Effect of Normal Force Intensity on Tactile Motion Speed Perception Based on Spatiotemporal Cue.

While the relative motion between the skin and objects in contact with it is essential to everyday tactile experiences, our understanding of how tactile motion is perceived via human tactile function is limited. Previous studies have explored the effect of normal force on speed perception under conditions where multiple motion cues on the skin (spatiotemporal cue, tangential skin deformation cue, and slip-induced vibration cue) were integrated. However, the effect of the normal force on speed perception in terms of each motion cue remains unclear since the multiple motion cues have not been adequately separated in the previously reported experiments. In this study, we aim to elucidate the effect of normal force in situations where the speed perception of tactile motion is based solely on a spatiotemporal cue. We developed a pin-array display which allowed us to vary the intensity of the normal force without causing tangential forces or slip-induced vibrations. Using the display, we conducted two psychophysical experiments. In Experiment 1, we found that the speed of the object was perceived to be 1.12-1.14 times faster when the intensity of the normal force was doubled. In Experiment 2, we did not observe significant differences in the discriminability of tactile speed caused by differences in normal force intensity. Our experimental results are of scientific significance and offer insights for engineering applications when using haptic displays that can only provide spatiotemporal cues represented by normal forces.

Alteration of microbial composition in the skin and blood in vasculitis.

Vasculitis is a systemic autoimmune disease characterized by leukocyte infiltration into blood vessels. Various microorganisms have been associated with the pathogenesis of vasculitis; however, the causal microbial agents and underlying mechanisms are not fully understood, possibly because of the technical limitations of pathogen detection. In the present study, we characterized the microbiome profile of patients with cutaneous vasculitis using comprehensive metagenome shotgun sequencing. We found that the abundance of the SEN virus was increased in the affected skin and serum of patients with vasculitis compared to healthy donors. In particular, the abundance of SEN virus reads was increased in the sera of patients with cutaneous arteritis. Among the bacteria identified, Corynebacteriales was the most differentially associated with vasculitis. Linear discriminant analysis effect size also indicated differences in the microbial taxa between patients with vasculitis and healthy donors. These findings demonstrate that vasculitis is associated with considerable alteration of the microbiome in the blood and skin and suggest a role for the infectious trigger in vasculitis.

Propionibacterium acnes is developing gradual increase in resistance to oral tetracyclines.

Propionibacterium acnes is an anaerobic bacterium that causes deep infection in organs and prosthetic joints, in addition to acne vulgaris. Many tetracycline-resistant P. acnes strains have been isolated because oral tetracyclines are frequently used as an acne treatment against P. acnes. In this study, we found a novel tetracycline resistance mechanism in P. acnes. Three doxycycline-resistant (MIC: 16 µg ml-1) strains were isolated from 69 strains in acne patients in Japan between 2010 and 2011. Additionally, six insusceptible strains (MIC: 1-2 µg ml-1) that had reduced susceptibility compared to susceptible strains (MIC: ≤0.5 µg ml-1) were identified. All doxycycline-resistant strains had a G1036C mutation in the 16S rRNA gene in addition to an amino acid substitution in the ribosomal S10 protein encoded by rpsJ. By contrast, insusceptible strains had an amino acid substitution in the S10 protein but no mutation in the 16S rRNA. When the mutant with decreased susceptibility to doxycycline was obtained in vitro, only the mutated S10 protein was found (MIC: 4 µg ml-1), not the mutated 16S rRNA gene. This result shows that the S10 protein amino acid substitution contributes to reduced doxycycline susceptibility in P. acnes and suggests that tetracycline resistance is acquired through a 16S rRNA mutation after the S10 protein amino acid substitution causes reduced susceptibility.

Relationship between the severity of acne vulgaris and antimicrobial resistance of bacteria isolated from acne lesions in a hospital in Japan.

