Polycyclic aromatic hydrocarbons (PAHs) are prevalent pollutants in the aquatic environment that can cause a wide range of toxic effects. Earlier studies have shown that toxicity of PAHs can be enhanced by ultraviolet (UV) radiation. In situ and laboratory exposures with Ceriodaphnia dubia were used to evaluate photoinduced toxicity of PAHs in wet-weather runoff and in turbid conditions. Exposure to UV increased the toxicity of PAH-contaminated sediment to C. dubia. Toxicity was removed when UV wavelengths did not penetrate the water column to the exposed organisms. A significant correlation was observed between in situ C. dubia survival and turbidity when organisms were exposed to sunlight. Stormwater runoff samples exhibited an increase in chronic toxicity (reproduction) to C. dubia when exposed to UV wavelengths as compared to C. dubia not exposed to UV wavelengths. Toxicity was reduced significantly in the presence of UV radiation when the organic fraction of stormwater runoff was removed. The PAHs are bound to the sediment and resuspended into the water column once the sediment is disturbed (e.g., during a storm). The in situ and laboratory results showed that photoinduced toxicity occurred frequently during low flow conditions and wet weather runoff and was reduced in turbid conditions.
The objective of this study was to evaluate the toxicity of sediments from the Grand Calumet River and Indiana Harbor Canal located in northwestern Indiana, USA. Toxicity tests used in this assessment included 10-day sediment exposures with the amphipod Hyalella azteca, 31-day sediment exposures with the oligochaete Lumbriculus variegatus, and the Microtox Solid-Phase Sediment Toxicity Test. A total of 30 sampling stations were selected in locations that had limited historic matching toxicity and chemistry data. Toxic effects on amphipod survival were observed in 60% of the samples from the assessment area. Results of a toxicity test with oligochaetes indicated that sediments from the assessment area were too toxic to be used in proposed bioaccumulation testing. Measurement of amphipod length after the 10-day exposures did not provide useful information beyond that provided by the survival endpoint. Seven of the 15 samples that were identified as toxic in the amphipod tests were not identified as toxic in the Microtox test, indicating that the 10-day H. azteca test was more sensitive than the Microtox test. Samples that were toxic tended to have the highest concentrations of metals, polycyclic aromatic hydrocarbons (PAHs), and polychlorinated biphenyls (PCBs). The toxic samples often had an excess of simultaneously extracted metals (SEM) relative to acid volatile sulfide (AVS) and had multiple exceedances of probable effect concentrations (PECs). Metals may have contributed to the toxicity of samples that had both an excess molar concentration of SEM relative to AVS and elevated concentrations of metals in pore water. However, of the samples that had an excess of SEM relative to AVS, only 38% of these samples had elevated concentration of metals in pore water. The lack of correspondence between SEM-AVS and pore water metals indicates that there are variables in addition to AVS controlling the concentrations of metals in pore water. A mean PEC quotient of 3.4 (based on concentrations of metals, PAHs, and PCBs) was exceeded in 33% of the sediment samples and a mean quotient of 0.63 was exceeded in 70% of the thirty sediment samples from the assessment area. A 50% incidence of toxicity has been previously reported in a database for sediment tests with H. azteca at a mean quotient of 3.4 in 10-day exposures and at a mean quotient of 0.63 in 28-day exposures. Among the Indiana Harbor samples, most of the samples with a mean PEC quotient above 0.63 ( i.e., 15 of 21; 71%) and above 3.4 ( i.e., 10 of 10; 100%) were toxic to amphipods. Results of this study and previous studies demonstrate that sediments from this assessment area are among the most contaminated and toxic that have ever been reported.
