A randomized, prospective study was conducted between October, 1994 and April, 1996 to compare the efficacy and safety of warfarin (group I) with dextran (group II) for the prevention of DVT after hip arthroplasty. 109 cases in 106 patients were included in the study. There were 60 cases in group I and 49 cases in group IL Risk factor for DVT were analysed before surgery and prophylactic modalities were performed. Color doppler was performed to all patients by one muskuloskeletal radiologist on 5th 8th post operative day and on 6 weeks after operation. DVT occurred in ten ( 16.6% ) of the 60 patients in group I, six ( 12.2% ) of the 49 patients in group II. but, this difference was not significant ( p= 0.582 ). Statistical analysis for the risk factors of age, sex, operation time, anesthetic method and operation method were performed and there were no statistical difference. Only statistical significance was a higher rates of DVT in cemented hip arthroplasty (p=0.028). There were seven proximal thigh DVT and nine calf DVT. We confirmed with sequential color doppler image that all cases of DVT except two complicated cases were resolved within 8 weeks after treatment: one case was expired for the reason of PE, and the other case had thigh hematoma during the treatment with warfarin. We could detect only one case of late onset DVT.
Arthroplasty* ; Dextrans ; Hematoma ; Hip* ; Humans ; Prospective Studies ; Risk Factors ; Thigh ; Venous Thrombosis* ; Warfarin

Reexpansion Pulmonary edema is the iatrogenic complication which develops in a lung that has been rapidly reinflated after varied period of collapse secondary to a pneumothorax or a pleural effusion of large volume. Its incidence is relatively low, but can sometimes lead to death. The prevention of this disease is known well, but the definite treatment method has not been known in severe case although there have been conventional ventilator therapy and some medications in mild case. Asynchronous differential lung ventilation is a new therapeutic modelity which is applied independently to bilateral lungs in respiratory failure patients secondary to ventilation-perfusion mismatch, preoperatively, intraoperatively or postoperatively. By asynchronous differential lung ventilation, we successfully treated a severe reexpansion pulmonary edema in 29 year old male patient. Therefore we suggest that asynchronous differential lung ventilation is the treatment of choice for severe reexpansion pulmonary edema.
Adult ; Humans ; Incidence ; Lung* ; Male ; Pleural Effusion ; Pneumothorax ; Pulmonary Edema* ; Respiration, Artificial ; Respiratory Insufficiency ; Ventilation* ; Ventilators, Mechanical

Pneumocystis carinii causes serious pulmonary infection in immunosuppressed patients. This study was undertaken to observe the cytoskeletal proteins of P. carinii by immuno-electron microscopy. P. carinii infection was experimentally induced by immunosuppression of Sprague-Dawley rats for seven weeks, and their lungs were used for the observations of this study. The gold particles localized actin, tropomyosin, and tubulin. The actin was irregularly scattered in the cytoplasm of the trophic forms but was much more concentrated in the inner space of the cell wall of the cystic forms called the inner electron-lucent layer. No significant amount of tropomyosin was observed in either trophic forms or cystic forms. The tubulin was distributed along the peripheral cytoplasm and filopodia of both the trophic and cystic forms rather than in the inner side of the cytoplasm. Particularly, in the cystic forms, the amount of tubulin was increased and located mainly in the inner electron-lucent layer of the cell wall where the actin was concentrated as well. The results of this study showed that the cell wall of P. carinii cystic forms is a structure whose inner side is rich in actin and tubulin. The location of the actin and tubulin in P. carinii suggests that the main role of these proteins is an involvement in the protection of cystic forms from the outside environment by maintaining rigidity of the cystic forms.
Actins/analysis ; Animals ; Cytoskeletal Proteins/*analysis ; Fungal Proteins/*analysis ; Histocytochemistry ; Microscopy, Immunoelectron ; Pneumocystis/*chemistry/cytology ; Rats ; Rats, Wistar ; Support, Non-U.S. Gov't ; Tropomyosin/analysis ; Tubulin/analysis

