The (in)effectiveness of anticipatory vibrotactile cues in mitigating motion sickness.

The introduction of (fully) automated vehicles has generated a re-interest in motion sickness, given that passengers suffer much more from motion sickness compared to car drivers. A suggested solution is to improve the anticipation of passive self-motion via cues that alert passengers of changes in the upcoming motion trajectory. We already know that auditory or visual cues can mitigate motion sickness. In this study, we used anticipatory vibrotactile cues that do not interfere with the (audio)visual tasks passengers may want to perform. We wanted to investigate (1) whether anticipatory vibrotactile cues mitigate motion sickness, and (2) whether the timing of the cue is of influence. We therefore exposed participants to four sessions on a linear sled with displacements unpredictable in motion onset. In three sessions, an anticipatory cue was presented 0.33, 1, or 3 s prior to the onset of forward motion. Using a new pre-registered measure, we quantified the reduction in motion sickness across multiple sickness scores in these sessions relative to a control session. Under the chosen experimental conditions, our results did not show a significant mitigation of motion sickness by the anticipatory vibrotactile cues, irrespective of their timing. Participants yet indicated that the cues were helpful. Considering that motion sickness is influenced by the unpredictability of displacements, vibrotactile cues may mitigate sickness when motions have more (unpredictable) variability than those studied here.

Self-motion perception without sensory motion.

Various studies have demonstrated a role for cognition on self-motion perception. Those studies all concerned modulations of the perception of a physical or visual motion stimulus. In our study, however, we investigated whether cognitive cues could elicit a percept of oscillatory self-motion in the absence of sensory motion. If so, we could use this percept to investigate if the resulting mismatch between estimated self-motion and a lack of corresponding sensory signals is motion sickening. To that end, we seated blindfolded participants on a swing that remained motionless during two conditions, apart from a deliberate perturbation at the start of each condition. The conditions only differed regarding instructions, a secondary task and a demonstration, which suggested either a quick halt ("Distraction") or continuing oscillations of the swing ("Focus"). Participants reported that the swing oscillated with larger peak-to-peak displacements and for a longer period of time in the Focus condition. That increase was not reflected in the reported motion sickness scores, which did not differ between the two conditions. As the reported motion was rather small, the lack of an effect on the motion sickness response can be explained by assuming a subthreshold neural conflict. Our results support the existence of internal models relevant to sensorimotor processing and the potential of cognitive (behavioral) therapies to alleviate undesirable perceptual issues to some extent. We conclude that oscillatory self-motion can be perceived in the absence of related sensory stimulation, which advocates for the acknowledgement of cognitive cues in studies on self-motion perception.

No increase of local recurrence rate in breast cancer patients treated with skin-sparing mastectomy followed by immediate breast reconstruction.

BACKGROUND: The aim of this study was to evaluate the incidence of local recurrence after SSM with IBR and to determine whether complications lead to postponement of adjuvant therapy. METHOD: Patients that underwent IBR after SSM between 2004 and 2011 were included. RESULTS: A total of 157 reconstruction procedures were performed in 147 patients for invasive breast cancer (n = 117) and ductal carcinoma in situ (n = 40). The median follow-up was 39 months [range 6-97]. Estimated 5-year local recurrence rate was 2.9% (95% CI 0.1-5.7). The median time to start adjuvant therapy was 27.5 days [range 19-92] in 18 patients with complications, and 23.5 days [range 8-54] in 46 patients without complications (p = 0.025). CONCLUSION: In our single-institution cohort, IBR after SSM carried an acceptable local recurrence rate. Complications caused a delay of adjuvant treatment but this was within guidelines and therefore not clinically relevant.

1-Nitropyrene as a marker for the mutagenicity of diesel exhaust-derived particulate matter in workplace atmospheres.

