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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 expression of rat 24p3, encoded by the Lcn2 gene, has been associated with rat mammary carcinomas initiated by the neu oncogene (Stoesz and Gould, 1995). In this study, we assign the Lcn2 gene to rat chromosome band 3q12 by genetic linkage analysis.

The rat is an extremely valuable model for studies of inherited susceptibility to breast cancer because the characteristics of rat mammary cancer and human breast cancer are so similar. There are now several rat models for studying sensitivity versus resistance, or cell autonomy versus non-cell-autonomy, for spontaneous and induced mammary cancers. It is known that the tumor-resistant Cop [20, 21] and WKy [8] strains carry dominant resistance genes that inhibit both spontaneous and induced mammary tumors. The WF and SD strains are known to carry dominant sensitivity genes that appear to increase susceptibility to induced but not spontaneous mammary tumors. The presence of both resistance and sensitivity genes in the Cop strain is intriguing, and provides a unique model for studying the interactions of both types of genes. It appears that the resistance genes together are at least partially dominant over the sensitivity gene in this model since the F1 rats develop only a few tumors. Yet another strain, the F344, has an intermediate sensitivity and has been shown to carry neither sensitivity or resistance genes. Thus, all these models and data indicate that sensitivity genes are not necessary for the development of mammary tumors, and neither are they sufficient. However, loss of resistance gene function is necessary but is not sufficient for mammary tumor development. Studies have shown that the sensitivity and resistance genes act directly within the mammary epithelial cells rather than globally in the rat. The products of these genes also do not appear to act at early steps in the carcinogenic process because there have been no observed effects of these genes on carcinogen metabolism or DNA adduct formation. It would appear that these genes act at later stages of mammary carcinogenesis. Identification and isolation of these genes should aid our understanding of the inherited components of human breast cancer. With the increasing availability of genetic markers and large-insert libraries for the rat genome, genetic and physical mapping studies are now a reality for the genes involved in mammary carcinogenesis of the rat. Such studies have already revealed the multigenic nature of this cancer, supporting the idea that the limited penetrance of BRCA1 and BRCA2 in human breast cancer is due to loci that modify the effects of the sensitivity genes. Assuming that human homologues of the Mcs genes exist, cloning the genes and defining the human homologues may provide a way to identify the risk for breast cancer development in women. Analysis of the function of such genes may also lead to the development of new drugs for chemoprevention and/or therapy of this lethal disease.

In this paper, patterns of allelic imbalances (Als) in chemically induced rat mammary, colon, and bladder tumors from (Wistar Furth x Fischer 344)F1 rats are described and compared. Male F1 rats were administered azoxymethane (AOM), and colon tumors were collected at 58 wk after treatment. Female F1 rats were given either N-nitroso-N-methylurea (NMU) or N-butyl-(hydroxybutyl)-nitrosoamine (BBN), and mammary and bladder tumors were collected at 15 and 52 wk after treatment, respectively. DNA was extracted from a subset of 18 of the largest tumors from each group, and a genome scan was performed by using polymerase chain reaction and 90 polymorphic microsatellite markers. Als, such as loss of heterozygosity, gene duplication, and microsatellite instability, were observed at low frequencies in all of the tumor models. Thirty random Als were observed in the AOM-induced colon tumors but only four in the NMU-induced mammary tumors. In both these models, all the tumors were classified as adenocarcinomas, and most of the Als observed were confined to single tumors with atypical histopathology. In contrast, 27 random Als were identified in the BBN-induced bladder tumors. Als were observed in both transitional-cell carcinomas and papillomas, although most were in the carcinomas. Statistical analysis of the Al data revealed no significant nonrandom Als within or among the tumor models, although several of the infrequently observed Al events identified in the rat tumors may also be observed in the corresponding human tumor type.

