Effectiveness of a shortened, clinically engaged anatomy course for physician assistant students.

There is little consensus among programs that train physician assistants (PAs) regarding how much time should be devoted to the study of anatomy, what should be included, or how it should be taught. Similar concerns led us to redesign anatomy for medical students and introduce clinically engaged anatomy, an approach designed in collaboration with clinical faculty. This approach presents anatomy entirely within the context of common clinical cases. This report examines whether clinically engaged anatomy could be adapted to the PA program, where students cover the basic sciences in half the time as medical students. We offered a modified version of clinically engaged anatomy to PA students in which time spent in self-directed learning activities was reduced relative to medical students. We compared their scores on an examination of long-term recall to students who took the previous course. Two classes who took clinically engaged anatomy, scored the same or significantly higher on every portion of the examination (P < 0.05). Students expressed high satisfaction with the course (Likert scale, 4.3-4.8/5 points). Compared to medical students who took clinically engaged anatomy, the data suggest that the tradeoff for reducing the time spent in self-directed learning was reduced skills in applying structure-function relationships and spatial reasoning to clinical problems. The data suggest clinically engaged anatomy can be effective in various educational settings, and can be readily adapted to clinical programs that vary in the depth that anatomy is covered. Nonetheless, careful assessments are needed to determine if the necessary tradeoffs are consistent with the goals of the profession.

Spectrum of orbital disease in South India: an aravind study of 6328 consecutive patients.

AIM: To review the incidence of orbital diseases in South India and to compare with other case series published. METHODS: Retrospective review of 6328 consecutive patients with orbital disease evaluated at Aravind Eye Hospital between January 1997 and December 2008. The main outcome measure was incidence of orbital disease in South Indian population, as determined by clinical and histopathologic criteria. A literature review was conducted to compare the results of this study with those of previously published reports. RESULTS: Of the 6328 patients, 2161 (34.1%) had inflammatory orbital disease, 1965 (31.0%) had systemic conditions involving the orbit, 1277 (20.1%) had neoplasm, 600 (9.4%) had congenital lesions, 308 (4.8%) had trauma, and 17 (0.2%) had vascular disease. Of the 2161 patients presenting with inflammatory disease, 1473 (68.1%) had idiopathic orbital inflammation, 270 (12.5%) had infection, 126 (5.8%) had dacryoadenitis, and 292 (13.5%) had other etiologies. Among the 1965 patients presenting with systemic disease involving the orbit, 1938 (98.6%) were diagnosed with thyroid orbitopathy, 22 (1.1%) with amyloidosis, and 5 (0.2%) with sarcoidosis. Of the 1277 patients with neoplasm, the tumor was vascular in 369 (28.8%), neural in 336 (26.3%), lymphoid or leukemic in 131 (10.2%), secondary neoplasm in 82 (6.4%), epithelial in 68 (5.3%), adipose in 53 (4.1%), metastatic in 39 (3.0%), and fibrous, fibro-osseous, striated muscle, histiocytic, and other cellular origin in 40 (3.1%), 37 (2.8%), 23 (1.8%), 21 (1.6%), and 78 (6.1%), respectively. Of the 600 patients with congenital lesions, 427 (71.1%) had dermoid and 170 (28.3%) had dermolipoma, followed by meningoencephalocele. CONCLUSIONS: The most common causes of orbital disease in South India are inflammatory (34.1%) and systemic conditions (31.0%). With the exception of higher incidence of inflammatory etiologies, these data are largely consistent with prior published reports.

Design, implementation, and evaluation of an innovative anatomy course.

Starting in 2004, a medical school gross anatomy course faced with a 30% cut in hours went through an extensive redesign, which transformed a traditional dissection course into a course with a clinical focus, learning societies, and extensive on-line learning support. Built into the redesign process was an extensive and ongoing assessment process, which included student focus groups, faculty development, surveys, and examinations. These assessments were used formatively, to enhance the course from year to year, and summatively, to determine how well the course was meeting the new learning objectives. The assessments from focus groups and faculty development prompted changes in support structures provided to students and the training and preparation of faculty. Survey results showed that, after student satisfaction declined the first year, satisfaction increased steadily through the fourth iteration as the course gained acceptance by students and faculty alike. There was a corresponding increase in the performance of students on course examinations. An additional examination given to students one and a half and three years after their anatomy course ended demonstrated the redesigned course's long-term effectiveness for retaining anatomical knowledge and applying it to clinical cases. Compared to students who took the original course, students who took the shorter, more clinical course performed as well, or better, on each section of the examination. We attribute these positive results to the innovative course design and to the changes made based on our formative assessment program.