Purpose of Review Compressive neuropathy of the ulnar nerve across the elbow is a common diagnosis encountered frequently within a hand and upper extremity clinical practice. Appropriate and timely evaluation, diagnosis, objective testing, and evidence-based decisions regarding treatment options are paramount in the optimal care of the patient with this pathology. An understanding of current literature is critical in determining and understanding best practices. Recent Findings A thorough review of the recent literature regarding physical examination, diagnostic testing, and nonoperative versus operative results was performed. Regarding physical examination, the glenohumeral internal rotation test and scratch collapse test are more effective and sensitive than traditional maneuvers such as Tinel's testing and the elbow flexion test. Electrodiagnostic testing, magnetic resonance imaging, and ultrasound evaluation have all been shown to be effective in diagnosing cubital tunnel syndrome. However, no single test has proven itself to be superior. Nonoperative treatment can be successful for mild cases of cubital tunnel syndrome. Surgical release techniques comparing open with endoscopic release are equivocal, and in situ release versus transposition techniques show that transposition should not be performed routinely. Summary The diagnosis and treatment of cubital tunnel syndrome do not have a well-defined algorithm based on current literature. The treating physician must therefore utilize the available information to determine a diagnostic and treatment plan individualized to the patient. More rigorous scientific studies are needed to determine the most effective surgical approaches for cubital tunnel syndrome. Keywords Cubital tunnel syndrome . Ulnar neuropathy . Ulnar nerve compression . Ulnar nerve transposition . Cubital tunnel release . In situ decompression This article is part of the Topical Collection on Compressive Neuropathies in the Upper Extremity
In response to noxious stimuli, planarians cease their typical ciliary gliding and exhibit an oscillatory type of locomotion called scrunching. We have previously characterized the biomechanics of scrunching and shown that it is induced by specific stimuli, such as amputation, noxious heat, and extreme pH. Because these specific inducers are known to activate Transient Receptor Potential (TRP) channels in other systems, we hypothesized that TRP channels control scrunching. We found that chemicals known to activate TRPA1 (allyl isothiocyanate (AITC) and hydrogen peroxide) and TRPV (capsaicin and anandamide) in other systems induce scrunching in the planarian species Dugesia japonica and, except for anandamide, in Schmidtea mediterranea. To confirm that these responses were specific to either TRPA1 or TRPV, respectively, we tried to block scrunching using selective TRPA1 or TRPV antagonists and RNA interference (RNAi) mediated knockdown. Unexpectedly, co-treatment with a mammalian TRPA1 antagonist, HC-030031, enhanced AITC-induced scrunching by decreasing the latency time, suggesting an agonistic relationship in planarians. We further confirmed that TRPA1 in both planarian species is necessary for AITC-induced scrunching using RNAi. Conversely, while co-treatment of a mammalian TRPV antagonist, SB-366791, also enhanced capsaicin-induced reactions in D. japonica, combined knockdown of two previously identified D. japonica TRPV genes (DjTRPVa and DjTRPVb) did not inhibit capsaicin-induced scrunching. RNAi of DjTRPVa/DjTRPVb attenuated scrunching induced by the endocannabinoid and TRPV agonist, anandamide. Overall, our results show that although scrunching induction can involve different initial pathways for sensing stimuli, this behavior’s signature dynamical features are independent of the inducer, implying that scrunching is a stereotypical planarian escape behavior in response to various noxious stimuli that converge on a single downstream pathway. Understanding which aspects of nociception are conserved or not across different organisms can provide insight into the underlying regulatory mechanisms to better understand pain sensation.
Supplementary Table 1. Lowest effect levels (LELs) in µM for each chemical before and after applying the biological relevancy cutoffs and inter-plate inconsistency checks in adult and regenerating planarians. The originial LELs were determined based on the statistically significant hits at each endpoint. The final LELs were based on the statistically and biologically significant hits (with biological relevance cutoffs and inconsistency check applied; see Methods and Zhang et al., 2018). The dash "-" represents the chemical was inactive. Final LELs which differed from the original LELs are shaded. Supplementary File 1 includes the details of how each individual hit was affected by either biologically relevancy cutoffs or the inter-plate inconsistency check.
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