@misc{orndorff_hamrick_smoak_havell_2006, title={Host and bacterial factors in listeriosis pathogenesis}, volume={114}, ISSN={["1873-2542"]}, DOI={10.1016/j.vetmic.2005.12.003}, abstractNote={Members of the Genus Listeria are ubiquitous environmental saprophytic microorganisms. If ingested they can cause a severe disseminated disease (listeriosis) that has a high mortality rate, the highest of any food-borne pathogen, even with antibiotic therapy. Central to the high mortality rate is the hallmark characteristic of the microorganism to grow intracellularly. The presence of listeriae in food processing plants has resulted in many outbreaks of human disease and large scale recalls of processed foods. Despite the ubiquity of the microorganism, the actual disease rate (those animals showing disease signs over those exposed) is quite low and disease is almost always associated with an underlying predisposition (pregnancy being the most common in otherwise normal individuals). There are many features of the pathogenesis of listeriosis that have remained mysterious despite the extensive use of the microorganism in the study of cell-mediated immunity and intracellular growth. Informational advances such as the sequence of the mouse and listerial genomes, and technical advances such as the discovery of listeria-susceptible mouse strains, may renew interest in the study of the natural pathogenesis of the disease. This may be further facilitated by studies that employ the natural inoculation route and mimic common predisposing conditions witnessed in victims of natural outbreaks.}, number={1-2}, journal={VETERINARY MICROBIOLOGY}, author={Orndorff, PE and Hamrick, TS and Smoak, IW and Havell, EA}, year={2006}, month={Apr}, pages={1–15} }
 @article{cesta_baty_keene_smoak_malarkey_2005, title={Pathology of end-stage remodeling in a family of cats with hypertrophic cardiomyopathy}, volume={42}, ISSN={["1544-2217"]}, DOI={10.1354/vp.42-4-458}, abstractNote={End-stage hypertrophic cardiomyopathy (ES-HCM), affecting 5-10% of human hypertrophic cardiomyopathy (HCM) patients, is characterized by relative thinning of the ventricular walls and septum with dilation of the ventricular lumen, decreased fractional shortening, and progression to heart failure. C. J. Baty and others recently documented similar progressive changes to ES-HCM in a family of four cats through serial echocardiograms. At the time of heart failure, these cats exhibited changes similar to those exhibited by human ES-HCM patients. Our objectives were to describe the pathologic alterations associated with ES-HCM and investigate the pathogenesis in three of the four cats. Grossly, there was left atrial dilation with relative thinning of the interventricular septum (IVS) and left ventricular free wall (LVFW). The left atrium contained large thrombi in two of the three cats, and all three cats died following thromboembolization of the aortic bifurcation. Histologically, all three cats had subendocardial and myocardial fibrosis, predominantly of the IVS and LVFW, and one cat had acute, multifocal, myocardial infarcts with mononuclear inflammatory cell infiltrates. The pathogenesis of ES-HCM is uncertain, but theories implicate occlusion of the coronary blood flow by thickening of the coronary vessels, coronary vascular thromboembolism or coronary vessel spasm, apoptosis of myocytes, and myocardial hypertrophy beyond the ability of the vasculature to supply blood. Apoptosis assays did not reveal any apoptotic myocytes. Considering the hypercoagulative state of these cats, coronary vascular thromboembolism could be a major contributing factor. We cannot exclude apoptosis or coronary vessel spasm on the basis of the data presented.}, number={4}, journal={VETERINARY PATHOLOGY}, author={Cesta, MF and Baty, CJ and Keene, BW and Smoak, IW and Malarkey, DE}, year={2005}, month={Jul}, pages={458–467} }
 @article{smoak_byrd_abu-issa_goddeeris_anderson_morris_yamamura_klingensmith_meyers_2005, title={Sonic hedgehog is required for cardiac outflow tract and neural crest cell development}, volume={283}, ISSN={["1095-564X"]}, DOI={10.1016/j.ydbio.2005.04.029}, abstractNote={The Hedgehog signaling pathway is critical for a significant number of developmental patterning events. In this study, we focus on the defects in pharyngeal arch and cardiovascular patterning present in Sonic hedgehog (Shh) null mouse embryos. Our data indicate that, in the absence of Shh, there is general failure of the pharyngeal arch development leading to cardiac and craniofacial defects. The cardiac phenotype results from arch artery and outflow tract patterning defects, as well as abnormal development of migratory neural crest cells (NCCs). The constellation of cardiovascular defects resembles a severe form of the human birth defect syndrome tetralogy of Fallot with complete pulmonary artery atresia. Previous studies have demonstrated a role for Shh in NCC survival and proliferation at later stages of development. Our data suggest that SHH signaling does not act directly on NCCs as a survival factor, but rather acts to restrict the domains that NCCs can populate during early stages (e8.5-10.5) of cardiovascular and craniofacial development.