Sēfer ḥaqîrôt hal-lēv : bi-lešôn aškenaz ; hû ḥibbûr nā'ē mālē mûsār we-ḥōkemôt ...

ḥibbērô ... Šelōmō Zelman ... Ben-...Šimʿôn Weṣlr ... miq-q"q Firda

Sēfer Maʿaśe H' : ... maʿaśîm gedôlîm we-niflā'îm ... bi-lešôn haq-qôdeš û-vi-lešôn aškenaz

[Simon Akiba Bär Ben-Josef]

Toxicity of aged gasoline exhaust particles to normal and diseased airway epithelia

Particulate matter (PM) pollution is a leading cause of premature death, particularly in those with pre-existing lung disease. A causative link between particle properties and adverse health effects remains unestablished mainly due to complex and variable physico-chemical PM parameters. Controlled laboratory experiments are required. Generating atmospherically realistic Aerosols and performing cell-exposure studies at relevant particle-doses are challenging. Here we examine gasoline-exhaust particle toxicity from a Euro-5 passenger car in a uniquely realistic exposure scenario, combining a smog chamber simulating atmospheric ageing, an aerosol enrichment System varying particle number concentration independent of particle chemistry, and an aerosol Deposition chamber physiologically delivering particles on air-liquid interface (ALI) cultures reproducing normal and susceptible health status. Gasoline-exhaust is an important PM source with largely unknown health effects. We investigated acute responses of fully-differentiated normal, distressed (antibiotics treated) normal, and cystic fibrosis human bronchial epithelia (HBE), and a proliferating, single-cell type bronchial epithelial cell-line (BEAS-2B). We show that a single, short-term exposure to realistic doses of atmospherically-aged gasoline-exhaust particles impairs epithelial key-defence mechanisms, rendering it more vulnerable to subsequent hazards. We establish dose-response curves at realistic particle-concentration levels. Significant differences between cell models suggest the use of fully differentiated HBE is most appropriate in future toxicity studies.

Sēfer Maʿaśe H' : do einn werṭ der tzilṭ wi H' huṭ gruśi nisim giṭon durch talmide ḥachomim ...

[Simon Akiba Bär Ben-Josef]

Stent placement vs. balloon angioplasty for popliteal artery treatment: two-year results of a prospective, multicenter, randomized trial.

PURPOSE To investigate the 2-year technical and clinical results of primary nitinol stent placement in comparison with percutaneous transluminal angioplasty (PTA) in the treatment of de novo lesions of the popliteal artery. METHODS The ETAP study (Endovascular Treatment of Atherosclerotic Popliteal Artery Lesions: balloon angioplasty vs. primary stenting; www.ClinicalTrials.gov identifier NCT00712309) is a prospective, randomized trial that enrolled 246 patients (158 men; mean age 72 years) who were randomly assigned to receive a nitinol stent (n=119) or PTA (n=127) for lesions averaging 42.3 mm in length. The results of the primary study endpoint were published. Secondary outcome measures and endpoints included primary patency (freedom from duplex-detected target lesion restenosis), target lesion revascularization (TLR), secondary patency, changes in ankle-brachial index and Rutherford class, and event-free survival (freedom from target limb amputation, TLR, myocardial infarction, and death). RESULTS In total, 183 patients (89 stent and 94 PTA) were available for the 2-year analysis. The primary patency rate was significantly higher in the stent group (64.2%) than in the PTA group (31.3%, p=0.0001). TLR rates were 22.4% and 59.5%, respectively (p=0.0001). When provisional stent placement in the PTA arm was not considered as TLR and loss in patency, the differences prevailed between the study groups but were not significant (64.2% vs. 56.1% for primary patency, respectively; p=0.44). A significant improvement in ABI and Rutherford category was observed at 2 years in both groups. CONCLUSION In treatment of obstructive popliteal artery lesions, provisional stenting reveals equivalent patency in comparison to primary stenting. However, the 2-year results of this trial suggest the possibility of a shift toward higher patency rates in favor of primary stenting.

Sēfer Ḥôvôt hal-levāvôt

mē-... Beḥay ... Bar-Yôsēf ...

Sēfer ḥaqîrôt hal-lēv : bi-lešôn aškenaz ; hû ḥibbûr nā'ē mālē mûsār we-ḥōkemôt ...

ḥibbērô ... Šelōmō Zelman ... Ben-...Šimʿôn Weṣlr ... miq-q"q Firda

Autophagy in malignant transformation and cancer progression.

Autophagy plays a key role in the maintenance of cellular homeostasis. In healthy cells, such a homeostatic activity constitutes a robust barrier against malignant transformation. Accordingly, many oncoproteins inhibit, and several oncosuppressor proteins promote, autophagy. Moreover, autophagy is required for optimal anticancer immunosurveillance. In neoplastic cells, however, autophagic responses constitute a means to cope with intracellular and environmental stress, thus favoring tumor progression. This implies that at least in some cases, oncogenesis proceeds along with a temporary inhibition of autophagy or a gain of molecular functions that antagonize its oncosuppressive activity. Here, we discuss the differential impact of autophagy on distinct phases of tumorigenesis and the implications of this concept for the use of autophagy modulators in cancer therapy.

Ester oder di belohnṭe ṭugend : in 4 abšniṭṭen in jidiš-ṭaiṭšer mundorṭ

fon Josef Herz

Ester oder di belohnṭe ṭugend : eine posse in fier abšniṭṭen jidiš daiṭšer mundarṭ als beilage tzum mišloaḥ-manos an purim

fon Josef Hertz

Sefer Ḳohelet Shelomoh : ʿal shem she-bo niḳhalu harbe devarim ṭovim mi-sefarim yeshanim ṿe-ḥadashim rabim ...

kol zeh ḳihel ṿe-asaf ... Shelomoh Zalman Londn

Sēfer Śimḥat han-nefeš : drinn werṭ gfundn gwiśi refues for dages un zorgn ; woś den laiṭn fil šedigṭ tz guf un nešome wen mn zi halṭ for borgn ...

[Elchanan Haendel Kirchhahn]

Sēfer Maʿaśe H' : do inn werṭ der tzilṭ wi H' J' hoṭ giṭon grośi nisim durch di talmide ḥachomim

[Simon Akiba Bär Ben-Josef]

The scaling of genetic diversity in a changing and fragmented world

Most species do not live in a constant environment over space or time. Their environment is often heterogeneous with a huge variability in resource availability and exposure to pathogens or predators, which may affect the local densities of the species. Moreover, the habitat might be fragmented, preventing free and isotropic migrations between local sub-populations (demes) of a species, making some demes more isolated than others. For example, during the last ice age populations of many species migrated towards refuge areas from which re-colonization originated when conditions improved. However, populations that could not move fast enough or could not adapt to the new environmental conditions faced extinctions. Populations living in these types of dynamic environments are often referred to as metapopulations and modeled as an array of subdivisions (or demes) that exchange migrants with their neighbors. Several studies have focused on the description of their demography, probability of extinction and expected patterns of diversity at different scales. Importantly, all these evolutionary processes may affect genetic diversity, which can affect the chance of populations to persist. In this chapter we provide an overview on the consequences of fragmentation, long-distance dispersal, range contractions and range shifts on genetic diversity. In addition, we describe new methods to detect and quantify underlying evolutionary processes from sampled genetic data.