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Rapid Biodegradation of Lindane Soil. The rapid degradation of lindane in soils after multiple treatments was studied under laboratory conditions. The rate of lindane disappearance increased with the increase in the frequency of application. After the fourth application of lindane, more than 85 % of the applied chemical was lost within 8 weeks (70 % in control soil). The rapid loss of lindane in the field for the long term experiment itself suggested that some lindane decomposing microrganisms had accumulated. A bacteria (Bacillus sp) was isolated as lindane decomposing microrganism.

The KCNE1 gene encodes a small protein, IsK, of 14.4 kDa, with a single transmembrane domain, and is part of a potassium channel expressed in the heart. This channel is thought to underly the very slow component of the cardiac delayed rectifying current which controls the duration and the degree of ventricular repolarization. This suggested that KCNE1 could be the morbid gene responsible for an autosomal recessive cardio-auditory disease, the Jervell and Lange-Nielsen syndrome, characterized by ventricular repolarization abnormalities and recurrent syncopes leading eventually to sudden death associated with a bilateral congenital deafness. By linkage analysis in four consanguinous families, using microsatellite markers of chromosome 21 as well as KCNE1 intragenic polymorphisms, we excluded KCNE1 as a candidate gene for Jervell and Lange-Nielsen syndrome. In addition, we described a new polymorphism, a G-to-A substitution at position 253, in the KCNE1 coding sequence detectable by SSCP analysis or RFLP.

Background KVLQT1 , the gene encoding the α-subunit of a cardiac potassium channel, is the most common cause of the dominant form of long-QT syndrome (LQT1-type), the Romano-Ward syndrome (RWS). The overall phenotype of RWS is characterized by a prolonged QT interval on the ECG and cardiac ventricular arrhythmias leading to recurrent syncopes and sudden death. However, there is considerable variability in the clinical presentation, and potential severity is often difficult to evaluate. To analyze the relationship between phenotypes and underlying defects in KVLQT1 , we investigated mutations in this gene in 20 RWS families originating from France. Methods and Results By PCR-SSCP analysis, 16 missense mutations were identified in KVLQT1 , 11 of them being novel. Fifteen mutations, localized in the transmembrane domains S2-S3, S4-S5, P, and S6, were associated with a high percentage of symptomatic carriers (55 of 95, or 58%) and sudden deaths (23 of 95, or 24%). In contrast, a missense mutation, Arg 555 Cys, identified in the C-terminal domain in 3 families, was associated with a significantly less pronounced QT prolongation (459±33 ms, n=41, versus 480±32 ms, n=70, P =.0012), and significantly lower percentages of symptomatic carriers (7 of 44, or 16%, P P Conclusions Our data show a wide KVLQT1 allelic heterogeneity among 20 families in which KVLQT1 causes RWS. We describe the first missense mutation in the C-terminal domain of KVLQT1, which is clearly associated with a fruste phenotype, which could be a favoring factor of acquired LQT syndrome.

Long QT syndrome (LQT) is a genetically heterogeneous inherited disorder that causes sudden death from cardiac arrhythmia. Four loci have been mapped to chromosomes 3, 4, 7 and 11 and three specific mutated genes for LQT syndrome have been identified. LQT2 results from mutations in the human ether-a-gogo-related gene, HERG, a cardiac potassium channel, whose protein product likely underlies Ikd the rapidly activating delayed rectifier current. By SSCP analysis and direct sequencing, we determined a new missense mutation in the HERG coding sequence, a G to A transition at position 1681 resulting in the substitution of threonine for a highly conserved alanine at codon 561. This mutation, Ala561Thr, in the coding sequence of the fifth membrane-spanning domain (S5) of the HERG protein seems to convey a risk of cardiac events in affected family members. In addition to a prolonged T wave of low amplitude on the surface ECG, a distinctive biphasic T-wave pattern was found in the left precordial leads of all affected subjects with the Ala561Thr mutation regardless of age, gender and beta blocking therapy.

Long QT syndrome (LQT) is an autosomal dominant cardiac disease characterized by ventricular arrhythmia. A first locus for LQT has been identified on chromosome 11p15.5 (LQT1), closely linked to HRAS. To refine the location of LQT1, microsatellites were genotyped in 8 French families and the following order was determined: tel-HRAS-DRD4-D11S922-D11S4046- IGF2-INS-TH-D11S1318-D11S1323-D11S1338-D11S90 9-D11S1346-cen. By haplotype analysis, 12 crossing-over events were identified in affected and unaffected subjects, delineating the LQT1 candidate region to 7 cM. This new delineated localization between D11S1318 and D11S1323 is in a more centromeric region than previously thought and is 5 cM proximal to HRAS.