Clinical Characteristics of the Patients Who Died Despite of Low APACHE II Score after Intensive Care / 대한마취과학회지

BACKGROUND: The acute physiology and chronic health evaluation (APACHE) II score is considered to be a precise predictor of mortality and a useful basic research tool. A lower APACHE II score means a better prognosis of patients, which means that these relatively low risk patients are more likely to benefit from the improved patient management than the higher predicted mortality admissions. Therefore, these patients are obvious targets for intensive care and for decreasing the level of intensive care unit (ICU) mortality. METHODS: This study reviewed the medical records of 729 patients, whose APACHE II scores on the ICU admission day were 10 or less, from June 1, 2001 to May 31, 2002 in University Hospital. The data of the patient's age, gender, disease category, first admission or readmission, APACHE II score, length of stay at the ICU and the hospital were reviewed. RESULTS: The average mortality rate of the patients who had an APACHE II score of 10 or less was 4.1%. The mortality of the cancer patients (8%) was significantly higher than the other disease groups. The mortality of the readmitted patients was significantly higher than the mortality of the patients who were admitted to the ICU for the first time. CONCLUSIONS: Among the patients in the ICU with a low APACHE II score, the mortality of cancer patients was high. The mortality of the readmitted patients was significantly higher than in those on the first admission.

Involvement of ROS and JNK1 in selenite-induced a poptosisin Chang liver cells

Selenium is a dietary essential trace nutrient with important biological roles. Selenocompounds were reported to induce apoptosis in many types of tumor cells. In this study, we investigated the signaling pathway involved in the selenite-induced apoptosis using Chang liver cells as a non-malignant cell model. The Chang liver cell apoptosis induced by selenite (10 mM) was confirmed by DNA fragmentation and typical apoptotic nuclear changes. Treatment of selenite increased intracellular reactive oxygen species (ROS) level and c-Jun N-terminal kinase1 (JNK1) phosphorylation. The selenite-induced cell death was attenuated by SP600125, a specific inhibitor of JNK, and by dominant negative JNK1 (DN-JNK1). Antioxidants such as glutathione (GSH), N-acetyl cysteine (NAC), curcumin, epigallocatechin gallate (EGCG) and epicatechin (EC) inhibited selenite-induced intracellular ROS elevation and JNK1 phosphorylation. Our results suggest that selenite-induced apoptosis in Chang liver cells was preceded by the ROS generation and JNK1 activation.

Direct Myocardial Depressant Effect of Desflurane: Mechanical and Electrophysiological Actions in Vitro / 대한마취과학회지

BACKGROUND: Desflurane actions on myocardial contractility and cellular electrophysiologic behavior were studied in isolated guinea pig and rat right ventricular papillary muscles. METHODS: The isometric force of isolated guinea pig ventricular papillary muscles was studied in normal and 26 mM K+ Tyrode's solution at various stimulation rates. Experiments using rat papillary muscles under normal Tyrode's solution at the rested-state (RS) and using guinea pig papillary muscles under low Na+ Tyrode's solution (25 mM) were performed to evaluate the effect of Ca2+ release from the sarcoplasmic reticulum (SR). Effects of desflurane on SR function in situ were examined by its effect on rapid cooling contractures (RCCs). Normal and slow action potentials (APs) were evaluated by using a conventional microelectrode technique. Finally, Ca2+ currents of isolated guinea pig ventricular myocytes were examined using the whole cell patch clamp technique. RESULTS: 1 MAC (minimum alveolar concentration: 6%) and 2 MAC desflurane were applied. 1 MAC and 2 MAC desflurane depressed guinea pig myocardial contractions by ~30% and ~60%, respectively, from RS to 3 Hz stimulation rates. 1 MAC (1.15%) and 2 MAC isoflurane depressed peak force by ~25% and ~45%, respectively. Contractile force after rest in rat and guinea pig myocardium under low Na+ Tyrode's solution showed modest depression. In the partially depolarized, adrenergically stimulated myocardium, 1 MAC and 2 MAC desflurane caused a marked depression of the late peak force (1 MAC:~60%, 2 MAC:~80%) with moderate changes of the early peak force (1 MAC: ~20%, 2 MAC: ~40%). RCCs were abolished at 1 MAC desflurane. Desflurane did not alter the peak amplitude or maximum depolarization rate of normal and slow APs, however, AP duration was significantly prolonged. In isolated guinea pig myocytes at room temperature, 1 MAC and 2 MAC desflurane caused a ~28% and ~55% decrease in Ca2+ currents, respectively. CONCLUSIONS: These results indicate that desflurane causes a dose-dependent depression of contractile force in isolated myocardium, which is comparable to that of isoflurane. The depression seems to be related, at least in part, to its ability to reduce inward Ca2+ currents through the cardiac membrane. Therefore, it is likely that various methods employed to enhance inward Ca2+ current may improve the hemodynamic depression induced by desflurane.

