To address the possible prognostic value of p53 and Bcl-2 proteins in non-small cell lung carcinomas (NSCLCs), the authors studied 43 cases of NSCLCs diagnosed between the years 1990 to 1995 at Pusan National University Hospital. The patients were treated either by pneumonectomy or lobectomy of the lung. The expression of p53 and Bcl-2 proteins was semiquantitatively analyzed in paraffin sections by immunohistochemical method and correlated with clinicopathologic prognostic parameters of NSCLCs. Overexpression of the p53 protein was found in 31 cases (72.1%) of the 43 NSCLCs. Overexpression of the p53 protein was significantly correlated with the decreasing degree of histologic differentiation, increasing tumor stage, and cigarette smoking. Bcl-2 expression was found in 19 cases (44.2%) of the 43 NSCLCs. Increased expression of the Bcl-2 protein was significantly correlated only with decreasing tumor stage. An inverse relationship was found between p53 and Bcl-2 proteins, but it was not statistically significant. Thus p53 and Bcl-2 proteins, as demonstrated immunohistochemically in routine paraffin sections, could be of value in prediction of the aggressiveness and prognosis of NSCLCs, in agreement with the central role of p53 and Bcl-2 proteins in the evolution of NSCLCs associated with cigarette smoking.
Busan ; Humans ; Immunohistochemistry ; Lung* ; Paraffin ; Pneumonectomy ; Prognosis ; Smoking

No abstract available.
Anemia, Hypoplastic, Congenital*

Hyperventilation is a common form of anesthetic management in neurosurgical patients with increased intracranial pressure. Acute hypocapnia through hyperventilation causes an increase in cerebrovascular resistance which decreases the cerebral blood flow within one minute. When the hyperventilation is sustained, the cerebral blood flow gradually rises toward normal. We performed this study for evaluation of the changes of acid-base balance in cerebrospinal fluid (CSF) according to duration of acute hyperventilation. We have studied 12 patients for elective surgery for cerebral aneurysm with a relatively clear mental state. The patients underwent induction of anesthesia with thiopental, fentanyl and vecuronium. After intubation, their ventilation was controlled and maintained at a PaCO2 of about 30 mmHg. Samples in arterial and lumbar CSF were obtained at hourly intervals for 6 hours after the onset of hyperventilation. The results were as follows: 1) The PaCO2 was low 30s mmHg and all arterial blood values were not changed throughout the period of observation. 2) The values of CSF were changed; the pH of CSF was increased for 3 hours and then gradually decreased after 4 hours, carbon dioxide tension was a steady state after an initial fall for 2 hours, HCO3-, was decreased from 2 hours and more significantly decreased after 5 hours, and the base excess was more significantly negative after 5 hours of hyperventilation. From the above data, we conclude that prolonged hyperventilation produces first a rise in CSF pH by decreased CSF PCO2 and then gradually a fall in CSF pH by decreasing CSF HCO3-, concentration, and measurable compensated acidosis in CSF was initiated within 5 hours after onset of hyperventilation.
Acid-Base Equilibrium ; Acidosis ; Anesthesia ; Carbon Dioxide ; Cerebrospinal Fluid ; Fentanyl ; Humans ; Hydrogen-Ion Concentration ; Hyperventilation* ; Hypocapnia ; Intracranial Aneurysm ; Intracranial Pressure ; Intubation ; Thiopental ; Vecuronium Bromide ; Ventilation

Background: Glutamate is the main excitatory neurotransmitter. Excessive glutamate causes excitatory toxicity and increases intracellular calcium, leading to neuronal death. Parvalbumin is a calcium-binding protein that regulates calcium homeostasis. Quercetin is a polyphenol found in plant and has neuroprotective effects against neurodegenerative diseases. Objectives: We investigated whether quercetin regulates apoptosis by modulating parvalbumin expression in glutamate induced neuronal damage. Methods: Glutamate was treated in hippocampal-derived cell line, and quercetin or vehicle was treated 1 h before glutamate exposure. Cells were collected for experimental procedure 24 h after glutamate treatment and intracellular calcium concentration and parvalbumin expression were examined. Parvalbumin small interfering RNA (siRNA) transfection was performed to detect the relation between parvalbumin and apoptosis. Results: Glutamate reduced cell viability and increased intracellular calcium concentration, while quercetin preserved calcium concentration and neuronal damage. Moreover, glutamate reduced parvalbumin expression and quercetin alleviated this reduction. Glutamate increased caspase-3 expression, and quercetin attenuated this increase in both parvalbumin siRNA transfected and non-transfected cells. The alleviative effect of quercetin was statistically significant in non-transfected cells. Moreover, glutamate decreased bcl-2 and increased bax expressions, while quercetin alleviated these changes. The alleviative effect of quercetin in bcl-2 family protein expression was more remarkable in non-transfected cells. Conclusions These results demonstrate that parvalbumin contributes to the maintainace of intracellular calcium concentration and the prevention of apoptosis, and quercetin modulates parvalbumin expression in glutamate-exposed cells. Thus, these findings suggest that quercetin performs neuroprotective function against glutamate toxicity by regulating parvalbumin expression.

