© 2015 Springer International Publishing Switzerland Although it is well established that heat conduction in unsaturated soil depends on liquid saturation, there are several models available to consider the changes in thermal conductivity during drying and wetting. The key factors affecting thermal conductivity of unsaturated soil are evaluated through a critical examination of these different models and their development. Depending on the principles and assumptions employed, these models are categorized into three groups: mixing models involving series/parallel elements; empirical models where thermal conductivity values at dry and saturated states are used; and mathematical models based on phase volume fractions. Experimental data for different soils are used to assess the quality of prediction for these models. It is found that all the existing models do not realistically account for pore structure or interface properties, and thus are not capable of properly predicting thermal conductivity as a function of liquid saturation. A conceptual model based on soil–water retention mechanisms, is proposed to overcome the pitfalls of the existing models and can be used to establish quantitative thermal conductivity models for variably saturated soils in the future.

Signaling through IL-2/IL-15Rβ (CD122) is essential for the differentiation and function of T cells and NK cells. A mAb against CD122 has been implicated to suppress autoimmune type 1 diabetes (T1D) development in animal models. However, the mechanisms remain poorly understood. We find that in vivo administration of an anti-CD122 mAb (CD122 blockade) restores immune tolerance in nonobese diabetic (NOD) mice via multiple mechanisms. First, CD122 blockade selectively ablates pathogenic NK cells and memory phenotype CD8+ T cells from pancreatic islets. In contrast, islet CD4+Foxp3+ Tregs are only mildly affected. Second, CD122 blockade suppresses IFN-γ production in islet immune cells. Third, CD122 blockade inhibits the conversion of islet Th17 cells into diabetogenic Th1 cells. Furthermore, a combination of anti-CD122 mAb and Treg-trophic cytokines (IL-2 or IL-33) enhances the abundance and function of islet Tregs. In summary, these data provide crucial mechanistic insights into CD122 blockade-mediated immunoregulation and support therapeutic benefits of this combinational treatment in T1D.

The Liver Imaging Reporting and Data System (LI-RADS) was created to standardize liver imaging in patients at high risk for hepatocellular carcinoma (HCC), and it uses a diagnostic algorithm to assign categories that reflect the relative probability of HCC, non-HCC malignancies, or benign focal liver lesions. In addition to major imaging features, ancillary features (AFs) are used by radiologists to refine the categorization of liver nodules. In the present document, we discuss and explain the application of AFs currently defined within the LI-RADS guidelines. We also explore possible additional AFs visible on contrast-enhanced ultrasonography (CEUS). Finally, we summarize the management of CEUS LI-RADS features, including the role of current and potential future AFs.

How tissue-resident macrophages (TRM) impact adaptive immune responses remains poorly understood. We report novel mechanisms by which TRMs regulate T cell activities at tissue sites. These mechanisms are mediated by the complement receptor of immunoglobulin family (CRIg). Using animal models for autoimmune type 1 diabetes (T1D), we found that CRIg⁺ TRMs formed a protective barrier surrounding pancreatic islets. Genetic ablation of CRIg exacerbated islet inflammation and local T cell activation. CRIg exhibited a dual function of attenuating early T cell activation and promoting the differentiation of Foxp3⁺ regulatory (Treg) cells. More importantly, CRIg stabilized the expression of Foxp3 in Treg cells, by enhancing their responsiveness to interleukin-2. The expression of CRIg in TRMs was postnatally regulated by gut microbial signals and metabolites. Thus, environmental cues instruct TRMs to express CRIg, which functions as an immune checkpoint molecule to regulate adaptive immunity and promote immune tolerance.

OBJECTIVE: To study the prevalence of extraglandular manifestations in primary Sjögrens syndrome (SS) among participants enrolled in the Sjögrens International Collaborative Clinical Alliance (SICCA) Registry. METHODS: A total of 1,927 participants in the SICCA registry were studied, including 886 participants who met the 2002 American-European Consensus Group (AECG) criteria for primary SS, 830 intermediate cases who had some objective findings of primary SS but did not meet AECG criteria, and 211 control individuals. We studied the prevalence of immunologic and hematologic laboratory abnormalities, specific rheumatologic examination findings, and physician-confirmed thyroid, liver, and kidney disease, as well as lymphoma among SICCA participants. RESULTS: Laboratory abnormalities, including hematologic abnormalities, hypergammaglobulinemia, and hypocomplementemia, frequently occurred among primary SS cases and were more common among the intermediate cases than among control participants. Cutaneous vasculitis and lymphadenopathy were also more common among primary SS cases. In contrast, the frequency of physician-confirmed diagnoses of thyroid, liver, and kidney disease and lymphoma was low and only primary biliary cirrhosis was associated with primary SS case status. Rheumatologic and neurologic symptoms were common among all SICCA participants, regardless of case status. CONCLUSION: Data from the international SICCA registry support the systemic nature of primary SS, manifested primarily in terms of specific immunologic and hematologic abnormalities. The occurrence of other systemic disorders among this cohort is relatively uncommon. Previously reported associations may be more specific to select patient subgroups, such as those referred for evaluation of certain neurologic, rheumatologic, or other systemic manifestations.