Single-Bit, Self-Powered Digital Counter Using a Wiegand Sensor for Rotary Applications.

This work explores energy harvesting from rotary motion using a Wiegand sensor, which is a magnetic sensor that induces a voltage pulse when the magnetization is reversed. The main feature of the Wiegand sensor is that a pulse is generated regardless of how slowly magnetism reversal occurs. Self-sustained sensors play major roles in advancing the Internet of Things (IoT) and wireless sensor networks (WSN). In this study, we identified a linear relationship between rotational motion, magnetic field reversal, and the rotational frequency generated by the Wiegand sensor. In addition, the maximum energy per pulse and its dependence were derived analytically. A maximum energy of 130 nJ per pulse was reported for the sensor used. We developed a single-bit, self-powered digital counter that was sufficiently driven with 38 nJ of energy. In this study, single rotations were measured without the need for external power.

A primary cardiac sarcoma presenting with superior vena cava obstruction.

Superior vena cava (SVC) obstruction leads to a constellation of symptoms and signs that encompass the SVC syndrome. Today, malignancy accounts for 65% of all cases. The most common neoplastic causes are non­small cell lung cancer (50%), small cell lung cancer (25%), lymphoma, and metastasis. Primary cardiac tumors are an extremely rare cause of SVC obstruction. We describe the case of a 48-year-old man who presented with dyspnea, confusion, and facial swelling with cyanosis. The patient developed life-threatening airway obstruction after administration of anxiolytic. The diagnosis of SVC obstruction secondary to a primary cardiac sarcoma was established based on clinical, radiologic, and post-mortem findings. This is one of very few reported cases of a primary cardiac sarcoma causing SVC obstruction.

Expression and function of mixed lineage kinases in dendritic cells.

Dendritic cells (DCs) sense the presence of conserved microbial structures in their local microenvironment via specific pattern recognition receptors (PRRs). This leads to a programme of changes, which include migration and activation, and enables them to induce adaptive T cell immunity. Mitogen-activated protein kinases (MAPKs) are implicated in this response, but the pathways leading from PRR ligation to MAPK activation, and hence DC activation, are not fully understood. Recent studies in the nervous system have suggested that the mixed lineage kinase (MLK) family of MAPK kinase kinase proteins may be involved as an intermediary step between PRRs and MAPKs. Therefore, in this study, we have used a well-established DC model to explore the role of MLKs in these cells. Messenger RNA for MLKs 2, 3, 4 and DLK and protein for MLKs 2, 3 and DLK are found in DC. DC activation in response to model PRR ligands, such as LPS or poly (I:C), is accompanied by phosphorylation of MLK3. In contrast, another known PRR ligand, zymosan, induces little MLK3 phosphorylation. Inhibition of MLK activity using a pharmacological inhibitor, CEP11004, blocks p38 and Jun N-terminal kinase (JNK) MAPK activation in response to LPS and poly (I:C), but not zymosan. The inhibition is associated with a block in DC activation as measured by cell-surface marker expression and cytokine secretion. Thus, MLKs are expressed in DC, and are implicated in DC activation, and the involvement of MLKs appears to be selective, depending on the nature of the DC stimulus.

JNK activation limits dendritic cell maturation in response to reactive oxygen species by the induction of apoptosis.

Dendritic cells (DC) sense infection in their local microenvironment and respond appropriately in order to induce T cell immunity. This response is mediated in part via the mitogen-activated protein kinase (MAPK) pathways. Hydrogen peroxide is present frequently in the inflammatory DC milieu and is known to activate MAPK. Therefore this study examines the role of hydrogen peroxide, both alone and in combination with lipopolysaccharide (LPS), in the regulation of activation of two key MAPK, p38 and JNK, regulation of phenotype, and regulation of apoptosis in human monocyte-derived DC. At low concentrations, hydrogen peroxide activates p38, but does not alter DC phenotype. At higher concentrations, hydrogen peroxide activates both p38 and JNK. Activation of JNK, which is associated with inhibition of tyrosine phosphatases in DC, is linked to the induction of DC apoptosis. An upstream JNK inhibitor (CEP11004) and a competitive JNK inhibitor (SP600125) both partially protected the DC from the proapoptotic effects of hydrogen peroxide. Unexpectedly, hydrogen peroxide and LPS synergize in inducing JNK activation and DC apoptosis. JNK-mediated apoptosis may limit damaging immune responses against neoepitopes generated by modification of self-antigens by reactive oxygen species present at sites of inflammation.