Synoptic climatological analysis of Red Sea Trough and non-Red Sea Trough rain situations over Israel

Winter (October to April) rainfall in Israel is caused mostly by migrating Mediterranean cyclones but certain rain situations are accompanied by a low pressure trough extending northward from the southern Red Sea towards the Eastern Mediterranean (EM) and the Levant. This system, the Red Sea Trough (RST) is one of the most frequent surface atmospheric circulation patterns over the southeastern Mediterranean, but most of the RSTs are not accompanied by rain. This paper presents a synoptic climatological comparative analysis between rain situations associated with RSTs, and those not connected with RSTs (non-RST rain, NRR). The RST situations were identified objectively with the aid of a new algorithm applied to the GEOS-1 reanalysis gridded data set from NASA, for the period of March 1985–November 1995. <br><br> Results show that RST rain is accompanied by a relatively narrow 500-hPa trough, located west of the Israeli coast-line and characterized by a deep southward penetration, while Non-RST-associated rain (NRR) is accompanied by a wider upper trough, located over the Israeli coast-line with a shallower southward penetration. We found a south-southwesterly wind vector anomaly at 200 hPa over Israel during RST rains, while during NRRs a similar wind vector anomaly pattern is observed east of Israel. There is a divergence center over, or a few degrees east of Israel during RST rains, while NRR is associated with a divergence value of nearly zero over Israel and a maximum divergence center located east of Israel. The moisture flux during NRR at 700 and 900 hPa is from the Mediterranean, while during RST rain there is a south-westerly moisture flux at 700 hPa from equatorial Africa to Israel and vicinity. A steeper temperature lapse-rate between 950–500 hPa was found during RST rain compared with NRR, resulting from a combination of cooling aloft together with heating near the surface

Tyrphostins that suppress the growth of human papilloma virus 16‐immortalized human keratinocytes

ABSTRACT Human papilloma virus 16 (HPV16) is considered to be the causative agent for cervical cancer, which ranks second to breast cancer in women's malignancies. In an attempt to develop drugs that inhibit the malignant transformation of HPV16-immortalized epithelial cells, we examined the effect of tyrphostins on such cells. We examined the effect of tyrphostins from four different families on the growth of HPV16-immortalized human keratinocytes (HF-1) cells. We found that they alter their cell cycle distribution, their morphology, and induce cell death by apoptosis. The effects of tyrphostins on HF-1 cells are different from their effects on normal keratinocytes. Growth suppression by AG555 and AG1478 is accompanied by 30% apoptosis in HF-1 cells, but this is not observed in normal keratinocytes. Tyrphostin treatment produces distinctive morphological changes in HF-1 cells and in normal keratinocytes; however, the culture organization of normal keratinocytes is less disrupted. These differential effects of the tyrphostins on HPV16-immortalized keratinocytes compared with their effects on normal keratinocytes suggests that these compounds are suitable candidates for the treatment of papilloma. Previous and present results indicate that group 1 tyrphostins, which inhibit Cdk2 activation, and group 2 tyrphostins, represented by AG1478, a potent epidermal growth factor receptor kinase inhibitor, induce cell cycle arrest; and, in the case of HF-1 cells, apoptosis and differentiation. Cells accumulate in the G 1 phase of the cell cycle at the expense of S and G 2 ϩ M. These compounds block the growth of normal keratinocytes without inducing apoptosis or differentiation, causing them to accumulate in G 1 . AG17, which belongs to group 4, exerts its antiproliferative effect mainly by increasing the fractions of cells in G 1 with a concomitant decrease in the fraction of cells in S and G 2 ϩ M