PURPOSE: The mechanical insights of death of cancer cells by ionizing radiation are not yet clearly defined. Recent evidences have demonstrated that radiation therapy may induce cell death via activation of signaling pathway for apoptosis in target cells. This study was designed whether ionizing radiation may activate the signaling cascades of apoptosis including caspase family cystein proteases, mitogen-activated protein (MAP) kinases, and transcriptional activation factors in target cells eventually leading to death. MATERIALS AND METHODS: HL-60 cell line in the log phase was used in this study and the culture media was RPMI 1640. The irradiation was done using the linear accelarator and the radiation does was 10 Gy, 20 Gy, and 30 Gy, respectively. The cell viability was tested by MTT assay and apoptosis was identified by the DNA fragmentation assay. JNK1 (cJun N-terminal kinase) and ERK (extracellular-signal regulated protein kinase) activity was analyzed by the in vitro Ig complex kinase assay. NF- kB (Nuclear Factor- kB) and AP-1 (activator protein-1) activity was assayed by the electrophoretic mobility sbift assay. RESULTS: Ionizing radiation decreased the viability of HL-60 cells in a time and dose dependent manner. Ionizing radiation-induced cell death of HL-60 cells may be an apo- ptotic death which was evidenced as apoptotic characteristic ladder pattern fragmentation of DNA over 20 Gy at 4 hours. Ionizing radiation specifically induced the activation of CPP32-like cystein protease rather than ICE-like protease of HL-60 cells in a time and dose dependent manner. The activation of CPP32-like cystein protease was also evidenced by the digestion of poly (ADP-ribose) polymerase with 30 Gy ionizing irradiation at 2 hours. The activity of JNK1 was transiently increased up to 3.6 fold by 30 Gy ionizing radiation at 2 hours. Ionizing radiation also rapidly activated the transcriptional activation factors including AP-1 and NF- kB at 10 or 30 min. CONCLUSION: These data suggested that ionizing radiation-induced apoptosis was mediated by the activation of CPP32-like cystein protease, JNK1, and transcriptional activation factors
Apoptosis ; Cell Death ; Cell Survival ; Culture Media ; Digestion ; DNA ; DNA Fragmentation ; HL-60 Cells ; Humans ; Peptide Hydrolases ; Phosphotransferases ; Radiation, Ionizing ; Transcription Factor AP-1 ; Transcriptional Activation

Sometimes, it is difficult to distinguish Churg-Strauss syndrome from idiopathic hypereosinophilic syndrome and there may be overlap syndrome in the differential diagnosis of systemic vasculitis with hypereosinophilia. Recently, we experienced a 42-year-old female patient who presented signs and symptoms of cardiac failure and neuropathy with peripheral hypereosinophilia. She had no history of asthma. She had erythematous skin lesions and distal digit necrosis. The cause of hypereosinophilia could not be identified. Skin and nerve biopsy revealed vasculitis with eosinophilic infiltration. Cardiac failure improved dramatically with steroid, inotropics and diuretics. Other symptoms including digital necrosis also improved. During steroid, tapering peripheral eosinophilia recurred. For maintenance therapy, we added daily cyclophosphamide to every-other-day prednisolone therapy. We report the case with a review of the literature.
Adult ; Asthma ; Biopsy ; Churg-Strauss Syndrome* ; Cyclophosphamide ; Diagnosis, Differential ; Diuretics ; Eosinophilia ; Eosinophils ; Female ; Heart Failure ; Humans ; Hypereosinophilic Syndrome* ; Necrosis ; Prednisolone ; Skin ; Systemic Vasculitis ; Vasculitis

