PURPOSE: The Professional Graduate Medical School (PGMS) was established in 2003 in South Korea to train doctors that had better humanities and various educational backgrounds. By comparing the learning styles between students of the Medical College (MC) and PGMS, we investigated the characteristics of these students. METHODS: The Kolb Learning Style Inventory (LSI) is used to determine learning preferences. It is composed of 12 statements on concrete experience, reflective observation, abstract conceptualization, and active experimentation. Six hundred nine students from all years of the 2 medical schools completed the Kolb LSI between June 1st and June 30th, 2008 (response rate: 91.4%). RESULTS: MC students preferred Kolb's 'assimilator (56.3%)' and 'diverger (25.6%)', and PGMS students preferred Kolb's 'assimilator (61.2%)' and 'converger (19.3%)'. PGMS students showed a higher preference for abstract conceptualization compared with MC students (adjusted Odds Ratio=2.191; 95% Confidence Interval=1.115~4.306). CONCLUSION: This study showed that the learning styles of PGMS and MC students differed. We can use this result not only in developing curricula and teaching strategies, but also in providing support to students.
Curriculum ; Humanities ; Humans ; Learning ; Republic of Korea ; Schools, Medical ; Students, Medical

Neuregulin-1 (NRG1) signaling participates in numerous neurodevelopmental processes. Although ErbB4, a key NRG1 receptor, is expressed in multiple regions in the adult animal brain, little is known about its expression in aged human brain. We show that ErbB4 immunoreactivity was shown regional difference in the hippocampus of age-matched control and that the distribution of these molecules was altered in Alzheimer's disease (AD) brains. Immunohistochemical characterization of the distribution of ErbB4 receptor in the hippocampus relative to pathology staging were performed in age-matched control (Braak stage I/II, n=5), early AD (Braak stage III/IV, n=5) and advanced AD(Braak stage V/VI, n=10). The intensity of ErbB4 immunoreactivity was higher in neurons of the CA2 than that in CA1 or CA3 in the age-matched control. Particularly, in the early AD, ErbB4 immunoreactivity was significantly increased in the apoptotic cells of the CA2 field. In the advanced AD, ErbB4 immunostaining was more intense in the apoptotic cell of the CA2 field. In the dentate gyrus (DG), ErbB4-positive granular cell density was gradually increased in proportion to the progression of pathology of AD brains. We have also found that ErbB4 immunostaining was increased in the nucleus, suggesting that the presenilin-dependent cleavage of ErbB4 generates the soluble ErbB4 ICD (intracellular domain) that translocalized to the nucleus. Together, these results provide the immunohistochemical analysis of ErbB4 receptor in the human hippocampus staged by the progression of pathology of AD.
Adult ; Aged ; Alzheimer Disease ; Animals ; Apoptosis ; Brain ; Cell Count ; Dentate Gyrus ; Hippocampus ; Humans ; Neuregulin-1 ; Neurons

PURPOSE: To determine the relationship between change in the expression of the p75 neurotrophin receptor (NTR) and transient receptor potential vanilloid 1 (TRPV1) after a spinal nerve injury with time. MATERIALS AND METHODS: The L5 and L6 spinal nerve of the rats were cut unilaterally. The spinal cord and dorsal root ganglion (DRG) were subjected to immunohistochemistry for p75 NTR and TRPV1. RESULTS: The immunoreaction (IR) for p75 NTR in the neuronal cytoplasm was persistently lower on the ipsilateral L5 and L6 DRG but higher in the satellite cells and fibers. The colocalization between p75 NTR and TRPV1 was increased temporarily in the L4 DRG in both sides. In the spinal cord, p75 NTR-IR decreased temporalily in the ipsilateral dorsal horn of the L4-L6 level and had recovered at 28 days after injury. CONCLUSION: These results show that a differential change in the expression of p75 NTR and TRPV1 is related to the different functional recovery of the sensory and motor system, and that increased colocalizations between p75 NTR and TRPV1 in a non-injured DRG might be related to the development of neuropathic pain after a peripheral nerve injury.
Animals ; Cytoplasm ; Diagnosis-Related Groups ; Ganglia, Spinal* ; Horns ; Immunohistochemistry ; Neuralgia ; Neurons ; Peripheral Nerve Injuries ; Rats* ; Receptor, Nerve Growth Factor* ; Spinal Cord* ; Spinal Nerve Roots* ; Spinal Nerves*