Efficacy of the Laryngeal Tube in General Anesthesia / 대한마취과학회지

BACKGROUND: A prototype airway management device, a laryngeal tube, has been recently introduced in Korea. This study was designed to assess the efficacy of the laryngeal tube for airway management under general anesthesia. METHODS: We studied thirty-six ASA physical status I and II patients undergoing general anesthesia. Anesthesia was induced with sleep dose propofol 2.0 mg/kg i.v., supplemented with fentanyl 1 microgram/kg, and maintained with 50% nitrous oxide and propofol. After inserting the laryngeal tube, its cuff was inflated using a balloon cuff gauge until the intracuff pressure reached approximately 65 cmH2O. Adequacy of ventilation was assessed by observing the end tidal carbon dioxide wave form, chest wall movement and by stethoscope auscultation. Oropharyngeal leak pressure was also measured. Changes in heart rate, blood pressure, end-tidal carbon dioxide, airway pressure and oxygen saturation before induction, before insertion, 2, 5 and 10 minutes after insertion and 5 minutes after incision were recorded. RESULTS: The first time success rate at achieving an effective airway was 30 in 36 (83%). The mean leak pressure was 22.9+/-4.6 mmHg. Heart rate, blood pressure, oxygen saturation, end-tidal carbon dioxide and airway pressure values remained stable during laryngeal tube insertion and during the surgical procedure. CONCLUSIONS: We conclude that the laryngeal tube is easy to place, allows adequate ventilation and has a lower incidence of complications. It may offer an alternative device for the oxygenation of non-intubated patients undergoing general anesthesia.

Association between Non-alcoholic Fatty Liver and Metabolic Diseases / 대한내분비학회지

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is known to be frequently associated with obesity, type 2 diabetes and dyslipidemia. Recently, the diagnosis of fatty liver disease, based on ultrasonographic findings, has increased. Therefore, we examined the association between NAFLD and various metabolic diseases, such as obesity, glucose intolerance, dyslipidemia, and hypertension or metabolic syndrome, and tried to find out whether NAFLD was independently related to insulin resistance. METHODS: From April to June 2000, 262 subjects, attending for routine physical check-ups, were screened. Of these, 115 one hundred fifteen subjects were studied, with the other 147 excluded due to significant alcohol consumption, evidence of viral or toxic hepatitis, significant liver or renal dysfunction, and overt thyroid disease. Fatty liver was diagnosed if the subject had a "bright" liver on ultrasonographic examination. All diagnoses were made by a single experienced radiologist. RESULTS: Of the 115 subjects. 30 (26%) showed NAFLD. 1. Systolic and diastolic blood pressures, body weight, serum total cholesterol, triglyceride, fasting insulin levels and HOMA IR (homeostasis model assessment insulin resistance index) were higher in the subjects with NAFLD than in the controls. 2. Multiple logistic regression analysis, including age, sex, BMI, waist to hip ratio, fasting serum glucose, lipids and insulin levels, HOMA IR, and hypertension showed that BMI, total cholesterol and HOMA IR were independently related with NAFLD. 3. 27% of the subjects with NAFLD showed metabolic syndrome, and 53% of subjects with metabolic syndrome had NAFLD. 4. The percentage of subjects who had more than two factors of metabolic syndrome was three times higher in the subjects with NAFLD compared to the controls. CONCLUSION: These results suggest that NAFLD may be independently related with insulin resistance. Metabolic diseases, such as glucose intolerance, obesity, dyslipidemia and hypertension, were more prevalent in the subjects with NAFLD than in the controls. Therefore, we should try to assess the status of the metabolic diseases, and treat them in patients with NAFLD.

