Local Magnetic Field Role in Star Formation

We highlight distinct and systematic observational features of magnetic field morphologies in polarized submm dust continuum. We illustrate this with specific examples and show statistical trends from a sample of 50 star-forming regions.Comment: 4 pages, 3 figures; to appear in the EAS Proceedings of the 6th Zermatt ISM Symposium "Conditions and Impact of Star Formation from Lab to Space", September 201

Magnetic Fields and Massive Star Formation

Massive stars ($M > 8$ \msun) typically form in parsec-scale molecular clumps that collapse and fragment, leading to the birth of a cluster of stellar objects. We investigate the role of magnetic fields in this process through dust polarization at 870 $\mu$m obtained with the Submillimeter Array (SMA). The SMA observations reveal polarization at scales of \lsim 0.1 pc. The polarization pattern in these objects ranges from ordered hour-glass configurations to more chaotic distributions. By comparing the SMA data with the single dish data at parsec scales, we found that magnetic fields at dense core scales are either aligned within $40^\circ$ of or perpendicular to the parsec-scale magnetic fields. This finding indicates that magnetic fields play an important role during the collapse and fragmentation of massive molecular clumps and the formation of dense cores. We further compare magnetic fields in dense cores with the major axis of molecular outflows. Despite a limited number of outflows, we found that the outflow axis appears to be randomly oriented with respect to the magnetic field in the core. This result suggests that at the scale of accretion disks (\lsim 10^3 AU), angular momentum and dynamic interactions possibly due to close binary or multiple systems dominate over magnetic fields. With this unprecedentedly large sample massive clumps, we argue on a statistical basis that magnetic fields play an important role during the formation of dense cores at spatial scale of 0.01 - 0.1 pc in the context of massive star and cluster star formation.Comment: Accepted for publication in Astrophysical Journa

Multi-scale physical properties of NGC 6334 as revealed by local relative orientations between magnetic fields, density gradients, velocity gradients, and gravity

We present ALMA dust polarization and molecular line observations toward 4 clumps (I(N), I, IV, and V) in the massive star-forming region NGC 6334. In conjunction with large-scale dust polarization and molecular line data from JCMT, Planck, and NANTEN2, we make a synergistic analysis of relative orientations between magnetic fields ($\theta_{\mathrm{B}}$), column density gradients ($\theta_{\mathrm{NG}}$), local gravity ($\theta_{\mathrm{LG}}$), and velocity gradients ($\theta_{\mathrm{VG}}$) to investigate the multi-scale (from $\sim$30 pc to 0.003 pc) physical properties in NGC 6334. We find that the relative orientation between $\theta_{\mathrm{B}}$ and $\theta_{\mathrm{NG}}$ changes from statistically more perpendicular to parallel as column density ($N_{\mathrm{H_2}}$) increases, which is a signature of trans-to-sub-Alfv\'{e}nic turbulence at complex/cloud scales as revealed by previous numerical studies. Because $\theta_{\mathrm{NG}}$ and $\theta_{\mathrm{LG}}$ are preferentially aligned within the NGC 6334 cloud, we suggest that the more parallel alignment between $\theta_{\mathrm{B}}$ and $\theta_{\mathrm{NG}}$ at higher $N_{\mathrm{H_2}}$ is because the magnetic field line is dragged by gravity. At even higher $N_{\mathrm{H_2}}$, the angle between $\theta_{\mathrm{B}}$ and $\theta_{\mathrm{NG}}$ or $\theta_{\mathrm{LG}}$ transits back to having no preferred orientation or statistically slightly more perpendicular, suggesting that the magnetic field structure is impacted by star formation activities. A statistically more perpendicular alignment is found between $\theta_{\mathrm{B}}$ and $\theta_{\mathrm{VG}}$ throughout our studied $N_{\mathrm{H_2}}$ range, which indicates a trans-to-sub-Alfv\'{e}nic state at small scales as well. The normalised mass-to-flux ratio derived from the polarization-intensity gradient (KTH) method increases with $N_{\mathrm{H_2}}$.Comment: 35 pages, 18 figures. Accepted by Ap

Financial toxicity in cancer patients and subsequent risk of repeat acute care utilization