PURPOSE: The authors studied the effect of the 3-AB, an inhibitor of poly(ADP-ribose)polymerase (PARP), on the changes of primary afferents and spinal cord after spinal nerve injury. METHOD: The L5 and L6 spinal nerve of the rats were cut, and 3-AB (10 mg/Kg) was injected intraperitoneally once per day. The animals were sacrificed 3 days, 7 days, 14 days and 28 days after nerve injury. Binding of isolectin B4 (IB4) and immunohistochemistry (IHC) of CGRP for the changes in primary afferents, IHC of NK1 for sensory neurons, and of cleaved caspase 3 and NeuN for the apoptotic changes in spinal neurons were performed. RESULT: Decreased binding of IB4 and immunoreactivity (IR) for CGRP, increase of IR for NK1, and cleaved caspase 3 in both neurons and glia in ipsilateral dorsal horn were observed after spinal nerve injury. These changes were attenuated, especially at between 3 days and 14 days, by administration of 3-AB. CONCLUSION: It is suggested that inhibition of PARP by 3-AB may attenuate alterations of primary afferents and spinal neurons, at least in early stage, after spinal nerve injury.
Animals ; Apoptosis ; Caspase 3 ; Horns ; Immunohistochemistry ; Lectins ; Neuroglia ; Neurons* ; Rats* ; Sensory Receptor Cells ; Spinal Cord ; Spinal Nerves*

PURPOSE: The authors studied the effect of the 3-AB, an inhibitor of poly(ADP-ribose)polymerase (PARP), on the changes of primary afferents and spinal cord after spinal nerve injury. METHOD: The L5 and L6 spinal nerve of the rats were cut, and 3-AB (10 mg/Kg) was injected intraperitoneally once per day. The animals were sacrificed 3 days, 7 days, 14 days and 28 days after nerve injury. Binding of isolectin B4 (IB4) and immunohistochemistry (IHC) of CGRP for the changes in primary afferents, IHC of NK1 for sensory neurons, and of cleaved caspase 3 and NeuN for the apoptotic changes in spinal neurons were performed. RESULT: Decreased binding of IB4 and immunoreactivity (IR) for CGRP, increase of IR for NK1, and cleaved caspase 3 in both neurons and glia in ipsilateral dorsal horn were observed after spinal nerve injury. These changes were attenuated, especially at between 3 days and 14 days, by administration of 3-AB. CONCLUSION: It is suggested that inhibition of PARP by 3-AB may attenuate alterations of primary afferents and spinal neurons, at least in early stage, after spinal nerve injury.
Animals ; Apoptosis ; Caspase 3 ; Horns ; Immunohistochemistry ; Lectins ; Neuroglia ; Neurons* ; Rats* ; Sensory Receptor Cells ; Spinal Cord ; Spinal Nerves*

BACKGROUND: There are many arguments that Helicobacter pylori is a protective factor or a risk factor for GERD. Some authors reported a high incidence of reflux esophagitis in patients who had received Helicobacter pylori eradication therapy. We studied the prevalence of pathologic gastroesophageal reflux in Helicobacter pylori positive peptic ulcer patients and the effects of Helicobacter pylori eradication therapy on development of pathologic gastroesophageal reflux. METHODS: A total of 44 patients with endoscopically documented peptic ulcer disease and Helicobacter pylori infection underwent 24-hour esophageal pH monitoring and received a week of triple therapy. After three months of cessation of triple therapy, patients underwent 24-hour esophageal pH monitoring again. 24-hour esophageal pH monitoring of 44 patients were compared before and after the triple therapy. Helicobacter pylori status was evaluated by Giemsa stain, rapid urease test and urea breath test at each examination. RESULTS: The patients were classified into cured and ongoing Helicobacter pylori infection group. In cured patients group, there was no significant difference in the prevalence of pathologic gastroesophageal reflux before and after Helicobacter pylori eradication (p=0.8). In 44 patients, 30 patients had pathologic gastroesophageal reflux before eradication. In these patients, 27 patients cured Helicobacter pylori infection and 3 patients were ongoing Helicobacter pylori infection. Among 27 patients who cured Helicobacter pylori infection, 5 patients recovered from pathologic gastroesophageal reflux after eradication. In patients without pathologic gastroesophageal reflux before eradication, the prevalence of pathologic gastroesophageal reflux was not associated with Helicobacter pylori eradication (p=1). CONCLUSION: We find that the prevalence of pathologic gastroesophageal reflux in patients with peptic ulcer is high before Helicobacter pylori eradication. We suggest that Helicobacter pylori eradication in patients with peptic ulcer disease is not associated with development of pathologic gastroesophageal reflux.
Azure Stains ; Breath Tests ; Esophageal pH Monitoring ; Esophagitis, Peptic ; Gastroesophageal Reflux ; Helicobacter pylori* ; Helicobacter* ; Humans ; Hydrogen-Ion Concentration* ; Incidence ; Peptic Ulcer* ; Prevalence ; Risk Factors ; Urea ; Urease