Activation of Mitogen-activated Protein Kinases in Hypoxia-induced Apoptosis of PC12 Cell

BACKGROUND: The Mitogen-activated Protein Kinase (MAPK) family is comprised of key regulatory proteins that control the cellular response to both proliferation and stress signals. Cell death is usually mediated through apoptosis regulated by extracellular factors. We investigated the apoptotic processes of PC12 cells induced by hypoxia and the activation of MAPKs in apoptosis. METHODS: PC12 cells were maintained in a RPMI 1640 medium containing 5% fetal bovine serum (FBS), 10% horse serum, and antibiotics. Hypoxia was induced in a humidified 37 degrees C incubator within a BBL GasPac Pouch. The apoptosis of PC12 cells was observed with an electron microscope and DNA laddering on agarose-gel electrophoresis. The phosphorylation of MAPKs was measured by an image analysis system after a Western blot. RESULTS: Hypoxic apoptosis occurred maximally when PC12 cells in 2% FBS and 5mM glucose media were incubated in an anaerobic state for 6 hours and then reoxygenated for 18 hours. The phosphorylation of MAPKs was observed 30 min after hypoxia and sustained for at least 2 hours. Phosphorylations of extracellular signal-regulated kinase (ERK) and p38 kinase were reduced after 4 hours of hypoxia, whereas those of c-Jun N-terminal kinase (JNK) persisted for 6 hrs Nerve Growth Factor (NGF). Significantly inhibited DNA fragmentation in hypoxia-induced apopto-sis of PC12 cells. NGF accentuated phosphorylation of ERK in both normoxia and hypoxia. Nerve growth factor (NGF) reduced the phosphorylation of JNK but did not affect the phosphorylation of p38 kinase. CONCLUSIONS: We established the conditions for PC12 cell apoptosis caused by hypoxia. These results suggest that activation of JNK and p38 kinase might be the apoptotic signals induced by hypoxia and regulated by different pathways. (J Korean Neurol Assoc 19(4):384~392, 2001)

Effects of prednisolone on eosinophils, IL-5, eosinophil cationic protein, EG2+ eosinophils, and nitric oxide metabolites in the sputum of patients with exacerbated asthma

Corticosteroids are considered to be one of the most effective medicine for asthma by suppressing airway inflammation. This study was carried out to investigate the effects of prednisolone in the sputum of exacerbated asthmatics. Clinical severity, cell differentials, levels of interleukin (IL)-5, eosinophil cationic protein (ECP), EG2+ eosinophils, and nitric oxide (NO) metabolites were measured. Sputum was examined 2 weeks apart in 13 exacerbated asthmatics before and after prednisolone treatment, and once in 12 stable asthmatics. We used a sandwich ELISA for IL-5, fluoroimmunoassay for ECP, immunohistochemical staining for EG2+ eosinophils, a NO metabolites assay using modified Griess reaction. Exacerbated asthmatics, in comparison with stable asthmatics, had significantly higher proportion of eosinophils, higher level of ECP, higher percentage of EG2+ eosinophils, and NO metabolites. Exacerbated asthmatics after treatment with prednisolone had reduced the proportions of eosinophils, reduced level of IL-5, ECP and percentage of EG2+ eosinophils. FEV1 was correlated with the proportion of eosinophils, ECP, and IL-5 respectively. These findings suggest that prednisolone is considered to be effective medicine for asthma by suppressing eosinophil activation through IL-5.

Effects of Nitric Oxide on the Maturation of Mouse Oocyte in vitro / 대한산부인과학회잡지

OBJECTIVE: Nitric oxide (NO) produced in ovary may contribute to follicle maturation, ovulation, oocyte maturation and luteinization. In this study, the effect of nitric oxide on the spontaneous maturation of mouse oocyte was observed. Method: The index of oocyte maturation was checked by the germinal vesicle breakdown (GVBD) and appearance of polar body (PB) under microscope in the denuded oocytes and oocyte-cumulus complexes (OCCs) from mouse ovarian follicles after 24 hours pregnant-mare serum gonadotropin treatment. RESULTS: The GVBD appeared 50 %, 1 hour and 80 %, 2 hrs after changes of oocytes from dibutyryl cAMP (dbcAMP, 0.5 mM) contained media into dbcAMP-free media. dbcAMP (0.5 mM) completely blocked the GVBD until 24 hrs but dbcGMP (5 mM) delayed the GVBD by 1 hr. Sodium nitroprusside, the NO generator, inhibited the GVBD dose-dependently at 2 hr incubation in denuded and OCCs. The appearance of GVBD was not different between control and dbcGMP or SNP in denuded oocytes and OCCs at 24 hrs incubation. The guanylate cyclase activity in denuded oocyte cytosol was not detected whereas the guanylate cyclase activity in OCCs cytosol was 1.3 nmole/min/mg protein which was increased about 3 times by SNP (100 micrometer). CONCLUSION: These results suggest that the NO in ovary may delay the spontaneous oocyte maturation in early stage by acting on the maturation signaling protein as well as guanylate cyclase.

