Influence of trip distance and population density on intra-city mobility patterns in Tokyo during COVID-19 pandemic.

This study investigates the influence of infection cases of COVID-19 and two non-compulsory lockdowns on human mobility within the Tokyo metropolitan area. Using the data of hourly staying population in each 500m×500m cell and their city-level residency, we show that long-distance trips or trips to crowded places decrease significantly when infection cases increase. The same result holds for the two lockdowns, although the second lockdown was less effective. Hence, Japanese non-compulsory lockdowns influence mobility in a similar way to the increase in infection cases. This means that they are accepted as alarm triggers for people who are at risk of contracting COVID-19.

Both IRBIT and long-IRBIT bind to and coordinately regulate Cl-/HCO3- exchanger AE2 activity through modulating the lysosomal degradation of AE2.

Anion exchanger 2 (AE2) plays crucial roles in regulating cell volume homeostasis and cell migration. We found that both IRBIT and Long-IRBIT (L-IRBIT) interact with anion exchanger 2 (AE2). The interaction occurred between the conserved AHCY-homologous domain of IRBIT/L-IRBIT and the N-terminal cytoplasmic region of AE2. Interestingly, AE2 activity was reduced in L-IRBIT KO cells, but not in IRBIT KO cells. Moreover, AE2 activity was slightly increased in IRBIT/L-IRBIT double KO cells. These changes in AE2 activity resulted from changes in the AE2 expression level of each mutant cell, and affected the regulatory volume increase and cell migration. The activity and expression level of AE2 in IRBIT/L-IRBIT double KO cells were downregulated if IRBIT, but not L-IRBIT, was expressed again in the cells, and the downregulation was cancelled by the co-expression of L-IRBIT. The mRNA levels of AE2 in each KO cell did not change, and the downregulation of AE2 in L-IRBIT KO cells was inhibited by bafilomycin A1. These results indicate that IRBIT binding facilitates the lysosomal degradation of AE2, which is inhibited by coexisting L-IRBIT, suggesting a novel regulatory mode of AE2 activity through the binding of two homologous proteins with opposing functions.

Geological implication of grain-size segregation in dense granular matter.

To the current common belief, grain size segregation in granular matter requires sufficient porosity. Therefore, grain size segregation found in a natural fault gouge could imply elevated fluid pressure and the reduced normal stress on fault, possibly caused by the frictional heat during an earthquake. To clarify whether fluidization is essential to grain size segregation, we conduct numerical simulation on a simple model of fault gouge in a plane shear geometry under constant volume condition: the volume fraction is fixed at 0.6, at which the granular system possesses yield stress. We observe apparent grain size segregation at this volume fraction, meaning that grain size segregation alone does not imply fluidization of granular matter. We also show that segregation is driven by the nonlinear velocity profile, and that the gravity is not essential to segregation. The physical condition tested here may be relevant to earthquake faults: the normal stress of 1 MPa, the sliding velocity of 1 m s-1, and the duration of 0.1 s.This article is part of the theme issue 'Statistical physics of fracture and earthquakes'.

Legionella Pneumonia Complicated with Acquired Fanconi Syndrome.

Legionella pneumonia is occasionally accompanied by renal complications; however, the cause of this remains unknown. We herein report a 70-year-old Japanese man with Legionella pneumonia who presented with hyponatremia, hypophosphatemia, and hypouricemia. The levels of urinary ß2-microglobulin and N-acetyl-ß-D-glucosaminidase were remarkably high, indicating severe renal tubular damage. The presence of glycosuria and aminoaciduria as well as increased fractional excretion of uric acid and decreased tubular reabsorption of phosphate indicated that the patient's condition was complicated with Fanconi syndrome. After antimicrobial therapy, the electrolyte abnormalities and renal tubular damage were completely resolved.

Reciprocal CD4+ T-cell balance of effector CD62Llow CD4+ and CD62LhighCD25+ CD4+ regulatory T cells in small cell lung cancer reflects disease stage.

PURPOSE: Small cell lung cancer (SCLC) possesses high tendency to disseminate. However, SCLC patients with paraneoplastic syndrome mediated by immunity against onconeural antigens remain in limited-stage disease (LD) without distant metastases. Cumulative evidence regulates that a balance between immune and regulatory T (Treg) cells determines the magnitude of immune responses to not only self-antigens but also tumor-associated antigens. The purpose of this study was to elucidate the immunologic balance induced in SCLC patients. EXPERIMENTAL DESIGN: We analyzed T cells in the peripheral blood of 35 consecutive SCLC patients, 8 long-term survivors, and 19 healthy volunteers. RESULTS: Purified CD4(+) T cells with down-regulated expression of CD62L (CD62L(low)) produced IFN-gamma, interleukin (IL)-4, and IL-17, thus considered to be immune effector T cells (Teff). Significantly more Teff cell numbers were detected in LD-SCLC patients than that of extended-stage SCLC (ED-SCLC). By contrast, induction of CD62L(high)CD25(+) CD4(+) Treg cells was significantly higher in ED-SCLC patients. Long-term survivors of SCLC maintained a high Teff to Treg cell ratio, whereas patients with recurrent disease exhibited a low Teff to Treg cell ratio. Teff cells in LD-SCLC patients included more IL-17-producing CD4(+) T cells (Th17). Moreover, dendritic cells derived from CD14(+) cells of LD-SCLC patients secreted more IL-23. CONCLUSION: These results show that CD4(+) T-cell balance may be a biomarker that distinguishes ED-SCLC from LD-SCLC and predicts recurrence. This study also suggests the importance of inducing Teff cells, particularly Th17 cells, while eliminating Treg cells to control systemic dissemination of SCLC.