Higgs-Boson Decay to Four Fermions Including a Single Top Quark Below ttˉt \bar t Threshold

The rare decay modes Higgs $\rightarrow$ four light fermions, and Higgs $\rightarrow$ single top-quark + three light fermions for $m_t<M_H<2m_t$, are presented, and phenomenologically interpreted. The angular correlation between fermion planes is presented as a test of the spin and intrinsic parity of the Higgs particle. In Higgs decay to single top, two tree-level graphs contribute in the standard model (SM); one couples the Higgs to $W^+W^-(\sim gM_W)$, and one to t\bar t(\sim g_{top\;yukawa}=m_t/246\GeV). The large Yukawa coupling for m_t>100\GeV makes the second amplitude competitive or dominant for most $M_H,m_t$ values. Thus the Higgs decay rate to single top directly probes the SM universal mechanism generating both gauge boson and fermion masses, and offers a means to infer the Higgs-$t \bar t$ Yukawa coupling when $H\rightarrow t \bar t$ is kinematically disallowed. We find that the modes $pp\rightarrow Xt\bar t(H\rightarrow t\bar b W^{(*)})$ at the SSC, and $e^+ e^-\rightarrow Z\,or\,\nu\bar{\nu} + (H\rightarrow t\bar b W^{(*)})$ at future high energy, high luminosity colliders, may be measureable if $2m_t$ is not too far above $M_H$. We classify non-standard Higgses as gaugeo-phobic, fermio-phobic or fermio-philic, and discuss the Higgs$\rightarrow$ single top rates for these classes.Comment: 30 pages, 6 figures (figures available upon request); VAND-TH-93/

Melatonin inhibira lipidnu peroksidaciju u jetri štakora uzrokovanu benzenom

We studied the antioxidative role of melatonin against benzene toxicity in rat liver. The inhibition of mitochondrial and microsomal lipid peroxidation differed between 24-hour (single-dose), 15-day, and 30-day treatments. Inhibition of mitochondrial lipid peroxidation was the highest after the single dose of melatonin, whereas highest microsomal inhibition was recorded after 30 days of melatonin treatment. No signifi cant difference was recorded between 15-day and 30-day treatments. Cytochrome P4502E1 (CYP4502E1) activity declined after the single-dose and 15-day melatonin treatment in the benzenetreated group, but it rose again, though not signifi cantly after 30 days of treatment. Liver histopathology generally supported these fi ndings. Phenol concentration in the urine samples declined in melatonin and benzene-treated rats. Our results show that melatonin affects CYP4502E1, which is responsible for benzene metabolism. Inhibition of its metabolism correlated with lower lipid peroxidation. In conclusion, melatonin was found to be protective against lipid peroxidation induced by benzene.Istražena je antioksidacijska uloga melatonina u zaštiti protiv toksičnoga djelovanja benzena u jetri štakora. Utvrđeno je da kratkoročno odnosno dugoročnije liječenje štakora melatoninom u različitoj mjeri štiti štakore istodobno izložene benzenu. Inhibicija lipidne peroksidacije mitohondrija i mikrosoma bila je različita nakon 24 h, 15 dana, odnosno 30 dana liječenja melatoninom. Najveća inhibicija lipidne peroksidacije mitohondrija zamijećena je nakon primjene jednokratne doze melatonina, dok je najizraženija inhibicija u mikrosomima zamijećena nakon 30 dana liječenja melatoninom. Slična istraživanja pokazuju da razina glutationa (GSH) najviše raste nakon 24 h liječenja melatoninom. Nije zamijećena razlika između liječenja u trajanju od 15 odnosno 30 dana. U štakora koji su uz benzen istodobno primali i melatonin razine citokroma P4502E1 pale su nakon 24 h odnosno 15 dana izloženosti. U štakora koji su primali samo melatonin te su razine nakon 30 dana statistički neznačajno porasle u odnosu na skupinu izloženu samo benzenu. Histopatološka analiza jetre načelno je potvrdila ove nalaze. Koncentracije fenola u mokraći bile su niže u štakora koji su istodobno primali melatonin i benzen. Ovi rezultati pokazuju da melatonin utječe na citokrom P4502E1, koji je odgovoran za metabolizam benzena. Inhibira li se njegov metabolizam, smanjuje se lipidna peroksidacija. Zaključak je da melatonin štiti od lipidne peroksidacije uzrokovane benzenom

