The use of magnetic field variations for positioning and navigation has been suggested by several researchers. In most of the applications, the magnetic field is used to determine the azimuth or heading. However, for indoor applications, accurate heading determination is difficult due to the presence of magnetic field anomalies. Here location fingerprinting methodology can take advantage of these anomalies. In fact, the more significant the local anomalies, the more unique the magnetic "fingerprint". In general, in each fingerprint, the more elements, the better for positioning. Unfortunately, magnetic field intensity data only consists of three components. Since true north (or magnetic north) is unknown, even with help of the accelerometer to detect the direction of the gravity, only two components can be extracted, i.e. the horizontal intensity and the vertical intensity (or total intensity and inclination). Furthermore, moving objects containing ferromagnetic materials and electronic devices may affect the magnetic field. Tests were carried out to investigate the feasibility of using magnetic field alone for indoor positioning. Possible solutions are discussed.

Location fingerprinting in wireless LAN (WLAN) positioning has received much attention recently. One of the key issues of this technique is generating the database of 'fingerprints'. The conventional method does not utilise the spatial correlation of measurements sampled at adjacent reference points (RPs), and the 'training' process is not an easy task. A new method based on kriging is presented in this paper. An experiment shows that the new method can not only achieve more accurate estimation, but can also greatly reduce the workload and save training time. This can make the fingerprinting technique more flexible and easier to implement.

Blockade of immune‐checkpoint programmed cell death protein 1 (PD‐1) or programmed cell death ligand 1 can enhance effector T‐cell responses. However, the lack of response in many patients to checkpoint‐inhibitor therapies emphasizes the need for combination immunotherapies to pursue maximal antitumor efficacy. We have previously demonstrated that antagonism of C‐X‐C chemokine receptor type 4 (CXCR4) by plerixafor (AMD3100) can decrease regulatory T (Treg)‐cell intratumoral infiltration. Therefore, a combination of these 2 therapies might increase antitumor effects. Here, we evaluated the antitumor efficacy of AMD3100 and anti‐PD‐1 (αPD‐1) antibody alone or in combination in an immunocompetent syngeneic mouse model of ovarian cancer. We found that AMD3100, a highly specific CXCR4 antagonist, directly down‐regulated the expression of both C‐X‐C motif chemokine 12 (CXCL12) and CXCR4 in vitro and in vivo in tumor cells. AMD3100 and αPD‐1 significantly inhibited tumor growth and prolonged the survival of tumor‐bearing mice when given as monotherapy. Combination of these 2 agents significantly enhanced antitumor effects compared with single‐agent administration. Benefits of tumor control and animal survival were associated with immunomodulation mediated by these 2 agents, which were characterized by increased effector T‐cell infiltration, increased effector T‐cell function, and increased memory T cells in tumor microenvironment. Intratumoral Treg cells were decreased, and conversion of Treg cells into T helper cells was increased by AMD3100 treatment. Intratumoral myeloid‐derived suppressor cells were decreased by the combined treatment, which was associated with decreased IL‐10 and IL‐6 in the ascites. Also, the combination therapy decreased suppressive leukocytes and facilitated M2‐to‐M1 macrophage polarization in the tumor. These results suggest that AMD3100 could be used to target the CXCR4‐CXCL12 axis to inhibit tumor growth and prevent multifaceted immunosuppression alone or in combination with αPD‐1 in ovarian cancer, which could be clinically relevant to patients with this disease.—Zeng, Y., Li, B., Liang, Y., Reeves, P. M., Qu, X., Ran, C., Liu, Q., Callahan, M. V., Sluder, A. E., Gelfand, J. A., Chen, H., Poznansky, M. C. Dual blockade of CXCL12‐CXCR4 and PD‐1‐PD‐L1 pathways prolongs survival of ovarian tumor‐bearing mice by prevention of immunosuppression in the tumor microenvironment. FASEB J. 33, 6596–6608 (2019). http://www.fasebj.org