@article{rogers_setzer_branch_chernoff_2004, title={Chemically induced supernumerary lumbar ribs in CD-1 mice: Size distribution and dose response}, volume={71}, ISSN={["1542-9733"]}, DOI={10.1002/bdrb.10055}, abstractNote={Abstract}, number={1}, journal={BIRTH DEFECTS RESEARCH PART B-DEVELOPMENTAL AND REPRODUCTIVE TOXICOLOGY}, author={Rogers, JM and Setzer, RW and Branch, S and Chernoff, N}, year={2004}, month={Feb}, pages={17–25} }
 @article{cisneros_branch_2004, title={Transplacental exposure to the DNA demethylating agent, 5-AZA-CdR, affects the sexual behavior of CD-1 male mice}, volume={25}, ISSN={["0161-813X"]}, DOI={10.1016/j.neuro.2003.09.002}, abstractNote={Intrauterine exposure to 5-AZA-2'-deoxycytidine (5-AZA-CdR) alters gene expression causing malformations, abnormal post-natal growth and altered reproductive capacity. To elucidate whether the phenomenon observed in 5-AZA-CdR in utero exposed male mice was a behavioral alteration, at gestation day (GD) 10, CD-1 pregnant mice were administered 1mg/kg i.p. of 5-AZA-CdR or saline solution. After parturition, the number and sex of pups were recorded. While litter size was not affected, the ratio of male to female offspring was altered in treated mice. To determine whether the phenotypic observation of male gender corresponded to the appropriate genotype, presence of Sry gene in 5-AZA-CdR F1 males was determined. At 3 months of age, the male sexual behavior test outlined by Chubb was conducted. Presence of vaginal plug and pregnancy were determined in the natural breeding phase. Mount latency and number of mounts per mouse were assessed in the behavioral test phase. In utero exposed male mice resulted in diminished mating behavior (as measured by vaginal plug presence, mount latency and number of mounts) and reduced sexual interest while exposed to a receptive female. While normal presence of Sry gene was observed, mating behavior was altered in exposed males suggesting that the reproductive alteration could be attributed to a behavioral phenomenon.}, number={3}, journal={NEUROTOXICOLOGY}, author={Cisneros, FJ and Branch, S}, year={2004}, month={Mar}, pages={411–417} }
 @article{cisneros_branch_2003, title={5-AZA-2 '-deoxycytidine (5-AZA-CdR): a demethylating agent affecting development and reproductive capacity}, volume={23}, ISSN={["0260-437X"]}, DOI={10.1002/jat.898}, abstractNote={Abstract}, number={2}, journal={JOURNAL OF APPLIED TOXICOLOGY}, author={Cisneros, FJ and Branch, S}, year={2003}, pages={115–120} }
 @article{cisneros_wilson_travlos_anderson_branch_2003, title={Susceptibility to postnatal growth retardation induced by 5- Aza-2 '-deoxycytidine in utero: Gender specificity and correlation with reduced insulin-like growth factor 1}, volume={72}, number={25}, journal={Life Sciences (Oxford, England)}, author={Cisneros, F. J. and Wilson, R. and Travlos, G. and Anderson, L. M. and Branch, S.}, year={2003}, pages={2887–2894} }
 @article{el-bayomy_smoak_branch_2002, title={Embryotoxicity of the pesticide mirex in vitro}, volume={22}, ISSN={["0270-3211"]}, DOI={10.1002/tcm.10016}, abstractNote={Abstract}, number={4}, journal={TERATOGENESIS CARCINOGENESIS AND MUTAGENESIS}, author={El-Bayomy, AA and Smoak, IW and Branch, S}, year={2002}, pages={239–249} }