The effects of oxygen radicals on the activity of nitric oxide synthase and guanylate cyclase

Reactive oxygen species such as superoxides, hydrogen peroxide (H2O2) and hydroxyl radicals have been suggested to be involved in the catalytic action of nitric oxide synthase (NOS) to produce NO from L-arginine. An examination was conducted on the effects of oxygen radical scavengers and oxygen radical-generating systems on the activity of neuronal NOS and guanylate cyclase (GC) in rat brains and NOS from the activated murine macrophage cell line J774. Catalase and superoxide dismutase (SOD) showed no significant effects on NOS or GC activity. Nitroblue tetrazolium (NBT, known as a superoxide radical scavenger) and peroxidase (POD) inhibited NOS, but their inhibitory actions were removed by increasing the concentration of arginine or NADPH respectively, in the reaction mixture. NOS and NO-dependent GC were inactivated by ascorbate/FeSO4 (a metal-catalyzed oxidation system), 2'2'-azobis-amidinopropane (a peroxy radical producer), and xanthine/xanthine oxidase (a superoxide generating system). The effects of oxygen radicals or antioxidants on the two isoforms of NOS were almost similar. However, H2O2 activated GC in a dose-dependent manner from 100 microM to 1 mM without significant effects on NOS. H2O2-induced GC activation was blocked by catalase. These results suggested that oxygen radicals inhibited NOS and GC, but H2O2 could activate GC directly.

The Epidemiologic and Clinical Study of Pulmonary Tuberculosis: Among Students at One Women's University for Recent 10 Years / 결핵

BACKGROUND: The prevalence of pulmonary tuberculosis has decreased progressively after the control of the tuberculosis began as national control. But as diabetes, malignancy, immunodeficiency disease recently tend to be increased, the tuberculosis become to the important national health problem. So, this study was designed to observe the state and the change of the prevalence and the clinical status of pulmonary tuberculosis for recent 10 years at one women's university. METHOD: We retrospectively investigated the epidemiology and the clinical status of 612 patients who were registered at the Ewha Womans University Health Center by analyzing records from 1983 to 1992. RESULTS: 1) The prevalence rate had been steadily decreased from 0.63% in 1983 to 0.11% in 1992. The prevalence of freshman and the incidence rate according to the entrance year while in the university significantly decreased since 1989. 2) In classifying by registered source, 45.6% of students were detected by annual periodical health examination, 34.5% by entrance physical examination, 12.0% by hospital, 5.4% by health center clinic, 2.5% by reentrance physical examination, sequentially. 3) The students with past history of tuberculosis were 70(11.4%) and 61(10%) suffered from pulmonary tuberculosis. The patients with family history of tuberculosis were 142(23.3%). 4) There were 530(86.6%) with minimal disease, 79(12.9%) with moderate and only 3(0.5%) with far advanced, when classified by the severity of disease. 5) The initial symptoms were mild breathing difficulty in 30.1%, sweating in 14.9%, fatigue in 14.3%, febrile sense in 11.7%, hemoptysis in 8.2%, sequentially. 6) The duration of treatment was 10.6+/-3.6 months in mild group, 14.9+/-5.2 months in the moderate group(P<0.05). 7) The side reactions of the drug were GI trouble in 7.2%, hepatitis in 1.8%, skin rash in 0.8% and streptomycin side in used patients in 9.1%. CONCLUSION: The prevalence of pulmonary tuberculosis among the students in one women's university was significantly lower than that of university students and 20-24 year-old age group announced in tuberculosis survey on a national scale, and significantly decreased since 1989. The treatment effect was desirable in student's group managed by university health center.

