Heparin Decreases in Tumor Necrosis Factor α (TNFα)-induced Endothelial Stress Responses Require Transmembrane Protein 184A and Induction of Dual Specificity Phosphatase 1.

Despite the large number of heparin and heparan sulfate binding proteins, the molecular mechanism(s) by which heparin alters vascular cell physiology is not well understood. Studies with vascular smooth muscle cells (VSMCs) indicate a role for induction of dual specificity phosphatase 1 (DUSP1) that decreases ERK activity and results in decreased cell proliferation, which depends on specific heparin binding. The hypothesis that unfractionated heparin functions to decrease inflammatory signal transduction in endothelial cells (ECs) through heparin-induced expression of DUSP1 was tested.

Homicide by poisoning.

By studying the number and method of homicidal poisoning in Miami-Dade County, Florida; New York City, NY; Oakland County, Michigan; and Sweden, we have confirmed that this is an infrequently established crime.Several difficulties come with the detection of homicidal poisonings. Presenting symptoms and signs are often misdiagnosed as natural disease, especially if the crime is committed in a hospital environment, suggesting that an unknown number of homicides go undetected.

Evaluation of postmortem serum and cerebrospinal fluid levels of thyroid-stimulating hormone with special regard to fatal hypothermia.

The aim of the present study was to undertake, during routine forensic work, a comprehensive analysis of the serum and cerebrospinal fluid (CSF) levels of thyroid-stimulating hormone (TSH) and to examine hypophyseal TSH immunopositivity in relation to the cause of death, with particular regard to fatal hypothermia. Medicolegal autopsy cases (n=120; within 48 h postmortem; survival time, <24 h), including cases of blunt injury (n=9), sharp instrument injury (n=8), fire fatality (n=18), mechanical asphyxiation (n=10), drowning (n=21), poisoning (n=6), hypothermia (n=10), and acute ischemic heart disease (n=38), were examined. Serum and CSF TSH concentrations were measured using an electrochemiluminescence immunoassay.

Postmortem biochemistry and immunohistochemistry of adrenocorticotropic hormone with special regard to fatal hypothermia.

Adrenocorticotropic hormone (ACTH) is involved in systemic reactions to stress. The aim of the present study was a comprehensive analysis of serum and cerebrospinal fluid (CSF) levels of ACTH, and the pituitary immunohistochemistry with special regard to fatal hypothermia in routine forensic autopsy cases (n=162: 5-97 years of age; 114 males and 48 females; 4 h to 3 days postmortem, median, 19.2 h).

Comparative evaluation of postmortem serum concentrations of neopterin and C-reactive protein.

The cellular immune response is accompanied by the release of neopterin. The level of neopterin in serum is increased in patients suffering from viral infections, autoimmune diseases, systemic inflammation, allograft rejection and malignant diseases, while that of C-reactive protein (CRP) is known to rise during inflammatory diseases and traumas. To investigate postmortem neopterin and CRP concentrations with regard to the cause of death, we examined cardiac and peripheral blood samples in 474 autopsy cases without advanced decomposition (0-96 years of age, 343 males and 131 females), 2.

Active stress kinases in proliferating endothelial cells associated with cytoskeletal structures.

It has become increasingly clear that stress-activated protein kinases have cytoplasmic substrates in addition to well-established transcription factor substrates in cell nuclei. The present study documented specific cytoplasmic locations of these enzymes in proliferating vascular cells. Immunofluorescent staining for active c-jun NH2-terminal kinase (JNK), the precipitation of JNK with microfilaments, and the loss of fiber-associated active JNK after cytochalasin treatment, but not nocodazole treatment, together indicate that active JNK is associated with stress fibers.