 @article{branch_henry-sam_2001, title={Altered Hox gene expression and cellular pathogenesis of 5-aza-2 '-deoxycytidine-induced murine hindlimb dysmorphogenesis}, volume={29}, ISSN={["0192-6233"]}, DOI={10.1080/019262301317226294}, abstractNote={ The DNA demethylating agent, 5-aza-2'-deoxycytidine (d-AZA), elicits temporally related morphological defects and altered gene expression in mouse hindlimbs. Segmental formation of limb regions (stylopod, zeugopod, and autopod) is partially dependent on Hox gene activation. The objective of this study was to understand the role of altered expression of key hox genes in the early pathogenesi s of d-AZA-induced hindlimb defects in mice. Semiquantitative RT-PCR was used to analyze hox gene expression (Hox C-11 and Hox A and D homologs, paralogs 9—13). Untreated and treated fore and hindlimb buds were collected 12 and 24 hours after IP injection (1 mg/kg) of d-AZA at 9 am on gestational (GD) 10 and processed for RT-PCR. Additional pregnant mice were treated similarly and whole embryos collected 12 and 24 hours posttreatment and processed for histopathological analysis. No changes in hox gene expression were detected in the forelimb tissue. There was a 2-fold down-regulation of hoxA-11 and C-11 in the 12-hour hindlimb bud tissue. No changes in the HoxD series were detected in the hindlimb bud tissue. The 12- and 24-hour untreated mice exhibited some of the morphological features consistent with physiological apoptosis. Most tissues of the treated mice exhibited cellular changes consistent with cell death associated with the cytotoxicity of the compound. The data reported supports the hypothesis that altered gene expression and not cytotoxicity alone is associated with d-AZA-induced hindlimb dysmorphogenesis . }, number={5}, journal={TOXICOLOGIC PATHOLOGY}, author={Branch, S and Henry-Sam, G}, year={2001}, pages={501–506} }
 @article{smoak_branch_2000, title={Glut-1 expression and its response to hypoglycemia in the embryonic mouse heart}, volume={201}, ISSN={["0340-2061"]}, DOI={10.1007/s004290050321}, abstractNote={The embryonic heart depends on glucose during early organogenesis. Glut-1 functions in constitutive glucose uptake in adult tissues and is the predominant glucose transporter in embryonic and fetal tissues. This study focuses on Glut-1 expression in the heart during normal organogenesis using immunohistochemistry for Glut-1 distribution, Western analysis for Glut-1 protein levels, and reverse transcriptase polymerase chain reaction for Glut-1 mRNA levels. The role of Glut in glucose uptake response to hypoglycemia in the embryonic heart is evaluated using the Glut inhibitor cytochalasin B. Cardiac Glut-1 expression is also evaluated after in vitro hypoglycemic exposure. Glut-1 levels are highest on gestational days 9-10, intermediate on gestational day 10.5, and lowest on gestational days 11.5-13.5 in the normal embryonic heart. Cardiac Glut-1 mRNA levels similarly decline between gestational days 9.5 and gd 13.5. Cytochalasin B produces a dose-dependent decrease in glucose uptake in hearts exposed to hypoglycemia for 30 min or 6 h, implicating Glut in this response. Glut-1 protein expression is unchanged after 2 or 6 h but increased after 12 and 24 h of hypoglycemia in the gestational day 9.5 heart. Thus, Glut-1 expression is prominent in the embryonic heart and is correlated with changes in cardiac glucose requirements during normal organogenesis. Glut activity increases in response to acute hypoglycemia and the expression of Glut-1 increases in response to prolonged hypoglycemia. These results support the importance of Glut-1 during normal cardiogenesis and in response to hypoglycemia in the embryonic heart.}, number={5}, journal={ANATOMY AND EMBRYOLOGY}, author={Smoak, IW and Branch, S}, year={2000}, month={May}, pages={327–333} }