}, number={2}, journal={DEVELOPMENTAL BIOLOGY}, author={Smoak, IW and Byrd, NA and Abu-Issa, R and Goddeeris, MM and Anderson, R and Morris, J and Yamamura, K and Klingensmith, J and Meyers, EN}, year={2005}, month={Jul}, pages={357–372} }
 @article{smoak_2004, title={Hyperglycemia-induced TGF beta and fibronectin expression in embryonic mouse heart}, volume={231}, ISSN={["1058-8388"]}, DOI={10.1002/dvdy.20123}, abstractNote={Cardiovascular defects are common in diabetic offspring, but their etiology and pathogenesis are poorly understood. Extracellular matrix accumulates in adult tissues in response to hyperglycemia, and transforming growth factor-beta1 (TGFβ1) likely mediates this effect. The objective of this study was to characterize TGFβ expression in the organogenesis-stage mouse heart and to evaluate TGFβ and fibronectin expression in embryonic mouse heart exposed to hyperglycemia. Prominent TGFβ1, and minimal TGFβ2 or TGFβ3, protein expression was demonstrated in embryonic day (E) 9.5–E13.5 hearts. Hyperglycemia for 24 hr produced significantly increased fibronectin, slightly increased TGFβ1, and unchanged TGFβ2 or TGFβ3, by immunohistochemistry. Increased TGFβ1 was demonstrated by enzyme-linked immunosorbent assay in embryonic fluid and isolated hearts after hyperglycemia for 24 hr, but not 48 hr. Hyperglycemia increased fibronectin protein and mRNA expression in embryonic hearts after 24 hr, and pericardial injection of TGFβ1 also increased fibronectin mRNA in the embryonic heart. It is proposed that TGFβ1 and fibronectin may play a role in diabetes-induced cardiac dysmorphogenesis. Developmental Dynamics 231:179–189, 2004. © 2004 Wiley-Liss, Inc.}, number={1}, journal={DEVELOPMENTAL DYNAMICS}, author={Smoak, IW}, year={2004}, month={Sep}, pages={179–189} }
 @article{ghatnekar_barnes_dow_smoak_2004, title={Hypoglycemia-induced changes in cell death and cell proliferation in the organogenesis-stage embryonic mouse heart (Retracted article. See vol 76, pg 278, 2006)}, volume={70}, ISSN={["1542-0760"]}, DOI={10.1002/bdra.20000}, abstractNote={Hypoglycemia is a side effect of diabetes therapy and causes abnormal heart development. Embryonic heart cells are largely resistant to teratogen-induced apoptosis.Hypoglycemia was tested for effects on cell death and cell proliferation in embryonic heart cells by exposing mouse embryos on embryonic day (E) 9.5 (plug = E0.5) to hypoglycemia (30-50 mg/dl glucose) in vivo or in vitro for 24 hr. Long-term effects of in vivo exposure on conceptus viability were evaluated at E18.5. Cell death was evaluated on E10.5 by: 1) two TUNEL assays in sectioned embryos to demonstrate DNA fragmentation; 2) confocal microscopy in whole embryos stained with Lysotracker; 3) flow cytometry in dispersed heart cells stained for TUNEL and myosin heavy chain (MHC) to quantify and characterize cell type susceptibility; and 4) immunohistochemistry (IHC) and Western analysis in sectioned embryos to evaluate potential involvement of caspase-3 active subunit and p53. Effects on cell proliferation were evaluated by IHC and Western analysis of proliferating cell nuclear antigen (PCNA).In vivo hypoglycemic exposure on E9.5 reduced viability in conceptuses examined on E18.5. Hearts examined on E10.5 demonstrated increased TUNEL and Lysotracker staining. In hearts of embryos exposed to hypoglycemia, flow cytometry demonstrated increased TUNEL-positive cells and cells dual-labeled for TUNEL and MHC. Protein expression of caspase-3 active subunit and p53 was increased and PCNA was markedly reduced in hearts of embryos exposed to hypoglycemia.Hypoglycemia reduces embryonic viability, induces significant cell death, and reduces cell proliferation in the E9.5 mouse heart, and these processes may involve active caspase-3 and p53.}, number={3}, journal={BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY}, author={Ghatnekar, GS and Barnes, JA and Dow, JL and Smoak, IW}, year={2004}, month={Mar}, pages={121–131} }