Although adriamycin is a potent chemotherapeutic agent, it elicits serious adverse effects, including cardiac toxicity. Evidence suggests that congestive heart failure induced by adriamycin is mediated by oxidative stress. We investigated whether regulators of adenosine A1 receptor and KATP channel, which have been demonstrated to mediate protective effects of ischemic -preconditioning in myocardium, are able to modulate adriamicin -induced impairment of cardiomyocyte. To study the effect of antioxidant, adenosine A1 receptor agonist & antagonist and KATP channel agonist & antagonist, ICR mice were pretreated with Cu,Zn -SOD, dimethyl thiourea, RPIA (R (-)N6 -(2 -Phenylisopropropyl)- adenosine, adenosine A1 receptor agonist), 8 -CPDPX (8 -Cyclopentyl -1, 3 -dipropylxanthine, adenosine A1 receptor antagonist), Pinacidil (KATP channel opener) and glibenclamide (KATP channel closer), followed by i.p injection with adriamycin. Mice were sacrificed day 1 or day 4 after adriamycin injection and cardiac toxicity was accessed by measurement of creatine phosphokinase (CK) levels in serum, immunohistochemistry using anti -Bcl -2 antibody and TUNEL histochemical assay. As expected, pretreatment of mice with Cu, Zn -SOD and DMTU reduced the frequency of TUNEL positive cells, indicating antioxidants protected cardiocytes from adriamycin -induced apoptosis. Interestingly, pretreatment with RPIA and pinacidil induced a significant decrease in adriamycin -induced cytotoxicity, whereas 8 -CPDPX and glibenclamide generated the opposite results. In Bcl -2 immunohistochemistry, an increased expression of Bcl -2 was found in all ADR treated groups, especially in glibenclamide pretreated group, and 8 -CPDPX pretreated groups, but Bcl -2 failed to protect myocytes from apoptosis. All ADR treated groups exhibited elevated levels of serum CK, compared with nomal controls, especially mice sacrificed at day 4 than those at day 1, and showed similar patterns of TUNNEL assay, reflecting heart tissue damages. This observation implicated cytoprotective roles of RPIA and pinacidil against adriamycin -induced cardiac toxicity. In conclusion, these results demonstrated that adriamycin -induced cardiotoxicity was associated with the generation of reactive oxygen species and that regulators including SOD, DMTU, RPIA and pinacidil elicited protective effects on this toxicity. In particular, pinacidil, the KATP channel opener, was more effective than RPIA, the adenosine A, receptor agonist, to attenate the adriamycin -induced cardiac toxicity.
Adenosine* ; Animals ; Antioxidants ; Apoptosis ; Creatine Kinase ; Doxorubicin* ; Glyburide ; Heart ; Heart Failure ; Immunohistochemistry ; In Situ Nick-End Labeling ; Mice ; Mice, Inbred ICR ; Muscle Cells ; Myocardium ; Myocytes, Cardiac ; Oxidative Stress ; Pinacidil ; Reactive Oxygen Species ; Receptor, Adenosine A1* ; Thiourea

Laminin, an extracellular matrix glycoprotein composed of three polypeptide chains such as alpha , beta, and gamma is distributed in basement membranes of epithelium, muscle, and nervous tissues. Laminin functions as an extracellular cytoskeleton and regulates the differentiation and polarization of cells adjacent to the basement membrane. Along with type IV collagen and heparan sulfate proteoglycan, laminin forms a spike -like structure in the renal glomerular basement membrane (GBM). It has been previously demonstrated that the distribution and immune reaction of laminin are changed in response to the conditions of glomerulonephritis and that laminin plays a role in the reformation of GBM as well as the regeneration of renal glomerular cells. In the present study, the profile of expression and distribution of laminin/laminin beta1 chain were examined in different developmental stages and upon adriamycin administration. Kidney obtained from fetuses (16, 18, and 20 days old) and infants (1 and 7 days old) of Sprague -Dawley rats were either cryosectioned for immunohistochemical assays or ultrathin -sectioned for electron microscopy using immunogold staining methods. The results were as follows: 1. Intensive expression of laminin was observed in the GBM and surrounding mesenchymal tissues obtained from 16, 18, and 20 days old fetuses and in the glomerulus from one day neonates, whereas the level of staining decreased in the glomerulus from 7 days old infants. 2. Immunogold particles were observed in the comma -shaped nephron, in particular in cisternae of rough endoplasmic reticulum, vesicles and nuclear membrane of endothelial cells and mesangial cells obtained from 18 days old fetuses. 3. The immune reactions of laminin beta1 chain were trace detected in the kidney from fetuses (16, 18, and 20 days old) and weakly in tissues surrounding blood capillary and mesangial tissues from one day old neonates. 4. After 24 hours following adriamycin treatment, the reactivity of laminin was slightly enhanced in the renal glomerulus, when compared with that of untreated controls. This enhancement persisted up to 1 week of adriamycin treatment. Laminin beta1 chain was weakly detectable, while further treatment with adriamycin for another 24 hours reduced the intensity of laminin beta1 chain. Taken together, these results suggest that laminin is localized in the GBM at the high level during early fetal stages but the expression levels decrease after birth. Moreover, administration with adriamycin may result in an increase in the immune reactivities of laminin and laminin beta1 chain by renal tissue damage followed by renal regeneration.
Animals ; Basement Membrane ; Capillaries ; Collagen Type IV ; Cytoskeleton ; Doxorubicin ; Endoplasmic Reticulum, Rough ; Endothelial Cells ; Epithelium ; Extracellular Matrix ; Fetus ; Glomerular Basement Membrane ; Glomerulonephritis ; Glycoproteins ; Heparan Sulfate Proteoglycans ; Humans ; Infant ; Infant, Newborn ; Kidney* ; Laminin* ; Mesangial Cells ; Microscopy, Electron ; Nephrons ; Nuclear Envelope ; Parturition ; Rats* ; Regeneration

