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Introduction: Many research reports revealed declining empathy in medical schools that continues in postgraduate years of training. Objective: The aim of this study is to examine the self-reported empathy levels of internal medicine (IM) residents in 3 community-based teaching hospitals. Methods: The Jefferson Scale of Physician Empathy, Health Professionals version, is an online, self-administered, questionnaire that was offered to 129 current and incoming residents at 1 osteopathic and 2 allopathic, IM training programs in Flint, Michigan. Results: Forty-five residents responded (35% response rate). Our residents’ cumulative mean empathy score was 112.5 with a SD of 12.72, which is comparable with the cumulative empathy scores for IM residents at university hospitals. There was an increase in empathy score from the beginning level of training, postgraduate year 0 (PGY0), to the PGY1 level, and a noticeable, although statistically non-significant, decrease in empathy score for both PGY2 and PGY3 residents. The graduating residents’ scores were higher compared with incoming residents. Conclusions: The cumulative mean empathy score in community-based IM residents showed an increase in the beginning of residents’ training and decrease in empathy score by the end of training. There were significant differences in empathy scores by level of training at individual hospitals. This might be related to different targeted curricula.

This case report documents a rare occurrence of pellagra in a chronic alcoholic individual, characterized by a pruritic rash and gastrointestinal symptoms. The patient, a Caucasian male in his 60s, with a history of alcohol use disorder, presented with worsening skin lesions and non-bloody diarrhea. Laboratory findings revealed significant deficiencies in niacin and related metabolites, confirming the diagnosis. Prompt initiation of niacin supplementation, dietary adjustments, and supportive care led to notable improvements. This case shows the critical importance of recognizing pellagra in chronic alcoholism, emphasizing the triad of symptoms - rash, diarrhea, and malnutrition - as key diagnostic markers. Early intervention holds the potential to significantly enhance the patient's well-being and prevent disease progression.

Interleukin-6 (IL-6) is a cytokine produced in response to a variety of inflammatory stimuli. Although IL-6 is often observed in increased amounts in acute respiratory distress syndrome, its role in the development of lung injury is unclear. The role of IL-6 was studied in the rat model of lung injury induced by the intra-alveolar deposition of IgG immune complexes. IL-6 induction, as determined by Northern blot analysis and bioactivity, was found as a function of time during the course of development of injury. Recombinant IL-6 instilled intratracheally at commencement of injury led to substantial reductions in lung vascular permeability, neutrophil accumulation, and levels of tumor necrosis factor (TNF)-alpha and macrophage inflammatory protein (MIP)-2 in bronchoalveolar lavage fluids. Conversely, blocking of intrinsic IL-6 by a neutralizing antibody resulted in increases in lung vascular permeability, neutrophil content, and TNF-alpha levels in bronchoalveolar lavage fluids. Rat alveolar macrophages stimulated in vitro with lipopolysaccharide in the presence of IL-6 showed a significant reduction in TNF-alpha expression. Together, these findings suggest that IL-6 acts as an intrinsic regulator of lung inflammatory injury after deposition of IgG immune complexes and that the protective effects of exogenously administered IL-6 may be in part linked to suppressed TNF-alpha production.

Many immune complex diseases are associated with deposits of specific immunoglobulin (Ig) classes and subclasses. Using an in vitro system for stimulating human peripheral blood mononuclear cells (PBMC) with immobilized Ig, patterns of cytokine production as a function of different Ig classes and subclasses were elucidated. Wells were coated with IgA, IgG1, IgG2, IgG3 or IgG4. Equivalent protein content on surfaces of wells was demonstrated by an ELISA for human kappa chain. Isolated human PBMC were added to Ig-coated wells and incubated for 24 hrs before supernatants were collected and assayed for cytokines by ELISA. The IgG subclasses showed differences in cytokine production stimulated from PBMC, with the relative stimulation for TNF[special characters omitted] being IgG2[special characters omitted]IgG3[special characters omitted]IgG1>IgG4 and for IL-6 production, IgG2[special characters omitted]IgG3>IgG1=IgG4. In contrast, the relative stimulation for IL-8 was IgG1=IgG2=IgG3=IgG4. IgA caused substantially less production of TNF[special characters omitted] when compared to IgG2, but similar levels of IL-8 were produced. Such differences may have important implications in the pathogenesis of immune complex mediated diseases. The above results suggested that PBMC production of TNF[special characters omitted] and IL-8 proceed via different signal transduction pathways. To investigate this possibility, inhibitors of second messenger systems were used to evaluate TNF[special characters omitted] and IL-8 production. PBMC were pretreated with inhibitors before adding the cells to IgG2-coated wells. After 4 hr, supernatant fluids were evaluated. The inhibitors of protein kinase C (PKC) completely inhibited TNF[special characters omitted] production while having no effect on IL-8 production. Gö6976 (an inhibitor specific for Ca++-dependent isoforms of PKC) inhibited generation of both TNF[special characters omitted] and IL-8, suggesting different isoforms of PKC may have opposing effects on IL-8 production. Inhibitors of protein tyrosine kinases and phospholipase C inhibited both TNF[special characters omitted] and IL-8 production, suggesting that both components are involved in cytokine production. Further, inhibitors of G proteins had differing effects. Pertussis toxin, which affects inhibitory G proteins, significantly inhibited IL-8 but not TNF[special characters omitted] production, while cholera toxin, an inhibitor of stimulatory G proteins, significantly inhibited TNF[special characters omitted] but not IL-8 production. These findings provide evidence for distinct signaling pathways of cytokine production from PBMC stimulated by immobilized Ig's.