Maḥzôr : ke-minhag aškenaz û-šeʿar qehillôt qedôšôt ; û-vô niklelû tefillôt šelôš regālîm we-hem pesaḥ, šāvûʿôt we-sûkkôt ... dizś maḥzer iz in lošn ha-koideš un ṭaiṭš gišṭelṭ

Übers. d. Hauptsacht.: Festtagsgebetbuch

Maḥzôr : ʿim lešôn aškenaz we-hadārat qôdeš ke-minhag aškenaz û-šʿar qehillôt qedôšôt û-mevûʿār bi-vē'ûr maspîq ; pērûš lešôn haq-qôdeš dāvār dāvûr ʿal ōfnāw be-mē'at devārîm we-rav ʿinyān ...

Text teilw. hebr., teilw. jidd.

Di šul-frage : redes fun di j[udiše] s[otzialisṭiše] a[rbeiṭer] p[arṭei] (P"Tz) raṭmener in lodzer šṭodṭ-raṭ, gehalṭen be-es di biudzšeṭ-debaṭen in nowember 1917

Digitalisat der Ausg. Warše [u.a.], 1920

Naie roš ḥoideš benšen ṭehine : nebsṭ šaʿarê demaʿôt teḥinnā ... šaʿarê raḥamîm, šaʿarê šāmayim, tefillat rāṣôn ... di ṭeḥine for dem šoifer blazen ...

Digitalisat der Ausg. Kroṭošin, [1875/85]

Sēfer mivḥar hap-penînîm

[Šelōmō Ben-Gabirol]

Kitve Ḥ. N. Byaliḳ u-mivḥar targumav

Byalik, Ḥ. N.

Ms. hebr. oct. 88 - Mivḥar ha-maʼamarim

Vorbesitzer: Eljāqīm Carmoly; Abraham Merzbacher

Ms. hebr. oct. 89 - Mivḥar ha-peninim

Vorbesitzer: Isaachi Castelnuovo; Elia Castelnuovo; Angelo Castelnuovo; Abraham Merzbacher

Calibration of cosmogenic noble gas production based on ³⁶Cl-³⁶Ar ages. Part 2. The ⁸¹Kr-Kr dating technique

We calibrated the ⁸¹Kr-Kr dating system for ordinary chondrites of different sizes using independent shielding-corrected ³⁶Cl-³⁶Ar ages. Krypton concentrations and isotopic compositions were measured in bulk samples from 14 ordinary chondrites of high petrologic type and the cosmogenic Kr component was obtained by subtracting trapped Kr from phase Q. The thus-determined average cosmogenic ⁷⁸Kr/⁸³Kr, ⁸⁰Kr/⁸³Kr, ⁸²Kr/⁸³Kr, and ⁸4Kr/⁸³Kr ratiC(Lavielle and Marti 1988; Wieler 2002). The cosmogenic ⁷⁸Kr/⁸³Kr ratio is correlated with the cosmogenic 22Ne/21Ne ratio, confirming that ⁷⁸Kr/⁸³Kr is a reliable shielding indicator. Previously, ⁸¹Kr-Kr ages have been determined by assuming the cosmogenic production rate of ⁸¹Kr, P(⁸¹Kr)c, to be 0.95 times the average of the cosmogenic production rates of ⁸⁰Kr and ⁸²Kr; the factor Y = 0.95 therefore accounts for the unequal production of the various Kr isotopes (Marti 1967a). However, Y should be regarded as an empirical adjustment. For samples whose ⁸⁰Kr and ⁸²Kr concentrations may be affected by neutron-capture reactions, the shielding-dependent cosmogenic (⁷⁸Kr/⁸³Kr)c ratio has been used instead to calculate P(⁸¹Kr)/P(⁸³Kr), as for some lunar samples, this ratio has been shown to linearly increase with (⁷⁸Kr/⁸³Kr)c (Marti and Lugmair 1971). However, the ⁸¹Kr-Kr ages of our samples calculated with these methods are on average ~30% higher than their ³⁶Cl-³⁶Ar ages, indicating that most if not all the ⁸¹Kr-Kr ages determined so far are significantly too high. We therefore re-evaluated both methods to determine P(⁸¹Kr)c/P(⁸³Kr)c. Our new Y value of 0.70 ± 0.04 is more than 25% lower than the value of 0.95 used so far. Furthermore, together with literature data, our data indicate that for chondrites, P(⁸¹Kr)c/P(⁸³Kr)c is rather constant at 0.43 ± 0.02, at least for the shielding range covered by our samples ([⁷⁸Kr/⁸³Kr]c = 0.119–0.185; [22Ne/21Ne]c = 1.083–1.144), in contrast to the observations on lunar samples. As expected considering the method used, ⁸¹Kr-Kr ages calculated either directly with this new P(⁸¹Kr)c/P(⁸³Kr)c value or with our new Y value both agree with the corresponding ³⁶Cl-³⁶Ar ages. However, the average deviation of 2% indicates the accuracy of both new ⁸¹Kr-Kr dating methods and the precision of the new dating systems of ~10% is demonstrated by the low scatter in the data. Consequently, this study indicates that the ⁸¹Kr-Kr ages published so far are up to 30% too high.

