Smoking and the sudden infant death syndrome: results from 1993-5 case-control study for confidential inquiry into stillbirths and deaths in infancy. Confidential Enquiry into Stillbirths and Deaths Regional Coordinators and Researchers.

OBJECTIVE--To investigate the effects of exposure to tobacco smoke and of parental consumption of alcohol and illegal drugs as risk factors for the sudden infant death syndrome after a national risk reduction campaign which included advice on prenatal and postnatal avoidance of tobacco smoke. DESIGN--Two year population based case-control study. Parental interviews were conducted for each infant who died and four controls matched for age and date of interview. SETTING--Three regions in England with a total population of 17 million people. SUBJECTS--195 babies who died and 780 matched controls. RESULTS--More index than control mothers (62.6% v 25.1%) smoked during pregnancy (multivariate odds ratio = 2.10; 95% confidence interval 1.24 to 3.54). Paternal smoking had an additional independent effect when other factors were controlled for (2.50; 1.48 to 4.22). The risk of death rose with increasing postnatal exposure to tobacco smoke, which had an additive effect among those also exposed to maternal smoking during pregnancy (2.93; 1.56 to 5.48). The population attributable risk was over 61%, which implies that the numbers of deaths from the syndrome could be reduced by almost two third if parents did not smoke. Alcohol use was higher among index than control mothers but was strongly correlated with smoking and on multivariate analysis was not found to have any additional independent effect. Illegal drug use was more common among the index parents, and paternal use of illegal drugs remained significant in the multivariate model (4.68; 1.56 to 14.05). CONCLUSIONS--This study confirms the increased risk of the sudden infant death syndrome associated with maternal smoking during pregnancy and shows evidence that household exposure to tobacco smoke has an independent additive effect. Parental drug misuse has an additional small but significant effect.     

Differential cytotoxicity and mycotoxin content among isolates of Fusarium moniliforme

Curvularia lunata was found causing (disseminated phaeohyphomycosis among a group of Nezara viridula (Insecta:Heteroptera) parasitizing vegetable crop Vigna unguiculata. Dark lesions were seen on pronotum and abdominal sterna. Experimental lesions were produced by applying 0.1 ml of 6.2 × 10⁸cfu/ml^–1 on abdominal sterna. Histopathology revealed that almost all internal organs and tissues showed extensive damage. It is interesting to note that C. lunata exhibited predeliction for chitinous tissues and elicited cellular immune response by granulocytes (phagocytosis). This is the first report of phaeohyphomycosis of an insect, extending the disease to invertebrates.A promising research career of one of the authors (Mrs. Vinita Dubey) was cut short by untimely death. This paper is dedicated to her memory.     

The Tau/A152T mutation,a risk factor for frontotemporal‐spectrum disorders,leads to NR2B receptor‐mediated excitotoxicity

We report on a novel transgenic mouse model expressing human full‐length Tau with the Tau mutation A152T (hTau^AT), a risk factor for FTD‐spectrum disorders including PSP and CBD. Brain neurons reveal pathological Tau conformation, hyperphosphorylation, mis‐sorting, aggregation, neuronal degeneration, and progressive loss, most prominently in area CA3 of the hippocampus. The mossy fiber pathway shows enhanced basal synaptic transmission without changes in short‐ or long‐term plasticity. In organotypic hippocampal slices, extracellular glutamate increases early above control levels, followed by a rise in neurotoxicity. These changes are normalized by inhibiting neurotransmitter release or by blocking voltage‐gated sodium channels. CA3 neurons show elevated intracellular calcium during rest and after activity induction which is sensitive to NR2B antagonizing drugs, demonstrating a pivotal role of extrasynaptic NMDA receptors. Slices show pronounced epileptiform activity and axonal sprouting of mossy fibers. Excitotoxic neuronal death is ameliorated by ceftriaxone, which stimulates astrocytic glutamate uptake via the transporter EAAT2/GLT1. In summary, hTau^AT causes excitotoxicity mediated by NR2B‐containing NMDA receptors due to enhanced extracellular glutamate.     

Two human ULBP/RAET1 molecules with transmembrane regions are ligands for NKG2D

We characterized two novel members of the RAET1/ULBP gene cluster, RAET1E and RAET1G. The encoded proteins were similar to the ULBP in their class I-like alpha1 and alpha2 domains, but differed in that, instead of being GPI-anchored, their sequences were type 1 membrane-spanning molecules. Both proteins were capable of being expressed at the cell surface. Both proteins bound the activating receptor NKG2D, and RAET1G bound the human CMV protein UL16. The expression of diverse NKG2D-binding molecules in different tissues and with different properties is consistent with multiple modes of infection- or stress-induced activation.     

Systematics ofNama (Hydrophyllaceae): Flavonoids and phyletic position of sect.Arachnoidea and sect.Cinerascentia

Eight flavonoids, four 6-oxygenated flavones, two methyl ethers of luteolin, apigenin 6,8-C-diglucoside and quercetin 3-O-glucoside, were isolated fromNama lobbii andN. rothrockii, sole members of sects.Arachnoidea andCinerascentia, respectively. Both taxa diverge markedly from other namas in morphology and chromosome number and their placement inNama has been questioned. The occurrence of 6-oxygenated flavones in these taxa adds to their already distinctive nature. Flavonoid evidence argues that both are more closely allied toEriodictyon than either is toNama.