Do learning approaches of medical students affect their satisfaction with problem-based learning?

The aim of this research was to determine the satisfaction of medical students with problem-based learning (PBL) and their approaches to learning to investigate the effect of learning approaches on their levels of satisfaction. The study group was composed of medical students from three different universities, which apply PBL at different levels in their curricula. The revised two-factor study process survey was applied to the study group to determine their approaches to learning as "deep" or "surface" learning. In addition, another survey of 20 questions was used to determine satisfaction levels of students with PBL and other variables. Of the study group, 64.6% were found to adopt a deep approach to learning, and we confirmed that these students were reasonably more satisfied with PBL.

Hippocampal neuron number loss in rats exposed to ingested sulfite.

Sulfite, which is continuously formed in the body during metabolism of sulfur-containing amino acids, is commonly used in preservatives. It has been shown that there are toxic effects of sulfite on many cellular components. The aim of this study was to investigate the possible toxic effects of sulfite on pyramidal neurons by counting cell numbers in CA1 and CA2-CA3 subdivisions of the rat hippocampus. For this purpose, male albino rats were divided into a control group and a sulfite group (25 mg/kg). Sulfite was administered to the animals via drinking water for 8 weeks. At the end of the experimental period, brains were removed and neurons were estimated in total and in a known fraction of CA1 and CA2-CA3 subdivisions of the left hippocampus by using the optical fractionator method--a stereological method. Results showed that sulfite treatment caused a significant decrease in the total number of pyramidal neurons in three subdivisions of the hippocampus (CA1 and CA2-CA3) in the sulfite group compared with the control group (p < 0.05, Mann Whitney U test). It was concluded that exogenous administration of sulfite causes loss of pyramidal neurons in CA1 and CA2-CA3 subdivisions of the rat hippocampus.

Bilateral symmetric junctional infarctions of the cerebellum: a case report.

The advances in neuroimaging have improved clinicoanatomic correlations in patients with stroke. Junctional infarct is a distinct term, used to describe border zone infarcts of the posterior fossa. We presented computed tomography (CT) and magnetic resonance imaging (MRI) findings in a rare case of bilateral symmetrical junctional infarcts between the superior cerebellar artery (SCA) and posterior inferior cerebellar artery (PICA) territories. In addition to precise knowledge of arterial territories required to achieve accurate localization of ischemic lesions on CT and MRI, the radiologist must also be aware of radiologic features and geographic territories of cerebellar arteries and their junctional infarctions.

The effect of in ovo ethanol exposure on retina and optic nerve in a chick embryo model system.

Ocular anomalies seen in children with fetal alcohol syndrome (FAS) suggest that ocular structures are sensitive to alcohol exposure during their development. This study was designed to investigate the effect of in ovo ethanol (EtOH) exposure on retinal development and myelinization of optic nerve fibers at an ultra structural level in a chick embryo model system. Prior to incubation, fertilized chicken eggs were injected once with 100 microl of either 0.9% NaCl (vehicle control), or EtOH solutions at different doses (10, 30, or 50%, v:v in 0.9% NaCl) into their air sacs and incubated at 37.5 degrees C and saturation humidity. On day 20 embryos were analyzed in terms of their viability and growth and the optic cups including the optic nerves were dissected out. Specimens were processed for electron microscopy (EM). Results showed that, EtOH significantly decreased the viability of chick embryos (P < 0.045), and caused significant prenatal growth retardation (P < 0.004) in a dose-dependant manner. Light microscopy of semi thin sections revealed that prenatal exposure to EtOH resulted in both retinal degeneration and optic nerve hypoplasia (P < 0.001) in a dose-dependant manner. EM revealed that a dose-dependant decrease in the number of myelinated nerve fibers was profound in groups exposed to EtOH (P < 0.001). Furthermore, the myelin coats observed were thinner than those seen in control embryos. In groups exposed to EtOH myelin sheets were unorganized and contained vacuolar structures in between them. The tissue in between the cells and optic nerve fibers, on the other hand, lost its intact appearance with vacuolar and vesicular structures in between them. In addition, the optic nerve fibers contained granular accumulations in EtOH exposed groups. A dose dependent degeneration was also observed in retinas of EtOH exposed groups. The effect of EtOH was profound in pigment epithelium (PE), inner plexiform layer (IPL), and ganglion cell layer (GC). Mitochondrial deficiencies, and alterations in melanin granule number and distribution dominated the defects seen in PE. On the other hand, EM findings of all the affected layers were suggestive of induced cell death in EtOH exposed groups. Thus, this study suggests retinal development with the emphasis on melanin pigmentation in PE and optic nerve myelinization as potential targets of prenatal EtOH exposure and discusses potential mechanisms of EtOH action on these tissues.

