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Abstract  Bone mineral density may be negatively influenced by hyperprolactinemia, which can be caused by atypic neuroleptics and antidepressants. Case description The present paper reports about a spontaneous rib fracture in a female patient (age 52) taking neuroleptics (mainly risperidone), antidepressants (mainly sertraline), and anxiolytics (mainly lorazepam). At the time of the fracture a severe osteoporosis and a strongly enhanced plasma prolactin level (117 ng/ml; normal values: 3–24 ng/ml) were detected. The latter one normalized 2 months after abandoning sertraline and risperidone. After this normalization, the patient did not report further accidents up to now. Discussion Enhancement of plasma prolactin levels is linked to the mechanism of action of risperidone. Mammoplasia and increased plasma prolactin can occur during SSRI (Selective Serotonin Reuptake Inhibitors) or trazodone administration. The role of anxiolytics is less clear. The causal relationship between osteoporosis and long-term use of neuroleptics and antidepressants was assessed using probability scores, more particularly the Naranjo probability scale and the Bradford-Hill criteria of causality. A score of 6/13 (probable) was obtained with the Naranjo scale, whereas all 9 Bradford-Hill criteria were fulfilled. Conclusion Although this case could not be fully explored, attention should be paid to bone mineral density loss in depressed patients taking a combined therapy of atypic antipsychotics and antidepressants. [ABSTRACT FROM AUTHOR]

Flexible electroluminescent (EL) lamps are fabricated onto woven textiles using a novel dispenser printing process. Dispenser printing utilizes pressurized air to deposit ink onto a substrate through a syringe and nozzle. This work demonstrates the first use of this technology to fabricate EL lamps. The luminance of the dispenser printed EL lamps is compared to screen-printed EL lamps, both printed on textile, and also commercial EL lamps on polyurethane film. The dispenser printed lamps are shown to have a 1.5 times higher luminance than the best performing commercially available lamp, and have a comparable performance to the screen-printed lamps. [ABSTRACT FROM AUTHOR]

Congenital long QT syndrome type 3 (LQT3) is caused by mutations in the gene SCN5A encoding the &agr;-subunit of the cardiac Na+ channel (Nav1.5). Functional studies of SCN5A mutations in the linker between domains III and IV, and more recently the C-terminus, have been shown to alter inactivation gating. Here we report a novel LQT3 mutation, L619F (LF), located in the domain I-II linker. In an infant with prolonged QTc intervals, mutational analysis identified a heterozygous missense mutation (L619F) in the domain I-II linker of the cardiac Na+ channel. Wild-type (WT) and mutant channels were studied by whole-cell patch-clamp analysis in transiently expressed HEK cells. LF channels increase maintained Na+ current (0.79 pA/pF for LF ; 0.26 pA/pF for WT) during prolonged depolarization. We found a +5.8mV shift in steady state inactivation in LF channels compared to WT (WT, V1/2=−64.0 mV; LF, V1/2=−58.2 mV). The positive shift of inactivation, without a corresponding shift in activation, increases the overlap window current in LF relative to WT (1.09 vs. 0.58 pA/pF), as measured using a positive voltage ramp protocol (−100 to +50 mV in 2s). The increase in window current, combined with an increase in non-inactivating Na+ current, may act to prolong the AP plateau and is consistent with the disease phenotype observed in patients. Moreover, the defective inactivation imposed by the L619F mutation implies a role for the I-II linker in the Na+ channel inactivation process. © 2003 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Congenital long QT syndrome type 3 (LQT3) is caused by mutations in the gene SCN5A encoding the α‐subunit of the cardiac Na+ channel (Nav1.5). Functional studies of SCN5A mutations in the linker between domains III and IV, and more recently the C‐terminus, have been shown to alter inactivation gating. Here we report a novel LQT3 mutation, L619F (LF), located in the domain I‐II linker. In an infant with prolonged QTc intervals, mutational analysis identified a heterozygous missense mutation (L619F) in the domain I‐II linker of the cardiac Na+ channel. Wild‐type (WT) and mutant channels were studied by whole‐cell patch‐clamp analysis in transiently expressed HEK cells. LF channels increase maintained Na+ current (0.79 pA/pF for LF ; 0.26 pA/pF for WT) during prolonged depolarization. We found a +5.8mV shift in steady state inactivation in LF channels compared to WT (WT, V1/2=−64.0 mV; LF, V1/2=−58.2 mV). The positive shift of inactivation, without a corresponding shift in activation, increases the overlap window current in LF relative to WT (1.09 vs. 0.58 pA/pF), as measured using a positive voltage ramp protocol (−100 to +50 mV in 2s). The increase in window current, combined with an increase in non‐inactivating Na+ current, may act to prolong the AP plateau and is consistent with the disease phenotype observed in patients. Moreover, the defective inactivation imposed by the L619F mutation implies a role for the I‐II linker in the Na+ channel inactivation process. © 2003 Wiley‐Liss, Inc. [ABSTRACT FROM AUTHOR]