SUSY model with R-parity violation, longlived charged slepton and quasistable matter

We construct SUSY $SU(3) \otimes SU(2)_{L} \otimes U(1)$ electroweak models with superweak R-parity. The scale of R-parity violation in one of the models is determined by the Majorana mass of neutrino and it is very small that leads to the existence of longlived ($T \geq O(10^{-4}sec$) lightest superparticle. If lightest superparticle is righthanded charged slepton that can be realized within gaugino dominated scenario then the phenomenology of such model differs in a drastic way from the standard SUSY phenomenology, in particular, longlived charged sleptons can form bound states with ordinary matter - quasistable supermatter (SUSY analogs of mu-atoms and muonium). We discuss possible manifestations of the existence of such longlived charged particle at LEP2, TEVATRON and LHC. We also construct $SU(3) \otimes SU(2)_{L} \otimes SU(2)_{R} \otimes U(1)$ model with Majorana mass and superweak R-parity violation.Comment: 12 pages, Latex, no figure

Molecular Epidemiology of Infant Botulism in California and Elsewhere, 1976–2010

Background. Infant botulism (IB), first identified in California in 1976, results from Clostridium botulinum spores that germinate, multiply, and produce botulinum neurotoxin (BoNT) in the immature intestine. From 1976 to 2010 we created an archive of 1090 BoNT-producing isolates consisting of 1012 IB patient (10 outpatient, 985 hospitalized, 17 sudden death), 25 food, 18 dust/soils, and 35 other strains. Methods. The mouse neutralization assay determined isolate toxin type (56% BoNT/A, 32% BoNT/B). Amplified fragment-length polymorphism (AFLP) analysis of the isolates was combined with epidemiologic information. Results. The AFLP dendrogram, the largest to date, contained 154 clades; 52% of isolates clustered in just 2 clades, 1 BoNT/A (n = 418) and 1 BoNT/B (n = 145). These clades constituted an endemic C. botulinum population that produced the entire clinical spectrum of IB. Isolates from the patient’s home environment (dust/soil, honey) usually located to the same AFLP clade as the patient’s isolate, thereby identifying the likely source of infective spores. C. botulinum A(B) strains were identified in California for the first time. Conclusions. Combining molecular methods and epidemiological data created an effective tool that yielded novel insights into the genetic diversity of C. botulinum and the clinical spectrum, occurrence, and distribution of IB in California

<i>Clostridium botulinum</i> Strain Af84 Contains Three Neurotoxin Gene Clusters: <i>Bont/A2</i>, <i>bont/F4</i> and <i>bont/F5</i>

<div><p>Sanger and shotgun sequencing of <i>Clostridium botulinum</i> strain Af84 type Af and its botulinum neurotoxin gene (<i>bont</i>) clusters identified the presence of three <i>bont</i> gene clusters rather than the expected two. The three toxin gene clusters consisted of <i>bont</i> subtypes A2, F4 and F5. The <i>bont/A2</i> and <i>bont/F4</i> gene clusters were located within the chromosome (the latter in a novel location), while the <i>bont/F5</i> toxin gene cluster was located within a large 246 kb plasmid. These findings are the first identification of a <i>C. botulinum</i> strain that contains three botulinum neurotoxin gene clusters.</p> </div

Alignment of the 2.4 and 4.2 regions of TcdR-related σ factors of selected toxigenic clostridia.

<p>Note the highly conserved Serine-Arginine-Glutamine (SRQ) motif in all 4.2 regions of the eight TcdR-related σ factors (i and ii). The alignment includes the 2.4 and 4.2 regions of: i) the TcdR-related σ factors UviA (<i>C. perfringens</i>), TcdR (<i>C. difficile</i>), TetR (<i>C. tetani</i>), BotR (<i>C. botulinum</i> type A) (adapted from <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097983#pone.0097983-Dupuy2" target="_blank">[27]</a>) and ii) the putative TcdR-related σ factors of <i>C. baratii</i> type F7, nonproteolytic <i>C. botulinum</i> type B4, <i>C. botulinum</i> type E3 and <i>C. botulinum</i> type F6. For comparison, (iii) four non-TcdR-related members of the σ⁷⁰ family found in <i>C. botulinum</i> type E3 strain Alaska (σ^E, σ^G, σ^H and σ^D) were also included in the alignment. BoxShade (<a href="http://www.ch.embnet.org/software/BOX_form.html" target="_blank">http://www.ch.embnet.org/software/BOX_form.html</a>) with a threshold of 0.5 was used for shading of identical amino acids (black) and similar amino acids (grey). Accession numbers are from GenBank. The zigzag sign represents the non-continuity of the 2.4 and 4.2 regions.</p

PCR amplification comparison of toxigenic and nontoxigenic <i>C. baratii</i> strains.

<p>Genomic DNA isolated from toxigenic (strain IBCA03-0045) (lanes 1–3) and nontoxigenic (strain IBCA08-0076) (lanes 4–6) <i>C. baratii</i> was used as templates. No template PCR (lanes 7–9) was used as a negative control. The PCR was performed with primer pairs specific for <i>bont/F7</i> (primers baratii58F and baratii60R, lanes 1, 4 and 7), the <i>uviA</i>-like gene (primers baratii1F and baratii2R, lanes 2, 5 and 8), and the 23S rRNA gene (primers baratii23sF1 and baratii23sR1, lanes 3, 6 and 9) of <i>C. baratii</i>. The toxigenic <i>C. baratii</i> strain was PCR-positive for both the <i>bont/F7</i> and the <i>uviA</i>-like genes (lanes 1 and 2), while the nontoxigenic strain was PCR-negative for both these genes (lanes 4 and 5). This finding suggests that the <i>C. baratii bont/F7</i> neurotoxin gene and the <i>uviA</i>-like gene are genetically linked. Note that both <i>C. baratii</i> strains were PCR-positive for the 23S rRNA gene that served as a positive control (lanes 3 and 6). M  =  Molecular weight markers (1 Kb Plus DNA Ladder, Invitrogen). The sizes (in base pairs) of the Molecular weight markers and the amplicons are presented at the left.</p