The effects of Moringa oleifera on blood glucose levels: A scoping review of the literature.

Diabetes is an increasingly problematic health concern in the United States. Moringa oleifera (M. oleifera) has been suggested as medication in the prevention or treatment of diabetes, but there is no convincing evidence of a causal relation between moringa and decreased blood sugar levels in humans. The purpose of this scoping review is to examine the effects of Moringa oleifera on blood glucose levels in rats and humans. A search of Scopus, Ovid Medline, Ovid Embase, IPA, and Web of Science and manual searching of bibliographies were performed for peer-reviewed English articles published between May 1, 2008 and May 1, 2018. This review included thirty studies. Out of seven human studies, five found that M. oleifera significantly reduced blood glucose levels in diabetic patients. Out of twenty-three animal studies, twenty-one found that administration of M. oleifera led to a statistically significant decrease in animal blood glucose levels. In human studies, moringa was mostly administered in a powdered leaf form, while in animal studies it was frequently administered to as an aqueous or ethanol-based extract. The review found statistical evidence that moringa decreased blood glucose; the evidence is not strong enough to recommend it as the default treatment for people with diabetes.

Resident macrophages reprogram toward a developmental state after acute kidney injury.

Acute kidney injury (AKI) is a devastating clinical condition affecting at least two-thirds of critically ill patients, and, among these patients, it is associated with a greater than 60% risk of mortality. Kidney mononuclear phagocytes (MPs) are implicated in pathogenesis and healing in mouse models of AKI and, thus, have been the subject of investigation as potential targets for clinical intervention. We have determined that, after injury, F4/80hi-expressing kidney-resident macrophages (KRMs) are a distinct cellular subpopulation that does not differentiate from nonresident infiltrating MPs. However, if KRMs are depleted using polyinosinic/polycytidylic acid (poly I:C), they can be reconstituted from bone marrow-derived precursors. Further, KRMs lack major histocompatibility complex class II (MHCII) expression before P7 but upregulate it over the next 14 days. This MHCII- KRM phenotype reappears after injury. RNA sequencing shows that injury causes transcriptional reprogramming of KRMs such that they more closely resemble that found at P7. KRMs after injury are also enriched in Wingless-type MMTV integration site family (Wnt) signaling, indicating that a pathway vital for mouse and human kidney development is active. These data indicate that mechanisms involved in kidney development may be functioning after injury in KRMs.

Parabiosis reveals leukocyte dynamics in the kidney.

The immune cellular compartment of the kidney is involved in organ development and homeostasis, as well as in many pathological conditions. Little is known about the mechanisms that drive intrarenal immune responses in the presence of renal tubular and interstitial cell death. However, it is known that tissue-resident leukocytes have the potential to have distinct roles compared with circulating cells. We used a parabiosis model in C57BL/6 CD45 congenic and green fluorescent protein transgenic mice to better understand the dynamics of immune cells in the kidney. We found F4/80Hi intrarenal macrophages exhibit minimal exchange with the peripheral circulation in two models of parabiosis, whether mice were attached for 4 or 16 weeks. Other intrarenal inflammatory cells demonstrate near total exchange with the circulating immune cell pool in healthy kidneys, indicating that innate and adaptive immune cells extensively traffic through the kidney interstitium during normal physiology. Neutrophils, dendritic cells, F4/80Low macrophages, T cells, B cells, and NK cells are renewed from the circulating immune cell pool. However, a fraction of double-negative T (CD4- CD8-) and NKT cells are long-lived or tissue resident. This study provides direct evidence of leukocyte sub-populations that are resident in the renal tissue, cells which demonstrate minimal to no exchange with the peripheral blood. In addition, the data demonstrate continual exchange of other sub-populations through uninflamed tissue.

Microsomal Prostaglandin E Synthase-1 Expression by Aortic Smooth Muscle Cells Attenuates the Differentiated Phenotype.

The development of numerous types of cardiovascular disease is associated with alteration of the vascular smooth muscle cell (SMC) phenotype. We have previously shown that abdominal aortic aneurysm progression in a mouse model of the disease is associated with reduced differentiation of SMCs within the lesion and that cyclooxygenase-2 (COX-2) is critical to initiation and progression of the aneurysms. The current studies used human aortic SMC (hASMC) cultures to better characterize mechanisms responsible for COX-2-dependent modulation of the SMC phenotype. Depending on the culture conditions, hASMCs expressed multiple characteristics of a differentiated and contractile phenotype, or a dedifferentiated and secretory phenotype. The pharmacological inhibition of COX-2 promoted the differentiated phenotype, whereas treatment with the COX-2-derived metabolite prostaglandin E2 (PGE2) increased characteristics of the dedifferentiated phenotype. Furthermore, pharmacological inhibition or siRNA-mediated knockdown of microsomal prostaglandin E synthase-1 (mPGES-1), the enzyme that functions downstream of COX-2 during the synthesis of PGE2, significantly increased expression of characteristics of the differentiated SMC phenotype. Therefore, our findings suggest that COX-2 and mPGES-1-dependent synthesis of PGE2 contributes to a dedifferentiated hASMC phenotype and that mPGES-1 may provide a novel pharmacological target for treatment of cardiovascular diseases where altered SMC differentiation has a causative role.

The Characteristics of Effective Cancer Education Media Interventions among African Americans: A Systematic Review.

Cancer incidence and mortality is a significant area of health disparity between African Americans and Caucasians. In the current article the authors used a systematic review design to examine the characteristics of different cancer media education intervention (CMEI) to increase access to cancer screenings for African Americans within a 30 year period (1980-2010). Ten computerized databases were searched using inclusion-exclusion criteria. Consequently, 179 potential studies were identified, and later reduced to 41 eligible studies through the inclusion-exclusion criteria. The eligible studies had a combined sample size of N = 12,764 respondents. The findings revealed that multi-media intervention strategies were the most common media intervention that led to increased cancer screenings among African Americans. The authors conclude with a call for social workers to be more involved in developing and following up with culturally appropriate media strategies that can increase the likelihood of early detection and successful treatment, thus reducing this important area of health disparity.