The use of 1-nitropyrene (1-NP) as a marker for the occupational exposure to diesel exhaust (DE) mutagens was investigated in workplace atmospheres contaminated with DE from a variety of emission sources, such as power supplies, forklifts, trucks, caterpillar vehicles, trains, ships' engines, and vehicles in city traffic. Total suspended particulate matter was collected by area sampling. The 1-NP content of acetone extracts of these samples as determined by gas chromatography-high resolution mass spectrometry varied from 0.080 to 17 micrograms/g acetone extractable matter, corresponding to air concentrations of 0.012 to 1.2 ng/m3. A sample collected in a rural area contained 0.0017 ng/m3 1-NP. The mutagenicity of the extracts was tested in the Salmonella typhimurium strains TA98 and TA1538, using the microsuspension assay with and without metabolic activation by an exogeneous metabolizing system (rat liver S9-fraction). In addition, the S. typhimurium strains YG1021 and YG1024 were used because of their high sensitivity towards the mutagenicity of nitro polycyclic aromatic hydrocarbons. When plotting the mutagenic potency of the air sample extracts as determined in the absence of liver S9 versus the particle-associated 1-NP level, a relatively high correlation (r = 0.80-0.91) was observed in all of the S. typhimurium strains. High correlations (r = 0.80-0.93) were also observed when plotting the results of mutagenicity testing after activation by S9 versus the outcome of chemical analysis. These results show that the 1-NP content of workplace air samples is associated with their mutagenic potency, suggesting that 1-NP may be used as a marker for occupational exposure to DE-derived particle-associated mutagens.

Assessment of occupational exposure to diesel exhaust. The use of an immunoassay for the determination of urinary metabolites of nitroarenes and polycyclic aromatic hydrocarbons.

In a repair shop for train engines a pilot study was conducted to investigate occupational exposure to diesel exhaust. 1-Nitropyrene was determined in stationary sampled total suspended particulate matter collected on 2 consecutive workdays. Air concentrations of particulate associated 1-nitropyrene varied from non-detectable to 5.6 ng/m3. In spot urine samples collected on Sunday, Monday and Tuesday urinary metabolites of polycyclic aromatic hydrocarbons and their nitro-substituted derivatives were determined using an immunoassay. In the urine samples of 3 diesel mechanics both cumulative and average excretion of urinary metabolites over 48 and 72 h were significantly enhanced (P < 0.05) as compared to the excreted levels in urine samples from 2 office clerks.

Interrelationship of protamine and platelet factor 4 in the neutralization of heparin.

To determine the interaction of platelet factor 4 (PF4) and protamine sulfate in the neutralization of heparin in plasma in vitro studies were carried out using a tritium-labeled heparin and a PF4 tagged with 14C. Plasmas treated with various combinations of PF4, protamine and heparin were chromatographed on Sephadex G200 and the fractions were tested for both radioactivity and antithrombin activity. PF4 was comparable to protamine in its ability to neutralize heparin, but the complexes formed with heparin were different. In contrast to protamine, when heparinized plasma was treated with an excess of PF4, no large PF4-heparin complexes were formed and none of the PF4-heparin complexes which did form were able to activate antithrombin III (ATIII). Also, incubation of PF4-neutralized, heparinized plasma at 37 degrees C did not result in liberation of heparin and prolongation of the thrombin clotting time as was found with protamine-neutralized plasma. The action of protamine and PF4 is complimentary. When half the neutralizing dose of each was added together to heparinized plasma, no immediate antithrombin activity remained. When a neutralizing dose of protamine was added to PF4-neutralized, heparinized plasma, the protamine displaced the PF4 from its complexes with heparin. The large protamine-heparin complexes which formed also contained PF4 but could not activate fresh ATIII as has been demonstrated with protamine-heparin complexes without PF4. On incubation of the protamine-PF4-neutralized, heparinized plasmas for 5 hours at 37 degrees C, the large complexes were broken down but no active heparin appeared. The results of these experiments may have some bearing on the amount of protamine needed for the neutralization of heparin following extracorporeal bypass procedures, when large amounts of PF4 may have been released from activated or disrupted platelets.