion. Thirty rabbits were divided into three groups, such as control(n=10), GSH(n=10) and PGE(n=10) groups. Acute hepatic ischemia was induced through the application of portal triad cross-clamping for 30 minutes, and thereafter hepatic reperfusion was induced with the removal of cross-clamping. A single bolus of 200 mg glutathione was injected 10 min before clamp in GSH group, and 200 ng/kg/min of PGE continuously from 10 min before clamp to 30 min after declamp in PGE group. AKBR and hepatic histological findings hefore clamp, 30 min after clamp, 5 min and 30 min after declamp, respectively were compared among 3 groups AKBR was markedly decreased during the clamping period in all groups (P<0.05). In control and PGE groups AKRR was significantly increased after reperfusion than before clamp (P<0.05), but was significantly lower than before clamp. Thirty minutes after reperfusion in GSH group AKBR returned to normal level and was significantly higher than in control group (P<0.05). On light tnicroscopic examination of liver biopsy, mild swollen hepatocytes in the centrilobular zone were seen at ischemia and reperfusion in control and GSH groups, but nearly normal hepatic architectures in PGE group. These results suggest that glutathione has some benefical effect on protection of hepatic dysfunction, and PGE1 on protection of hepatocellular injury during hepatic ischemia and reperfusion.
Alprostadil* ; Biopsy ; Constriction ; Glutathione* ; Hemorrhage ; Hepatectomy ; Hepatocytes ; Ischemia* ; Liver ; Liver Transplantation ; Prostaglandins E ; Rabbits* ; Reactive Oxygen Species ; Reperfusion Injury ; Reperfusion* ; Warm Ischemia

Eosinophilic gastritis is a rare disease that is characterized by eosinophilic infiltration of the bowl wall tissue, and the presentation of symptoms varies depending on the affected site. It is likely that eosinophil-active cytokines play important roles in this disease. A 22-year old man presented with abdominal pain and vomiting. Endoscopic gastric biopsy revealed eosinophilic infiltration, and the serum level of Interleukin (IL)-5 was increased. Gastric emptying was moderately delayed in this patient. The patient was treated with steroid and he showed dramatic clinical improvement with disappearance of the eosinophilic infiltration of the gastric mucosa, normalization of the serum level of IL-5 and improvement of the gastric emptying time. There has been few case reports of eosinophilic gastritis that have described the change of the serum level of cytokines and the gastric emptying. We report here on a case of eosinophilic gastritis and the patient showed elevated serum level of cytokines and delayed gastric emptying. The patient improved after being treated with steroid.
Abdominal Pain ; Biopsy ; Cytokines ; Enteritis ; Eosinophilia ; Eosinophils ; Gastric Emptying ; Gastric Mucosa ; Gastritis ; Humans ; Interleukin-5 ; Interleukins ; Rare Diseases ; Vomiting

Many fungi including Penicillium, Aspergillus, Gliocladium, and Thermoascus produce an epipolythiodioxopiperazine class of fungal metabolite, gliotoxin, which contirbutes the pathogenesis of fungal infection as an immunomodulator and cytotoxic agent. This study is designed to define the mechanism by which gliotoxin exerts the cytotoxic effect of gliotoxin on human promyelocytic leukemic cells, HL-60. Gliotoxin induces the apoptosis of HL-60 cells which is characterized by the ladder pattern fragmentation of DNA. Gliotoxin induces the activation of DEVD-specific cysteine protease in a time- and dose-dependent rnanner. It also increases the phosphotransferase activities of c-Jun N-terminal kinase1 (JNK1) and p38 in gliotoxin-treated HL-60 cells. Furthermore, gliotoxin decreases the activation of transcriptional activator, actiating protein (AP-1) and NF-kB. These results suggest that gliotoxin induces the apoptotic death of HL-60 cells via activation of DEVD- specific caspase as well as mitogen activated protein kinases (MAP kinases) including JNK1 and p38, and inhibition of transcriptional activators, AP-1 and NF-kB.
Apoptosis* ; Aspergillus ; Caspase 3 ; Cysteine Proteases ; DNA ; Fungi ; Gliocladium ; Gliotoxin* ; HL-60 Cells* ; Humans ; Mitogen-Activated Protein Kinases ; NF-kappa B ; Penicillium ; Thermoascus ; Transcription Factor AP-1 ; Transcription Factors