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Evidence shows that those living in rural communities experience consistently worse health outcomes than their urban and suburban counterparts. One proven strategy to address this disparity is to increase the physician supply in rural areas through graduate medical education (GME) training. However, rural hospitals have faced challenges developing training programs in these underserved areas, largely due to inadequate federal funding for rural GME. The Consolidated Appropriations Act of 2021 (CAA) contains multiple provisions that seek to address disparities in Medicare funding for rural GME, including funding for an increase in rural GME positions or "slots" (Section 126), expansion of rural training opportunities (Section 127), and relief for hospitals that have very low resident payments and/or caps (Section 131). In this Invited Commentary, the authors describe historical factors that have impeded the growth of training programs in rural areas, summarize the implications of each CAA provision for rural GME, and provide guidance for institutions seeking to avail themselves of the opportunities presented by the CAA. These policy changes create new opportunities for rural hospitals and partnering urban medical centers to bolster rural GME training, and consequently the physician workforce in underserved communities.

EXECUTIVE SUMMARY The number of rural hospital mergers has increased substantially in recent years. A commonly reported reason for merging is to increase access to capital. However, no empirical evidence exists to show whether capital expenditures increased at rural hospitals after a merger. We used a difference-in-differences approach to determine whether total capital expenditures changed at rural hospitals after a merger. The comparison group (rural hospitals that did not merge during the 2012 through 2015 study period) was weighted using inverse probability of treatment weights. The key outcome measure was logged total capital expenditures.Merging resulted in a 26% increase in capital expenditures and also was associated with a significant improvement in plant age. The postmerger improvement in plant age may have been partially attributable to merger-related accounting changes and partially attributable to increased capital expenses, possibly on long-term asset renovations and replacement.These findings suggest that through mergers, rural hospital board members and executives who have accepted or are considering a merger may improve a hospital's ability to increase capital expenditures. Further, increased capital investments in rural hospitals may be an important signal to the community that the acquirer intends to keep the rural hospital open and continue providing some volume and level of services within the community. Future research should determine how capital is spent after a merger.

Background Immunosuppression therapy after lung transplantation fails to prevent bronchiolitis obliterans syndrome (BOS) in many patients, primarily a disease of the small airways. We have reported that BOS is associated with a lack of suppression of cytotoxic mediators, and proinflammatory cytokines, in peripheral blood T, NKT-like (particularly CD8+) and NK cells. We also showed a loss of glucocorticoid receptor (GCR) in proinflammatory lymphocytes after transplant. It is unknown whether these proinflammatory lymphocytes target the small and/or large airways in BOS. Methods Blood, bronchoalveolar lavage, large proximal, and small distal airway brushings were collected from patients with BOS (n = 10), stable lung transplant patients (n = 18), and healthy aged-matched controls (n = 10). Intracellular cytotoxic mediators (perforin/granzyme B), proinflammatory cytokines (IFNγ/TNFα), and expression of GCR were determined in lymphocytes subsets from cultured blood using flow cytometry. Results Increases in CD8 T cells, NKT-like cells, and NK cells were found in the small distal airways in BOS compared with stable patients and controls. An increase in perforin, granzyme B, IFNγ, TNFα, and a loss of GCR from these lymphocyte subsets was also found in BOS. GCR expression by CD8+ T cells from small airways correlated with FEV1 (R = 0.834, P = 0.039). Many of these changes significantly differed from those in the large airways. Conclusions BOS is associated with increased cytotoxic/proinflammatory CD8+ T, NKT-like, and NK cells in the small airways. Treatments that increase GCR in these lymphocyte subsets may improve graft survival.

Objective To determine whether individuals from surgery-specific service areas with a low supply of general surgeons (GSs) are at increased risk for ruptured appendicitis (ruptured appendicitis is an indicator of surgical access). Background The increased health care costs and morbidity linked to appendiceal rupture are considered preventable in most cases with timely access to surgery. Among the factors thought to affect an individual's access to surgery for appendicitis is the relative supply of GSs. The maldistribution of GSs is targeted by a Medicare bonus payment although the impact of GS supply on surgical access has yet to be fully described. Methods Patients discharged from acute care and ambulatory surgery facilities in North Carolina from 2007 to 2009 were pooled for observational analysis. Using ICD-9-CM (International Classification of Diseases, Ninth Revision, Clinical Modification) codes, cases were identified as ruptured or unruptured. GS shortage levels based on supply were calculated at the surgical service area level and tested for an association with an individual's risk of rupture using logistic regression. Results Living in a service area with less than 3 GSs per 100,000 people significantly increases the probability of rupture in individuals with appendicitis, compared with living in a service area with at least 5 GSs per 100,000. Conclusions The supply of GSs does affect access to surgical services for appendicitis. Expanding on this finding, the recently instituted HPSA (health professional shortage area) surgical incentive payment from the Affordable Care Act should be evaluated closely for its effectiveness. Enhancing supply in critical shortage areas could reduce appendiceal rupture and improve surgical access more generally.

Lymphocytic bronchiolitis (LB) has been shown to be an important factor for the subsequent development of obliterative bronchiolitis (OB). We have previously shown that OB, which limits long-term survival after lung transplantation, is associated with lack of suppression of peripheral blood T-cell granzyme B, interferon (IFN)-gamma, and tumor necrosis factor (TNF)-alpha. However, the role of these proinflammatory mediators in LB is unknown. We hypothesized that these proinflammatory mediators may also be increased during LB episodes despite standard immunosuppression regimens.T-cell intracellular cytokine profiles and granzyme B were studied in whole blood, bronchoalveolar lavage samples, and bronchial brushings from stable lung transplant patients with LB and from healthy controls, using multiparameter flow cytometry.There was a significant increase in peripheral blood T-cell granzyme B and CD8 T-cell IFN-gamma and TNF-alpha in patients with LB compared with control and stable groups and a decrease in CD25CD127CD3CD8 T regulatory cells in stable and LB transplant patients compared with controls. No changes were noted in the airways.LB is associated with inadequate suppression of peripheral blood T-cell granzyme B, IFN-gamma, and TNF-alpha. Drugs that effectively reduce these proinflammatory mediators may improve current protocols for treating LB and possibly reduce subsequent progression to OB in lung transplant patients.

