The process of curricular integration and its effects on anatomical knowledge retention.

Introduction: Integration has been recognized as an important aspect of medical education. After transitioning from a discipline-specific to a systems-based preclinical curriculum, we examined faculty perceptions of the integrated approach and also whether it would lead to better anatomy knowledge retention.

Methods: To understand faculty perspectives, we reviewed curricular materials, interviewed block directors, and observed educational sessions.

Using ultrasound to teach living anatomy to non-medical graduate students.

Purpose: Ultrasound technology is used to supplement gross anatomy instruction in many medical sciences programs. However, this technology is not common practice for anatomy instruction in nonmedical graduate-level courses. Ultrasound sessions provide a clear view of local anatomy and could help graduate students transfer anatomical content from a didactic context onto a living, moving body.

Inflammatory bowel disease, colorectal cancer and type 2 diabetes mellitus: The links.

The co-occurrence of the three disease entities, inflammatory bowel disease (IBD), colorectal cancer (CRC), type 2diabetes mellitus (T2DM) along with inflammation and dismicrobism has been frequently reported. Some authors have even suggested that dysbiosis could be the link through a molecular crosstalk of multiple inflammatory loops including TGFβ, NFKB, TNFα and ROS among others. This review focuses on the inflammatory process along with the role of microbiota in the pathophysiology of the three diseases.

Curricular response to increase recall and transfer of anatomical knowledge into the obstetrics/gynecology clerkship.

Deficits in retention of anatomy knowledge from the preclinical years to clinical application on the wards have been well documented in the medical education literature. We developed and evaluated a web and laboratory-based curriculum to address deficits in anatomy knowledge retention and to increase anatomy knowledge recall through repetition and application of clinical concepts during the obstetrics and gynecology (Ob/Gyn) core clinical clerkship. Using principles of adult learning and instructional design, a curriculum was designed consisting of (1) interactive, case-based e-modules reviewing clinically relevant anatomical topics and (2) a hands-on laboratory session reinforcing the content of the e-modules, with the practice of clinical techniques using anatomical cadaveric dissections.

Anatomical knowledge retention in third-year medical students prior to obstetrics and gynecology and surgery rotations.

Surgical anatomy is taught early in medical school training. The literature shows that many physicians, especially surgical specialists, think that anatomical knowledge of medical students is inadequate and nesting of anatomical sciences later in the clinical curriculum may be necessary. Quantitative data concerning this perception of an anatomical knowledge deficit are lacking, as are specifics as to what content should be reinforced.

Can anatomists teach living anatomy using ultrasound as a teaching tool?

The utilization of bedside ultrasound by an increasing number of medical specialties has created the need for more ultrasound exposure and teaching in medical school. Although there is a widespread support for more vertical integration of ultrasound teaching throughout the undergraduate curriculum, little is known about whether the quality of ultrasound teaching differs if performed by anatomists or clinicians. The purpose of this study is to compare medical students' evaluation of ultrasound anatomy teaching by clinicians and anatomists.

Design for learning: adapting the microscopic anatomy laboratory to adult learners.

Medical school curricula are undergoing transformational change in response to calls for integrating content across courses and years to enable better retention and application and for individualizing learning to meet the diverse backgrounds and thus differing needs of students. To address the related teaching challenges, faculty can employ solid principles of adult learning and instructional design and use teaching strategies that stimulate different learning styles. We developed laboratory sessions that follow a learner-centered instructional design model we refer to as "PLHET," reflecting the steps of preparing, linking, hooking, engaging, and transferring learning, and also applied teaching strategies that reflect Kolb's four styles of learning (accommodative, divergent, assimilative, and convergent).

Exposure to particulate hexavalent chromium exacerbates allergic asthma pathology.

Airborne hexavalent chromate, Cr(VI), has been identified by the Environmental Protection Agency as a possible health threat in urban areas, due to the carcinogenic potential of some of its forms. Particulate chromates are produced in many different industrial settings, with high levels of aerosolized forms historically documented. Along with an increased risk of lung cancer, a high incidence of allergic asthma has been reported in workers exposed to certain inhaled particulate Cr(VI) compounds.

Blocking cyclophilins in the chronic phase of asthma reduces the persistence of leukocytes and disease reactivation.

