Comparison of Team-Based Learning versus Traditional Lectures in Neuroanatomy: Medical Student Knowledge and Satisfaction.

Neuroanatomy is often considered a difficult subject to teach, due to its broad scope, multitude of terms, and high degree of complexity. Thus, newer educational strategies that facilitate learning while also stimulating students by allowing increased student autonomy and group discussions should be carefully considered. This study aimed to evaluate the impact of introducing team-based learning (TBL) in the traditional discipline of neuroanatomy and to measure student knowledge acquisition and perception relative to traditional lectures (TL). A quasi-experimental, nonrandomized study was performed using two consecutive TBL classes (intervention group, n = 157 students, 25% content using TBL) with a TL class (control group, n = 76). Team-based learning sessions included all stages according to the classic description of the method. Student knowledge acquisition was assessed in regularly scheduled tests during the discipline, and their perception regarding TBL was evaluated using a questionnaire (developed by the authors). The groups presented a similar sociodemographic profile (sex and age) and the same performance in another anatomy discipline before the study. Team-based learning was significantly associated with greater acceptance, higher motivation, better student perception, and feelings that the methodology was able to integrate clinical and basic sciences. Nevertheless, according to tests, knowledge acquisition was similar between the TBL and lectures. In conclusion, since TBL is comparable to TL for knowledge acquisition, TBL seems to be a promising strategy to improve the teaching of neuroanatomy in medical schools. It fosters group discussions and increases satisfaction and the perception of integration between clinical and basic sciences.

Tumour necrosis factor receptors and apoptosis of alveolar macrophages during early infection with attenuated and virulent Mycobacterium bovis.

Apoptosis of macrophages has been reported as an effective host strategy to control the growth of intracellular pathogens, including pathogenic mycobacteria. Tumour necrosis factor-α (TNF-α) plays an important role in the modulation of apoptosis of infected macrophages. It exerts its biological activities via two distinct cell surface receptors, TNFR1 and TNFR2, whose extracellular domain can be released by proteolysis forming soluble TNF receptors (sTNFR1 and sTNFR2). The signalling through TNFR1 initiates the majority of the biological functions of TNF-α, leading to either cell death or survival whereas TNFR2 mediates primarily survival signals. Here, the expression of TNF-α receptors and the apoptosis of alveolar macrophages were investigated during the early phase of infection with attenuated and virulent mycobacteria in mice. A significant increase of apoptosis and high expression of TNFR1 were observed in alveolar macrophages at 3 and 7 days after infection with attenuated Mycobacterium bovis but only on day 7 in infection with the virulent M. bovis. Low surface expression of TNFR1 and increased levels of sTNFR1 on day 3 after infection by the virulent strain were associated with reduced rates of apoptotic macrophages. In addition, a significant reduction in apoptosis of alveolar macrophages was observed in TNFR1(-/-) mice at day 3 after bacillus Calmette-Guérin infection. These results suggest a potential role for TNFR1 in mycobacteria-induced alveolar macrophage apoptosis in vivo. In this scenario, shedding of TNFR1 seems to contribute to the modulation of macrophage apoptosis in a strain-dependent manner.

Splenectomy increases atherosclerotic lesions in apolipoprotein E deficient mice.

BACKGROUND: Atherosclerosis is an inflammatory immune disease associated with lipid accumulation in the intima layer of arteries. The spleen plays an important immune function, but its influence in development of atherosclerosis remains unclear. Evaluation of the role of the spleen in atherosclerosis is justified due to the high frequency of total splenectomies. In this work, the effect of splenectomy on the development of atherosclerosis in apolipoprotein E (ApoE) deficient mice was investigated. METHODS: ApoE deficient mice were divided into a sham-operated control group (CT) and a splenectomized group (SP). Thirty days after surgery, animals were fed a high fat western diet. After 8 wk, mice were euthanized and their blood, heart, and aorta were subjected to analysis. Atherosclerotic lesion areas in the aortic root were stained with hematoxylin-eosin and quantified by morphometry. The atherosclerotic lesions in the thoracic and abdominal portions of aorta were determined by assessing the percentage of the luminal surface area stained by Sudan IV. Total serum cholesterol and anti-oxidized LDL antibodies were measured. RESULTS: Levels of total serum cholesterol did not vary significantly after splenectomy. Anti-oxidized LDL IgG antibodies were similar between groups. However, compared with the control group, lesions in the aortic root were significantly larger in splenectomized mice (P<0.01). These data were confirmed by the increase of atherosclerotic area in the thoracic and abdominal portions of aorta in splenectomized mice. CONCLUSIONS: These data indicate that splenectomy increases atherosclerotic lesions in ApoE deficient mice fed an atherogenic diet, suggesting an atheroprotector role of the spleen.

Antibody response of autogenous splenic tissue implanted in the abdominal cavity of mice.

There is still controversy about the immunologic function of autotransplanted splenic tissue. In this study, splenic autotransplantation was performed in the abdominal cavity of mice, and the plaque-forming cell (PFC) assay was used to investigate the frequency of antibody-forming cells in response to sheep red blood cell (SRBC) immunization. BALB/c mice were divided into four groups according to the location of the autogenous graft: intraomental (IO), free peritoneal splenosis (FPS), retroperitoneal (RP), and nongrafted control (CT). Thirty days after surgery the mice were immunized intraperitoneally with SRBCs, and 4 days later splenic immunoglobulin M anti-SRBC-secreting cells were determined by counting the number of PFCs. All the immunized mice showed increased numbers of PFCs that were about 2 logs higher than those in the the nonimmunized controls (P < 0.005). The frequencies of anti-SRBC-producing cells in the tissues grafted in various sites of the abdominal cavity (IO, FPS, RP), in the normal spleen from nonoperated controls (CT), or in the sham-operated control group (SCT) were not notably different (5582 +/- 2475 PFC/10(7) cells for IO; 4849 +/- 1856 for FPS; 6604 +/- 2903 for RP; 5940 +/- 5029 for CT; and 6172 +/- 2203 for SCT). Similar histology with small architectural variations was observed in all implants; less white pulp was involved, and there was more congestion in the red pulp, with extensive sinusoids and reticular fiber proliferation. This study shows that the T cell-dependent antibody response in implanted splenic tissues is as efficient as in the intact spleen, with no difference between the graft sites studied. This immune response does not depend on the slight architectural variations observed in the splenic implants.