Effects of second generation tetracyclines on penicillin-epilepsy-induced hippocampal neuronal loss and motor incoordination in rats.

Epileptic seizures cause pathological changes such as sclerosis and pyramidal neuronal loss in the hippocampus. Experimentally, epilepsy can be induced by application of various chemicals directly to the cerebral cortex. In this study, epilepsy was induced in rats by intracortical application of 500 IU penicillin G, and the effect of minocycline and doxycycline on the resulting motor incoordination (rotarod) and hippocampal neuronal loss in CA1, CA2 and CA3 fields (optical fractionator method) were investigated. The rotarod performance was reduced in the epilepsy group to 285.1+/-6.9 s (P<0.05 vs. sham-300 s). Minocycline and doxycycline increased this performance to 297.4+/-1.0 s and 296.9+/-1.2 s respectively. No significant difference was detected between minocycline and doxycycline. The present results also showed that the number of neurons (x10(3)) in the sham group was 150+/-9. In the penicillin-epileptic rats, the number was decreased to 105+/-7 (P<0.01). Minocycline, but not doxycycline (125+/-8), significantly increased the number to 131+/-3 (P<0.05). In conclusion, the second generation tetracycline minocycline decreased the loss of hippocampal neurons and motor incoordination in penicillin-epileptic rats. Minocycline could protect against a variety of neurological insults including epilepsy.

Grape seed extract has superior beneficial effects than vitamin E on oxidative stress and apoptosis in the hippocampus of streptozotocin induced diabetic rats.

We aimed to investigate the effects of grape seed extract (GSE) and vitamin E (Vit E) on oxidative stress and apoptosis in the hippocampus of streptozotocin-induced diabetic rats. In Control, Diabetic, and Diabetic treated with GSE (Diabetic+GSE) and vitamin E (Diabetic+Vit E) groups, oxidative stress index (OSI), TUNEL staining and Bcl-2, Bcl-XL, Bax, caspase-3, -9, and -8, Cyt-c, TNF-α, and NF-κB gene expressions were evaluated. OSI was significantly increased in the plasma and hippocampus of the Diabetic compared to Control group and decreased in Diabetic+GSE and Diabetic+Vit E groups compared to Diabetic. TUNEL positive neurons significantly increased in the hippocampus of the Diabetic group compared to Control and decreased in Diabetic+GSE (more prominently) and Diabetic+Vit E groups compared to Diabetic. In the hippocampus of the Diabetic group, Bcl-2 and Bcl-XL gene expressions were significantly decreased; Bax, caspase-3, -9, and -8, Cyt-c, TNF-α, and NF-κB gene expressions were significantly increased compared to Control. In Diabetic+GSE and Diabetic+Vit E groups, Bcl-2 gene expressions were significantly increased; Bcl-XL gene expressions did not differ compared to the Diabetic group. The expression of Bax, caspase-3, -9, and -8, Cyt-c, TNF-α, and NF-κB genes in the Diabetic+GSE group and the expression of caspase-3 and -9, TNF-α, and NF-κB genes in the Diabetic+Vit E group were significantly decreased compared to Diabetic. In conclusion, GSE (more prominently) and vitamin E decreased oxidative stress and neuronal apoptosis occurring in the hippocampus of diabetic rats.

SEM examination of the dorsal lingual papillae of pregnant rats.

To our knowledge there are no histomorphological studies examining the lingual papillae in pregnancy. Therefore, this present study was planned. The purpose of this study was to clarify different physiological results and to investigate whether there are any changes on the dorsal surface of the rat tongue during pregnancy. On days 7 and 14 of pregnancy, superficial epithelial configurations of the lingual papillae (circumvallate, fungiform, filiform) in pregnant rats were examined by scanning electron microscopy (SEM). It was found that there were some differences in topographic configurations of these papillae in pregnant rats compared with controls. The obtained changes by SEM may reflect something which occurs in the lingual papillae during pregnancy in rat. There may be a correlation between the alterations of some hormone levels in pregnancy and some morphological changes of the lingual papillae.

Effect of nifedipine on hippocampal neuron number in penicillin-induced epileptic rats.

