Interactive effects of mosquito control insecticide toxicity, hypoxia, and increased carbon dioxide on larval and juvenile eastern oysters and hard clams.

Mosquito control insecticide use in the coastal zone coincides with the habitat and mariculture operations of commercially and ecologically important shellfish species. Few data are available regarding insecticide toxicity to shellfish early life stages, and potential interactions with abiotic stressors, such as low oxygen and increased CO2 (low pH), are less understood. Toxicity was assessed at 4 and 21 days for larval and juvenile stages of the Eastern oyster, Crassostrea virginica, and the hard clam, Mercenaria mercenaria, using two pyrethroids (resmethrin and permethrin), an organophosphate (naled), and a juvenile growth hormone mimic (methoprene). Acute toxicity (4-day LC50) values ranged from 1.59 to >10 mg/L. Overall, clams were more susceptible to mosquito control insecticides than oysters. Naled was the most toxic compound in oyster larvae, whereas resmethrin was the most toxic compound in clam larvae. Mortality for both species generally increased with chronic insecticide exposure (21-day LC50 values ranged from 0.60 to 9.49 mg/L). Insecticide exposure also caused sublethal effects, including decreased swimming activity after 4 days in larval oysters (4-day EC50 values of 0.60 to 2.33 mg/L) and decreased growth (shell area and weight) in juvenile clams and oysters after 21 days (detected at concentrations ranging from 0.625 to 10 mg/L). Hypoxia, hypercapnia, and a combination of hypoxia and hypercapnia caused mortality in larval clams and increased resmethrin toxicity. These data will benefit both shellfish mariculture operations and environmental resource agencies as they manage the use of mosquito control insecticides near coastal ecosystems.

A non-radiolabelled ferriprotoporphyrin IX biomineralisation inhibition test for the high throughput screening of antimalarial compounds.

Intraerythrocytic malaria parasites produce large amounts of toxic ferriprotoporphyrin IX (FP) during their digestion of host cell haemoglobin. The inhibition of biomineralisation of FP to haemozoin (or beta-haematin) by antimalarial drugs underlies their mode of action. We have developed an in vitro microassay for testing the inhibition of biomineralisation by drugs. It is based on the detection by optical density measurement of solubilised beta-haematin remaining after contact with drugs. The assay uses a 192-microM haemin chloride solution in dimethyl sulfoxide, 96-well filtration microplates as well as normal microplates; it lasts 18-24h and requires a spectrophotometer. We determined by this assay the IC(50) of chloroquine phosphate (28microM) and quinine base (324microM) and showed that unlike previous methods it is insensitive to inorganic anions. We also determined the activity of synthetic dyes and plant extract to determinate the interference of coloured compounds on the accuracy of the test. We found that methylene blue, thionine (IC(50) 38 and 87microM, respectively), and an extract of plants that contains quinoline derivatives, inhibited the biomineralisation of FP regardless of their intrinsic colour.

A congenital hand deformity: Dupuytren's disease.

A 10-month-old child presented with a lack of extension at the distal interphalangeal joint. Despite the absence of trauma, a provisional diagnosis of mallet finger led to treatment using a short dorsal splint. Four months later the flexion had increased and included the proximal interphalangeal joint. Palpation revealed a palmar cord on the lateral aspect of the finger. Surgery disclosed a typical Dupuytren cord and the histology supported this diagnosis. There was no known family history of the disease. There was no sign of recurrence 27 months after surgery in this case of Dupuytren's disease that was present at birth.