Effects of Calcium Antagonists on the PC12 Cell Damage Induced by Hypoxia

Hypoxia-induced cell damage is known to be mediated by increase in intracellular calcium. In the present study, the effect of calcium channel blockers on the hypoxia-induced cell damage was investigated in iat pheochromocytoma cells line, PC12 cells. The cultured cells were exposed to hypoxia under 95% N2 plus 5% C02 gas phase and incubated in the media devoid of fetal bovine seruril The cell demage was assessed by measuring the release of lactate dehydrogenase (LDH) from the cells into the incubation media. Exposure of the cells to hypoxia for 2 hours caused a 28% of the total LDH to be released from cells -into media. The pretreatment of the cells with 1 mM each of diltiazem, nifedipine, and verapamil depressed the LDH release to the extent of 52%, 42%, and 30% inhibition, respectively. The inhibitory effects of diltiazem and verapamil were more marked at 1 mM than at 10 mM. The influx of 45 Ca2+ into the cells was rapidly increased within 2 minutes after exposure of the cells to hypoxia. Diltiazem at 1 mM almost completely inhibited Ca2+ influx, while nifedipine and verapamil exhibited only, 30% inhibition of Ca2- influx. The results lend support to the notion that mcreased intracellular calcium triggers a series of cascade reactions leadmg to cell death. It is suggested that the inhibitory effects of various calcium antagonists on hypoxia-induced cell damage differ from each other in their potency.

Distribution of Thiol-specific Antioxidant Protein Immunoreactivity in the Mammalian Central Nervous Systern

Thiol-specific antioxidant protein (TSA) is the antioxidant protein which specifically inhibits the inactivation of various enzymes by a nonenzymatic mixedfunction oxidation (MFO) system containing a sulfhydryl compound as reducing equivalent but not by the MFO system containing a nonsulf hydryl reducing equivalent. TSA was isolated and purified from Saccharomyces cerevisiae and bovine brain. But localization in the brain and physiological role of TSA as an antioxidant enzyme a-re known very little. The localization of TSA protein in the rat brain and rabbit spinal cord was examined with polygonal antibodies to bovine TSA made in rabbit. Tissues were fixed with 4% paraformaldehyde, frozen in dry ice, sectioned on a sliding microtome, incubated with these antibodies, and then processed for avidin-biotin peroxidase complex staining. The irrimunoreactive (IR) cellular element for TSA in the central nervous system - ne-om The IR product for TSA was mainly located m neuronal soma and proximal part of neuronal process such as apical dendnte of pyranudal cell of the cerebral cortex. The glial cell, blood vessel and nucleus of neuron did not show the TSA IR TSA IR neurons were found at every nucleus and cortex mcluding cerebral cortex, hippocampus, corpus striatum, cerebellar cortex, thalamus, septum and spinal gray matter. In hypoxia rabbit spinal cord, there were dense and light IR neurons, and the former was considered to be miured by hypoxic msult These results indicate that TSA is ubiquitous protem in neurons of mammalian central nervous system and show uneven distribution among individual neurons in same nucleus and different nucleus. And TSA may be induced by increased oxidative pressure after ischemia.

Effects of Experimental Ischemia on Expression of Protein Kinase C Isozyme in Rat Neocortex

Ischemia leads to a complex sequence of events culmination in the loss of functional integrity of the nervous system and, ultimately, in neuronal cell death. Intracellular accumulation of calcium ions following ischemia may alter protein kinase C(PKC) activity. But nature of change of the PKC activity depending on duration and degree of ischemia is not well understood. To understand the effect of the experimental focal ischemia on expression of PKC isozyme, we investigated the expression of PKC gamma, beta, alpha immunocytochemically and activities of cytochrome oxidase(CO) histochemically in focal ischemic brain of the rat. Two groups of focal ischemic infarction were produced in two groups of Sprague Dawley rats(200-300 gm) : Group I, Clip compression of left middle cerebral artery(MCA) for 10min and releases and sacrificed 48 hr later ; Group II, Electric coagulation of left MCA and killed 2-24 hr later. In the group I, CO activity and immunoreactivity(IR) for PKC gamma and beta were decreased generally in the left MCA territory, especially in layers II through IV of ischemic cortex. In the group II, decrease of CO activities and marked increase of three PKC isozyme IRs were noted in the layers I through IV. The isozymes displayed different localization in the control cortex, but the IRs of three isozymes markedly increased in the ischmic region, so that the difference among IR patterns disappeared. Although vacuolation and decrease of number of IR neuron were noted, there were remaining IR pyramidal neurons arounf vacuole in layers IV/V showing dense immuostaining in the cell body and apical dendrite. These results indicate that 10min acute ischemia inhibits activity of PKC gamma and beta and that prolonged ischemia longer than 2hr induces the expression of three PKC isozymes. Inhibition and possible induction of PKC are proposed to represent a critical step during ischemic neuronal injury.

Comparison of measurements of airway resistance during panting and quiet breathing / 결핵

No abstract available.

Effects of psychotropic drugs on phospholipase C and protein kinase C in vitro / 신경정신의학

No abstract available.