 @article{joyner_smoak_2004, title={In vivo hyperglycemia and its effect on Glut-1 expression in the embryonic heart}, volume={70}, ISSN={["1542-0760"]}, DOI={10.1002/bdra.20046}, abstractNote={Maternal diabetes exposes embryos to periods of hyperglycemia. Glucose is important for normal cardiogenesis, and Glut-1 is the predominant glucose transporter in the embryo.Pregnant mice were exposed to 6 or 12 hr hyperglycemia during organogenesis using intraperitoneal (IP) injections of D-glucose on gestational day (GD) 9.5 (plug = GD 0.5). Embryos were examined for morphology and total cardiac protein, and embryonic hearts were evaluated for Glut-1 protein and mRNA expression immediately after treatment (GD 9.75, GD 10.0), as well as on GD 10.5 and GD 12.5.IP glucose injections were effective in producing sustained maternal hyperglycemia. Maternal hyperglycemia for 6 or 12 hr on GD 9.5, followed by normoglycemia, produced a decrease in overall size and total cardiac protein in embryos evaluated on GD 10.5 but no difference on GD 12.5. Cardiac Glut-1 expression was immediately upregulated in embryos exposed to 6 or 12 hr maternal hyperglycemia. On GD 10.5, cardiac Glut-1 expression was not different in embryos exposed to maternal hyperglycemia for 6 hr but was downregulated in embryos exposed for 12 hr. On GD 12.5, cardiac Glut-1 expression in embryos exposed to maternal hyperglycemia on GD 9.5 for 6 or 12 hr, followed by normoglycemia, was not different from controls. The temporal pattern was the same for Glut-1 protein and mRNA expression.Hyperglycemia-induced alterations in Glut-1 expression likely interfere with balance of glucose available to the embryonic heart that may affect cardiac morphogenesis.}, number={7}, journal={BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY}, author={Joyner, NT and Smoak, IW}, year={2004}, month={Jul}, pages={438–448} }
 @article{hamrick_horton_spears_havell_smoak_orndorff_2003, title={Influence of pregnancy on the pathogenesis of listeriosis in mice inoculated intragastrically}, volume={71}, ISSN={["1098-5522"]}, DOI={10.1128/IAI.71.9.5202-5209.2003}, abstractNote={ABSTRACT Pregnancy increases the risk of listeriosis, a systemic disease caused by Listeria monocytogenes . However, there is incomplete agreement on the reasons for this increased risk. We examined two features of listeriosis in gravid and nongravid female mice following intragastric (gavage) inoculation, namely, (i) disease severity (measured by lethality) and (ii) listerial infectivity (measured by liver and spleen colonization levels up to 120 h postinoculation). Two listerial strains of differing serotype (1/2a and 4nonb) were initially employed. Neither strain produced a lethal infection in nonpregnant female mice (dose range, 10 6 to 10 9 CFU/mouse), and only the 4nonb strain produced lethalities in pregnant mice (dose range, 10 6 to 10 8 CFU/mouse). The 4nonb strain also produced a higher level of liver and spleen colonization than the 1/2a strain following gavage administration. (The two strains showed similar levels of colonization if parenterally administered.) Both strains were equally capable of binding to and forming plaques upon cultured mouse enterocytes. The ability of the 4nonb strain to produce a lethal infection in pregnant animals did not correlate with an increased incidence or level of liver and spleen colonization over that in nonpregnant females. However, the lethality rate did correlate well with the rate at which embryos and their surrounding decidual covering became infected, suggesting that intrauterine infection could be responsible for the increased disease severity in the gravid females.}, number={9}, journal={INFECTION AND IMMUNITY}, author={Hamrick, TS and Horton, JR and Spears, PA and Havell, EA and Smoak, IW and Orndorff, PE}, year={2003}, month={Sep}, pages={5202–5209} }
 @article{ghatnekar_gracz_smoak_2002, title={C-13-NMR study of hypoglycemia-induced glycolytic changes in embryonic mouse heart}, volume={66}, ISSN={["0040-3709"]}, DOI={10.1002/tera.10103}, abstractNote={Glucose metabolites can be detected in embryonic mouse tissues using 13C-NMR spectroscopy. The advantage of this method is in its chemical specificity and the ability to follow metabolic changes.In this study, CD-1 mice were mated and embryos excised on gestational day (GD) 10.5 (plug = GD 0.5). Hearts were isolated and cultured in 150 mg/dl glucose (normoglycemic medium) or 40 mg/dl glucose (hypoglycemic medium) for 6 hr. 13C-labeled glucose comprised 62%-64% of total glucose in the culture medium. Pre- and postculture media were treated with deuterated water (D2O), and 13C spectra were obtained using a Bruker Avance 500 MHz spectrometer operating at 11.744 tesla (125.7 MHz for 13C). NMR spectra demonstrated