Propionibacterium acnes and Staphylococcus epidermidis are normal skin inhabitants that are frequently isolated from lesions caused by acne, and these micro-organisms are considered to contribute to the inflammation of acne. In the present study, we examined the antimicrobial susceptibilities and resistance mechanisms of P. acnes and S. epidermidis isolated from patients with acne vulgaris in a university hospital in Japan from 2009 to 2010. Additionally, we analysed the relationship between the antimicrobial resistance of P. acnes and the severity of acne vulgaris. Some P. acnes strains (18.8 %; 13/69) were resistant to clindamycin. All strains had a mutation in the 23S rRNA gene, except for one strain that expressed erm(X) encoding a 23S rRNA methylase. Tetracycline-resistant P. acnes strains were found to represent 4.3 % (3/69) of the strains, and this resistance was caused by a mutation in the 16S rRNA gene. Furthermore, three strains with reduced susceptibility to nadifloxacin (MIC = 16 µg ml(-1)) were detected. When analysing the correlation between the antimicrobial resistance of P. acnes and S. epidermidis, more than 80 % of the patients who carried clindamycin-resistant P. acnes also carried clindamycin-resistant S. epidermidis. However, no epidemic strain that exhibited antimicrobial resistance was detected in the P. acnes strains when analysed by PFGE. Therefore, our results suggest that the antimicrobial resistance of P. acnes is closely related to antimicrobial therapy. Additionally, those P. acnes strains tended to be frequently found in severe acne patients rather than in mild acne patients. Consequently, the data support a relationship between using antimicrobial agents and the emergence of antimicrobial resistance.

Paracrine cytokine mechanisms underlying the hyperpigmentation of seborrheic keratosis in covered skin areas.

We previously reported that increased expression of the endothelin (EDN)1/EDNB receptor (EDNBR) as well as the stem cell factor (SCF)/SCF receptor (c-KIT) linkages is mainly responsible for the activation of melanocytes in the epidermal hyperpigmentation of ultraviolet (UV)-B melanosis and lentigo senilis (LS). In this study, we characterized seborrheic keratosis (SK) to examine the paracrine cytokine mechanism(s) involved in its epidermal hyperpigmentation by reverse transcription polymerase chain reaction, immunohistochemistry and western blotting analyses. In contrast to our previous study which showed the upregulated expression of EDN1 and EDNBR at the transcriptional and translational levels in the epidermis of SK, we observed unexpectedly that the cytokine SCF and its receptor c-KIT are not upregulated, but are downregulated at both the gene and protein levels. We established SK cell lines to examine whether SK basaloid cells are less sensitive to SCF-inducible stimulation than are normal human keratinocytes (NHK). Comparison of the stimulatory effects of interleukin (IL)-1α or tumor necrosis factor (TNF)-α on SCF production between SK cells and NHK demonstrated that SK cells do not respond to IL-1α or TNF-α to stimulate production of SCF, whereas a significant stimulation of SCF is elicited by those same cytokines in NHK. These finding underscore a role of phenotypic changes in melanogenic cytokine production in the epidermis between SK and LS/UV-B melanosis.

Glycolic acid chemical peeling improves inflammatory acne eruptions through its inhibitory and bactericidal effects on Propionibacterium acnes.

Glycolic acid chemical peeling is effective for treating comedones, and some clinical data show that it also improves inflammatory eruptions. The purpose of this study was to identify the mechanism of glycolic acid chemical peeling to improve inflammatory acne. To assess growth inhibitory and bactericidal effects of glycolic acid on Propionibacterium acnes in vitro, we used an agar diffusion method and a time-kill method. To reveal bactericidal effects in vivo, we established an agar-attached method which correlated well with the ordinary swab-wash method, and we used the agar-attached method to compare the numbers of propionibacteria on the cheek treated with glycolic acid chemical peeling. Our results show that 30% glycolic acid (at pH 1.5, 3.5 and 5.5) formed growth inhibitory circles in the agar diffusion method, but the diameters of those circles were smaller than with 1% nadifloxacin lotion or 1% clindamycin gel. In the time-kill method, 30% glycolic acid (at pH 1.5 and 3.5) or 1% nadifloxacin lotion reduced the number of P. acnes to less than 100 CFU/mL within 5 min. In contrast, in 30% glycolic acid (at pH 5.5) or in 1% clindamycin gel, P. acnes survived for more than 4 h. Chemical peeling with 35% glycolic acid (at pH 1.2) decreased the number of propionibacteria on the cheeks of patients compared with untreated controls (P < 0.01). Our results demonstrate that glycolic acid has moderate growth inhibitory and bactericidal effects on P. acnes, and that chemical peeling with glycolic acid works on inflammatory acne via those effects.