 @article{branch_chernoff_brownie_francis_1999, title={5-AZA-2 '-deoxycytidine-induced dysmorphogenesis in the rat}, volume={19}, ISSN={["0270-3211"]}, DOI={10.1002/(sici)1520-6866(1999)19:5<329::aid-tcm3>3.3.co;2-j}, abstractNote={5-aza-2′-deoxycytidine (d-AZA) causes temporally related defects in the developing mouse. Treatment of 1.0 mg/kg on gestation day (GD) 8 results in axial skeletal defects; on GD9, cleft palate and vertebral defects; on GD10, hindlimb phocomelia; and on GD11, digital defects. An unusual aspect of d-AZA teratogenicity in mice is that the phocomelia appears to be specific to the hindlimb, and the forelimb is not similarly affected regardless of treatment day. The current study was initiated to evaluate the embryonic response of another species, the rat, to this unique teratogen. Pregnant Sprague Dawley (CD) rats were treated with d-AZA or vehicle control. The compound was administered i.p. on GD9, 10, 11, or 12 to parallel developmental staging of the mouse. The highest dose (1.0 mg/kg) elicited effects indicating increased sensitivity to the compound in the rat as compared to the mouse. GD9 treatment was characterized by massive resorptions; GD10, by a predominance of axial skeletal defects and cleft palate; GD11, by a predominance of forelimb phocomelia and missing ribs; and GD12 by hindlimb phocomelia and forelimb digit defects. These data indicate significant differences in the developmental responses to d-AZA of the mouse and the rat. This may reflect interspecies differences in the temporal expression of genes involved in morphogenesis and/or the methylation patterns of such genes. Molecular data generated in the mouse will be compared to that of the rat to further characterize the developmental dynamics responsible for the interspecies differences. Teratogenesis Carcinog. Mutagen. 19:329–338, 1999. © 1999 Wiley-Liss, Inc.}, number={5}, journal={TERATOGENESIS CARCINOGENESIS AND MUTAGENESIS}, author={Branch, S and Chernoff, N and Brownie, C and Francis, BM}, year={1999}, pages={329–338} }
 @article{barnes_smoak_branch_1999, title={Expression of glucose-regulated proteins (GRP78 and GRP94) in hearts and fore-limb buds of mouse embryos exposed to hypoglycemia in vitro}, volume={4}, ISSN={["1355-8145"]}, DOI={10.1379/1466-1268(1999)004<0250:EOGRPG>2.3.CO;2}, abstractNote={Hypoglycemia, the classic inducer of glucose-related protein (GRP) synthesis, is dysmorphogenic in rodent embryos and detrimentally affects the heart. This study compares GRP induction in a target vs non-target tissue by evaluating GRP expression in hearts and fore-limb buds of mouse embryos following exposure to hypoglycemia in vitro. Gestational day 9.5 embryos were exposed to 2, 6, and 24 h of either mild (80 mg/dl glucose) or severe (40 mg/dl glucose) hypoglycemia using the method of whole-embryo culture. GRP78 increased in a dose- and time-dependent fashion in embryonic hearts exposed to either 40 mg/dl or 80 mg/dl glucose, whereas GRP94 levels increased in hearts only after 24 h of hypoglycemia. In contrast to the heart, GRP induction in fore-limb buds occurred only with GRP78 following the most severe level and duration of hypoglycemia. RT-PCR analysis demonstrated an elevation in GRP78 and GRP94 message levels in embryonic hearts following severe hypoglycemia. However, mRNA levels did not increase in response to mild hypoglycemia. Overall, these data demonstrate the preferential induction of GRPs in the heart as compared to fore-limb buds in mouse embryos exposed to hypoglycemia. Increases in GRP protein levels may be a more reliable biomarker of stress than message levels. However, both tissues and methods should be examined for enhanced biomarker sensitivity.}, number={4}, journal={CELL STRESS & CHAPERONES}, author={Barnes, JA and Smoak, IW and Branch, S}, year={1999}, month={Dec}, pages={250–258} }
