Exercise as medicine: Providing practitioner guidance on exercise prescription.

The purpose of this study was to examine the effect of a practitioner education program (consisting of education on exercise guidelines and exercise prescription) on practitioner (i) confidence in prescribing exercise and (ii) rate of prescribing exercise. A pre-post study design was utilized. A two-session practitioner education and a toolbox of resources was developed and implemented in January 2020, targeting 12 eligible practitioners at a large primary care and functional medicine office in New York City. A three-question confidence survey was given pre and post. Fifty randomly selected charts were reviewed at baseline (pre), and 25 charts were reviewed monthly for 3 months (February - April 2020) post. There were significant increases and a large effect size in both confidence in prescribing exercise (30% to 89% [p = .020, Phi = 0.596]) and individualizing an exercise prescription between pre- and post-education sessions (20% to 78% [p = .023, Phi = 0.578]). There was also a sustained and significant increase (24% to 63% [p < .001, Phi = 0.379]) in exercise prescription over the three-month period following the education sessions. No statistically significant data was obtained regarding increasing the rate of physical activity among patients. The evidence from this study demonstrates the effectiveness of increasing practitioner confidence and uptake of exercise prescription through education sessions that provide them with the knowledge and tools to properly assess patients' activity level and offer individualized exercise recommendations.

Complement factor B activation in patients with preeclampsia.

Preeclampsia is a leading cause of maternal and fetal morbidity and mortality. Bb, the active fragment of complement factor B (fB), has been reported to be a predictor of preeclampsia. However, conflicting results have been found by some investigators. We hypothesized that the disagreement in findings may be due to the racial/ethnic differences among various study groups, and that fB activation is significant in women of an ethnic minority with preeclampsia. We investigated the maternal and fetal levels of Bb (the activated fB fragment) in pregnant women of an ethnic minority with or without preeclampsia. We enrolled 291 pregnant women (96% of an ethnic minority, including 78% African-American). Thirteen percent of these were diagnosed with preeclampsia. Maternal venous blood was collected from all participants together with fetal umbilical cord blood samples from 154 deliveries in the 291 women. The results were analyzed using the Mann-Whitney U test and multivariate analyses. Maternal Bb levels were significantly higher in the preeclamptic group than in the nonpreeclamptic group. Levels of Bb in fetal cord blood were similar in both groups. Subgroup analyses of African-American patients' results confirmed the study hypothesis that there would be a significant increase in Bb in the maternal blood of the preeclamptic group and no increase in Bb in the fetal cord blood of this group. These results suggest that a maternal immune response through complement fB might play a role in the development of preeclampsia, particularly in African-American patients.

Two Plasmodium rhomboid proteases preferentially cleave different adhesins implicated in all invasive stages of malaria.

Invasion of host cells by the malaria pathogen Plasmodium relies on parasite transmembrane adhesins that engage host-cell receptors. Adhesins must be released by cleavage before the parasite can enter the cell, but the processing enzymes have remained elusive. Recent work indicates that the Toxoplasma rhomboid intramembrane protease TgROM5 catalyzes this essential cleavage. However, Plasmodium does not encode a direct TgROM5 homolog. We examined processing of the 14 Plasmodium falciparum adhesins currently thought to be involved in invasion by both model and Plasmodium rhomboid proteases in a heterologous assay. While most adhesins contain aromatic transmembrane residues and could not be cleaved by nonparasite rhomboid proteins, including Drosophila Rhomboid-1, Plasmodium falciparum rhomboid protein (PfROM)4 (PFE0340c) was able to process these adhesins efficiently and displayed novel substrate specificity. Conversely, PfROM1 (PF11_0150) shared specificity with rhomboid proteases from other organisms and was the only PfROM able to cleave apical membrane antigen 1 (AMA1). PfROM 1 and/or 4 was thus able to cleave diverse adhesins including TRAP, CTRP, MTRAP, PFF0800c, EBA-175, BAEBL, JESEBL, MAEBL, AMA1, Rh1, Rh2a, Rh2b, and Rh4, but not PTRAMP, and cleavage relied on the adhesin transmembrane domains. Swapping transmembrane regions between BAEBL and AMA1 switched the relative preferences of PfROMs 1 and 4 for these two substrates. Our analysis indicates that PfROMs 1 and 4 function with different substrate specificities that together constitute the specificity of TgROM5 to cleave diverse adhesins. This is the first enzymatic analysis of Plasmodium rhomboid proteases and suggests an involvement of PfROMs in all invasive stages of the malaria lifecycle, in both the vertebrate host and the mosquito vector.