Research Spotlight

Tan, M., A. Mamun, H. Kitzman, S. R. Mandapati and L. Dodgen (2017). “Neighborhood disadvantage and allostatic load in african american women at risk for obesity-related diseases.” Prev Chronic Dis 14: 1-15.

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INTRODUCTION: African American women have higher rates of obesity and related chronic disease than other demographic groups. The poorer health of African American women compared with other groups may be explained by allostatic load, or cumulative physiologic stress, due to chronic socioeconomic disadvantage. The objective of this study was to evaluate neighborhood and individual factors contributing to allostatic load in African American women at risk for obesity-related diseases. METHODS: This study evaluated the relationship of allostatic load with neighborhood disadvantage, individual socioeconomic determinants, and synergism between neighborhood and socioeconomic disadvantage, along with health behaviors and other factors as mediators in African American women. Our sample consisted of 220 African American women at risk of obesity-related diseases enrolled in the Better Me Within program (mean [standard deviation] age, 50.1 [11.2] y; mean [standard deviation] body mass index, 36.7 [8.4] kg/m(2)). Allostatic load score for each participant was calculated by summing the number of biomarkers (of 9 biomarkers) that were determined to be in the high-risk quartile. RESULTS: Poisson regression of neighborhood disadvantage and individual socioeconomic determinants found that neighborhood disadvantage, but not education level or household income, was significantly associated with allostatic load (beta = 0.22, SE, 0.10, P = .04). Tests for mediators showed that household income and alcohol consumption partially mediated the relationship between allostatic load score and neighborhood disadvantage but were not significant. CONCLUSION: More research is necessary to determine the mechanisms by which neighborhoods can exacerbate and attenuate cumulative disadvantage among African American women. Policies and interventions that focus on neighborhood health may improve the outcomes of individual-level health interventions among women who reside in disadvantaged communities.

Souza, R. F. and S. J. Spechler (2017). “Oesophagus: A new candidate for the progenitor cell of barrett metaplasia.” Nat Rev Gastroenterol Hepatol: 2017 Nov [Epub ahead of print].

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In Barrett oesophagus, the distal oesophagus is lined by an abnormal columnar epithelium that has both gastric and intestinal features and is predisposed to malignant transformation1. Barrett oesophagus develops through metaplasia, the process in which one adult tissue type replaces another in response to injury, and its pathogenesis typically begins with oesophageal injury from GERD1. With ongoing GERD, damaged stratified squamous epithelium is replaced by metaplastic, single-layer, columnar epithelium which, presumably, is more resistant to GERD injury. This process must involve GERD-induced molecular reprogramming of key developmental transcription factors (transcommitment) in the progenitor cells giving rise to the metaplastic epithelium2.

Testa, G. and L. Johannesson (2017). “The ethical challenges of uterus transplantation.” Curr Opin Organ Transplant 22(6): 593-597.

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PURPOSE OF REVIEW: As the techniques of uterus transplantation have evolved, culminating in a birth in 2014, the ethical debate has been enriched by several considerations. Uterus transplantation raises issues because of its unique features of being temporary, nonlifesaving, experimental, and expensive, with established alternatives. RECENT FINDINGS: Uterus transplantation entails risks for the recipient related to multiple surgeries and immunosuppression, yet studies have shown that women see infertility as a distressing element in their lives, justifying the risks. The alternative of surrogacy has its own ethical issues, and adoption does not provide for genetic progeny. Although patient decisions are susceptible to inconsistent reasoning, misconception of risks or wishful thinking, a carefully drafted and clearly explained informed consent can represent a valid ethical response in balancing risks and benefits. There is no evidence of increased risks for children born from uterus transplant. For living donors, the risks of hysterectomy are known and can be explained to facilitate proper informed consent. Allocation of deceased donor organs needs to be determined, as guidelines for other organs cannot readily be applied. Cost is an issue, as the procedure is expensive and not covered by insurance. SUMMARY: In this rapidly advancing field, a strong ethical foundation is needed to guide regulations and legislation.

Frazee, R., C. C. Burlew, J. Regner, R. McIntyre, E. Peltz, C. Cribari, J. Dunn, L. Butler, P. Reckard, S. Dissanaike, K. Karimi, C. Behnfield, N. Melo and D. Margulies (2017). “Outpatient laparoscopic appendectomy can be successfully performed for uncomplicated appendicitis: A southwestern surgical congress multicenter trial.” Am J Surg 214(6): 1007-1009.

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BACKGROUND: Many laparoscopic procedures are now performed on an outpatient basis. We hypothesize laparoscopic appendectomy can be safely performed as an outpatient procedure. METHODS: Seven institutions adopted a previously described outpatient laparoscopic appendectomy protocol for uncomplicated appendicitis. Patients were dismissed unless there was a clinical indication for admission. Patient demographics, success with outpatient management, time of dismissal, morbidity, and readmissions were analyzed. RESULTS: Two hundred six men and one hundred seventy women with a mean age of 35.4 years were included in the protocol. Seventy-eight patients (21%) had pre-existing comorbidities. 299 patients (80%) were managed as outpatients. There were no conversions to open appendectomy. Postoperative morbidity was 5%. The time of patient dismissals was evenly distributed throughout the day and night. Twelve patients (3%) required readmission. Outpatient follow-up occurred in 63% of patients. CONCLUSIONS: An outpatient laparoscopic appendectomy protocol was successfully applied at multiple institutions with low morbidity and low readmission rates. Application of this practice nationally could reduce length of stay and decrease overall health care costs for acute appendicitis.

Alaoui, L., G. Palomino, S. Zurawski, G. Zurawski, S. Coindre, N. Dereuddre-Bosquet, C. Lecuroux, C. Goujard, B. Vaslin, C. Bourgeois, P. Roques, R. Le Grand, O. Lambotte and B. Favier (2017). “Early siv and hiv infection promotes the lilrb2/mhc-i inhibitory axis in cdcs.” Cell Mol Life Sci: 2017 Nov [Epub ahead of print].

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Classical dendritic cells (cDCs) play a pivotal role in the early events that tip the immune response toward persistence or viral control. In vitro studies indicate that HIV infection induces the dysregulation of cDCs through binding of the LILRB2 inhibitory receptor to its MHC-I ligands and the strength of this interaction was proposed to drive disease progression. However, the dynamics of the LILRB2/MHC-I inhibitory axis in cDCs during early immune responses against HIV are yet unknown. Here, we show that early HIV-1 infection induces a strong and simultaneous increase of LILRB2 and MHC-I expression on the surface of blood cDCs. We further characterized the early dynamics of LILRB2 and MHC-I expression by showing that SIVmac251 infection of macaques promotes coordinated up-regulation of LILRB2 and MHC-I on cDCs and monocytes/macrophages, from blood and lymph nodes. Orientation towards the LILRB2/MHC-I inhibitory axis starts from the first days of infection and is transiently induced in the entire cDC population in acute phase. Analysis of the factors involved indicates that HIV-1 replication, TLR7/8 triggering, and treatment by IL-10 or type I IFNs increase LILRB2 expression. Finally, enhancement of the LILRB2/MHC-I inhibitory axis is specific to HIV-1 and SIVmac251 infections, as expression of LILRB2 on cDCs decreased in naturally controlled chikungunya virus infection of macaques. Altogether, our data reveal a unique up-regulation of LILRB2 and its MHC-I ligands on cDCs in the early phase of SIV/HIV infection, which may account for immune dysregulation at a critical stage of the anti-viral response.