Use of mistletoes by the Grey Go‐away‐bird (Corythaixoides concolor,Musophagidae) in a semi‐arid savannah,south‐west Zimbabwe

Mistletoes are preferred nesting sites for many bird species in a range of habitats. However, no studies have examined the use of mistletoes by nesting birds in the semi‐arid savannah. We studied nesting in mistletoe and its role in determining nesting success in the Grey Go‐away‐bird in south‐west Zimbabwe. We modelled the effects of mistletoe, mistletoe abundance, nest microclimate, concealment and nest height on daily survival rates (DSR) using program MARK. A constant survival model was best fitted for the Grey Go‐away‐bird suggesting a constant nest survival rate across the nesting period. Mistletoe nests had lower DSR than nests placed elsewhere in the canopy. Mistletoe abundance and nest height had a positive association with DSR whereas visibility distance, microclimate and concealment were negatively associated with DSR. Overall, survival for nests in mistletoe was 22.1% compared with 90.5% for nests in other substrates over the 50‐day nesting period. In conclusion, the low nest survival in mistletoe suggests either that the factors used to select mistletoe as nest sites by these birds are poor predictors of nest success or that nesting in mistletoe may be maladaptive.     

A molecular genetic linkage map of mouse chromosome 2

Interspecific backcross mice were used to create a molecular genetic linkage map of chromosome 2. Genomic DNAs from N2 progeny were subjected to Southern blot analysis using molecular probes that identified the Abl, Acra, Ass, C5, Cas-1, Fshb, Gcg, Hox-5.1, Jgf-1, Kras-3, Ltk, Pax-1, Prn-p, and Spna-2 loci; these loci were added to the 11 loci previously mapped to the distal region of chromosome 2 in the same interspecific backcross to generate a composite multilocus linkage map. Several loci mapped near, and may be the same as, known mutations. Comparisons between the mouse and the human genomes indicate that mouse chromosome 2 contains regions homologous to at least six human chromosomes. Mouse models for human diseases are discussed.     

An interspecific backcross linkage map of mouse chromosome 8

We have established a 67-cM molecular genetic linkage map of mouse chromosome 8 by interspecific backcross analysis. Genes that were mapped in this study include Act-6, Aprt, Aprt-ps1, Emv-2, Es-N, Hp, Insr, Mt-1, Plat, Psx-8, Ucp, and Zfp-4. New regions of homology were established between mouse chromosome 8 and human chromosomes 8 and 19. A conserved linkage group was identified between mouse chromosome 8 and human chromosome 16. The map will be useful for establishing linkage of other markers to mouse chromosome 8.     

Increased Stimulated Release and Uptake of Dopamine in Nucleus Accumbens After Repeated Cocaine Administration as Measured by In Vivo Voltammetry

Electrically stimulated dopamine (DA) release (overflow) and uptake were measured with in vivo voltammetry in the nucleus accumbens (N ACC) of anesthetized rats that had previously received repeated cocaine treatments. Electrically stimulated DA release was induced by a 10-s stimulation in the medial forebrain bundle (2-ms, 200-microA, biphasic pulses at 100 Hz). DA overflow and uptake were measured with fast chronoamperometry using a Nafion-plated, carbon fiber electrode. Animals given repeated doses of cocaine (10 mg/kg s.c. from day 1 to 5, 20 mg/kg s.c. from day 6 to 10) showed marked increases in DA uptake (5.47 +/- 0.28 vs. 2.93 +/- 0.26 microM/s) and in stimulated DA overflow (27.3 +/- 1.1 vs. 18.9 +/- 1.3 microM) compared with DA uptake and stimulated overflow in saline control animals. The increased uptake was shown to be independent of the increased overflow. Uptake was monitored as a function of stimulation current, and the data were extrapolated to zero stimulation, resulting in calculated rates of uptake of 2.43 and 3.71 microM/s in the control and cocaine-treated groups, respectively. These effects were found to be temporary, as there were no significant differences in stimulated release or uptake between saline control animals and animals given 10 days of cocaine followed by a 10-day abstinence period. These alterations in the N ACC produced by repeated cocaine administration may be a compensatory response to prolonged uptake blockade of synaptic DA.     