Hypoxic injury during neonatal development in murine brain: correlation between in vivo DTI findings and behavioral assessment.

Preterm birth results in significant neurodevelopmental disability. A neonatal rodent model of chronic sublethal hypoxia (CSH), which mimics effects of preterm birth, was used to characterize neurodevelopmental consequences of prolonged exposure to hypoxia using tissue anisotropy measurements from diffusion tensor imaging. Corpus callosum, cingulum, and fimbria of the hippocampus revealed subtle, yet significant, hypoxia-induced modifications during maturation (P15-P51). Anisotropy differences between control and CSH mice were greatest at older ages (>P40) in these regions. Neither somatosensory cortex nor caudate putamen revealed significant differences between control and CSH mice at any age. We assessed control and CSH mice using tests of general activity and cognition for behavioral correlates of morphological changes. Open-field task revealed greater locomotor activity in CSH mice early in maturation (P16-P18), whereas by adolescence (P40-P45) differences between control and CSH mice were insignificant. These results may be associated with lack of cortical and subcortical anisotropy differences between control and CSH mice. Spatial-delayed alternation and free-swim tasks in adulthood revealed lasting impairments for CSH mice in spatial memory and behavioral laterality. These differences may correlate with anisotropy decreases in hippocampal and callosal connectivities of CSH mice. Thus, CSH mice revealed developmental and behavioral deficits that are similar to those observed in low birth weight preterm infants.

Neurodevelopment of C57B/L6 mouse brain assessed by in vivo diffusion tensor imaging.

Heterogeneous spatiotemporal patterns of C57B/L6 murine brain maturation during the first 7 weeks after birth (i.e. P15 to P45) were assessed in vivo by diffusion tensor imaging (DTI) at 9.4 T. Maps of apparent diffusion coefficient (ADC) and fractional anisotropy (FA) were used to assess developmental changes. Because directionally encoded color (DEC) maps provide an efficient and straightforward way to visualize anisotropy direction, they were used to highlight the orientation-dominant anisotropic tissues. In the corpus callosum, the increases in FA (approximately 0.4 to approximately 0.6 from P15 to P45) were primarily dominant in the medial-lateral direction, whereas the ADC decreased slightly (approximately 0.8 x 10(-3) to approximately 0.5 x 10(-3) mm(2)/s from P15 to P45). Similar increases in FA (approximately 0.3 to approximately 0.4 from P15 to P45) and decreases in ADC (approximately 0.8 x 10(-3) to approximately 0.5 x 10(-3) mm(2)/s from P15 to P45) were found in the cingulate, but these anisotropic changes were dominant in the anterior-posterior direction. In the caudate putamen, there were significant FA increases (approximately 0.1 to approximately 0.2 from P15 to P45) dominant in the dorsal-ventral and anterior-posterior directions, whereas the ADC increased rapidly early in development (approximately 0.3 x 10(-3) to approximately 0.7 x 10(-3) mm(2)/s from P15 to P17). There were no significant changes in tissue anisotropy in the somatosensory regions (whisker, forelimb), but the ADC decreased slightly (approximately 0.7 x 10(-3) to approximately 0.5 x 10(-3) mm(2)/s from P15 to P45). Although the major differences in DEC values were mainly observed in white matter pathways, other cortical and subcortical regions showed some potential morphological changes that were consistent with classical histological findings. In summary, these results show that high-resolution DTI at high magnetic fields allows detection and quantification of brain structures throughout normal development in C57B/L6 mice in vivo.

Should we continue teaching anatomy by dissection when ...?

The central role that human dissection has long held in clinical education is being reevaluated in many institutions. Despite the impression that many institutions are abandoning dissection, very few have and most of those have reinstated dissection within a few years. What are the inherent qualities that lead institutions back to dissection? In our efforts to redesign a shortened dissection course, our consultations with a broad range of clinicians lead us to understand how the rhythms of clinical practice are modeled and developed in the small-group setting of the dissection laboratory. Following further consultation with colleagues who have experimented with different models of anatomy instruction, we discuss three themes in support of dissection. First, problem-solving in the dissection laboratory develops the habits-of-mind of clinical practice. Second, relating dissection to imaging modalities develops the spatial reasoning skills needed to understand computer simulations, interpret imaging data, and interact with surgeons, radiologists, and patients. Third, the human face of dissection fosters self-reflection and integration of the cognitive and affective skills required for medical practice. Through group process, the collaborative effort of dissection teams develops essential of attributes of clinical professionalism.