Specialized Learning in Antlions (Neuroptera: Myrmeleontidae), Pit-Digging Predators, Shortens Vulnerable Larval Stage

Unique in the insect world for their extremely sedentary predatory behavior, pit-dwelling larval antlions dig pits, and then sit at the bottom and wait, sometimes for months, for prey to fall inside. This sedentary predation strategy, combined with their seemingly innate ability to detect approaching prey, make antlions unlikely candidates for learning. That is, although scientists have demonstrated that many species of insects possess the capacity to learn, each of these species, which together represent multiple families from every major insect order, utilizes this ability as a means of navigating the environment, using learned cues to guide an active search for food and hosts, or to avoid noxious events. Nonetheless, we demonstrate not only that sedentary antlions can learn, but also, more importantly, that learning provides an important fitness benefit, namely decreasing the time to pupate, a benefit not yet demonstrated in any other species. Compared to a control group in which an environmental cue was presented randomly vis-à-vis daily prey arrival, antlions given the opportunity to associate the cue with prey were able to make more efficient use of prey and pupate significantly sooner, thus shortening their long, highly vulnerable larval stage. Whereas “median survival time,” the point at which half of the animals in each group had pupated, was 46 days for antlions receiving the Learning treatment, that point never was reached in antlions receiving the Random treatment, even by the end of the experiment on Day 70. In addition, we demonstrate a novel manifestation of antlions' learned response to cues predicting prey arrival, behavior that does not match the typical “learning curve” but which is well-adapted to their sedentary predation strategy. Finally, we suggest that what has long appeared to be instinctive predatory behavior is likely to be highly modified and shaped by learning

Aneuploidy and prognosis of non-small-cell lung cancer: a meta-analysis of published data

In lung cancer, DNA content abnormalities have been described as a heterogeneous spectrum of impaired tumour cell DNA histogram patterns. They are merged into the common term of aneuploidy and probably reflect a high genotypic instability. In non-small-cell lung cancer, the negative effect of aneuploidy has been a subject of controversy inasmuch as studies aimed at determining the survival–DNA content relationship have reported conflicting results. We made a meta-analysis of published studies aimed at determining the prognostic effect of aneuploidy in surgically resected non-small-cell lung cancer. 35 trials have been identified in the literature. A comprehensive collection of data has been constructed taking into account the following parameters: quality of specimen, DNA content assessment method, aneuploidy definition, histology and stage grouping, quality of surgical resection and demographic characteristics of the analysed population. Among the 4033 assessable patients, 2626 suffered from non-small-cell lung cancer with aneuploid DNA content (overall frequency of aneuploidy: 0.65; 95% CI: (0.64–0.67)). The DerSimonian and Laird method was used to estimate the size effects and the Peto and Yusuf method was used in order to generate the odds ratios (OR) of reduction in risk of death for patients affected by a nearly diploid (non-aneuploid) non-small-cell lung cancer. Survivals following surgical resection, from 1 to 5 years, were chosen as the end-points of our meta-analysis. Patients suffering from a nearly diploid tumour benefited from a significant reduction in risk of death at 1, 2, 3 and 4 years with respective OR: 0.51, 0.51, 0.45 and 0.67 (P< 10−4for each end-point). 5 years after resection, the reduction of death was of lesser magnitude: OR: 0.87 (P = 0.08). The test for overall statistical heterogeneity was conventionally significant (P< 0.01) for all 5 end-points, however. None of the recorded characteristics of the studies could explain this phenomenon precluding a subset analysis. Therefore, the DerSimonian and Laird method was applied inasmuch as this method allows a correction for heterogeneity. This method demonstrated an increase in survival at 1, 2, 3, 4 and 5 years for patients with diploid tumours with respective size effects of 0.11, 0.15, 0.20, 0.20 and 0.21 (value taking into account the correction for heterogeneity;P< 10−4for each end-point). Patients who benefit from a surgical resection for non-small-cell lung cancer with aneuploid DNA content prove to have a higher risk of death. This negative prognostic factor decreases the probability of survival by 11% at one year, a negative effect deteriorating up to 21% at 5 years following surgery. © 2001 Cancer Research Campaign http://www.bjcancer.co