Recent Publications by CFE Educators

PURPOSE

Despite being well suited to provide the breadth of care needed in rural areas, few general internists become rural physicians. Little formal rural residency training is available and no formal curricula exist. For over 25 years the University of Washington School of Medicine has provided elective WWAMI (Washington, Wyoming, Alaska, Montana, Idaho) rural residency rotations to expose residents to the rewards and challenges of rural practice. This study identified the characteristics of outstanding rural residency rotations.

METHOD

The key preceptors at three outstanding rural residency sites were interviewed about their experiences, teaching strategies, and opinions about curriculum. Their responses were categorized. Seven university-based residents and eight training at WWAMI sites recorded and rated the value of over 1,500 learning encounters.

RESULTS

The preceptors agreed that outstanding rotations were led by enthusiastic preceptors who served as role models for excellence. These preceptors provided residents with meaningful responsibilities and emphasized independent decision making based on the history and physical examination. They stressed supervised independence and self-directed learning with frequent structured feedback for residents. The residents rated the learning value of patient encounters in rural locations significantly higher than that of those in university clinics.

CONCLUSIONS

Exceptional rural residency experiences involve excellent role models who provide meaningful responsibility and emphasize core skills using a learner-centered approach. Rural training experiences should be supported, and the suggestions of outstanding preceptors should be used to develop and disseminate a curriculum that will better prepare residents for rural practice.

Left ventricular outflow tract stroke distance (SD) can be measured using pulsed-wave Doppler echocardiography, and is independent of body size. Moreover, persons with structurally normal hearts (heart rate 55 beats/min) had SD > 0.18 m, and those with a heart rate > 95 beats/min had SD 0.22 m; outside of these parameters, low- and high-output states are likely to exist, and suspicion of these can be confirmed by calculation of minute distance (normal range 9.7 to 20.5 m/min).

PURPOSE

We explore the history of testosterone in the context of medical and scientific developments.

MATERIALS AND METHODS

A review of the scientific and historical literature was conducted.

RESULTS

The origins and effects of testosterone have been recognized throughout the history of humankind. Hunter performed testicular transplantation experiments in 1767 while studying tissue transplantation techniques, and almost a century later Berthold linked the physiological and behavioral changes of castration to a substance secreted by the testes. Brown-Séquard gave birth to the field of organotherapy in 1889 when he announced that his auto-injection of testicular extracts resulted in rejuvenated physical and mental abilities. Steinach and Niehans expanded upon Brown-Séquard's work with rejuvenation treatments involving vasoligation, tissue grafts and cellular injections. In 1935 David et al isolated the critical ingredient in organotherapeutic treatments, testosterone.

CONCLUSIONS

The effects of the powerful hormone testosterone continue to inspire research and controversy 65 years later.

Many studies indicate that blood pressure control systems can attenuate pain (hypoalgesia) of short duration; however, we recently found exaggerated nociceptive responses (hyperalgesia) of persistent duration in the spontaneously hypertensive rat (SHR). Here, we used SHR, Dahl Salt-Sensitive (SS), and normotensive control rats to evaluate the contribution of sustained elevations in arterial pressure to nociceptive responses. Compared with Sprague-Dawley and/or Wistar-Kyoto controls, SHR were 1) hypoalgesic in the hot plate test and 2) hyperalgesic in longer latency tail and paw-withdrawal tests and in two models of inflammatory nociception. These differences were not observed between SS and salt-resistant controls fed a high-salt diet. Inflammatory hyperalgesia in SHR was correlated with neither paw edema nor the number of Fos-positive spinal cord neurons. Our results indicate that "pain" phenotype of the SHR is not restricted to hypoalgesia. This phenotype is related to genetic factors or to the autonomic systems that control blood pressure and not to sustained elevations in blood pressure, differences in spinal neuron activity, or inflammatory edema.

Idiopathic pulmonary fibrosis is a progressive and usually fatal lung disease characterized by fibroblast proliferation and extracellular matrix remodeling, which result in irreversible distortion of the lung's architecture. Although the pathogenetic mechanisms remain to be determined, the prevailing hypothesis holds that fibrosis is preceded and provoked by a chronic inflammatory process that injures the lung and modulates lung fibrogenesis, leading to the end-stage fibrotic scar. However, there is little evidence that inflammation is prominent in early disease, and it is unclear whether inflammation is relevant to the development of the fibrotic process. Evidence suggests that inflammation does not play a pivotal role. Inflammation is not a prominent histopathologic finding, and epithelial injury in the absence of ongoing inflammation is sufficient to stimulate the development of fibrosis. In addition, the inflammatory response to a lung fibrogenic insult is not necessarily related to the fibrotic response. Clinical measurements of inflammation fail to correlate with stage or outcome, and potent anti-inflammatory therapy does not improve outcome. This review presents a growing body of evidence suggesting that idiopathic pulmonary fibrosis involves abnormal wound healing in response to multiple, microscopic sites of ongoing alveolar epithelial injury and activation associated with the formation of patchy fibroblast-myofibroblast foci, which evolve to fibrosis. Progress in understanding the fibrogenic mechanisms in the lung is likely to yield more effective therapies.

The proto-oncogene products erbB-l (EGF-Receptor) and erbB-2 (HER-2/neu), distinct members of the epidermal growth factor receptor family, are frequently overexpressed in squamous cell carcinoma of the head and neck (SCCHN). The accumulation of these transmembrane proteins may lead to significant amounts of the respective extracellular receptor domains (ECD) that are shed from the tumour cell surface and enter blood circulation, thus representing potential serum tumour markers. For erbB-l and erbB-2, we determined the ECD serum levels with enzyme-linked immunosorbent assays and evaluated the protein expression in tumour tissue by immunohistochemistry. The present study included 49 patients (37 untreated, 12 recurrences) and the same number of age- and sex-matched healthy controls. In 24 patients ECD serum levels were determined before and 6 weeks after surgery. Mean ECD serum levels for erbB-1 and erbB-2 were 54.8+/-1.6 and 153.7+/-6.1 fmol/ml in cancer patients, and 54+/-1.5 and 147.9+/-4.5 fmol/ml in healthy controls, respectively. There was no significant difference between untreated and recurrent disease. Serum ECD follow-ups 6 weeks after surgery revealed a significant 12.3% decline of erbB-1 but no change of erbB-2 values. Immunohistochemistry showed strong staining for erbB-1 in 78% and erbB-2 in 47% of the SCCHN specimens. No correlation was detectable between receptor ECD serum levels and receptor tissue expression, tumour stage, and tumour differentiation. Hence, ECD serum levels of erbB-1 and erbB-2 are not considered to be valuable tumour markers in SCCHN.