Recent Publications by CFE Educators

Affinity-purified goat anti-rabbit immunoglobulin G (GAR) was conjugated with (3H)-propionyl succinimidate and used to localize substance P (SP), enkephalin (ENK), and serotonin immunoreactive sites in the spinal dorsal horn and medulla of the rat and cat. Autoradiographic localization was demonstrated on paraffin, frozen, Vibratome, and 2 micron plastic sections. The latter were obtained from radiolabeled Vibratome sections that were embedded in epoxy resin. The distribution of SP, ENK, and serotonin demonstrated by radioimmunocytochemistry was comparable to that observed on semiadjacent sections using peroxidase-antiperoxidase (PAP) immunocytochemistry. The autoradiograms, however, were generated using primary antibody concentrations up to five times more dilute than concentrations used for the PAP procedure. Indirect radioimmunocytochemistry using a (3H) anti-immunoglobulin G second antibody can be used to localize a variety of monoclonal and polyclonal antisera. It is quantifiable at the light microscopic level and can be potentially used with peroxidase histochemistry to double label immunoreactive structures at the ultrastructural level.

Doctors are encouraged to look upon each patient as a learning experience ( Wyngaarden , 1979). Case-oriented learning begins in the clinical years of medical school and continues throughout the professional career of the doctor. Clinical cases, or anecdotes, have the potential of producing accurate, relevant and meaningful learning for the clinician even though they are uncontrolled in a scientific sense. However, unusual or atypical cases can also result in erroneous learning which can negatively affect patient care. The purpose of this article is to identify difficulties in this form of subjective learning which can lead to suboptimal doctor practice patterns. Six actual clinical cases are briefly described to illustrate how inaccurate learning distorted subsequent clinical problem-solving by doctors. Suggestions are then made for ameliorating this difficulty.

Through combined ultrastructural localization of ENK immunoreactivity and [3H]5-HT uptake sites, it was found that 5-HT radiolabeled axons contact ENK immunoreactive cell bodies and small dendrites in the cat superficial dorsal horn. While some contacts displayed both pre- and postsynaptic specializations, the majority lacked a definitive synaptic cleft and postsynaptic density. These results suggest that 5-HT-containing axons, presumably derived from the medullary nucleus raphe magnus, directly influence spinal opiod antinociceptive activity.

A patient with Waldenström's macroglobulinemia who presented with pleuropulmonary manifestations is described. The course was complicated by recurrent Streptococcus pneumoniae infections despite pneumococcal immunization.

Although the midbrain periaqueductal gray (PAG) is thought to have a major role in an endorphin-mediated analgesia system, little is known about its neuroanatomical organization. To determine the microcircuitry within the PAG through which exogenous and endogenous opiates may act, we analyzed the synaptic organization of normal and immunoreactive enkephalin (ENK)-labeled profiles in the caudal PAG, a region of particular interest because of its effectiveness in generating analgesia. Examination of the normal fine structure of this region demonstrated that there is no characteristic synaptic morphology that distinguishes individual regions of the caudal PAG (ventromedial, ventrolateral and dorsolateral) from one another. In all 3 regions of the caudal PAG, axodendritic synapses are the predominant form of synaptic interaction making up 93-97% of all synapses counted. Axosomatic synapses are much less common, as are presumed axoaxonic and dendrodendritic synapses. In the caudal ventral PAG, the largest population of ENK-labeled axonal boutons are found presynaptic to unlabeled, centrally placed dendrites. Much less frequently, immunoreactive ENK-containing boutons are found presynaptic to neuronal perikarya or vesicle-containing profiles. Thus, these results suggest that the dendrites of neurons intrinsic to the PAG are the most probable site of opiate action in the caudal ventral PAG.

Eighteen patients with lupus erythematosus (LE) and pleural effusions were evaluated. Fourteen patients had lupus pleuritis and four had pleural effusions of other etiologies. All patients were symptomatic, and the presenting signs and symptoms did not help distinguish between lupus pleuritis and pleural effusions of other causes. The presence of LE cells confirmed the diagnosis of lupus pleuritis in seven of eight patients. In 11 of 13 patients with lupus pleuritis, the pleural fluid antinuclear antibody (ANA) titer was greater than or equal to 1:160, and in nine of 13 patients with lupus pleuritis, the pleural fluid to serum (PF/S) ANA ratio was greater than or equal to 1. In the four patients with LE and a pleural effusion of another etiology, the pleural fluid ANA titer was negative in two and low titer in two (1:40, 1:80); the pleural fluid to serum ANA titer was always less than one. Of 67 patients with pleural effusions of other etiologies, the pleural fluid ANA was negative. The signs and symptoms of lupus pleuritis are nonspecific, however; the findings of LE cells in pleural fluid confirms the diagnosis and a high pleural fluid ANA titer (greater than or equal to 1:160) and a PF/S ANA ratio of greater than or equal to 1 strongly supports the diagnosis.

