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The paper deals with brief information about expedition of 1932 that investigated Kyiv and Zhytomyr Polissian industry of the past and modern times. The expedition led by O. Ohloblin comprised the Taras Shevchenko All-Ukrainian Historical museum representatives. There is a short characteristic of the expedition report in the paper. The document is kept in the archives of the Institute of History of Ukraine and the Institute of Archaeology of Ukraine, as well as in the Central State Archive of the Higher Governing Bodies of Ukraine. Fragments of the report concerning two unknown faience factories of the early 19th century in the villages Zaruddia and Piniazevychi in the Irsha river downstream area are presented. One of them belonged to Branitskys.

The breast cancer gene BRCA1 has previously been cloned from both human and mouse. We cloned a fragment of the rat Brca1 homologue in order to map it and explore its biological function. Partial cDNA fragments of the rat Brca1 homologue were isolated by RT-PCR. Sequence analysis revealed that the RING-finger domain is well conserved among rat, mouse and human. Rat Brca1 mRNA was expressed in most tissues studied with the highest level in testis, consistent with studies in human and mouse. Next, intron 6-containing DNA fragments were amplified by PCR from WKY and WF rat strains. The splicing sites between exon 6 and exon 7 are conserved between rat and human. Partial sequencing of the rat Brca1 intron 6 revealed a polymorphism of a pentanucleotide TTTTG repeat between the WKY and WF strains. With this intragenic microsatellite marker, we were able to map precisely the rat Brca1 gene to chromosome 10 using a genetic linkage study of (WKY x WF)F1 x WF backcross rats. Brca1 cosegregates with marker BAND3A, and is flanked by R5123 and R5842. Using this polymorphic marker, we also investigated the loss of heterozygosity (LOH) of the Brca1 microsatellite marker in carcinogen- or radiation-induced mammary carcinomas in (WF x F344)F1 female rats. No LOH or somatic microsatellite instability was detected in 18 DMBA-induced tumors studied. Only one LOH of the F344 allele was observed in 26 radiation-induced tumors tested. Ribonuclease protection assays demonstrated that Brca1 mRNA levels are similar in normal rat mammary glands and mammary carcinomas of various etiologies, including those induced by DMBA, NMU, activated-neu and activated-ras oncogenes.

Recombinant inbred BXH-2 mice spontaneously produce a B-tropic murine leukemia virus (MuLV) beginning early in life and have a high incidence of spontaneous myeloid leukemia. These traits are not characteristic of the progenitor strains (C57BL/6J and C3H/HeJ) or of 11 other recombinant inbred BXH strains. Genetic analysis has shown that the virus is not transmitted through the germ line, suggesting that the virus is passed from one generation to the next by horizontal transmission. An additional ecotropic proviral locus was detected in some mice of this strain after several generations of inbreeding. We show that BXH ecotropic virus was transmitted to other strains when fostered on viremic BXH-2 mice and that these mice go on to develop tumors of hematopoietic origin. Our earlier finding that virus is expressed early in gestation suggested that the ecotropic MuLV is also transmitted in utero. In order to determine the stage at which the ecotropic MuLV is transmitted in utero, preimplantation stage embryos were transferred to the uteri of recipient ecotropic virus-negative mice. These mice were found to be negative for the presence of the ecotropic MuLV, suggesting that transplacental transmission of the ecotropic virus readily occurs in BXH-2 mice. Although other viruses, including human lentiviruses, are transmitted across the placental barrier, transplacental transmission of MuLV is a rare event. Thus, the BXH-2 mouse strain may contribute to our understanding of the mechanism of transplacental transmission and pathogenesis and offers a potential new model for use in drug therapy of exogenously transmitted viruses related to lentiviruses.

Chronic treatment of rats with the synthetic estrogen diethylstilbestrol is known to induce the formation of pituitary tumors, and such tumor induction is highly dependent on the strain of rat used. We examined three previously discovered restriction fragment length polymorphisms in rats to determine whether these correlated with susceptibility to tumor formation. The results indicate that the presence of particular alleles of the polymorphic N-ras and retinoblastoma (Rb) genes does not correlate with tumor susceptibility. A polymorphism upstream of the rat prolactin (Prl) gene is due to the presence or absence of an Alu-like sequence. Results of this study indicate that animals bearing the allele lacking this Alu-like insertion are more likely to develop larger pituitary tumors in response to diethylstilbestrol than are animals in which the Prl allele contains the insertion. In addition, we show that the N-ras, Rb, and Prl genes are dispersed in the rat genome and that the polymorphic alleles of the Prl genes are segregating as classical Mendelian alleles. These results suggest that the difference in the Prl gene itself or in some closely linked gene is related to tumor resistance or susceptibility.

The goal of this study was to evaluate a correspondence weight control program, and to assess the impact of three program elements (weekly homework, interim weigh-ins, and participation deposits) individually and in combination. All treated participants received 15 weekly standard lessons by mail. Three program features were varied factorially: a) homework assignments, b) interim weigh-ins and c) a deposit refunded contingent on returning homework and/or attending interim weigh-ins. Participants were assigned randomly to active treatment conditions or a delayed treatment control group. Among treated males (N = 14), initial average weight loss and BMI reduction were 9.6 kg and 3.1 respectively; average net weight loss and BMI reduction at one year follow-up were 5.8 kg and 1.9 respectively. Among treated females (N = 128), initial average weight loss and BMI reduction were 3.1 kg and 1.2 respectively; average net weight loss and BMI reduction at one year were 2.3 kg and .88 respectively. Women in all treated groups, except lessons only, showed a greater BMI reduction than untreated controls at the end of treatment. Women in conditions including both homework and interim weigh-ins had greater initial BMI reductions (M = 1.6) than those who received lessons only (M = .76). At one year, net BMI reductions were comparable across all treated groups. Of the 42 women initially registered in conditions that included both homework and weigh-ins, 12 who denied joining other programs lost at least 4.5 kg (M = 7.1) during treatment, and 7 had a net loss of at least 4.5 kg (M = 8.0) at one year without apparent involvement in any other program.