Measurement of the Positive Muon Anomalous Magnetic Moment to 0.20 ppm.

We present a new measurement of the positive muon magnetic anomaly, a_{µ}≡(g_{µ}-2)/2, from the Fermilab Muon g-2 Experiment using data collected in 2019 and 2020. We have analyzed more than 4 times the number of positrons from muon decay than in our previous result from 2018 data. The systematic error is reduced by more than a factor of 2 due to better running conditions, a more stable beam, and improved knowledge of the magnetic field weighted by the muon distribution, ω[over ˜]_{p}^{'}, and of the anomalous precession frequency corrected for beam dynamics effects, ω_{a}. From the ratio ω_{a}/ω[over ˜]_{p}^{'}, together with precisely determined external parameters, we determine a_{µ}=116 592 057(25)×10^{-11} (0.21 ppm). Combining this result with our previous result from the 2018 data, we obtain a_{µ}(FNAL)=116 592 055(24)×10^{-11} (0.20 ppm). The new experimental world average is a_{µ}(exp)=116 592 059(22)×10^{-11} (0.19 ppm), which represents a factor of 2 improvement in precision.

AICAR inhibits ceramide biosynthesis in skeletal muscle.

BACKGROUND: The worldwide prevalence of obesity has lead to increased efforts to find therapies to treat obesity-related pathologies. Ceramide is a well-established mediator of several health problems that arise from adipose tissue expansion. The purpose of this study was to determine whether AICAR, an AMPK-activating drug, selectively reduces skeletal muscle ceramide synthesis. METHODS: Murine myotubes and rats were challenged with palmitate and high-fat diet, respectively, to induce ceramide accrual, in the absence or presence of AICAR. Transcript levels of the rate-limiting enzyme in ceramide biosynthesis, serine palmitoyltransferase 2 (SPT2) were measured, in addition to lipid analysis. Student's t-test and ANOVA were used to assess the association between outcomes and groups. RESULTS: Palmitate alone induced an increase in serine palmitoyltransferase 2 (SPT2) expression and an elevation of ceramide levels in myotubes. Co-incubation with palmitate and AICAR prevented both effects. However, ceramide and SPT2 increased with the addition of compound C, an AMPK inhibitor. In rats fed a high-fat diet (HFD), soleus SPT2 expression increased compared with normal chow-fed littermates. Moreover, rats on HFD that received daily AICAR injections had lower SPT2 levels and reduced muscle ceramide content compared with those on HFD only. CONCLUSIONS: These results suggest that AICAR reduces ceramide synthesis by targeting SPT2 transcription, likely via AMPK activation as AMPK inhibition prevented the AICAR-induced improvements. Given the role of skeletal muscle ceramide in insulin resistance, it is tempting to speculate that interventions that activate AMPK may lead to long-term ceramide reduction and improved metabolic function.

Changes in lymphocyte and Langerhans cell populations in allergic and irritant contact dermatitis.

We observed in situ changes in lymphocyte subpopulations and Langerhans cells during allergic and irritant contact dermatitis using immunohistochemical staining methods with monoclonal antibodies to cell surface antigens. In both types of contact dermatitis, there was a perivascular infiltrate of T lymphocytes, with helper/inducer T cells predominating. B cells were absent, and natural killer cells were absent or sparse. During the course of allergic contact dermatitis, Langerhans cells showed a striking sequential change in location, with the cells first in the epidermis, then perivascularly in the dermis (days 1-14), and returning to the epidermis (days 14-21). In irritant contact dermatitis, the Langerhans cells were initially identified in the epidermis and then appeared diffusely in the dermis (days 1-2). The numbers in the dermis then decreased abruptly (day 4). They were again identified in normal numbers in the epidermis (day 21). The response of Langerhans cells appears to be different between allergic and irritant contact dermatitis.

Embryonic maturation of sensory terminals of primate facial hairs.

The present study examines the sequence of maturation of sensory nerve terminals that can be identified on primate facial guard hairs. At birth, the sensory innervation of both guard and vellus hairs is mature in that lanceolate, Ruffini, and free nerve ending (FNE) terminals can be identified and resemble those of the adult. Presumptive lanceolate terminals can be identified at the beginning of the third trimester of gestation, and other axons present are either Ruffini or FNEs, but definite identification is not possible. In the latter half of the second trimester only axons arranged circumferentially are present, resembling FNE or Ruffini terminals. Some of these axons directly abut the hair follicle and might eventually become lanceolate endings. The earliest nerve terminals associated with hairs cytologically resemble FNE or Ruffini terminals. At the onset of hair differentiation in the early part of the second trimester, nerves were always associated with developing epithelial hair placodes. Branching Schwann cells in the axons radiating toward the epidermis in these youngest embryos studied were best identified by electron microscopy. The early development of afferent nerve fibers in hairy skin provides an anatomical substrate for the known reflexogenic activity of primate embryos. Adequate cytologic criteria are thus available for the identification of sensory terminals in growing, differentiating, and presumably regenerating axons in primate hairy skin.