AIM: Epileptic seizures lead to neuronal loss in the hippocampus. Experimental epilepsy can be induced by direct application of various chemicals to cerebral cortex. Nifedipine is an L-type voltage-dependent calcium channel blocker. In spite of several studies that show the seizure-suppressing effects of nifedipine, it has been shown that nifedipine does not suppress but conversely increases epileptic seizures. Similarly, contradictory effects of nifedipine have been reported, such as neuroprotection, failed neuroprotection and neurotoxicity. We therefore aimed to investigate the effect of nifedipine on hippocampal neuronal loss in penicillin induced epileptic rats in this study. MATERIAL AND METHODS: The effect of nifedipine on total hippocampal neuron number was estimated by using the optical fractionator method (an unbiased stereological method) in penicillin-G induced epileptic rats. RESULTS: The total number of hippocampal neurons in the control group was 183687 ± 3184. In the penicillin-induced group, the total neuron number significantly decreased to 146318 ± 3042 compared to the control group. In the nifedipine group, the neuron number significantly decreased to 128873 ± 1157 compared to both control and penicillin-induced groups. CONCLUSION: Nifedipine increased neuronal loss and did not suppress epileptic seizures in penicillin-induced epileptic rats. Nifedipine could not protect against hippocampal neuronal loss in penicillin-induced epileptic rats.

Comparison of the calcaneal pitch angle and modified projection area per length squared method for medial longitudinal arch evaluation of the foot.

OBJECTIVE: To compare the calcaneal pitch angle (CPA) values measured on direct lateral radiographs of feet, and the modified projection area per length squared (PAL), which was calculated as a new method for the evaluation of the medial longitudinal arch (MLA) of the foot. MATERIAL AND METHODS: Direct lateral radiographs of patients who had weightbearing feet radiographies for any reason except trauma were retrospectively obtained from the archives. Direct lateral radiographs of the feet were printed and a transparent sheet was placed on it. A straight line was drawn between the most plantar process of the calcaneus and the head of the first metatarsal bone for the calculation of the PAL of the MLA. Two semilunar arcs were drawn upon this straight line. PAL1 and PAL2 were estimated using a point-counting technique. The CPA, lateral talo-calcaneal angles (LTCA), and talo-first metatarsal angles (TFMA) were measured. The correlations between PAL1, PAL2 of right and left feet and CPA, LTCA, and TFMA were explored. RESULTS: Fifty patients (27 females, 23 males) with a mean age of 40.12 (4-78) years were evaluated. Significant correlations were detected between PAL1, PAL2 and CPA, and TFMA for both right and left feet (p<0.05). CONCLUSION: A significant correlation was detected between the modified PAL method as a new technique and the standard CPA method for MLA evaluation. The PAL method is suggested as a simple and practical method for MLA evaluation.

Effects of different corticosteroids on the brain weight and hippocampal neuronal loss in rats.

Equivalent antiinflammatory doses of steroids including betamethasone, methylprednisolone and dexamethasone were administered in the neonatal period in a rat model. In situ cell death in hippocampus quantified by Terminal Deoxynucleated Transferase Nick-End Labeling and on ratio of brain to body weight was investigated. Apoptotic index (AI) was significantly higher in methylprednisolone, and high dose dexamethasone groups than the other groups. AI in "Cornu ammonis 1" (CA1) and "Cornu ammonis 3" (CA3) subregions of high dose dexamethasone group was the highest among the five groups tested. AI in CA3 subregions of methylprednisolone group was also significantly higher than the control, betamethasone and low dose dexamethasone groups. AI in CA1 subregion were not different among control, betamethasone, methylprednisolone and low dose dexamethasone groups. In addition, high dose dexamethasone resulted significant decrease in the ratio of brain weight to body weight in comparison to all other groups tested. In conclusion, betamethasone and low dose dexamethasone may be better alternative treatments among agents tested in this study for chronic lung disease (CLD).

Increased tunel positive cells in CA1, CA2, and CA3 subfields of rat hippocampus due to copper and ethanol co-exposure.

