A Qualitative Exploration of a User-Centered Model for Smartwatch Comfort Using Grounded Theory

Smartwatch comfort is a fundamental factor that significantly influences the user experience and provides crucial guidance for the evolution of wearable technology. However, there is currently a lack of a comprehensive theoretical model to describe the dimensions of smartwatch comfort and their corresponding influencing factors. Therefore, the present study employed a bottom-up grounded theory approach to construct a user-centered model for smartwatch comfort. Through the coding of in-depth interviews with 64 smartwatch users, we discovered that smartwatch comfort encompasses both physiological dimensions (e.g., pressure and foreign body sensation) and psychological dimensions (e.g., perceived intelligence and satisfaction of needs). Furthermore, the features of smartwatches, including physical attributes (e.g., size and material) and functionalities (e.g., interoperability and automation capabilities), directly impact the comfort experience. Additionally, individual and contextual factors can explain variations in the comfort experience of smartwatches. Users with different physiological characteristics (e.g., wrist size and body sensitivity) and psychological needs (e.g., utilitarian or hedonic needs) are influenced differently by the factors of smartwatches that affect their comfort experience. The adaptability of smartwatches across different contexts (including task context, social context, and temporal context) is also a significant influencing factor on comfort. This substantive grounded theory provides crucial guidance for the selection of core variables in future quantitative research and contributes to the development of smarter, more comfortable, and user-centric smartwatches.</p

D6D activity is higher in tumor tissue than in adjacent non-tumor tissue.

<p>(<b>a</b>) The activity of biomarkers of D6D in B16 melanoma. <i>Upper:</i> Gas chromatography showing the differences in LA, ETA and AA content between B16 melanoma and adjacent non-tumor tissue. <i>Lower</i>: The ratios of ETA/LA and AA/LA indicate D6D enzyme activity. **<i>P</i><0.01, n = 4. (<b>b</b>) Activity of biomarkers of D6D in LLC tumors. <i>Upper:</i> Gas chromatography showing the differences in LA, ETA and AA content between LLC tumor and adjacent non-tumor tissue. <i>Lower</i>: The ratios of ETA/LA and AA/LA indicate D6D enzyme activity. **<i>P</i><0.01, n = 4. (<b>c</b>) D6D mRNA levels in tumor and adjacent non-tumor tissue. **<i>P</i><0.01, n = 3. (<b>d</b>) Western blot showing D6D protein levels in tumor and adjacent non-tumor tissue. (<b>e</b>) Correlation of the activity of biomarkers of D6D (based on ETA/LA and AA/LA ratios) with tumor size. (<b>f</b>) Correlation of D6D mRNA levels with tumor size.</p

Vγ2Vδ2 T cells that accumulated in tissue compartments could mount effector function and produce anti-TB cytokine.

<p>Shown are ELISPOT data for IPP-driven IFNγ+ cellular response in lymphocytes from blood, lung and liver collected from four Mtb-infected macaques at 4–6 weeks after the infection. Data were subtracted from values of glucose/medium control and expressed here as IFNγ+ Vγ2Vδ2 T cells in 10∧6 lymphocytes. IPP stimulates activation of only Vγ2Vδ2 T cells but not other immune cells.</p

TCR CDR3 spetratyping revealed predominance of a selected CDR3 length in expanded Vγ2Vδ2 T cells in kidney/liver tissue compartments in late local Mtb infection.

