Synaptic dysfunction occurs early in senile dementias, presumably as a result of decreased levels of functional synaptic proteins as found in autopsied brains of patients with Alzheimer's disease (AD) or frontotemporal dementia (FTD). Plasma neuronal‐derived exosomes (NDEs) were recovered by precipitation and immunoabsorption from 12 patients with AD, 16 with FTD, and 28 controls in a cross‐sectional study, and from 9 patients with AD, 10with FTD, and 19 controls in a longitudinal study. Six synaptic proteins in NDE extracts were quantified by ELISAs and normalized for exosome amounts. NDE levels of synaptophysin, synaptopodin, synaptotagmin‐2, and neurogranin were significantly lower in patients with FTD and ADthan in controls, but those of growth‐associated protein 43 and synapsin 1 were reduced only in patients with AD. Functionally relevant phosphorylation of synapsin 1 serine 9 was reduced in patients with FTD and AD, although total synapsin 1 protein was higher in FTD than in controls. NDE levels of synaptotagmin, synaptophysin, and neurograninwere decreased yearsbeforedementia inpatientswithFTD and AD.NDElevelsof synaptopodin, synaptotagmin, and synaptophysin, but not of amyloid β‐peptide 42 or P‐T181‐tau, were correlated significantly with cognition assessed bymini‐mental state examination or AD assessment scale‐cognitive subscale. NDE synaptic proteins may be useful preclinical indices and progression measures in senile dementias.—Goetzl, E. J., Kapogiannis, D., Schwartz, J. B., Lobach, I. V., Goetzl, L., Abner, E. L., Jicha, G. A., Karydas, A.M., Boxer, A., Miller, B. L. Decreased synaptic proteins in neuronal exosomes of frontotemporal dementia and Alzheimer's disease. FASEB J. 30, 4141–4148 (2016). www.fasebj.org

Efficient intercellular transfer of RNAs, proteins, and lipids as protected exosomal cargo has been demonstrated in the CNS, but distinct physiologic and pathologic roles have not been well defined for this pathway. The capacity to isolate immunochemically human plasma neuron‐derived exosomes (NDEs), containing neuronspecific cargo, has permitted characterization of CNS‐derived exosomes in living humans. Constituents of the amyloid β‐peptide (Aβ)42‐generating system now are examined in 2 distinct sets of human neural cells by quantification in astrocyte‐derived exosomes (ADEs) and NDEs, enriched separately from plasmas of patients with Alzheimer's disease (AD) or frontotemporal dementia (FTD) andmatched cognitively normal controls. ADE levels of β‐site amyloid precursor protein‐cleaving enzyme 1 (BACE‐1), γ‐secretase, soluble Aβ42, soluble amyloid precursor protein (sAPP)β, sAPPα, glial‐derived neurotrophic factor (GDNF), P‐T181‐tau, and P‐S396‐tau were significantly (3‐ to 20‐fold) higher than levels in NDEs for patients and controls. BACE‐1 levels also were a mean of 7‐fold higher in ADEs than in NDEs from cultured rat type‐specific neural cells. Levels of BACE‐1 and sAPPβ were significantly higher and of GDNF significantly lower in ADEs of patients with AD than in those of controls, but not significantly different in patients with FTD than in controls. Abundant proteins of the Aβ42 peptide‐generating system in ADEs may sustain levels in neurons. ADE cargo proteins may be useful for studies of mechanisms of cellular interactions and effects of BACE‐1 inhibitors in AD.—Goetzl, E. J., Mustapic, M., Kapogiannis, D., Eitan, E., Lobach, I. V., Goetzl, L., Schwartz, J. B., Miller, B. L. Cargo proteins of plasma astrocyte‐derived exosomes in Alzheimer's disease. FASEB J. 30, 3853–3859 (2016) www.fasebj.org

The objective of this article was to review the existing standards of practice regarding trauma which occurs during pregnancy. The design of this study was to review the available data from the surgical and obstetrical literature regarding trauma during pregnancy. The design was also to incorporate the contemporary recommendations from the trauma resuscitation courses relating to trauma during pregnancy. Trauma occurs in 5% of pregnancies. A fetus is not considered to be viable until week 25. Motor vehicle accidents account for more than 50% of all trauma during pregnancy, with 82% of fetal deaths occurring during these automobile accidents. With life threatening trauma a 50% fetal loss rate exists. As anatomy, physiology, and even laboratory findings change during pregnancy, the clinician must consider both patients, the mother and fetus. Following blunt trauma abruption of the placenta is the more common cause of fetus loss. Anterior abdominal penetrating trauma almost never fails to injury the uterus and fetus in the last half of pregnancy. Preventive strategies exist in the areas of social violence, automobile restraints and use of alcohol and drugs by the mother. Perimortem caesarian section is rarely successful. Trauma during pregnancy is uncommon, but with increasing trauma severity leads to increased fetal loss. Preventive strategies exist and when admitted monitoring standards should be followed.

To examine maternal temperature changes after epidural analgesia. A prospective cohort of nulliparas at term was monitored with hourly maternal tympanic temperatures after epidural analgesia (n=99). Temperature response after epidural analgesia was examined in the group as a whole. Subsequently, mean maternal temperature curves were compared between women who remained afebrile throughout labor (n=77) and women who developed intrapartum fever with body temperature greater than 100.4 degrees F (n=22). Baseline maternal characteristics were assessed. Women who later developed intrapartum fever had a higher mean temperature within 1 hour after epidural analgesia. In contrast, women who remained afebrile had no increase in core temperature. During the first 4 hours after epidural analgesia initiation, women who later develop intrapartum fever have an increase in mean tympanic temperature of 0.33 degrees F per hour. Epidural analgesia is not associated with increased temperature in the majority of women. Hyperthermia is an abnormal response confined to a minority subset, which occurs immediately after exposure. Our findings do not support a universal perturbation of maternal thermoregulation after epidural analgesia. II.