No abstract available.
Lung Transplantation* ; Lung*

BACKGROUND: Laparoscopic cholecystectomy has emerged rapidly as a popular alternative to tradidonal laparotomy and cholecystectomy in the management of cholelithiasis. The advantages of shorter hospital stay, more rapid return to normal activities are combined with less pain associated with the small limited incisions. But it has some disadvantages related to insufflation of a large amount of carbon dioxide into peritoneal cavity. METHODS: To investigate ventilatory and hemodynamic changes during laparoscopic cholecystectomy, we observed the changes in blood pressure (systole, diastole, mean), heart rate, end-tidal carbon dioxide tension (PerCO2), arterial carbon dioxide tension(PaCO2), and arterial oxygen tension(PaO2) at intervals during general anesthesia with controlled ventilation (tidal volume: 10 mg/kg, ventilatory rate: 10 breaths/min). RESULTS: Mean arterial pressure was increased significantly until 30 minutes after carbon dioxide insufflation(p<0.05). Heart rate was not changed significantly throughout the operation. End-tidal carbon dioxide tension and arterial carbon dioxide tension were increased significantly during carbon dioxide insufflation(p<0.01), but arterial oxygen tension was not decreased significantly throughout the operation. CONCLUSIONS: This study described 19 patients who underwent laparoscopic cholecystectomy and analyzed the changes in hemodynamic and ventilatory parameters. It is important for anesthesiologist to monitor ventilation and hemodynamics carefully because the patients with cardiac or pulmonary diseases may be adversely affected by the hypercarbia associated with carbon dioxide insufflation.
Anesthesia, General ; Arterial Pressure ; Blood Pressure ; Carbon Dioxide ; Cholecystectomy ; Cholecystectomy, Laparoscopic* ; Cholelithiasis ; Diastole ; Heart Rate ; Hemodynamics ; Humans ; Insufflation ; Laparoscopy ; Laparotomy ; Length of Stay ; Lung Diseases ; Oxygen ; Peritoneal Cavity ; Ventilation

BACKGROUND: Recently many studies reported that the postoperative pain was prevented or decreased from preoperative regional anesthesia by preventing the establishment of central sensitization(pre-emptive analgesia). Therefore, we evaluated the efficacy of preincisional lidocaine infiltration on the postoperative pain. METHODS: We conducted a study to compare preinfiltrating group with 1% lidocaine (30 ml), postinfiltrating group with 1% lidocaine (30 ml) and non-infiltrating group in 45 patients scheduled for elective inguinal herniorrhaphy. During operation, all patients received a general anesthesia with thiopental, isoflurane and nitrous oxide in oxygen. Postoperatively, pain scores on visual analogue scale (VAS) and on verbal rating scale(VRS) at rest, coughing and movement from supine into sitting position were assessed. Also the time to first request for an on-demand postoperative analgesics and the total dose of postoperative analgesics were assessed. And the number of patients who didn't require any analgesics during postoperative period was assessed. RESULTS: The VAS and VRS at rest, coughing, movement were low in preinfiltrating group than in non-infiltrating group and postinfiltrating group postoperatively, but it was statistically significant only in early postoperative period. The time to first request for an on-demand postoperative analgesics occurred later in preinfiltrating group than in non-infiltrating group and in postinfiltrating group and the total dose of supplemental analgesics (ketorolac) was smaller in the preinfiltrating group than in non-infiltrating group and postinfiltrating group, and the patients without analgesic treatment was less in the preinfiltrating group than in non-infiltrating group and postinfiltrating group, but it was not statistically significant. CONCLUSIONS: In patients with inguinal herniorrhaphy, we can not support the pre-emptive analgesia clinically with preincisional lidocaine infiltration.
Analgesia ; Analgesics ; Anesthesia, Conduction ; Anesthesia, General ; Anesthetics ; Cough ; Herniorrhaphy* ; Humans ; Isoflurane ; Lidocaine* ; Nitrous Oxide ; Oxygen ; Pain, Postoperative* ; Postoperative Period ; Thiopental

The authors report a case of posterior fossa dural arteriovenous malformation with increased intracranial pressure. It was fed left occipital artery, posterior auricular artery, posterior meningeal branch of vertebral artery, and meningohypophyseal artery of left internal carotid artery. Treatment has been tried with transcatheter embolization using gelfoam and ivalon, intracranial clipping of feeders, ligation of external carotid artery, and radiation therapy. The unusual clinical manifestations such as visual disturbance and hearing impairment are discussed.
Arteries ; Arteriovenous Malformations* ; Carotid Artery, External ; Carotid Artery, Internal ; Gelatin Sponge, Absorbable ; Hearing Loss ; Intracranial Pressure ; Ligation ; Vertebral Artery

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