Design principles for developing an efficient clinical anatomy course.

The exponential growth of medical knowledge presents a challenge for the medical school curriculum. Because anatomy is traditionally a long course, it is an attractive target to reduce course hours, yet designing courses that produce students with less understanding of human anatomy is not a viable option. Faced with the challenge of teaching more anatomy with less time, we set out to understand how students employ instructional media to learn anatomy inside and outside of the classroom. We developed a series of pilot programs to explore how students learn anatomy and, in particular, how they combine instructional technology with more traditional classroom and laboratory-based learning. We then integrated what we learned with principles of effective instruction to design a course that makes the most efficient use of students' in-class and out-of-class learning. Overall, we concluded that our new anatomy course needed to focus on transforming how medical students think, reason, and learn. We are currently testing the hypothesis that this novel approach will enhance the ability of students to recall and expand their base of anatomical knowledge throughout their medical school training and beyond.

Neonatal hypoxia suppresses oligodendrocyte Nogo-A and increases axonal sprouting in a rodent model for human prematurity.

Premature human infants frequently suffer from periventricular leukomalacia (PVL) characterized by the loss of central myelinated tracts in the brain [Neuropathology, 22 (2002) 193]. Rodent chronic sublethal hypoxia (CSH) from P3 to 33 (postnatal day 3-33) provides a model for PVL characterized by cerebral ventriculomegaly and reductions in cerebral white matter volume [Brain Res. Dev. Brain Res. 111 (1998) 197; Proc. Natl. Acad. Sci. USA 100 (2003) 11718]. Here, we demonstrate that mice exposed to CSH from P3 to P33 followed by normoxia from P33 to P75 continue to exhibit a locomotor hyperactivity that resembles behavioral changes observed in some human children with very low birth weights. Because periventricular white matter is specifically lost in PVL, we examined the expression of oligodendrocyte proteins. Hypoxic rearing dramatically decreases the level of the axon outgrowth inhibitor Nogo-A in oligodendrocytes of CNS white matter at P12. The Nogo-A decrease exceeds the moderate decrease in another myelin protein, myelin associated glycoprotein (MAG). Although myelin protein expression returns to normal by maturity (P75), persistent abnormalities in axonal trajectories are detectable. Anterograde axonal tracing from motor cortex demonstrates ectopic corticofugal fibers in the corticospinal tract (CST), corpus callosum, and caudate nucleus of adult animals reared in CSH. Thus, hypoxia-induced reduction in myelin-derived axon outgrowth inhibitors appears to contribute axonal misconnection to the pathology of very low birth weight infants.

Chronic neonatal hypoxia leads to long term decreases in the volume and cell number of the rat cerebral cortex.

Preterm birth results in significant neurodevelopmental disability. The neonatal rodent model of chronic sublethal hypoxia faithfully mimics the effect of preterm birth on the developing brain. We employed this model to test the hypothesis that the hypoxia that accompanies preterm birth results in inappropriate signaling of apoptotic mechanisms in developing brain. We performed cortical cell counts, determinations of neuronal size and Western analyses of the apoptosis related proteins, Bcl-2 and Bax, in rat pups who were raised in chronic hypoxia (FiO2 9.5%) beginning on postnatal day 3 (P3) and extending for either 10 (P13) or 30 (P33) days. A third group of animals was exposed to 30 days of hypoxia followed by an additional 30 days in a normoxic environment (P63) to assess the potential for recovery from the initial effects of hypoxia. Age matched control pups were raised in room air throughout the experimental time period. Assessment of cortical cell number revealed a 25% reduction (P < 0.01) in total cell number following 30 days of hypoxic rearing. Glia were significantly reduced by 34% and 41% after 10 and 30 days of hypoxia, respectively, while neuron numbers were only significantly reduced (14%) after 30 days of hypoxia. Animals exposed to a hypoxic environment for 30 days followed by 30 days in a normoxic environment revealed some recovery of glial cell numbers, but no significant recovery of neuronal cell numbers. Measurement of cell size at both P13 and P33 revealed that neurons of layer III were significantly smaller in cross-sectional area in hypoxic compared with control rats (P < 0.01). However, no significant difference was noted in neuronal size following 30 days of normoxic recovery. Western blot analyses of Bcl-2 and Bax protein levels demonstrated a ratio favorable to Bax at multiple time points during the period of hypoxic exposure. These data suggest that chronic exposure to hypoxia during the perinatal period alters the production and maintenance of glial and neuronal cells and that glia and neurons demonstrate differential patterns of vulnerability and recovery following subsequent periods of normoxic exposure. It is hypothesized that the mechanisms responsible for these alterations in cortical cell number may depend on the state of differentiation of the different cell types at the time of hypoxic exposure.