Genetic Analysis of Mouse T Haplotypes Using Mutations Induced by Ethylnitrosourea Mutagenesis: The Order of T and Qk Is Inverted in T Mutants

The t region of mouse chromosome 17 exhibits recombination suppression with wild-type chromatin. However, the region has resisted classical genetic dissection because of a lack of defined variants. Mutations induced by N-ethyl-N-nitrosourea (ENU) at the Brachyury (T), quaking (qk), and tufted (tf) loci of the mouse tw5 haplotype have now allowed the analysis of crossovers between two complete t haplotypes. A classical breeding analysis of the complete t haplotypes, tw5 and t12, utilizing the newly induced markers, reveals two inversions in t chromatin: one involving T and qk, and one involving tf and the H-2 complex. Moreover, the recombination frequency between the loci of T and qk is reduced compared to the frequency reported in normal chromatin. These two inversions are a sufficient explanation for the recombination inhibition with normal chromatin exhibited by t haplotypes isolated from the wild. Furthermore, the reduced recombination frequency between T and qk may indicate that the proximal gene rearrangement is not a simple inversion.     

SOS regulatory elements are essential for UPEC pathogenesis

Epithelial cells are highly regarded as the first line of defense against microorganisms, but the mechanisms used to control bacterial diseases are poorly understood. A component of the DNA damage repair regulon, SulA, is essential for UPEC virulence in a mouse model for human urinary tract infection, suggesting that DNA damage is a key mediator in the primary control of pathogens within the epithelium. In this study, we examine the role of DNA damage repair regulators in the intracellular lifestyle of UPEC within superficial bladder epithelial cells. LexA and RecA coordinate various operons for repair of DNA damage due to exogenous and endogenous agents and are known regulators of sulA. UPEC strains defective in regulation of the SOS response mediated by RecA and LexA display attenuated virulence in immunocompetent mice within the first 6 h post infection. RecA and LexA regulation of the SOS regulon is dispensable in immunocompromised mice. These data suggest that epithelial cells produce sufficient levels of DNA damaging agents, such that the bacterial DNA damage repair response is essential, as a means to control invading bacteria. Since many pathogens interact with the epithelium before exposure to professional phagocytes, it is likely that adaptation to oxidative radicals during intracellular growth provides additional protection from killing by innate immune phagocytes.     

Retroviral insertions in the VISION database identify molecular pathways in mouse lymphoid leukemia and lymphoma

AKXD recombinant inbred (RI) strains develop a variety of leukemias and lymphomas due to somatically acquired insertions of retroviral DNA into the genome of hematopoetic cells that can mutate cellular proto-oncogenes and tumor suppressor genes. We generated a new set of tumors from nine AKXD RI strains selected for their propensity to develop B-cell tumors, the most common type of human hematopoietic cancers. We employed a PCR technique called viral insertion site amplification (VISA) to rapidly isolate genomic sequence at the site of provirus insertion. Here we describe 550 VISA sequence tags (VSTs) that identify 74 common insertion sites (CISs), of which 21 have not been identified previously. Several suspected proto-oncogenes and tumor suppressor genes lie near CISs, providing supportive evidence for their roles in cancer. Furthermore, numerous previously uncharacterized genes lie near CISs, providing a pool of candidate disease genes for future research. Pathway analysis of candidate genes identified several signaling pathways as common and powerful routes to blood cancer, including Notch, E-protein, NFκB, and Ras signaling. Misregulation of several Notch signaling genes was confirmed by quantitative RT-PCR. Our data suggest that analyses of insertional mutagenesis on a single genetic background are biased toward the identification of cooperating mutations. This tumor collection represents the most comprehensive study of the genetics of B-cell leukemia and lymphoma development in mice. We have deposited the VST sequences, CISs in a genome viewer, histopathology, and molecular tumor typing data in a public web database called VISION (Viral Insertion Sites Identifying Oncogenes), which is located at . Keith C. Weiser and Bin Liu are authors that contributed equally to this work.     

Quantification of angiogenesis in estrogen receptor-positive and negative breast carcinoma

Background

The objective of this study was to evaluate angiogenesis according to CD34 antigen expression in estrogen receptor (ER)-positive and negative breast carcinomas.

Methods

This study comprised 64 cases of infiltrating ductal carcinoma in postmenopausal women divided into two groups: Group A: ER-positive, n = 35; and Group B: ER-negative, n = 29. The anti-CD34 monoclonal antibody was used as a marker for endothelial cells. Microvessel count was carried out in 10 fields per slide using a 40× objective lens (magnification 400×). Statistical analysis of the data was performed using Student's t-test (p < 0.05).

Results

The mean number of vessels stained with the anti-CD34 antibody in the estrogen receptor-positive and negative tumors was 23.51 ± 1.15 and 40.24 ± 0.42, respectively. The number of microvessels was significantly greater in the estrogen receptor-negative tumors (p < 0.001).

Conclusion

ER-negative tumors have significantly greater CD34 antigen expression compared to ER-positive tumors.