 @article{fritz_smoak_branch_1999, title={Hexokinase I expression and activity in embryonic mouse heart during early and late organogenesis}, volume={112}, ISSN={["0301-5564"]}, DOI={10.1007/s004180050417}, abstractNote={Hexokinase (HK) catalyzes the first step in glucose metabolism, that is, the conversion of glucose to glucose-6-phosphate (G6P). Four HK isoforms have been identified, of which HK-I is predominant in embryonic and fetal tissues. HK-I has been studied in preimplantation embryos and in fetal stages, but little is known about its activity or expression in the early postimplantation embryo. We evaluated HK-I expression, HK-I activity, and glycolytic metabolism in the embryonic mouse heart during early [gestational day (gd) 9.5] and late (gd 13.5) organogenesis. Immunohistochemistry demonstrated that HK-I is localized mainly in the heart at both stages, with stronger expression on gd 13.5. Densitometry after SDS-PAGE/western analysis confirmed higher immunodetectable HK-I protein levels in hearts on gd 13.5 vs gd 9.5. By contrast, RT-PCR demonstrated higher HK-I mRNA expression on gd 9.5 vs gd 13.5. Similarly, cardiac HK-I activity (conversion of glucose to G6P) and glycolysis (conversion of glucose to lactate) were higher on gd 9.5 than on gd 13.5. These results suggest a complex regulation of HK-I expression and activity in the embryonic heart during organogenesis, involving a change in the intrinsic activity of the enzyme with development. HK-I appears to play an important role in glucose metabolism during this critical stage of cardiogenesis.}, number={5}, journal={HISTOCHEMISTRY AND CELL BIOLOGY}, author={Fritz, HL and Smoak, IW and Branch, S}, year={1999}, month={Nov}, pages={359–365} }
 @article{branch_francis_rosen_brownie_held_chernoff_1998, title={Differentially expressed genes associated with 5-Aza-2'-deoxycytidine-induced hindlimb defects in the Swiss Webster mouse}, volume={12}, DOI={10.1002/(sici)1099-0461(1998)12:3<135::aid-jbt1>3.0.co;2-m}, abstractNote={5‐Aza‐2′‐deoxycytidine (d‐AZA) inhibits methylation of DNA, a process that serves as an epigenetic regulator of gene expression. We have shown that d‐AZA causes temporally related defects in mice. Gestational day (GD) 10 treatment induced severe long‐bone defects of the hindlimb but not the forelimb. Exposure of younger embryos (GD 8 or 9) does not induce similar defects in forelimbs. This limb‐dependent response suggests that methylation alterations in genes specific for fore‐ or hindlimbs may contribute to the observed pattern of defects. Subtraction hybridization (SH) studies were conducted to identify differential expression of DNA subsequent to the administration of d‐AZA to mice on GD 10. Hindlimb buds collected from both treated and untreated embryos at 4, 12, and 24 hours post‐treatment were used. A clone isolated from the untreated sample (down‐regulation in treated tissue) was identified as a member of the murine B1 family of repetitive sequences. The two other clones isolated from the treated tissue (up‐regulation) were homologous to avian myogenic regulatory protein mRNA and activin receptor type II gene. Both species are active during embryogenesis. These findings suggest that the isolated clones may have roles in abnormal embryonic development when inappropriately expressed. © 1998 John Wiley & Sons, Inc. J Biochem Toxicol 12: 135–141, 1998}, number={3}, journal={Journal of Biochemical and Molecular Toxicology}, author={Branch, S. and Francis, B. M. and Rosen, M. B. and Brownie, C. F. and Held, G. A. and Chernoff, N.}, year={1998}, pages={135–141} }
 @article{branch_hall_blackshear_chernoff_1998, title={Infectious dermatitis in a ball python (Python regius) colony}, volume={29}, number={4}, journal={Journal of Zoo and Wildlife Medicine}, author={Branch, S. and Hall, L. and Blackshear, P. and Chernoff, N.}, year={1998}, pages={461–464} }