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Patients with cancer can develop neurologic deficits that frequently, but not exclusively, arise from intracranial involvement by malignancy. In this case series, we highlight 3 patients with new focal neurologic deficits in the setting of hematologic cancers without baseline intracranial disease. The first, with Waldenstrom macroglobulinemia, develops bradyphrenia, inattention, and disorientation. Patients 2 and 3 have diagnoses of chronic lymphocytic leukemia (CLL), with one experiencing a first lifetime seizure and the other right hemiparesis, rash, headache, and intermittent speech arrest. A description of the pathophysiology of the final diagnosis, suggestive imaging characteristics, and historical outcomes follows to improve future diagnostic precision.

As the penetration of renewables increases, air conditioners (ACs), whose electricity consumptions account for a large share, present tremendous potential in providing load regulating service to maintain the power supply–demand balance. In this paper, an analytical model for the dynamic aggregated power and schedulable capacity of ACs is presented, where the safe protocol (SP) is utilized to eliminate the power oscillations caused by temperature setpoint shifting. Based on this, the response potential of ACs is quantified by the evaluation indexes in the dimensions of capacity and time. Besides, an optimal dispatch strategy is proposed to implement the coordination of air conditioning resources in the response stage and recovery stage, by which not only the reliable load regulation service can be provided, but also the influences on users can be minimized. Simulation studies demonstrate the effectiveness of the proposed method.

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As the pressure of supply–demand balance increases with the high penetration of renewable energy resources, it is widely accepted that demand side resources including air conditioners (ACs) play an important role in providing ancillary services to the grid. In this paper, air conditioning loads are modeled as a kind of virtual energy storage device based on their inherent thermal storage capacity. It is investigated that air conditioning loads can provide regulation service with certain storage power output and ramping rate limits as a result of minimum on/off time requirements. Simulation studies demonstrate the effectiveness of the proposed method by coordinating ACs to track a regulation signal.

Perivascular adipose-derived stem cells (PV-ADSCs) could differentiate into smooth muscle cells (SMCs), participating in vascular remodeling. However, its underlying mechanism is not well explored. Our previous single-cell RNA-sequencing dataset identified a unique expression of matrix Gla protein (MGP) in PV-ADSCs compared with subcutaneous ADSCs. MGP involves in regulating SMC behaviors in vascular calcification and atherosclerosis. In this study, we investigated MGP’s role in PV-ADSCs differentiation toward SMCs in vitroand in vascular remodeling in vivo. PV-ADSCs were isolated from perivascular regions of mouse aortas. Quantitative reverse transcription–polymerase chain reaction (qRT-PCR), Western blot, and immunofluorescence confirmed higher MGP expression in PV-ADSCs. The MGP secretion increased along PV-ADSCs differentiation toward SMCs in response to transforming growth factor–beta 1 (TGF-β1). Lentivirus knockdown of MGP markedly promoted the bone morphogenetic protein 2 (BMP2) expression and phosphorylation of SMAD1/5/8 in PV-ADSCs, subsequently inhibiting its differentiation toward SMCs. Such inhibition could be partially reversed by further application of BMP2 inhibitors. On the contrary, exogenous MGP inhibited BMP2 expression and SMAD1/5/8 phosphorylation in PV-ADSCs, thereby promoting its differentiation toward SMCs. Transplantation of cultured PV-ADSCs, which was pretreated by MGP knockdown, in mouse femoral artery guide-wire injury model significantly alleviated neointimal hyperplasia. In conclusion, MGP promoted the differentiation of PV-ADSCs toward SMCs through BMP2/SMAD-mediated signaling pathway. This study offers a supplement to the society of perivascular tissues and PV-ADSCs.