The rat is an extremely valuable model for studies of inherited susceptibility to breast cancer because the characteristics of rat mammary cancer and human breast cancer are so similar. There are now several rat models for studying sensitivity versus resistance, or cell autonomy versus non-cell-autonomy, for spontaneous and induced mammary cancers. It is known that the tumor-resistant Cop [20, 21] and WKy [8] strains carry dominant resistance genes that inhibit both spontaneous and induced mammary tumors. The WF and SD strains are known to carry dominant sensitivity genes that appear to increase susceptibility to induced but not spontaneous mammary tumors. The presence of both resistance and sensitivity genes in the Cop strain is intriguing, and provides a unique model for studying the interactions of both types of genes. It appears that the resistance genes together are at least partially dominant over the sensitivity gene in this model since the F1 rats develop only a few tumors. Yet another strain, the F344, has an intermediate sensitivity and has been shown to carry neither sensitivity or resistance genes. Thus, all these models and data indicate that sensitivity genes are not necessary for the development of mammary tumors, and neither are they sufficient. However, loss of resistance gene function is necessary but is not sufficient for mammary tumor development. Studies have shown that the sensitivity and resistance genes act directly within the mammary epithelial cells rather than globally in the rat. The products of these genes also do not appear to act at early steps in the carcinogenic process because there have been no observed effects of these genes on carcinogen metabolism or DNA adduct formation. It would appear that these genes act at later stages of mammary carcinogenesis. Identification and isolation of these genes should aid our understanding of the inherited components of human breast cancer. With the increasing availability of genetic markers and large-insert libraries for the rat genome, genetic and physical mapping studies are now a reality for the genes involved in mammary carcinogenesis of the rat. Such studies have already revealed the multigenic nature of this cancer, supporting the idea that the limited penetrance of BRCA1 and BRCA2 in human breast cancer is due to loci that modify the effects of the sensitivity genes. Assuming that human homologues of the Mcs genes exist, cloning the genes and defining the human homologues may provide a way to identify the risk for breast cancer development in women. Analysis of the function of such genes may also lead to the development of new drugs for chemoprevention and/or therapy of this lethal disease.

We have mapped 11 novel, anonymous genetic markers to rat chromosome 2. The rat ceruloplasmin gene (Cp) had been previously mapped to chromosomes 2 and 7q11--q13 by two different methods. To resolve the assignment and to localize the Cp gene on the rat genetic linkage map, we used linkage analysis to confirm that rat Cp lies on chromosome 2.

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.

We have observed restriction fragment length polymorphisms for the N-ras and retinoblastoma (Rb) genes between rat strains that are susceptible or resistant to induction of pituitary tumors by diethylstilbestrol (DES). Thirteen other proto-oncogenes tested displayed the same restriction patterns between all samples. The N-ras polymorphism is observed with more than one restriction nuclease and the N-ras and Rb polymorphisms are not a result of DES treatment. The N-ras polymorphism is inherited in a Mendelian fashion and there appear to be two separate loci in the rat genome that are detected by the N-ras probe. For both the N-ras and Rb genes there is an 'extra' fragment in the tumor-resistant animals that is not seen in the susceptible rats. These polymorphisms may indicate regions of the genome that play a role in determining susceptibility to pituitary tumors or any of a number of other chemically induced tumors.

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.

Photolumineseent methods are proposed for the determination of the built-in field E, the graded layer thickness, and the main recombination parameters: the diffusion and diffusion-drift lengths, the surface recombination velocities on the illuminated and back surfaces, and the emission internal efficiency. [Russian Text Ignored].

This article describes experiences in designing and implementing an elective program to teach effective communication and counseling skills to medical students. Although studies have identified its importance, effective communication is rarely part of the closely supervised experience of students. Yet, most graduates enter a practice situation where effective patient-doctor communication must be established to ensure patient cooperation in diagnosis and treatment of disease. Physicians must also frequently assist patients in making decisions to which they become committed because they feel involved in the decision-making process. For these reasons, communication skills, presently one of the least developed aspects of training programs for students, must extend beyond interviewing techniques which result in simple information gathering and encompass the entire counseling approach. The approach to effective teaching of communciation skills as described is applicable to all clinical areas. In addition, it provides skill training in problem-solving counseling which is often demanded of most practicing physicians.

New photoluminescent methods are used to investigate the parameters of graded band-gap Alx, Ga1−xAs solid solutions of direct-band composition, grown by the liquid-phase-epitaxial processes, with linear band-gap variation. The layer thicknesses, built-in field E, diffusion and diffusion-drift lengths, internal quantum yield of interband photoluminescence, as well as recombination velocities on the illuminated and back surfaces are determined. Variations of the recombination parameters along the layer thickness and as a function of the solid-solution composition gradient are investigated. A decrease of the diffusion length and an increase of the surface recombination velocity for large composition gradients are attributed to an increase of the defect concentration. [Russian Text Ignored].