<p>Shown are the Vδ2 TCR CDR3 profiles revealed by Genescan-based spectratyping as previously described <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030631#pone.0030631-Zhou1" target="_blank">[22]</a>. The numbers of nucleotides in the different CDR3 lengths were determined in control experiments <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030631#pone.0030631-Zhou1" target="_blank">[22]</a>, and were expressed as predicted numbers of amino acids. A short line at the bottom of each histogram represents the predicted CDR3 length of 12 aa. The profiles of CDR3 lengths in Vδ2 TCR cDNA from blood, spleen and lung of the Mtb-infected macaques were diverse without a restricted selection of a single CDR3 length. In contrast, Vδ2 TCR cDNA derived from expanded Vγ2Vδ2 T cells in kidney or liver tissues of four infected macaques exhibited predominance of a selected CDR3 length. A selected CDR3 length was consistent with the clonal dominance of TCR sequence analyses in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030631#pone-0030631-g003" target="_blank">Fig. 3</a>.</p

Clonal immune responses of Mycobacterium-specific gammadelta T cells in tuberculous and non-tuberculous tissues during M. tuberculosis infection

Background: We previously demonstrated that unvaccinated macaques infected with large-dose M.tuberculosis(Mtb) exhibited delays for pulmonary trafficking of Ag-specific alphabeta and gammadelta T effector cells, and developed severe lung tuberculosis(TB) and "secondary" Mtb infection in remote organs such as liver and kidney. Despite delays in lungs, local immunity in remote organs may accumulate since progressive immune activation after pulmonary Mtb infection may allow IFNgamma-producing gammadelta T cells to adequately develop and traffic to lately-infected remote organs. As initial efforts to test this hypothesis, we comparatively examined TCR repertoire/clonality, tissue trafficking and effector function of Vgamma2Vdelta2 T cells in lung with severe TB and in liver/kidney without apparent TB. Methodology/Principal Findings: We utilized conventional infection-immunity approaches in macaque TB model, and employed our decades-long expertise for TCR repertoire analyses. TCR repertoires in Vgamma2Vdelta2 T-cell subpopulation were broad during primary Mtb infection as most TCR clones found in lymphoid system, lung, kidney and liver were distinct. Polyclonally-expanded Vgamma2Vdelta2 T-cell clones from lymphoid tissues appeared to distribute and localize in lung TB granuloms at the endpoint after Mtb infection by aerosol. Interestingly, some TCR clones appeared to be more predominant than others in lymphocytes from liver or kidney without apparent TB lesions. TCR CDR3 spetratyping revealed such clonal dominance, and the clonal dominance of expanded Vgamma2Vdelta2 T cells in kidney/liver tissues was associated with undetectable or low-level TB burdens. Furthermore, Vgamma2Vdelta2 T cells from tissue compartments could mount effector function for producing anti-mycobacterium cytokine. Conclusion: We were the first to demonstrate clonal immune responses of mycobacterium-specific Vgamma2Vdelta2 T cells in the lymphoid system, heavily-infected lungs and lately subtly-infected kidneys or livers during primary Mtb infection. While clonally-expanded Vgamma2Vdelta2 T cells accumulated in lately-infected kidneys/livers without apparent TB lesions, TB burdens or lesions appeared to impact TCR repertoires and tissue trafficking patterns of activated Vgamma2Vdelta2 T cells

Polyclonally-expanded Vγ2Vδ2 T cells from lymphoid tissues appeared to distribute and localize in lung TB granuloms after Mtb infection by aerosol.

<p>Shown are individual Vδ2 TCR clones isolated from lymphocytes of lung tissues from five Mtb-infected macaques. The immunohistochenistry data showing infiltration and distribution of Vγ2Vδ2 T cells in TB granulomas were shown in the previous publication <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030631#pone.0030631-Huang2" target="_blank">[18]</a>. Flow cytometry data indicating cellular expansion of Vγ2Vδ2 T cells in CD3+ T cells isolated from the lung tissues were described in the text. Note polyclonal Vδ2 TCR sequences and sub-dominant clones in cDNA derived from lung lymphocytes in which expansion of Vγ2Vδ2 T cells was detected. Clones present in blood and spleen were marked as described in the legend of <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030631#pone-0030631-g001" target="_blank">Fig. 1</a>.</p

Broad T cell repertoire in Vγ2Vδ2 T-cell subpopulation in lymphoid system during primary Mtb infection of macaques.