Knowledge of the environmental factors affecting leaf element stoichiometry patterns can reveal nutrient fluxes of ecosystems and their responses to global change. However, understanding of continental patterns of leaf nitrogen (N) and phosphorus (P) stoichiometry in relation to solar radiation is still insufficient. We compiled available data on leaf N and P concentrations for over 1,500 species of Chinese terrestrial plants extracted from publications and acquired surface solar radiation related indexes including global radiation, direct radiation, diffuse radiation, photosynthetically active radiation (PAR) and ultraviolet‐B radiation (UVB), and other related climate indexes for 173 sites to explore the relationships between leaf N and P stoichiometry and solar radiation especially including its direct, diffuse, and spectral components for the first time at a continental scale. We found that leaf N and P concentrations were positively related to global radiation and direct radiation but negatively related to diffuse radiation. Leaf N and P concentrations were positively related to PAR but negatively related to UVB. Solar radiation had both direct associations and indirect associations mediated by temperature, precipitation, and so on with leaf N and P stoichiometry; furthermore, the direct associations, when solar radiation was indicated by spectral components, were greater than the indirect associations. So when predicting the effects of global dimming on ecosystem nutrient fluxes, we must distinguish the roles of direct, diffuse, and spectral components of solar radiation. Our study has implications for all future macroecological researches involving the effects of solar radiation on ecosystems. Solar radiation and elements are two of the main factors determining ecosystem structure and process. However, the large‐scale biogeographical patterns of leaf nitrogen (N) and phosphorus (P) in relation to solar radiation are not yet fully understood. Especially, solar radiation at Earth surface is the sum of direct radiation and diffuse radiation, and it falls in the ultraviolet, visible, and infrared portion of the spectrum. However, the associations between these components of solar radiation and leaf N, P, and N:P are unknown. To deepen understanding the underlying mechanisms by which solar radiation as a composite and polychromatic factor affects nutrient fluxes, we compiled available data on leaf N and P concentrations for over 1,500 species of Chinese terrestrial plants and acquired solar radiation‐related indexes including global radiation, direct and diffuse radiation, and specific solar spectral radiation—photosynthetically active radiation (PAR) and ultraviolet‐B radiation (UVB), and other related climate indexes for 173 sites to explore the relationships between solar radiation and leaf N and P stoichiometry at a continental scale. Our study showed that leaf N and P concentrations increased with global radiation, possibly due to the effects of global radiation on plant photosynthesis and various soil biogeochemical processes. Leaf N and P concentrations increased with direct radiation but decreased with diffuse radiation; leaf N and P concentrations increased with PAR and but decreased with UVB. These phenomena may be owed to the different effects of solar radiation components on ecosystem processes. In addition, solar radiation had both direct associations and indirect associations mediated by temperature, precipitation, and so on with leaf N and P stoichiometry; furthermore, the direct associations, when solar radiation was indicated by spectral components, were greater than the indirect associations. So when predicting the effects of global dimming on ecosystem nutrient fluxes, we must distinguish the roles of direct, diffuse, and spectral components of solar radiation. That's what's so special about solar radiation. Leaf N and P increase with direct radiation and decrease with diffuse radiation at a continental scaleLeaf N and P increase with photosynthetically active radiation and decrease with ultraviolet‐B radiation at a continental scaleDirect associations between solar spectrums and leaf N and P are greater than their indirect associations mediated by climate