The component parts and development of a comprehensive system to evaluate and improve teaching in a school of medicine are described by the author in this paper. This system integrates quantitative measures of teaching (student/resident ratings of classroom and clinical teaching), descriptive documentation (faculty teaching load, innovations, and research on teaching), and qualitative judgments (peer review) on the full spectrum of instruction in medicine. Medical school policies have standardized evaluation criteria, instrumentation, and procedures while granting departments flexibility in conducting peer review. The results of two studies indicate that the evaluation system described here has had a positive impact both on the improvement of teaching and on academic promotions.

To clarify the circuitry through which opioid compounds modulate spinal and trigeminal nociceptive transmission, we have examined the synaptic associations formed by leucine-enkephalin-containing (enkephalin) neurons in the superficial dorsal horn of the cat. As described previously, punctate enkephalin immunoreactivity is concentrated in the marginal layer (lamina I) and in both the outer and inner layers of the substantia gelatinosa (lamina IIo and IIi). In colchicine treated cats, enkephalin perikarya are most numerous in lamina I and at the border between laminae I and II. Ultrastructural analysis reveals that enkephalin cells receive a diverse afferent input. The majority of afferent inputs are presynaptic to the enkephalin dendrites; few axosomatic synapses are seen. Among these presynaptic axonal profiles are unlabeled axons which resemble primary afferent terminals, including the characteristic central axonal varicosity. Enkephalin dendrites are also postsynaptic to enkephalin immunoreactive axons. Two types of enkephalin axonal profiles appear in the superficial dorsal horn. Class I profiles are only found in lamina I. These are large profiles which form few synapses; those synapses made are axodendritic. Class II enkephalin axons are smaller and are distributed in both layers I and II. While Class II axons most commonly form axo-dendritic synapses, they also form axo-axonic synapses with flat vesicle-containing profiles; the latter are generally presynaptic to the enkephalin terminals. Serial analysis further revealed that both the enkephalin and the flat vesicle-containing profile synapse onto a common dendrite. Although enkephalin axons frequently lie adjacent to round vesicle-containing profiles, anatomical evidence that opioid axons form synapses with this type of ending was not found. An additional type of enkephalin vesicle containing-profile is found in layer IIi; its morphological features do not clearly distinguish its axonal or dendritic origin. These endings are typically postsynaptic to unlabelled central endings, and provide minimal presynaptic input to other elements in the neuropil. Like some class II axons, these labelled profiles contain vesicles which cluster at the membrane immediately adjacent to unlabelled central axons. These results indicate that spinal enkephalin neurons receive a variety of synaptic inputs. These include inputs which may derive from primary afferent axons. Enkephalin neurons, in turn, influence nociceptive transmission predominantly through postsynaptic mechanisms. Finally, while we did not observe enkephalin terminals presynaptic in an axoaxonic relationship, the possibility that enkephalin neurons modulate the excitability of fine fiber nociceptive and nonnociceptive afferents via "nonsynaptic interactions" is discussed.

This study was designed to investigate the frequency and diagnostic importance of the pleuropulmonary manifestations of the postcardiac injury syndrome. A retrospective study of 35 patients (2 to 76 years old) with clearly defined postcardiac injury syndrome is presented. Twenty-one cases followed cardiac surgery, and 14 appeared after myocardial infarction. The onset of the syndrome was an average of 20 days following injury. The major clinical findings were pleurisy (91 percent; 32/35), fever (66 percent; 23/35), pericardial rub (63 percent; 22/35), dyspnea (57 percent; 20/35), rales (51 percent; 18/35), pleural rub (46 percent; 16/35), elevated erythrocyte sedimentation rate (96 percent; 25/26), and leukocytosis (49 percent; 17/35). The chest roentgenogram was abnormal in 94 percent (33/35). Pleural effusion was present in 83 percent (29/35), parenchymal infiltrates in 74 percent (26/35), and an enlarged cardiac silhouette in 49 percent (17/35). Analysis of pleural fluid was performed on 16 samples from 12 patients and revealed a bloody exudate with a pH greater than 7.40. The data presented document that pleuropulmonary involvement is a common manifestation of postcardiac injury syndrome. In addition, we discuss how these findings can be used to differentiate this syndrome from other clinical entities that may appear following cardiac injury, ie, parapneumonic effusions, congestive heart failure, and pulmonary embolism.