BackgroundAcute care (AC) visits by cancer patients are costly sources of healthcare resources and can exert a financial burden of oncology care both for individuals with cancer and healthcare systems. We sought to identify whether cancer patients who reported more severe initial financial toxicity (FT) burdens shouldered excess risks for acute care utilization.MethodsIn 225 adult patients who participated in the Economic Strain and Resilience in Cancer (ENRICh) survey study of individuals receiving ambulatory cancer care between March and September 2019, we measured the baseline FT (a multidimensional score of 0–10 indicating the least to most severe global, material, and coping FT burdens). All AC visits, including emergency department (ED) and unplanned hospital admissions, within 1-year follow-up were identified. The association between the severity of FT and the total number of AC visits was tested using Poisson regression models.ResultsA total of 18.6% (n = 42) of patients had any AC visit, comprising 64.3% hospital admissions and 35.7% ED visits. Global FT burden was associated with the risk of repeat AC visits within 1-year follow-up (RR = 1.17, 95% CI 1.07–1.29, P < 0.001 for every unit increase), even after adjusting for sociodemographic and disease covariates. When examining subdimensions of FT, the burden of depleted FT coping resources (coping FT) was strongly associated with the risk of repeat AC visits (RR = 1.27, 95% CI 1.15–1.40, P < 0.001) while material FT burden showed a trend toward association (RR = 1.07, 95% CI 0.99–1.15, P = 0.07).ConclusionIn this prospective study of acute oncology care utilization outcomes among adult cancer patients, FT was a predictor of a higher burden of acute care visits. Patients with severely depleted material and also practical and social coping resources were at particular risk for repeated visits. Future studies are needed to identify whether early FT screening and intervention efforts may help to mitigate urgent acute care utilization burdens

Notch signaling contributes to the maintenance of both normal neural stem cells and patient-derived glioma stem cells

<p>Abstract</p> <p>Background</p> <p>Cancer stem cells (CSCs) play an important role in the development and recurrence of malignant tumors including glioma. Notch signaling, an evolutionarily conserved pathway mediating direct cell-cell interaction, has been shown to regulate neural stem cells (NSCs) and glioma stem cells (GSCs) in normal neurogenesis and pathological carcinogenesis, respectively. However, how Notch signaling regulates the proliferation and differentiation of GSCs has not been well elucidated.</p> <p>Methods</p> <p>We isolated and cultivate human GSCs from glioma patient specimens. Then on parallel comparison with NSCs, we inhibited Notch signaling using γ-secretase inhibitors (GSI) and assessed the potential functions of Notch signaling in human GSCs.</p> <p>Results</p> <p>Similar to the GSI-treated NSCs, the number of the primary and secondary tumor spheres from GSI-treated GSCs decreased significantly, suggesting that the proliferation and self-renewal ability of GSI-treated GSCs were attenuated. GSI-treated GSCs showed increased differentiation into mature neural cell types in differentiation medium, similar to GSI-treated NSCs. Next, we found that GSI-treated tumor spheres were composed of more intermediate progenitors instead of CSCs, compared with the controls. Interestingly, although inhibition of Notch signaling decreased the ratio of proliferating NSCs in long term culture, we found that the ratio of G2+M phase-GSCs were almost undisturbed on GSI treatment within 72 h.</p> <p>Conclusions</p> <p>These data indicate that like NSCs, Notch signaling maintains the patient-derived GSCs by promoting their self-renewal and inhibiting their differentiation, and support that Notch signal inhibitor GSI might be a prosperous candidate of the treatment targeting CSCs for gliomas, however, with GSI-resistance at the early stage of GSCs cell cycle.</p

Convergent Evidence from Mouse and Human Studies Suggests the Involvement of Zinc Finger Protein 326 Gene in Antidepressant Treatment Response

OBJECTIVES: The forced swim test (FST) is a commonly used model to predict antidepressant efficacy. Uncovering the genetic basis of the model may unravel the mechanism of antidepressant treatment. METHODS: FVB/NJ (FVB) and C57BL/6J (B6) were first identified as the response and non-response strains to fluoxetine (a serotonin-specific reuptake inhibitor antidepressant) treatment in the mouse FST. Simple-interval (SIM) and composite-interval (CIM) mappings were applied to map the quantitative trait loci (QTLs) of the anti-immobility effect of fluoxetine in FST (FST(FLX)) in 865 male B6×FVB-F2 mice. The brain mRNA expressions of the gene with the maximum QTL-linkage signal for FST(FLX) after the FST were compared between B6 and FVB mice and also compared between fluoxetine and saline treatment. The association of the variants in the human homologue of the mouse FST(FLX)-QTL gene with major depressive disorder (MDD) and antidepressant response were investigated in 1080 human subjects (MDD/control = 582/498). RESULTS: One linkage signal for FST(FLX)-QTL was detected at an intronic SNP (rs6215396) of the mouse Zfp326 gene (maximal CIM-LOD = 9.36). The Zfp326 mRNA expression in the FVB thalamus was significantly down-regulated by fluoxetine in the FST, and the higher FVB-to-B6 Zfp326 mRNA expressions in the frontal cortex, striatum and hypothalamus diminished after fluoxetine treatment. Two coding-synonymous SNPs (rs2816881 and rs10922744) in the human homologue of Zfp326, ZNF326, were significantly associated with the 8-week antidepressant treatment response in the MDD patients (Bonferroni-corrected p = 0.004-0.028). CONCLUSIONS: The findings suggest the involvement of the Zfp326 and ZNF326 genes in antidepressant treatment response