Copper (Cu) is an essential element for life. However, it is toxic at excessive doses, whereas exposure to ethanol (EtOH) has known to cause morphological changes, degeneration, and neuronal loss in central nervous system. A previous investigation by the authors' group showed that Cu and EtOH co-treatment cause severe hippocampal neuronal loss in CA1, CA2, and CA3 subfields of rat hippocampus. This study was designed to analyze the possible mechanism(s) of action of this effect. In addition, the possible neurogenesis in response to a potent neurodegenerative treatment in rat hippocampus was analyzed. Results demonstrated that Cu and EtOH induced neuronal loss in rat hippocampus was in correlation with the increased cell death analyzed on the basis of TdT-mediated dUTP nick end labeling (TUNEL) assay. On the other hand, neuronal regenerative activity was detectable in analyzed CA1, CA2, and CA3 subfields of the rat hippocampus analyzed on the basis of 5-bromo-2'-deoxy-uridine (BrdU) labeling assay; however, this activity in treated group was not significantly different from that of control group.

Penicillin-induced epilepsy model in rats: dose-dependant effect on hippocampal volume and neuron number.

This study was designed to evaluate the penicillin-induced epilepsy model in terms of dose-response relationship of penicillin used to induce epilepsy seizure on hippocampal neuron number and hippocampal volume in Sprague-Dawley rats. Seizures were induced with 300, 500, 1500 and 2000IU of penicillin-G injected intracortically in rats divided in four experimental groups, respectively. Control group was injected intracortically with saline. Animals were decapitated on day 7 of treatment and brains were removed. The total neuron number of pyramidal cell layer from rat hippocampus was estimated using the optical fractionator method. The volume of same hippocampal areas was estimated using the Cavalieri method. Dose-dependent decrease in hippocampal neuron number was observed in three experimental groups (300, 500 and 1500IU of penicillin-G), and the effects were statistically significant when compared to the control group (P<0.009). Dose-dependent decrease in hippocampal volume, on the other hand, was observed in all three of these groups; however, the difference compared to the control group was only statistically significant in 1500IU of penicillin-G injected group (P<0.009). At the dose of 2000IU penicillin-G, all animals died due to status seizures. These results suggest that the appropriate dose of penicillin has to be selected for a given experimental epilepsy study in order to demonstrate the relevant epileptic seizure and its effects. Intracortical 1500IU penicillin-induced epilepsy model may be a good choice to practice studies that investigate neuroprotective mechanisms of the anti-epileptic drugs.

Granule cell apoptosis induced by overdose copper and ethanol is counterbalanced by co-induced cellular proliferation in rat dentate gyrus.

Copper (Cu) is an essential element for life, however, is toxic at excessive doses, whereas exposure to ethanol (EtOH) has been known to cause morphological changes, degeneration and neuronal loss in central nervous system (CNS). In this study, the effect of overdose co-exposure to Cu and EtOH on dentate gyrus was investigated in rats. Analysis of apoptotic cell death on the basis of TdT-mediated dUTP nick end labeling (TUNEL) assay revealed that the rate of apoptosis was increased by 1.84 folds in treated group in comparison to that in controls (p < 0.0001). Analysis of cell proliferation on the basis of 5-bromo-2'-deoxy-uridine labeling assay, on the other hand, revealed a 1.49 fold increase in treated group when compared to controls (p < 0.006). Total number of granule cells in dentate gyrus of each group was estimated using the optical fractionator method. The results showed that mean granule cell number in dentate gyrus was 4.64% lower in treated group than that in control group, but this difference was not statistically significant (p > 0.05). These results suggest that the apoptotic effect of overdose Cu and EtOH on granule cells of dentate gyrus may be counterbalanced by the co-induced cellular proliferation, thereby maintaining the total granule cell number unaltered.

Effect of copper overload together with ethanol uptake on hippocampal neurons.

Copper is an essential trace element which forms an integral component of many enzymes. While trace amounts of copper are needed to sustain life, excess copper is extremely toxic in the brain. Also, ethanol intake causes morphological changes in the brain. The present study aims to investigate effects of copper overload with ethanol intake in hippocampal neuron numbers of rat brain. Control and experimental group of rats (n = 6 for each group) were fed ad libitum. Experimental group were given ethanol with copper in drinking water each day for ten days. Control group animals were given only drinking water during this period. Afterwards, animals were decapitated and their brains were removed by craniotomy. Frozen brains were cut by a cryostat. Sections collected via systematic random sampling were stained with hematoxylin and eosin. On microscopic images obtained from pyramidal cell layers in hippocampus, total neuron numbers were estimated using the optical fractionator method. We observed that pyramidal neuron numbers in the subdivisions of hippocampus were significantly lower in the experimental group than in the control group. These results suggest that copper overdose with ethanol intake can cause neuronal loss in hippocampus of rat brain.