Cross-linking cellular prion protein triggers neuronal apoptosis in vivo

Neuronal death is a prominent, but poorly understood, pathological hallmark of prion disease. Notably, in the absence of the cellular prion protein (PrPC), the disease-associated isoform, PrPSc, appears not to be intrinsically neurotoxic, suggesting that PrPC itself may participate directly in the prion neurodegenerative cascade. Here, cross-linking PrPC in vivo with specific monoclonal antibodies was found to trigger rapid and extensive apoptosis in hippocampal and cerebellar neurons. These findings suggest that PrPC functions in the control of neuronal survival and provides a model to explore whether cross-linking of PrPC by oligomeric PrPSc can promote neuronal loss during prion infection.     

Aerosol composition of urban and desert origin in the Eastern Mediterranean. I

Aerosol samples were collected in Tel-Aviv, Israel, during two different atmospheric situations, clear days and dust storms, and were analyzed for shape, size distribution, elemental composition, and presence of sulfate in individual particles. Results of two cases are presented in this paper. In both cases about 80% of the 0.2 to 2.0 µm particles contained sulfate. On the clear day over 50% of the total were pure sulfates while 27% were mixed sulfates; on the dusty day 63% were mixed sulfates — desert particles coated with sulfate — and only 20% were pure sulfates. The sulfate content of the desert particles was fairly high, on the order of 0.1 g sulfate g^?1 of desert particles. A possible explanation of this phenomenon may be heterogeneous nucleation of SO₂ on the surfaces of insoluble desert particles during their passage over the Mediterranean.     

Prion-induced amyloid heart disease with high blood infectivity in transgenic mice

We investigated extraneural manifestations in scrapie-infected transgenic mice expressing prion protein lacking the glycophosphatydylinositol membrane anchor. In the brain, blood, and heart, both abnormal protease-resistant prion protein (PrPres) and prion infectivity were readily detected by immunoblot and by inoculation into nontransgenic recipients. The titer of infectious scrapie in blood plasma exceeded 10(7) 50% infectious doses per milliliter. The hearts of these transgenic mice contained PrPres-positive amyloid deposits that led to myocardial stiffness and cardiac disease.     

Axonopathy and transport deficits early in the pathogenesis of Alzheimer's disease

We identified axonal defects in mouse models of Alzheimer's disease that preceded known disease-related pathology by more than a year; we observed similar axonal defects in the early stages of Alzheimer's disease in humans. Axonal defects consisted of swellings that accumulated abnormal amounts of microtubule-associated and molecular motor proteins, organelles, and vesicles. Impairing axonal transport by reducing the dosage of a kinesin molecular motor protein enhanced the frequency of axonal defects and increased amyloid-beta peptide levels and amyloid deposition. Reductions in microtubule-dependent transport may stimulate proteolytic processing of beta-amyloid precursor protein, resulting in the development of senile plaques and Alzheimer's disease.     

Water distribution analysis of a linear move irrigator by aerial survey and RTK-GNSS monitors

Precision Agriculture - Irrigation uniformity in a semi-arid climate remains one of the main factors of water use efficiency (WUE) regardless of the level of agronomic advance, since over- and...     

Asymmetric growth of citrus fruit peel induced by localized application of gibberellins in lanolin pastes

Lanolin pastes containing 0.02–1.0% gibberellin A₄₊₇(GA₄₊₇) were applied to one side of developing citrus fruitlets and caused thickening of the peel in the proximity of the treated zone. Enlargement of albedo (= the white portion of citrus peel) cells was involved, as revealed by scanning electron microscopy. The flavedo (= the coloured portion of the peel) and the pulp were not affected by the hormone. Gibberellin A₃ was slightly less active than GA₄₊₇. Cultivars with a naturally thick peel, such as ‘Marsh’ grapefruit (Citrus paradisi Macf.) and ‘Shamouti’ orange (Citrus sinensis (L.) Osbeck) responded more strongly than thin-peel cultivars. The role of gibberellins in the differential growth of citrus fruit tissues is discussed.     

A field investigation of the use of the pedometer for the early detection of lameness in cattle

The efficacy of the pedometer to predict lameness earlier than the appearance of the clinical signs in a herd of dairy cows was investigated by correlating pedometric activity (PA) with clinical cases of lameness. The computer program was set to identify cows with a reduction of 5% or more in PA compared with their own previous 10 days average; these animals were then examined for clinical lameness. At the same time, every lame cow was checked to see if and when its PA was reduced. Forty-six cows showed a reduced PA; 38 cases of lameness were identified by either a reduction in PA or clinical observation; of these, 21 lame cows (45.7%) showed a reduction in PA of 5% or more, 7 to 10 days prior to the appearance of clinical signs. This cohort comprised 55.3% of the lame cows. In 92% of the lame cows identified by PA, the decrease was above 15%.     

Anchorless prion protein results in infectious amyloid disease without clinical scrapie

In prion and Alzheimer's diseases, the roles played by amyloid versus nonamyloid deposits in brain damage remain unresolved. In scrapie-infected transgenic mice expressing prion protein (PrP) lacking the glycosylphosphatidylinositol (GPI) membrane anchor, abnormal protease-resistant PrPres was deposited as amyloid plaques, rather than the usual nonamyloid form of PrPres. Although PrPres amyloid plaques induced brain damage reminiscent of Alzheimer's disease, clinical manifestations were minimal. In contrast, combined expression of anchorless and wild-type PrP produced accelerated clinical scrapie. Thus, the PrP GPI anchor may play a role in the pathogenesis of prion diseases.