<p>Shown are individual Vδ2 TCR clones isolated from PBL (left) and lymphocytes of spleen tissues (right) from 5 Mtb-infected macaques. The flow cytometry data indicating cellular expansion of Vγ2Vδ2 T cells in spleen were described in the text. Note that spleen lymphocytes in which major expansion of Vγ2Vδ2 T cells was seen were used for RNA isolation, cDNA synthesis and Vδ2 TCR sequence analyses. Note polyclonal sequences of Vδ2 TCR in cDNA derived from spleen lymphocytes and PBLs. Frequencies were expressed as the number of individual clones among the total analyzed clones. Similar data indicating polyclonal representation of Vγ2Vδ2 T cells in PBL before Mtb infection were also seen (data not shown). CDR3 were presumably indicated based on the definition for TCR β CDR3 <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030631#pone.0030631-Du1" target="_blank">[9]</a>. D indicates diversity region; N indicates non-determining region of TCR receptor genes. Clones marked by ‘♦’ were present in the blood, lung and kidney (2717). Clones marked by ‘’ and ‘•’ were present in the blood, lung and spleen(3055 and 2823). Clones marked by ‘▴’ and ‘▪’ were present in the blood and lung(2722).</p

P values derived from statistical analyses of frequencies of dominant Vδ2 clonotypes between different tissues compartments (n = 5).

#<p>p value = 0.0041(**, very significant) when frequencies of dominant Vδ2 clonotypes in blood were compared with those in spleen(Blood vs Spleen). Individual dominant Vδ2 clonotypes were defined if they comprised >20% of the clones identified in a tissue compartment or blood from a macaque. Frequencies of dominant Vδ2 clonotypes among total TCR clones in a compartment from five macaques (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030631#pone-0030631-g001" target="_blank">Figs. 1</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030631#pone-0030631-g002" target="_blank">2</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030631#pone-0030631-g003" target="_blank">3</a>) were calculated and analyzed for statistical significance between different tissue compartments using two-tailed Fisher exact test. We also statistically compared percentage numbers for total distinct Vδ2-bearing clones between different tissues compartments (n = 5), and found similar trends of results suggesting that Vδ2 repertoires in blood and lung were significantly broader than those in liver and kidney(data not shown).</p

Some Vδ2 T cell clones of Vγ2Vδ2 T-cell subpopulation appeared to be more predominant than others in lately Mtb-infected liver or kidney.

<p>The localization of Vγ2Vδ2 T cells in interstitial tissues of kidney or liver were shown in the previous publication <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030631#pone.0030631-Huang2" target="_blank">[18]</a>. Expansion of Vγ2Vδ2 T cells in CD3+ T cells isolated from the kidney or liver tissues were described in the text. Note that three macaques(2717, 3055, 2935) exhibited dominance of a single clone or oligo-clones bearing a same length of CDR3 in TCR cDNA derived from kidney lymphocytes in which expansion of Vγ2Vδ2 T cells was detected. In cDNA derived from liver lymphocytes, a dominance of a single TCR clone or clones with a restricted CDR3 length was also noted in three macaques (2717, 2823, 2935). Clones marked by ‘♦’were present in the blood,lung and kidney(2717).</p

Reducing D6D expression or activity suppresses tumor growth.

<p>(<b>a</b>) Effect of D6D-RNAi knockdown on B16 melanoma growth. **<i>P</i><0.001; n = 8 for both groups. (<b>b</b>) Effect of the D6D selective inhibitor SC-26196 on B16 melanoma growth. **<i>P</i><0.0001; control, n = 7; treated, n = 8. (<b>c</b>) Effect of D6D-RNAi knockdown on LLC tumor growth. *<i>P</i><0.05; n = 8 for both groups. (<b>d</b>) Effect of the D6D selective inhibitor SC-26196 on LLC tumor growth. **<i>P</i><0.01; control, n = 7; treated, n = 10. (<b>a–d</b>) <i>Upper left</i>: Representative tumor sizes. <i>Upper right</i>: Average tumor weight at the end of the experiment. <i>Lower</i>: Tumor growth rate during the 14-day experimental period.</p