Effects of Experimental Focal Ischemia of PV- and Calbindin-Immunoreactive Neuron of Rat Neocortex

To understand the changes in expression of calcium binding proteins(CaBP) during the experimental focal ischemia, expression of two kinds of CaBP, paralvumin(PV) and calbindin D-28K(Calbindin), immunocytochemically, and activities of cytochrome oxidase(CO) and acetylcholinesterase(AchE), histochemically, in focal ischemic brain of the rat were investigated. Two groups of focal ischemic infarction were produced in Sprague Dawley rats(200-350 mg):Group I, Clip compression of left middle cerebral artery(MCA) for 5-10 mins and release;Group II, Electric coagulation of left MCA for 2-24 hrs. In the group I, CO activity and PV- and Calbindin-immunoreactivity(IR) were decreased in the left MCA territory, and decreased in number of PV- and Calbindin-IR neurons and degree of IR, but AchE activity was nearly same as that of control cortex. In the group II, decrease of CO and AchE activities, and marked increase of PV- and Calbindin IRs were noted on neuropil in the layers I through VI of ischemic region. Characteristically pyramidal cells, which did not express the both CaBPs in the control cortex, of layer V of ischemic cortex showed PV- and Calbindin Irs in the cell body and apical dendrite. These findings suggest that 1) PV- and Calbindin-IR neurons, mainly non-pyramidal cells, are more vulnerable than pyramidal cell to ischemic injury, 2) CaBP may have some roles in hypoxic neuronal injury, and 3) PV and Calbindin-immunocytochemistry can be used as useful technique in evaluation of experimental ischemia.

A Study on the Seasonal Occurrence of Asthma in Children

Well known predisposing factors of asthmatic attack are emotional factors, autonomic nerve dysfunctions, immunologic factors, endocrinologic factors and respiratory track infections. In addition, environmental factors are also important. Meteorological factors-temperature, air pre-ssure, relative humidity-seem to bo the mail triggering agents. According to our clinical experience, the hospotal admission rate of asthmatic children is hi-gher in certain seasons than in other seasons. In response to this observation, a study was conducted to determine the effects of weather and respiratory tract infections on the occurren-ce of asthmatic children in the department of Pediatrics at Severance Hospital, Yonsei Univers-ity, College of Medicine from Jan. 1976 to Dec. 1980. Meteorological data was supplied by the Central Meteorological Office, Seoul, Korea. Results were as follows; 1. The admission rate of asthmatic children was the higher in Autumn (10.8%) than in other seasons. 2. The monthly admission rate of asthmatic children was the highest in September (5.3%) and the lowest in January (0.3%). 3. During the period of rapid decrease of temperature from the highest monthly mean temp-erature in a year, the admission rate of asthmatic children was the highest. The monthly mean temperature of this period was under 18.6degrees C(16~21degrees C). 4. The admission rates of asthmaftic children are tend to be increased at the monthly mean relative humidity range of 66~72% (the average 67.2%). 5. During the period of an increase of monthly average range of temperature, the admission rate of asthmatic children is also increased. 6. During the period of rapid fluctuation of air pressure, the admission rate of asthmatic chil-dren is also increased. 7. There was no significant correlation between asthmatic attacks and respiratory infections.

Clinical Study on Neonatal Meningitis

A clinical study was made on 58 cases of neonatal meningitis occuring under the age of 1 month in the department of Pediatrics at Severance Hospital, yonsei University College of Medicine, from Jan. 1, 1965 to Dec. 31, 1978. 1. The sex ratio of male and female was approximately 1.8:1. 2. Neonatal predisposing factors significantly associated with meningitis were omphalitis(14 cases), skin infection (11 cases), birth injury (9 cases), pneumonia(8 cases), etc. Most common maternal predisposing factors were difficult labor (12 cases). 3. In 25 out of the 58 cases cultered, the most common organism was E. coli(32%), next common Staphylococcus coagulase(+) (24%), followed by beta-Streptococcus (16%). 4. The most common presenting symptoms were nonspecific in nature-a elevated or subnormal temperature, poor feeding, irritability, jaundice and vomiting in order of frequency. 5. The presence of poor moro reflex, neck stiffness, unconsciousness, or convulsion correlated significantly with the high mortality rate. 6. Complications included subdural effusion(8 cases), convulsion(6 cases), Candida infection (6 cases), hydrocphalus(2 cases), and cerebral hemorrhage (2 cases) in order of frequency. 7. In the 58 cases there were 25 mortalities, or 43.1%.