PURPOSE: The purpose of this study was to demonstrate effects of a critical pathway (CP) for stroke patients seen in emergency rooms (ER). METHODS: The CP developed by the CP committee consisted of 8 criteria: behavior of doctors and nurses, laboratory tests, Image testing, medication, treatment, activity, and nutrition. According to application of CP, a control group (n=17) and experimental group (n=17) were defined. Time was checked by the electronic medical records. RESULTS: Use of CP for stroke patients in the ER, resulted in a decreased length of stay in ER (t=2.341, p=.026), and time required for image testing (t=2.623, p=.021), and an increased number of patients using rtPA (chi2=4.802, p=.049). Time required for neurology doctor contact, for neurology doctor to see patient in the ER, and for report of blood tests decreased, but there were no statistical significance. CONCLUSION: Quick responses are most important in the ER, so CP for these patients is a very effective patient management tool. To reduce delay in stroke diagnosis, continuous education programs for similar symptoms are necessary. CPs for other patients in the ER should be developed, and studies on cost and satisfaction, as well as length of stay, should be done.
Critical Pathways ; Electronics ; Electrons ; Emergencies ; Hematologic Tests ; Humans ; Length of Stay ; Neurology ; Stroke

Background: Stroke is caused by disruption of blood supply and results in permanent disabilities as well as death. Chlorogenic acid is a phenolic compound found in various fruits and coffee and exerts antioxidant, anti-inflammatory, and anti-apoptotic effects. Objectives: The purpose of this study was to investigate whether chlorogenic acid regulates the PI3K-Akt-Bad signaling pathway in middle cerebral artery occlusion (MCAO)-induced damage. Methods: Chlorogenic acid (30 mg/kg) or vehicle was administered peritoneally to adult male rats 2 h after MCAO surgery, and animals were sacrificed 24 h after MCAO surgery.Neurobehavioral tests were performed, and brain tissues were isolated. The cerebral cortex was collected for Western blot and immunoprecipitation analyses. Results: MCAO damage caused severe neurobehavioral disorders and chlorogenic acid improved the neurological disorders. Chlorogenic acid alleviated the MCAO-induced histopathological changes and decreased the number of terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells. Furthermore, MCAO-induced damage reduced the expression of phospho-PDK1, phospho-Akt, and phospho-Bad, which was alleviated with administration of chlorogenic acid. The interaction between phospho-Bad and 14-3-3 levels was reduced in MCAO animals, which was attenuated by chlorogenic acid treatment. In addition, chlorogenic acid alleviated the increase of cytochrome c and caspase-3 expression caused by MCAO damage. Conclusions The results of the present study showed that chlorogenic acid activates phospho-Akt and phospho-Bad and promotes the interaction between phospho-Bad and 14-3-3 during MCAO damage. In conclusion, chlorogenic acid exerts neuroprotective effects by activating the Akt-Bad signaling pathway and maintaining the interaction between phosphoBad and 14-3-3 in ischemic stroke model.

Herein is a retrospective study of 220 cases of open heart surgery at Yeungnam University Hospital from April, 1984 to March, 1987 anti the anesthetic methods employed. Among the 226 caaes, there were 169 cases of congenital acyanotic disease, 21 cases of congenital cyanotic disease and 36 cases were acquired heart disease. One hundred fourteen cases were male and 112 were female. The mean age of patients with congenital heart disease was 9.2+/-7.9 gears and it was 34.2+/-13.8 years in acquired heart disease. The primarily utilized premedicants were morphine, hydroxyzine and glycopyrrolate. Induction agents included thiopental in the congenital acyanotic group, ketamine in the congenital cyanotic group and morphine and Valium in the acquired heart disease group. Mainten- ance agents were mainly halothane+N2O in the congenital acyanotic group, ketamine in the congenital cyanotic group and morphine with or without inhalation agents in the acquired heart disease group. Muscle relaxants such as succinylcholine and pancuroniurn were used in the early days of open heart surgery, but recently vecurnnium has been utilized for intubation and maintenance of muscle relaxation. The duration of cardiopulmonary bypass, aortic cross clamp, surgery and anesthesia were longer in the order of congenital acyanotic, congenital cyanotic and acquired heart disease group. Overall the mortality rate was 3.1%, and the main cause of death was respiratory failure (42.9%) .
Anesthesia* ; Cardiopulmonary Bypass ; Cause of Death ; Diazepam ; Female ; Glycopyrrolate ; Heart Defects, Congenital ; Heart Diseases ; Heart* ; Humans ; Hydroxyzine ; Inhalation ; Intubation ; Ketamine ; Male ; Morphine ; Mortality ; Muscle Relaxation ; Respiratory Insufficiency ; Retrospective Studies ; Succinylcholine ; Thiopental ; Thoracic Surgery*

