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Using data from 3,120 farm households surveyed in 2000 and 2006, the paper tests for factors that affect the degree and extent of households’ participation in the rural land rental market. The survey period coincided with the full implementation of the Comprehensive Agrarian Reform Program (CARP) which imposes restriction on the conveyance and transfer (including rental) of all lands awarded under the program. Econometric results show that the rural land rental market is not functioning efficiently. Transaction costs in land leasing are significant resulting in high proportion of nonparticipants and incomplete adjustment toward desired cultivated area for households that participate in the market. Moreover, the poor and landless have limited access to the land rental market since participation in the market is not determined by agricultural ability but is strongly influenced by endowment of land and access to formal credit. While households with less land tend to rent-in more land, the demand for land increases for household owning land more than five hectares. On the other hand, the wealth bias of rural credit market is creating more barriers for the poor to access land. The poor has been able to participate in the rental market through share tenancy arrangements but dependence on informal credit markets constrains them to operate desired cultivated area. The twin effects of inefficient land rental market and credit market imperfections can offset labor advantages of family farms and cause farms to operate below optimal level. The need to achieve an efficient farm size is critical for rural development and should be viewed separately from land ownership. In particular, the land rental market plays a critical role in access to land by the poor and in households’ adjustment to an optimal farm size. It would thus be desirable for the government to improve the regulatory framework for the land rental market to operate efficiently.

HMG-CoA reductase inhibitors, such as Lovastatin and Simvastatin, cause cell cycle arrest by interfering with the mitogenic activity of mitogens present in culture media. Cells are induced to pause in G1 and can readily resume growth upon removal of the enzymatic block. Estrogens, acting via their nuclear receptor, are mitogens for different normal and transformed cell types, where they foster cell cycle progression and cell division. In estrogen-responsive MCF-7 human breast cancer cells, but not in non responsive cells, 17 beta-estradiol (E2) induces cells arrested with Lovastatin or Simvastatin to proliferate in the presence of inhibitor, without restoring HMG-CoA reductase activity or affecting the protein prenylation pattern. Mitogenic stimulation of G1-arrested MCF-7 cells with E2 includes primary transcriptional activation of c-fos, accompanied by transient binding in vivo of the estrogen receptor and/or other factors to the ERE and the estrogen-responsive DNA region of this proto-oncogene, as detected by dimethylsulphate genomic footprinting analysis. Mitogenic stimulation of growth-arrested MCF-7 cells by E2 occurs, under these conditions, without evident activation of ERK-1 and -2 kinases, and thus independently from the mitogen-responsive signal transduction pathways that converge on these enzymes.

Estrogens exert a key biological role in mammary gland epithelial cells and promote breast carcinogenesis and tumor progression. We recently identified a new large set of estrogen responsive genes from breast cancer (BC) cells by DNA microarray analysis of the gene expression profiles induced by 17beta-estradiol in ZR-75.1 and MCF-7 cells. The purpose of the present study was to test whether the expression pattern of hormone regulated genes from this set identifies estrogen receptor (ERalpha) positive, hormone responsive BC cells. To this aim, we carried out in silico metanalysis of ERalpha positive and ERalpha negative human BC cell line transcriptomes, focusing on two sets of 171 and 218 estrogen responsive genes, respectively. Results show that estrogen dependent gene activity in hormone responsive BC cells is significantly different from that of non-responsive cells and, alone, allows to discriminate these two cellular phenotypes. Indeed, we have identified 61 genes whose expression profile specifically marks ERalpha positive BC cells, suggesting that this gene set may be exploited for phenotypic characterization of breast tumors. This possibility was tested with data obtained by gene expression profiling of BC surgical samples, where the ERalpha positive phenotypes were highlighted by the expression profile of a subset of 27 such hormone responsive genes and four additional BC marker genes, not including ERs. These results provide direct evidence that the expression pattern of a limited number of estrogen responsive genes can be exploited to assess the estrogen signaling status of BC cells both in vitro and ex-vivo. Copyright 2004 Wiley-Liss, Inc.

The authors evaluate the positivity of the tumor markers CEA, AFP, TPA and ferritin among an homogeneous group of 500 patients suffering from a chronic hepatopathy and positive for HBsAg. The obtained results show a significant increase of TPA, AFP and Ferritin (70.4%, 20% and 24% respectively of the examined patients), while CEA is increased only in the 3.2%. The correlation between the positivity of these markers and possible evolution of the chronic hepatopathy is at present under investigation.

Estrogen hormones are potent mitogens for certain target tissues, where they stimulate cell growth by inducing recruitment of quiescent cells in cycle and by fostering cell cycle progression. To define the molecular bases of the mitogenic action of these steroid hormones, the pattern of "immediate-early" gene expression was monitored during the early phases of estrogen stimulation of rat uterine cells in vivo. Nuclear run-on transcription and/or Northern blot RNA analysis indicate that c-jun, junB, jun-D, c-fos, TIS 1 (also called NGFI-B or nur/77) and TIS 8 (zif-268, krox24, egr-1, or NGFI-A) genes are all transiently activated in the uterus (up to 20-fold) within 30-120 min after treatment of adult ovariectomized rats with a mitogenic dose of 17b-estradiol. Conversely, JE gene mRNA accumulates progressively in estrogen-stimulated uterine cells, whereas TIS 11 and 21 genes are only slightly responsive to the hormone (less than twofold induction) and fos B,fra-1,fra-2,krox20 (egr-2), TIS 7 and 10, KC, and c-rel mRNAs are undetectable in rat uterus either before or after estrogen treatment. Stimulation in the presence of cycloheximide shows that only c-jun, jun-D, c-fos, and JE gene activations are primary responses to the hormone in rat uterine cells. These findings establish the direct mitogenic role of estrogen and identify for the first time a specific genetic program activated by these steroid hormones during stimulation of target cell proliferation. Furthermore, since most of the activated genes encode for transcription factors, these results enable us to envision how the mitogenic signal transmitted by the hormone can be elaborated and amplified within target cells by the products of estrogen-responsive genes, leading to a cascade of growth-dependent gene regulation, cell cycle progression, and, ultimately, cell division.