For 26 days in mid‐June and July 2000, a research group comprised of U.S. Navy, NASA, and university scientists conducted the Puerto Rico Dust Experiment (PRIDE). In this paper we give a brief overview of mean meteorological conditions during the study. We focus on our findings on African dust transported into the Caribbean utilizing a Navajo aircraft and AERONET Sun photometer data. During the study midvisible aerosol optical thickness (AOT) in Puerto Rico averaged 0.25, with a maximum >0.5 and with clean marine periods of ∼0.08. Dust AOTs near the coast of Africa (Cape Verde Islands and Dakar) averaged ∼0.4, 30% less than previous years. By analyzing dust vertical profiles in addition to supplemental meteorology and MPLNET lidar data we found that dust transport cannot be easily categorized into any particular conceptual model. Toward the end of the study period, the vertical distribution of dust was similar to the commonly assumed Saharan Air Layer (SAL) transport. During the early periods of the study, dust had the highest concentrations in the marine and convective boundary layers with only a weak dust layer in the SAL being present, a state usually associated with wintertime transport patterns. We corroborate the findings of Maring et al. [2003] that in most cases, there was an unexpected lack of vertical stratification of dust particle size. We systematically analyze processes that may impact dust vertical distribution and speculate that dust vertical distribution predominately influenced by flow patterns over Africa and differential advection coupled with fair weather cloud entrainment, mixing by easterly waves, and regional subsidence.

Motor control, which relies on constant communication between motor and sensory systems, is crucial for spine posture, stability and movement. Adaptions of motor control occur in low back pain (LBP) while different motor adaption strategies exist across individuals, probably to reduce LBP and risk of injury. However, in some individuals with LBP, adapted motor control strategies might have long-term consequences, such as increased spinal loading that has been linked with degeneration of intervertebral discs and other tissues, potentially maintaining recurrent or chronic LBP. Factors contributing to motor control adaptations in LBP have been extensively studied on the motor output side, but less attention has been paid to changes in sensory input, specifically proprioception. Furthermore, motor cortex reorganization has been linked with chronic and recurrent LBP, but underlying factors are poorly understood. Here, we review current research on behavioral and neural effects of motor control adaptions in LBP. We conclude that back pain-induced disrupted or reduced proprioceptive signaling likely plays a pivotal role in driving long-term changes in the top-down control of the motor system via motor and sensory cortical reorganization. In the outlook of this review, we explore whether motor control adaptations are also important for other (musculoskeletal) pain conditions.

We analyzed the postmortem blood of a total of 100 fatal cases for beta-hydroxybutyric acid (BHBA). In 25 cases of sudden and unexpected death of alcoholics we found pathologically increased levels of BHBA of 1260 to 47 200 (median 8000) µmol/L. This led us to the diagnosis of an alcoholic ketoacidosis (AKA) as cause of death in these cases. The control group of 69 postmortem cases revealed that BHBA concentrations below 500 can be regarded as normal, and values up to 2500 µmol/L as elevated. Our study shows that BHBA values over 2500 µmol/L could lead to death, if no medical attention is sought. During storage we did not find any indication of postmortem formation or decomposition of BHBA in blood in vitro or in the corpses. In our opinion, BHBA should be considered the diagnostic marker of choice for the postmortem determination of alcoholic ketoacidosis (AKA) as the cause of death. The classical indications of such deaths are: unexpected death of a chronic alcoholic; none or only traces of ethanol in the blood; increased acetone blood concentration; and neither autopsy, histology, microbiology, nor toxicology reveal the cause of death. In six further cases a diabetic ketoacidosis (DKA) was diagnosed as the cause of death.

Fear of movement (FOM) can be acquired by a direct aversive experience such as pain or by social learning through observation and instruction. Excessive FOM results in heightened disability and is an obstacle for recovery from acute, subacute, and chronic low back pain (cLBP). FOM has further been identified as a significant explanatory factor in the Fear Avoidance (FA) model of cLBP that describes how individuals experiencing acute back pain may become trapped into a vicious circle of chronic disability and suffering. Despite a wealth of evidence emphasizing the importance of FOM in cLBP, to date, no related neural correlates in patients were found and this therefore has initiated a debate about the precise contribution of fear in the FA model. In the current fMRI study, we applied a novel approach encompassing: (1) video clips of potentially harmful activities for the back as FOM inducing stimuli; and (2) the assessment of FOM in both, cLBP patients (N = 20) and age- and gender-matched pain-free subjects (N = 20). Derived from the FA model, we hypothesized that FOM differentially affects brain regions involved in fear processing in patients with cLBP compared to pain-free individuals due to the recurrent pain and subsequent avoidance behavior. The results of the whole brain voxel-wise regression analysis revealed that: (1) FOM positively correlated with brain activity in fear-related brain regions such as the amygdala and the insula; and (2) differential effects of FOM between patients with cLBP and pain-free subjects were found in the extended amygdala and in its connectivity to the anterior insula. Current findings support the FOM component of the FA model in cLBP.