Apert's syndrome is rare autosomal dominant defect characterized by craniosynostosis, midface hypoplasia and symmetrical syndactyly. Multiple surgical procedures will be needed for the child with this syndrome. Especially surgery for craniosynostosis is most often performed between 2 and 6 months of life, a period of physiologic anemia. Perioperative complications can occur from numerous sources-massive blood loss, venous air embolism, cerebral edema, hypothermia and hazardous airway management, thus more monitoring, large bored central venous line and early transfusion are recommended. We report a case of 5 month-old female Apert patient undergoing frontal bone advancement and cranioplasty. At the end of uneventful surgery, we removed endotracheal tube in operating room and permitted early feeding because the procedure was limited above the orbital ridge. As soon as feeding the patient presented cyanosis with generalized seizure. Patient was immediately intubated, sucked out secretions and inhaled with oxygen. Blood gas showed moderate hypoxemia which was improved by oxygen therapy. Suspicious aspiration pneumonia was marked on chest film but disappered I week later. The condition was favorable thereafter and discharged without complication. Keypoints in management of Aperts syndrome are close observation, early detection and preventive treatment of possible complications in perioperative period. (Korean J Anesthesiol 1995; 29: 300~303)
Airway Management ; Anemia ; Anoxia ; Brain Edema ; Child ; Craniosynostoses ; Cyanosis ; Embolism, Air ; Female ; Frontal Bone ; Humans ; Hypothermia ; Infant ; Operating Rooms ; Orbit ; Oxygen ; Perioperative Period ; Pneumonia, Aspiration ; Seizures ; Syndactyly ; Thorax

Schwannomas are slow-growing benign tumors originating from the Schwann cells of the peripheral nerve sheaths. Herein, we report the first documented case of a schwannoma presenting as a painful nipple mass in a 32-year-old woman. This mass initially developed six years ago following a period of breastfeeding. Breast magnetic resonance imaging (MRI) scans revealed an iso-intense mass, with an approximate size of 2.2 cm, on a T1-weighted image with internal cystic changes. The mass exhibited heterogeneously delayed enhancement and restricted diffusion.Surgical excision was performed, and the diagnosis of cutaneous plexiform nipple schwannoma was confirmed histopathologically. A literature review revealed that the MRI findings of the nipple mass in our case were consistent with the common features of a schwannoma.

Glutamate is a representative excitatory neurotransmitter. However, excessive glutamate exposure causes neuronal cell damage by generating neuronal excitotoxicity. Excitotoxicity in neonates caused by glutamate treatment induces neurological deficits in adults. The 14–3-3 family proteins are conserved proteins that are expressed ubiquitously in a variety of tissues. These proteins contribute to cellular processes, including signal transduction, protein synthesis, and cell cycle control. We proposed that glutamate induces neuronal cell damage by regulating 14–3-3 protein expression in newborn animals. In this study, we investigated the histopathological changes and 14–3-3 proteins expressions as a result of glutamate exposure in the neonatal cerebral cortex. Rat pups at post-natal day 7 were intraperitoneally administrated with vehicle or glutamate (10 mg/kg). Animals were sacrificed 4 h after treatment, and brain tissues were fixed for histological study. Cerebral cortices were isolated and frozen for proteomic study. We observed serious histopathological damages including shrunken dendrites and atypical neurons in glutamate-treated cerebral cortices. In addition, we identified that 14–3-3 family proteins decreased in glutamate-exposed cerebral cortices using a proteomic approach. Moreover, Western blot analysis provided results that glutamate treatment in neonates decreased 14–3-3 family proteins expressions, including the β/α, ζ/δ, γ, ε, τ, and η isoforms. 14–3-3 proteins are involved in signal transduction, metabolism, and anti-apoptotic functions. Thus, our findings suggest that glutamate induces neonatal neuronal cell damage by modulating 14–3-3 protein expression.