The BCR/ABL oncogene, generated by the t(9;22)(q34;q11) chromosomal translocations known as the Philadelphia chromosome (Ph), is associated with virtually all human chronic myelogenous leukemia (CML), and is also associated with 20% of the adult and 5% of the pediatric cases of acute lymphoblastic leukemia (ALL). v-Abl, the oncogene of the Abelson murine leukemia virus (A-MuLV) originally found to cause pre-B cell leukemia/lymphoma when introduced into newborn mice by intraperitoneal or intravenous injection, was created by a recombination event that fused viral gag sequences to c-abl sequences, deleting the Abl SH3 domain and accumulating point mutations in the process. Using a mouse bone marrow transduction and transplantation model, we have previously shown that expression of BCR/ABL in mouse bone marrow cells rapidly (in approximately 3 weeks) induced a myeloproliferative disease (MPD) resembling human CML, while v-Abl rapidly (in approximately 4 weeks) induced B-ALL along with a minor expansion of v-Abl-infected myeloid cells. It has long been shown that the Abl carboxyl terminal region is required for the lymphoid cell transformation by v-Abl both in vivo and in vitro. We decided to investigate the role of the Abl carboxyl terminal region in BCR/ABL- and v-Abl-leukemogenesis using the mouse bone marrow transduction and transplantation model. We found that the Abl carboxyl terminal region is required for v-Abl-induced B-ALL, as expected. But, interestingly, v-Abl without C-terminus (v-Abl/p160/ΔC) induced a MPD in mice, similar to that induced by BCR/ABL, with a relative long latency (approximately 3 months in average). On the other hand, BCR/ABLΔC still induced MPD efficiently, similar as wild type BCR/ABL. These results demonstrated the Abl carboxyl terminal region is required for the induction of acute lymphoblastic leukemia by v-Abl but not for the induction of MPD by BCR/ABL or v-Abl. The results also suggested that v-Abl has a capacity to induce MPD, albeit much weaker than that of BCR/ABL and much weaker than v-Abl's capacity to induce B-ALL. The role of the ABL carboxyl terminal region in BCR/ABL-induced B-ALL and the mechanism by which the Abl carboxyl terminal region contributes to the lineage-specific transformation are under investigation. Such research will shed lights into the mechanism of lineage-specific leukemogenesis and help to identify therapeutic targets for lymphoid malignancies.

The BCR/ABL oncogene, generated by the t(9;22)(q34;q11) chromosomal translocations known as the Philadelphia chromosome (Ph), is associated with virtually all human chronic myelogenous leukemia (CML), and is also associated with 20% of the adult and 5% of the pediatric cases of acute lymphoblastic leukemia (ALL). v-Abl, the oncogene of the Abelson murine leukemia virus (A-MuLV) originally found to cause pre-B cell leukemia/lymphoma when introduced into newborn mice by intraperitoneal or intravenous injection, was created by a recombination event that fused viral gag sequences to c-abl sequences, deleting the Abl SH3 domain and accumulating point mutations in the process. Using a mouse bone marrow transduction and transplantation model, we have previously shown that expression of BCR/ABL in mouse bone marrow cells rapidly (in approximately 3 weeks) induced a myeloproliferative disease (MPD) resembling human CML, while v-Abl rapidly (in approximately 4 weeks) induced B-ALL along with a minor expansion of v-Abl-infected myeloid cells. It has long been shown that the Abl carboxyl terminal region is required for the lymphoid cell transformation by v-Abl both in vivo and in vitro. We decided to investigate the role of the Abl carboxyl terminal region in BCR/ABL- and v-Abl-leukemogenesis using the mouse bone marrow transduction and transplantation model. We found that the Abl carboxyl terminal region is required for v-Abl-induced B-ALL, as expected. But, interestingly, v-Abl without C-terminus (v-Abl/p160/ΔC) induced a MPD in mice, similar to that induced by BCR/ABL, with a relative long latency (approximately 3 months in average). On the other hand, BCR/ABLΔC still induced MPD efficiently, similar as wild type BCR/ABL. These results demonstrated the Abl carboxyl terminal region is required for the induction of acute lymphoblastic leukemia by v-Abl but not for the induction of MPD by BCR/ABL or v-Abl. The results also suggested that v-Abl has a capacity to induce MPD, albeit much weaker than that of BCR/ABL and much weaker than v-Abl’s capacity to induce B-ALL. The role of the ABL carboxyl terminal region in BCR/ABL-induced B-ALL and the mechanism by which the Abl carboxyl terminal region contributes to the lineage-specific transformation are under investigation. Such research will shed lights into the mechanism of lineage-specific leukemogenesis and help to identify therapeutic targets for lymphoid malignancies.