Statewide Evaluation of the California Medical Supervision Program Using Cholinesterase Electronic Laboratory Reporting Data: An Update.

The California Medical Supervision Program is designed to protect agricultural workers from overexposure to Toxicity Category I and II organophosphate (OP) and carbamate (CB) pesticides by routinely monitoring their blood cholinesterase (ChE) activity levels. ChE testing is conducted at State-approved laboratories and electronically reported to the Department of Pesticide Regulation (DPR) and the Office of Environmental Health Hazard Assessment (OEHHA) for review. In 2015, OEHHA and DPR evaluated the effectiveness of the Program by analyzing ChE data from pesticide handlers performed between 2011 and 2013, which revealed issues with the data quality that hindered the evaluation process.

Assessment of the in vitro toxicity of the disinfection byproduct 2,6-dichloro-1,4-benzoquinone and its transformed derivatives.

An emerging class of unregulated disinfection byproducts, halobenzoquinones (HBQs), has gained recent interest following suggestions of enhanced toxicity compared to regulated disinfection byproducts. While the kinetics of HBQ hydrolysis in water have been well characterized, the stability of HBQs in cell culture media, a critical parameter when evaluating toxicity in vitro, has been overlooked. The objective of this study was: (1) to contrast the stability of a prevalent HBQ, 2,6-dichloro-1,4-benzoquinone (DCBQ), in cell culture media and water, and (2) to evaluate the cytotoxicity of parent and transformed DCBQ compounds as well as the ability of these compounds to generate intracellular reactive oxygen species (ROS) in normal human colon cells (CCD 841 CoN) and human liver cancer cells (HepG2).

Developmental Exposure to 2,2',4,4'-Tetrabromodiphenyl Ether Permanently Alters Blood-Liver Balance of Lipids in Male Mice.

Polybrominated diphenyl ethers (PBDEs) were used as flame-retardant additives starting 1965 and were recently withdrawn from commerce in North America and Europe. Approximately 1/5 of the total U.S.

Does Axillary Reverse Mapping Prevent Lymphedema After Lymphadenectomy?

Background: We hypothesized that disconcerting lymphedema rates in both sentinel lymph node biopsy (SLNB) and axillary lymph node dissection (ALND) may be because of unrecognized vunerable variations in arm lymphatic drainage within the axilla. Axillary reverse mapping (ARM) facilitates identification and avoidance of arm lymphatics within the axilla and its use may reduce lymphedema.

Methods: This institutional review board-approved study from June 2007 to December 2013 involved patients undergoing SLNB with or without ALND, or ALND alone.

Cathepsin L acutely alters microvessel integrity within the neurovascular unit during focal cerebral ischemia.

During focal cerebral ischemia, the degradation of microvessel basal lamina matrix occurs acutely and is associated with edema formation and microhemorrhage. These events have been attributed to matrix metalloproteinases (MMPs). However, both known protease generation and ligand specificities suggest other participants.

Management of Pneumatosis Intestinalis in a Pediatric Burn Patient.

Pneumatosis intestinalis is gas in the wall of the gastrointestinal tract. It is not well described in pediatric burn patients. The authors present the case of a 23-month-old girl who sustained 40% total body surface area deep-partial and full-thickness burns as well as a grade two inhalational injury.

Increased expression of fibronectin and the alpha 5 beta 1 integrin in angiogenic cerebral blood vessels of mice subject to hypobaric hypoxia.

The extracellular matrix (ECM) is an important regulator of angiogenesis and vascular remodeling. We showed previously that angiogenic capillaries in the developing CNS express high levels of fibronectin and its receptor alpha5beta1 integrin, and that this expression is developmentally downregulated. As cerebral hypoxia leads to an angiogenic response, we sought to determine whether angiogenic vessels in the adult CNS re-express fibronectin and the alpha5beta1 integrin.

Responses of endothelial cell and astrocyte matrix-integrin receptors to ischemia mimic those observed in the neurovascular unit.

Background And Purpose: Apposition of endothelial cells and astrocyte foot processes to the basal lamina matrix is postulated to underlie the cerebral microvessel permeability barrier. Focal cerebral ischemia induces rapid loss of select matrix-binding integrins from both cell compartments in the nonhuman primate. This study is the first to examine the conditions underlying integrin loss from these cell-types during ischemia in vitro and their relation to the changes in vivo.

The rapid decrease in astrocyte-associated dystroglycan expression by focal cerebral ischemia is protease-dependent.

During focal cerebral ischemia, the detachment of astrocytes from the microvascular basal lamina is not completely explained by known integrin receptor expression changes. Here, the impact of experimental ischemia (oxygen-glucose deprivation (OGD)) on dystroglycan expression by murine endothelial cells and astrocytes grown on vascular matrix laminin, perlecan, or collagen and the impact of middle cerebral artery occlusion on alphabeta-dystroglycan within cerebral microvessels of the nonhuman primate were examined. Dystroglycan was expressed on all cerebral microvessels in cortical gray and white matter, and the striatum.

Fibronectin- and vitronectin-induced microglial activation and matrix metalloproteinase-9 expression is mediated by integrins alpha5beta1 and alphavbeta5.

Early in the pathogenesis of multiple sclerosis, the blood-brain barrier is compromised, which leads to deposition of the plasma proteins fibronectin and vitronectin in cerebral parenchyma. In light of our previous finding that microglial activation in vitro is strongly promoted by fibronectin and vitronectin, we set out to examine the possibility that modulation of microglial activation by fibronectin or vitronectin is an important regulatory mechanism in vivo. In an experimental autoimmune encephalomyelitis mouse model of demyelination, total brain levels of fibronectin and vitronectin were strongly increased and there was a close relationship between fibronectin and vitronectin deposition, microglial activation, and microglial expression of matrix metalloproteinase-9.

Microglial activation and matrix protease generation during focal cerebral ischemia.

Local environmental conditions contribute to the activation state of cells. Extracellular matrix glycoproteins participate in cell-cell boundaries within the microvascular and extravascular tissues of the central nervous system and provide a scaffold for the local environment. These conditions are altered during focal cerebral ischemia (and other central nervous system disorders) when extracellular matrix boundaries are degraded or when matrix proteins in the vascular circulation enter the neuropil as the microvascular permeability barrier is degraded.

Systemic priming-boosting immunization with a trivalent plasmid DNA and inactivated murine cytomegalovirus (MCMV) vaccine provides long-term protection against viral replication following systemic or mucosal MCMV challenge.

We previously demonstrated that vaccination of BALB/c mice with a pool of 13 plasmid DNAs (pDNAs) expressing murine cytomegalovirus (MCMV) genes followed by formalin-inactivated MCMV (FI-MCMV) resulted in complete protection against viral replication in the spleen and salivary glands following sublethal intraperitoneal (i.p.) challenge.