Characterization of pharmaceuticals, personal care products, and polybrominated diphenyl ethers in lake sturgeon serum and gametes.

Recent research suggests contaminants of emerging concern (CECs) are widespread and environmentally relevant concentrations can impact fishes. However, little is known about impacts of CECs to long-lived or rare species. The objective of this study was to characterize CEC concentrations in lake sturgeon (Acipenser fulvescens) serum and gametes. Blood serum was collected non-lethally from lake sturgeon at four lower Great Lakes basin sites: Detroit, upper Niagara, lower Niagara, and St. Lawrence rivers; additionally, gametes were collected from lake sturgeon in the St. Lawrence River. Samples were analyzed for pharmaceuticals and personal care products (PPCPs) and polybrominated diphenyl ethers (PBDEs). Overall, 44 different PPCPs were identified in serum and gamete samples across sites, with 22 PPCPs identified in at least 25% of serum samples and three PPCPs identified in 25% of gamete samples. PPCP concentrations in serum and gametes ranged from 0.00208 to 130 ppb and 0.00538-190 ppb, respectively. NMDS ordination revealed differences in the presence and concentrations of PPCPs in lake sturgeon serum across sites, however, N,N-diethyl-meta-toluamide (DEET), hydrocortisone, benztropine, and amitriptyline were detected in at least one serum sample at all sites. Additionally, DEET, 10-hydroxy-amitriptyline, and sertraline were detected in ≥25% of gamete samples collected from the St. Lawrence River. Twenty-six PBDE congeners were identified in 25% of serum samples and 24 were identified in 25% of gamete samples. PBDEs in serum were present across all sites and in gametes of St. Lawrence River lake sturgeon, and total PBDE concentrations in serum and gametes ranged from 0.184 to 12.7 ppb and 0.0826-0.44 ppb, respectively. Managers of lake sturgeon populations may need to consider the impacts of CECs if reproductive, developmental, behavioral, growth effects, or mortality are observed in the Great Lakes basin or other areas that are impacted by increased exposures to PPCPs and PBDEs.

Death due to apparent intravenous injection of tapentadol.

This case report describes a 34-year-old male who died as the result of tapentadol toxicity. This case apparently represents the first reported description of a death because of this drug. The toxicologic features of this case, namely concentrations of tapentadol in the femoral blood and heart blood, 1.05 and 3.20 mg/L, respectively, may assist other individuals in evaluating deaths where tapentadol concentration is a factor. Analysis of the blood based upon enzyme-linked immunosorbent assays, liquid chromatography-mass spectrometry, and gas chromatography-mass spectrometry revealed no other substance of significance, only nicotine and cotinine, and the autopsy findings were consistent with an opiate-type drug overdose, and indicated no competing cause of death.

In vitro effects of enamel matrix derivative on microvascular cells.

BACKGROUND: Periodontal regeneration requires a coordinated series of events that includes not only the recruitment of periodontal ligament (PDL)-specific cells, but vascular cells as well. The mechanisms of action of enamel matrix derivative (EMD) are poorly understood, and its effects on vascular cells are unknown. The objective of this study was to examine the extent to which EMD affects angiogenesis and PDL cell recruitment. METHODS: The effects of EMD on human microvascular endothelial cells (HMVECs) were determined by examining proliferation, chemotaxis, angiogenesis, and migration. Proliferation was determined using water-soluble tetrazolium salt (WST)-1 reagent. Chemotaxis was determined using microporous-culture well inserts. Angiogenesis was assessed on plates containing matrigel. The effects of HMVECs on the migration of PDL cells were assessed by evaluating PDL cell outgrowth from collagen gels cultured in the presence of HMVECs on fibrin matrix and surrounded by fibronectin-containing fibrin clots at 24 hours. Effects of EMD on PDL expression of vascular endothelial cell (VEGF) types (A, B, C, and D) and isoforms were determined using reverse transcription-polymerase chain reaction (RT-PCR). Production of VEGF, platelet-derived growth factor (PDGF)-AA, PDGF-BB, PDGF-AB, and transforming growth factor (TGF)-beta1 by EMD-stimulated PDL cells was assessed quantitatively in conditioned media using specific enzyme-linked immunosorbent assays (ELISAs). RESULTS: EMD at concentrations <50 microg/ml resulted in significant (P <0.05) stimulation of HMVEC proliferation. Compared to baseline, EMD also stimulated a 100% increase in HMVEC chemotaxis when PDL cells were present (P <0.05). All doses of EMD tested (25, 50, and 100 microg/ml) increased angiogenesis in vitro. HMVECs, in combination with EMD at a concentration of 100 microg/ml, stimulated a 750% increase in migration of PDL cells from collagen gels into fibrin clots compared to controls when neither was present. RT-PCR results indicated that PDL cells expressed VEGF-A, -B, and -C and multiple isoforms of VEGF-A, including VEGF(121), VEGF(165), and VEGF(189), whether or not EMD was present in the culture media. ELISAs determined a 400% increase in VEGF concentration by PDL C cells in EMD-stimulated conditioned media and a similar increase in TGF-beta(1)-stimulated media. CONCLUSIONS: It is likely that EMD stimulates angiogenesis directly by stimulating endothelial cells and indirectly by stimulating the production of angiogenic factors (VEGF) by PDL cells. Importantly, the data are consistent with the concept that EMD enhances bidirectional communication between HMVEC and PDL cells during angiogenesis associated with healing.