Disrupted synaptic development in the hypoxic newborn brain.

Infants born prematurely risk significant life-long cognitive disability, representing a major pediatric health crisis. The neuropathology of this cohort is accurately modeled in mice subjected to sublethal postnatal hypoxia. Massively parallel transcriptome analysis using cDNA microchips (9,262 genes), combined with immunohistochemical and protein assays, reveals that sublethal hypoxia accentuates genes subserving presynaptic function, and it suppresses genes involved with synaptic maturation, postsynaptic function, and neurotransmission. Other significantly affected pathways include those involved with glial maturation, vasculogenesis, and components of the cortical and microtubular cytoskeleton. These patterns reveal a global dysynchrony in the maturation programs of the hypoxic developing brain, and offer insights into the vulnerabilities of processes that guide early postnatal cerebral maturation.

Correlation of Web usage and exam performance in a human anatomy and development course.

Course materials for a Human Anatomy and Development Course were placed on the World Wide Web (WWW). The materials included a lab manual, lecture notes and slides, faculty-generated atlases, Web links, and examinations. The lab manual, lecture notes, and atlases were also provided as black-and-white hardcopy. The Office of Education assigned students a code name that allowed them to use the Web site and take exams anonymously. Student Web use was tracked and correlated with their performance on the final examination. Overall use patterns revealed that most students used the Web site to prepare for examinations, but not for daily studying. Old examinations were the most accessed documents; lecture notes were the least accessed. The access patterns of the students with top 20, middle 20 (closest to the mean), and bottom 20 scores on the final examination were compared. In general, there was little difference between the middle and top groups. Students in the bottom group used computer resources significantly less than the other groups. In a second analysis, the 10 students who used the Web site most frequently scored below the mean. The study suggests that interactive exercises will be heavily used, but that the preparation of all course materials for the WWW may not be an efficient use of institutional resources.

Paracrine and autocrine functions of neuronal vascular endothelial growth factor (VEGF) in the central nervous system.

Recent data have demonstrated that vascular endothelial growth factor (VEGF) is expressed by subsets of neurons, coincident with angiogenesis within the developing cerebral cortex. Here we investigate the characteristics of VEGF expression by neurons and test the hypothesis that VEGF may serve both paracrine and autocrine functions in the developing central nervous system. To begin to address these questions, we assayed expression of VEGF and one of its potential receptors, Flk-1 (VEGFR-2), in the embryonic mouse forebrain and embryonic cortical neurons grown in vitro. Both VEGF and Flk-1 are present in subsets of post-mitotic neurons in vivo and in vitro. Moreover, VEGF levels are up-regulated in neuronal cultures subjected to hypoxia, consistent with our previous results in vivo. While the abundance of Flk-1 is unaffected by hypoxia, the receptor exhibits a higher level of tyrosine phosphorylation, as do downstream signaling kinases, including extracellular signal-regulated protein kinase, p90RSK and STAT3a, demonstrating activation of the VEGF pathway. These same signaling components also exhibited higher tyrosine phosphorylation levels in response to exogenous addition of rVEGFA(165). This activation was diminished in the presence of specific inhibitors of Flk-1 function and agents that sequester VEGF, resulting in a dose-dependent increase in apoptosis in these neuronal cultures. Further, inhibition of MEK resulted in increased apoptosis, while inhibition of phosphatidylinositol 3-kinase had no appreciable affect. In addition to the novel function for VEGF that we describe in neuronal survival, neuronal VEGF also affected the organization and differentiation of brain endothelial cells in a three-dimensional culture paradigm, consistent with its more traditional role as a vascular agent. Thus, our in vitro data support a role for neuronal VEGF in both paracrine and autocrine signaling in the maintenance of neurons and endothelia in the central nervous system.