We experienced a case of a 38 year old women in whom an alpha-fetoprotein producing carcinoma originated in the rectum. The patient had symptoms of hematochezia and bowel habit change, and a rectal examination revealed an ulcerative mass at the midrectum. The mass size was 6.5 cm 6 cm. The serum alpha-fetoprotein measured preoperatively was 9336 ng/ml, and the serum (carcinoembryonic antigen) was 6.4 ng/ml. The serum level of alpha-fetoprotein decreased to 830 ng/ml thirteen days after a low anterior resection. The tumor mass was a poorly differentiated adenocarcinoma. Using an immunohistochemical staining method, we detected alpha-fetoprotein producing cells in the tumor mass. During the follow up, the serum alpha-fetoprotein level began to increase continuously, and an abdomin opelvic CT scan showed a systemic, local tumor recurrence. Based on our experience with this patient and a review of the literature on the few cases previously reported, it seems that alpha-fetoprotein producing colorectal carcinamas have a tendency to produce frequent blood-borne metastasis and are associated with a poor prognosis.
Adenocarcinoma ; Adult ; alpha-Fetoproteins* ; Colorectal Neoplasms ; Female ; Follow-Up Studies ; Gastrointestinal Hemorrhage ; Humans ; Neoplasm Metastasis ; Prognosis ; Rectal Neoplasms* ; Rectum ; Recurrence ; Tomography, X-Ray Computed ; Ulcer

BACKGROUND: Diverse injury to central nervous system results in proliferation and hypertrophy of astrocytes. The hallmark of this response is enhanced expression of the major intermediate filament protein of astrocyte, glial fibrillary acidic protein(GFAP). These obsevations suggested that GFAP may be a useful biochemical indicator of neurotoxicity. This study is designed for investigating the chronological effects of the thiamine deficiency on the astrogrial GFAP immunoreactivity in the rat forebrain, and for comparing the difference between time-sequenital morphological changes of luxol fast blue-cresyl violet stain reported in previous study and GFAP immunoreactivity. METHODS: A total of 40 healthy Sprague-Dawley strain rats, weighing about 200gm were used as experimental animals(10 control, 30 thiamine deficient rats). Pyrithiamine was injected intraperitonially for 9 days and thiamine deficient diet was continuously supplied until sacrifice. Thiamine deficient rats were subdivided into 3 groups according to thiamine deficient state. Immunohistochemical stains for GFAP in the regions of thalamus, medial mammillary nucleus and CA1 sector in hippocampus were performed by free floating method in cell culture plate. All preperations were observed with light microscope. RESULTS: GFAP immunoactivities at thalamus were tracely positive(+) in controls, strongly positive(+++) in group I, and moderately positive(++) in group II and III. But GFAP immunoactivities at medial mammillary nucleus were tracely positive( ) in controls, moderately positive(++) in group I and III , and strongly positive(+++) in group II. At the CA1 region of hippocampus, the immunoactivities were weakly positive in controls , strongly positive(+++) in group I and II, and moderately positive(++) in group III. The diverse patterns of GFAP immunoreactivities in each vulnerable site were different from the previous morphological study. In luxol-fast and cresyl violet staining, the neuronal damage and necrosis were marked in group III, group II, and group I, in that order, which findings are consistent in all regions. CONCLUSIONS: Different patterns of time-sequential GFAP immunoactivities at each vulnerable site suggest that there are regional differences in sensitivity and resistance to thiamine deficiency.
Animals ; Astrocytes ; Cell Culture Techniques ; Central Nervous System ; Coloring Agents ; Diet ; Glial Fibrillary Acidic Protein* ; Hippocampus ; Hypertrophy ; Intermediate Filaments ; Necrosis ; Neurons ; Prosencephalon* ; Pyrithiamine ; Rats* ; Rats, Sprague-Dawley ; Thalamus ; Thiamine Deficiency* ; Thiamine* ; Viola