Das Werkchen Sa'ar has-samayim, angeblich von Ibn-Esra

Ai.

Alteration of CEACAM1 gene transcription in prostate cancer cells: The role of AR, Sp2, and HDAC

Cell to cell adhesion molecule (CEACAM1), a type II tumor suppressor, has been found to be down-regulated in prostate cancer cells. The mechanism that causes CEACAM1's down-regulation in tumorigenesis is unknown. Here we show that the transcriptional activity of CEACAM1 is decreased in prostate cancer cells. This decrease is not due to methylation of the CEACAM1's promoter, but rather to the alteration of transcription factors regulating CEACAM1 expression. ^ Since androgen/androgen receptors (AR) are potent regulators of prostate growth and differentiation, their role on CEACAM1 gene transcription was examined. The androgen receptor could directly increase CEACAM1 transcriptional activity in a ligand dependent manner by interacting with an AR consensus element that resides in the CEACAM1 promoter. However, AR binding to the CEACAM1 promoter is not related to the loss of CEACAM1 during prostate cancer progression. ^ Further analysis enabled us to determine the particular region in the CEACAM1 promoter that mediates a decrease in CEACAM1 transcriptional activity in prostate cancer cells. Upon further examination, we found that this CEACAM1 promoter region interacts with the Sp1, Sp2, and Sp3 transcription factors. However, only Sp2 expression was found to increase in prostate cancer cells. Inhibiting Sp2 from binding to the CEACAM1 promoter caused an increase in CEACAM1 transcriptional activity in prostate cancer cells. In addition, over-expressing Sp2 in normal prostate cells resulted in a decrease in CEACAM1 transcriptional activity and endogenous protein expression. These observations suggest that Sp2 is a transcription repressor of CEACAM1. Furthermore, prostate cancer cells treated with trichostatin A (TSA), a specific histone deacetylase (HDAC) inhibitor, activated CEACAM1 transcriptional activity. This implies that HDACs are involved in CEACAM1 transcriptional activity. Mutation of the Sp2 DNA binding region on the CEACAM1 promoter inhibited TSA activation of CEACAM1 transcriptional activity. This indicates that HDACs inhibit CEACAM1 transcriptional activity through Sp2. Base on these results, we propose that Sp2 is critical for down-regulating CEACAM1 expression, and one mechanism by which Sp2 represses CEACAM1 expression is by recruiting HDAC to the CEACAM1 promoter in prostate cancer cells. Collectively, these findings provide novel insights into mechanisms that cause the down-regulation of CEACAM1 expression in prostate cancer cells. ^

Ms. hebr. qu. 34 Film - Sheṭar shel "rodefe tsedaḳah"

Digitalisat des Mikrofilms (MF 4429)

Ms. hebr. qu. 35 Film - Sheṭar shel "rodefe tsedaḳah"

Digitalisat des Mikrofilms (MF 4430)

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