Flagellin is a subunit protein of the flagellum, a whip-like appendage that enables bacterial motility. Traditionally, flagellin was viewed as a virulence factor that contributes to the adhesion and invasion of host cells, but now it has emerged as a potent immune activator, shaping both the innate and adaptive arms of immunity during microbial infections. In this review, we summarize our understanding of bacterial flagellin and host immune system interactions and the role flagellin as an adjuvant, anti-tumor and radioprotective agent, and we address important areas of future research interests.

Background: Hashimoto's thyroiditis (HT) has been found to coexist with differentiated thyroid cancer (DTC) in surgical specimens, but an association between the two conditions has been discounted by the medical literature. Therefore, we performed this study to determine any potential relationship between HT and the risk of developing DTC. Methods: We collected data for thyrotropin (TSH), thyroxine (T 4 ), thyroid peroxidase antibody (TPO-Ab) titers, surgical pathology, and weight-based levothyroxine (LT 4 ) replacement dose for patients who were referred for thyroid surgery. Patients with HT at final pathology were studied further. To estimate thyroid function, patients with preoperative hypothyroid HT (Hypo-HT) were divided into three equal groups based on their LT 4 replacement: LT 4 -Low (<0.90 lg/kg), LT 4 -Mid (0.90-1.43 lg/kg), and LT 4 -High (>1.43 lg/kg). A group of preoperatively euthyroid (Euth-HT) patients but with HT by pathology was also studied. All subjects were also grouped based on their TPO-Ab titer in TPO-high (titer >1:1000) or TPO-low/negative (titer <1:1000 or undetectable) groups. The relationship of HT and DTC was studied extensively. Results: Of 2811 subjects, 582 had HT on surgical pathology, 365 of whom were Euth-HT preoperatively. DTC was present in 47.9% of the Euth-HT, in 59.7% of LT 4 -Low, 29.8% of LT 4 -Mid, and 27.9% of LT 4 -High groups. The relative risk (RR) for DTC was significantly elevated for the Euth-HT and LT 4 -Low groups ( p < 0.001), but not for the LT 4 -Mid or LT 4 -High replacement dose groups. TPO-low/negative status conferred an increased RR in the Euth-HT and LT 4 -Low replacement dose groups ( p < 0.001 both), while TPO-high status decreased it in Euth-HT group ( p < 0.05) and made it nonsignificant in the LT 4 -Low group. Conclusions: HT pathology increases the risk for DTC only in euthyroid subjects and those with partially functional thyroid glands (LT 4 -Low) but not in fully hypothyroid HT (LT 4 -Mid and LT 4 -High). High TPO-Ab titers appear to protect against DTC in patients with HT.

Compressed sensing (CS) is a mathematical framework that reconstructs data from highly undersampled measurements. To gain acceleration in acquisition time, CS has been applied to MRI and has been demonstrated on diverse MRI methods. This review discusses the important requirements to qualify MRI to become an optimal application of CS, namely, sparsity, pseudo-random undersampling, and nonlinear reconstruction. By utilizing concepts of transform sparsity and compression, CS allows acquisition of only the important coefficients of the signal during the acquisition. A priori knowledge of MR images specifically related to transform sparsity is required for the application of CS. In this paper, Section I introduces the fundamentals of CS and the idea of CS as applied to MRI. The requirements for application of CS to MRI is discussed in Section II, while the various acquisition techniques, reconstruction techniques, the advantages of combining CS and parallel imaging, and sampling mask design problems are discussed in Section III. Numerous applications of CS in MRI due to its ability to improve imaging speed are reviewed in section IV. Clinical evaluations of some of the CS applications recently published are discussed in Section V. Section VI provides information on available open source software that could be used for CS implementations.

Thyroid cancer is usually surrounded by a significant number of immune reactive cells. Tumor associated lymphocytes as well as background lymphocytic thyroiditis is frequently mentioned in pathology reports of patients operated for thyroid cancer. The nature of this lymphocytic reaction in not well understood. Evidently, the fact that cancer can survive in this adverse microenvironment speaks for immune regulation. We characterized the lymphocytic infiltration that accompanies thyroid cancer and compared it to that present in thyroid autoimmunity. We found that double-negative (DN) T cells were significantly more abundant in thyroid cancer than in thyroid autoimmunity. Although FOXP3+ Tregs were also present, DN T cells were the dominant cell type associated with thyroid cancer. Furthermore, upon stimulation, the DN T cells associated with cancer remained unchanged while the few (<5%) DN T cells associated with thyroid autoimmunity increased in numbers (>20%). CD25 expression on DN T cells remained unchanged after stimulation which suggests that the increase in the absolute number of DN T cells in thyroid autoimmunity was at the expense of inactivation of single positive T cells. We concluded that in the setting of thyroid cancer, DN T cells appear to suppress tumor immunity. In contrast, in thyroid autoimmunity, DN T cells were barely present and only increased at the expense of inactivated, single positive T cells upon induction. Together, these findings suggest that thyroid cancer associated DN T cells might regulate proliferation and effector function of T cells and thereby contribute to tumor tolerance and active avoidance of tumor immunity.

Progesterone and luteal blood flow effects of an i.u. 2-h infusion of 0.25 mg/h of prostaglandin F 2a (PGF) that simulated a natural pulse of 13,14-dihydro-15-keto-PGF (PGFM) were compared to the effects of a single bolus i.u. injection of PGF (4 mg) that induced complete luteolysis in heifers. Blood sampling and an estimate of the percentage of luteal area with colour-Doppler signals of blood flow were performed every 2 min for 20 min and less frequently thereafter for 6 h. After the beginning of PGF infusion or a bolus injection, progesterone increased to a peak at 14 and 10 min respectively, and was accompanied by an increase in blood flow in the bolus group but not in the infusion group. Progesterone then decreased for 1 or 2 h and was accompanied by a continued elevation in blood flow in the PGF bolus group and by a slight increase in the PGF infusion group. Progesterone then rebounded in both groups, but the rebound was greater in the infusion group. Blood flow decreased during the descending arm of the progesterone rebound. Cortisol and prolactin began to increase 6 min after the bolus PGF injection but did not increase during or after PGF infusion. The increases in cortisol, prolactin and blood flow after a PGF bolus treatment but not during a simulated PGFM pulse indicated that the bolus treatment was pharmacologic, and its use may lead to faulty conclusions on the nature of physiologic luteolysis. The comparisons between progesterone and blood flow are novel.