BACKGROUND Allograft rejection remains a major cause of morbidity and mortality following lung transplantation and is associated with an increased expression of T-cell proinflammatory cytokines. We have recently shown that peripheral blood T-cell proinflammatory cytokine production was significantly reduced in stable lung transplant patients consistent with immunosuppression therapy. However, analysis of inflammatory cytokine profiles in bronchoalveolar lavage (BAL) T cells may be more relevant than peripheral blood T cells for assessing graft status. METHODS To investigate the immunomodulatory effects of currently used immunosuppressive regimens on BAL T-cell cytokine production, whole blood and BAL from stable lung transplant patients and control volunteers was stimulated in vitro and cytokine production by CD8+ and CD4+ T-cell subsets determined using multiparameter flow cytometry. RESULTS There was a significant decrease in T-cell proinflammatory cytokine production in BAL compared with blood from control subjects but not transplant patients. Anti-inflammatory cytokine IL-4 was increased in BAL compared with blood from both groups. There was a significant increase in IFNgamma, IL-2, IL-4, TGFbeta, and TNFalpha production by CD8 T cells and IFNgamma and TNFalpha production by CD4 T cells in BAL from transplant patients compared with controls. CONCLUSIONS We have shown decreased T-cell pro- and anti-inflammatory cytokine production in BAL compared with blood in control subjects but not in stable lung transplant patients. Current immunosuppression protocols have limited effect on T-cell proinflammatory cytokine production in BAL but do upregulate anti-inflammatory cytokines IL-4 and TGFbeta. Drugs that effectively reduce T-cell proinflammatory cytokine production in BAL may improve current protocols for reducing graft rejection in these patients.

BACKGROUND Alveolar macrophages are a major source of inflammatory cytokines and chemokines involved in the pathogenesis of lung transplant rejection and are derived from blood monocytes that migrate to the lung. Levels of monocyte cytokines and chemokines that may be relevant in transplant rejection have not previously been determined in transplant recipients. We hypothesized that production of these inflammatory mediators by blood monocytes may be up-regulated despite the use of potent immunosuppression therapy. METHOD To investigate this, whole blood from 9 stable lung transplant recipients and 12 control volunteers was stimulated with lipopolysaccharide in vitro, and intracellular chemokine and cytokine production were determined with multiparameter flow cytometry. RESULTS Monocyte production of chemokines interleukin (IL)-8, monocyte chemotactic protein (MCP)-1, and MCP-3, and anti-inflammatory cytokine IL-10 were significantly increased in the lung transplant group, but IL-6, tumor necrosis factor-alpha, IL-1alpha, IL-12, macrophage inflammatory protein-1alpha, macrophage inflammatory protein-1beta, and transforming growth factor-beta levels were unchanged. CONCLUSIONS Because MCP-3 is a major chemoattractant for leukocytes to sites of antigenic challenge and is a natural ligand for MCP-1 receptor, this novel finding has important implications for the pathogenesis of lung transplant rejection. We now provide evidence that current immunosuppression protocols have a limited effect on monocyte inflammatory cytokine production and do not adequately suppress monocyte IL-8, MCP-1, and MCP-3 chemokine production. Drugs that modulate the action of these chemokines may improve current protocols for reducing graft rejection. Intracellular chemokine and cytokine analysis with flow cytometry may be a more accurate indicator of immunosuppression than drug levels in these patients.

SHIPP, N. J., G. C. SCROOP, S. C. JACKSON, M. D. HOLMES, A. T. THORNTON, and C. J. GORE. Rectal Temperature Correction Overestimates the Frequency of Exercise-Induced Hypoxemia. Med. Sci. Sports Exerc., Vol. 36, No. 7, pp. 1111–1116, 2004. Exercise-induced hypoxemia (EIH) occurs in an uncertain proportion of endurance trained athletes. Whereas blood gas measurements must be corrected for core temperature at the time of sampling, the commonly used rectal temperature readings may not be the most appropriate. Ten males [mean peak oxygen uptake, VO2peak, 65.4 ± 7.0 mL·kg−1·min−1] performed incremental treadmill exercise from rest to exhaustion with radial artery blood samples collected at the end of each 2-min workload for gas analysis. The thermogenic effect of exercise was monitored with rectal, arterial blood, and esophageal temperature probes, and the values obtained at all three sites, simultaneous with blood sampling, were used to correct the standard blood gas measurements made at 37°C. The mean increase in rectal temperature across exercise (1.4 ± 0.4°C) was approximately half that recorded in radial arterial blood (2.3 ± 0.5°C) and the esophagus (2.4 ± 0.5°C). In consequence, the uncorrected fall in PaO2 across exercise of 15.4 ± 8.2 mm Hg was reduced to 8.4 ± 7.7 mm Hg when corrected for rectal temperature, and to 2.9 ± 7.4 and 2.1 ± 8.8 mm Hg when corrected for arterial blood and esophageal temperatures. Using a fall of ≥10 mm Hg as the index of EIH, the proportion in the 10 subjects in the present study fell from 80% (uncorrected) through 50% (rectal correction) to 20% (arterial blood and esophageal corrections). When correcting arterial blood gas values for the thermogenic effects of exercise, the proportion of athletes meeting the definition of EIH depends on the site of core temperature measurement.