Allergic asthma is characterized by acute influxes of proinflammatory leukocytes in response to allergen stimulation, followed by quiescent (chronic) periods between allergen challenges, during which sustained, low-level inflammation is evident. These chronic phases of disease are thought to be mediated by populations of leukocytes persisting within airways and tissues. The lack of any in situ proliferation by these cells, along with their limited lifespan, suggests that a continual recruitment of leukocytes from the circulation is needed to maintain disease chronicity.

A cell-impermeable cyclosporine A derivative reduces pathology in a mouse model of allergic lung inflammation.

Although the main regulators of leukocyte trafficking are chemokines, another family of chemotactic agents is cyclophilins. Intracellular cyclophilins function as peptidyl-prolyl cis-trans isomerases and are targets of the immunosuppressive drug cyclosporine A (CsA). Cyclophilins can also be secreted in response to stress factors, with elevated levels of extracellular cyclophilins detected in several inflammatory diseases.

Syndecan-1 regulates cell migration and fibronectin fibril assembly.

Corneal scarring is a major cause of blindness worldwide and can result from the deposition of abnormal amounts of collagen fibers lacking the correct size and spacing required to produce a clear cornea. Collagen fiber formation requires a preformed fibronectin (FN) matrix. We demonstrate that the loss of syndecan1 (sdc1) in corneal stromal cells (CSC) impacts cell migration rates, the sizes and composition of focal and fibrillar adhesions, the activation of integrins, and the assembly of fibronectin into fibrils.

Loss of syndecan-1 is associated with malignant conversion in skin carcinogenesis.

Syndecan-1 (sdc-1) is a cell surface proteoglycan that mediates the interaction of cells with their matrix, influencing attachment, migration, and response to growth factors. In keratinocytes, loss of sdc-1 delays wound healing, reduces migration, and increases Transforming growth factor beta (TGFbeta) 1 expression. In this study we show that sdc-1 expression is significantly reduced in basal cell, squamous cell, and metastatic human skin cancers compared to normal human skin.

Primary dermal fibroblasts derived from sdc-1 deficient mice migrate faster and have altered alphav integrin function.

ABSTRACT The goal of this study is to determine whether dermal fibroblasts lacking syndecan-1 (sdc1) show differences in integrin expression and function that could contribute to the delayed skin and corneal wound healing phenotypes seen in sdc-1 null mice. Using primary dermal fibroblasts, we show that after 3 days in culture no differences in alpha-smooth muscle actin were detected but sdc-1 null cells expressed significantly more alphav and beta1 integrin than wildtype (wt) cells. Transforming growth factor beta1 (TGFbeta1) treatment at day 3 increased alphav- and beta1-integrin expression in sdc-1 null cells at day 5 whereas wt cells showed increased expression only of alphav-integrin.

BALB/c and C57BL6 mouse strains vary in their ability to heal corneal epithelial debridement wounds.

Genetically engineered mice are usually produced on a mixed genetic background and can be derived from several mouse strains including 129SvJ, C57BL6, and BALB/c. To determine whether differences in recurrent corneal epithelial erosions (RCEEs), corneal epithelial stem cell deficiency (CESCD), and cell migration rate vary between two different mouse strains (BALB/c and C57BL6), 8-week mice were subjected to 1.5 (small) or 2.

Inflammatory bowel disease in rats: bacterial and chemical interaction.

Aim: To develop a novel model of colitis in rats, using a combination of iodoacetamide and enteropathogenic E. coli (EPEC), and to elucidate the pathophysiologic processes implicated in the development of ulcerative colitis (UC).

Methods: Male Sprague-Dawley rats (n = 158) were inoculated intrarectally on a weekly basis with 4 different combinations: (a) 1% methylcellulose (MC), (b) 100 microL of 6% iodoacetamide (IA) in 1% MC, (c) 200 microL containing 4 x 10(8) colony factor units (CFU) of EPEC, and (d) combined treatment of (IA) followed by bacteria (B) after 2 d.

Reduced migration, altered matrix and enhanced TGFbeta1 signaling are signatures of mouse keratinocytes lacking Sdc1.

We have reported previously that syndecan-1 (Sdc1)-null mice show delayed re-epithelialization after skin and corneal wounding. Here, we show that primary keratinocytes obtained from Sdc1-null mice and grown for 3-5 days in culture are more proliferative, more adherent and migrate more slowly than wt keratinocytes. However, the migration rates of Sdc1-null keratinocytes can be restored to wild-type levels by replating Sdc1-null keratinocytes onto tissue culture plates coated with fibronectin and collagen I, laminin (LN)-332 or onto the matrices produced by wild-type cells.