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

Radiometric 81Kr dating identifies 120,000-year-old ice at Taylor Glacier, Antarctica

We present successful 81 Kr-Kr radiometric dating of ancient polarice. Krypton was extracted from the air bubbles in four∼350-kg polar ice samples from Taylor Glacier in the McMurdo Dry Valleys, Antarctica, and dated using Atom Trap Trace Analysis (ATTA). The 81 Kr radiometric ages agree with independent age estimates obtained from stratigraphic dating techniques with a mean abso-lute age offset of 6±2.5 ka. Our experimental methods and sampling strategy are validated by (i) 85 Kr and 39 Ar analyses that show the samples to be free of modern air contamination and (ii)air content measurements that show the ice did not experience gas loss. We estimate the error in the 81 Kr ages due to past geomagnetic variability to be below 3 ka. We show that ice from the previous interglacial period (Marine Isotope Stage 5e, 130–115 ka before present) can be found in abundance near the surface of Taylor Glacier. Our study paves the way for reliable radiometric dating of ancient ice in blue ice areas and margin sites where large samples are available, greatly enhancing their scientific value as archives of old ice and meteorites. At present, ATTA 81Kr analysis requires a 40–80-kg ice sample; as sample requirements continue to decrease, 81 Kr dating of ice cores is a future possibility.

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)

Mivḥar ha-shirah ha-ʿIvrit : le-mi-yom ḥatom ketave ha-ḳodesh ʿad-gelot Yiśraʾel me-ʿal adamat Sefarad bi-shenat 5252

arukh u-metukan ʿal-yede Ḥayim Berodi ... Meʾir Ṿiner

Ṿi azoy lebn Poylishe Yidn in di geṭos : geleyenṭ oyf der 16ṭer yoriḳer ḳonferenz fun Yidishn Ṿisenshaftlekhn Insṭiṭuṭ, Nyu-Yorḳ, dem 11ṭn Yanuʾar 1942

Shloyme Mendelson

Sefer Divre Yaʿaḳov : kolel shishah ʿaśar derushim niflaʾim, le-moʿadim ṿe-yamim noraʾim, reʿayonot ʿamuḳim, metubalim be-maʾamre RaZaL u-meshalim metuḳim, divre ḥokhmah u-musar, orḥot tsedeḳ u-mesharim le-ʿorer

ḥubar me-iti Yaʿakov b. la.a.a. Shelomoh Ṭaṿshunsḳi