resonances for 13C-glucose in preculture normoglycemic and hypoglycemic media. Postculture spectra for normoglycemic and hypoglycemic media demonstrated 13C-glucose signals as well as a signal for 13C-lactate. Area under the curve (AUC) was measured for the [1-(13)C-glucose] resonance from preculture media and the [3-(13)C-lactate] resonance from postculture media. The ratios of AUC for postculture [3-(13)C-lactate] to preculture [1-(13)C-glucose] were calculated and found to be higher in hypoglycemic than in normoglycemic media.Our results confirm earlier findings using radiolabeled substrates and suggest that 13C-NMR spectroscopy can be used to study glucose metabolism in isolated embryonic hearts exposed to hypoglycemia.NMR effectively measures glucose and its metabolite, lactate, in the same spectrum and thus determines metabolic flux in the isolated embryonic heart after exposure to hypoglycemia and normoglycemia. This method could evaluate glucose metabolism in embryonic tissues following other teratogenic exposures.}, number={5}, journal={TERATOLOGY}, author={Ghatnekar, GS and Gracz, HS and Smoak, IW}, year={2002}, month={Nov}, pages={267–272} }
 @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={Mirex is a pesticide that is environmentally stable, accumulates in body tissues, and is embryo- and feto-toxic at high concentrations in vivo. This study is the first to evaluate the effects of mirex on organogenesis-stage embryos in vitro. Mouse embryos were exposed on gestation day 8.5 for 24 h in whole-embryo culture to mirex at 100, 200, or 400 microg/ml dissolved in xylene and compared with xylene-treated controls (1, 2, or 4 microl/ml, respectively) and untreated controls. Embryos were evaluated for malformations, somite number, total protein content, and visceral yolk sac circulation. Potential embryotoxic mechanisms were evaluated by using PCNA stain for cell proliferation and the TUNEL assay for apoptotic cell death. Mirex-exposed embryos demonstrated increased malformation rates and decreased total embryonic protein contents at > or =200 microg/ml mirex, and decreased somite numbers and VYS circulation at > or =100 microg/ml mirex, compared with xylene-treated controls. There was no difference in PCNA levels or TUNEL staining in mirex-treated embryos compared with xylene-treated controls or untreated controls. Thus, mirex is embryotoxic in vitro to early organogenesis stage mouse embryos at concentrations > or =100 microg/ml, but the effects do not appear to be mediated by changes in cell proliferation or apoptotic cell death.}, number={4}, journal={TERATOGENESIS CARCINOGENESIS AND MUTAGENESIS}, author={El-Bayomy, AA and Smoak, IW and Branch, S}, year={2002}, pages={239–249} }
 @article{abu-issa_smyth_smoak_yamamura_meyers_2002, title={Fgf8 is required for pharyngeal arch and cardiovascular development in the mouse}, volume={129}, number={19}, journal={Development (Cambridge, England)}, author={Abu-Issa, R. and Smyth, G. and Smoak, I. and Yamamura, K. and Meyers, E. N.}, year={2002}, pages={4613–4625} }
 @misc{smoak_2002, title={Hypoglycemia and embryonic heart development}, volume={7}, ISSN={["1093-4715"]}, DOI={10.2741/smoak}, abstractNote={Abnormal embryonic development is a complication of the diabetic pregnancy, and heart defects are among the most common and detrimental congenital malformations of the diabetic embryopathy. Hypoglycemia is a common side effect of diabetes therapy and is a potential teratogen. An association between hypoglycemia and congenital defects has been difficult to demonstrate in humans, but in vivo and in vitro animal studies have illustrated the importance of glucose as a substrate for normal development. Hypoglycemia alters embryonic heart morphology, producing abnormal looping and chamber expansion, decreased myocardial thickness, disorganized layers, and decreased overall size. Hypoglycemia decreases embryonic heart rate and vascularity, and it alters embryonic heart metabolism by increasing glucose uptake and glycolysis. Hypoglycemia also affects protein expression in the embryonic heart, increasing the expression of glucose regulated proteins, hexokinase, and glucose transport protein. Thus, hypoglycemia interferes with normal cardiogenesis and alters morphology, function, metabolism, and expression of certain proteins in the developing heart. It is likely that these factors contribute to heart defects observed in the diabetic embryopathy, but the definitive link has yet to be made. Future studies are expected to further elucidate mechanisms mediating hypoglycemia-induced cardiac dysmorphogenesis.}, journal={FRONTIERS IN BIOSCIENCE-LANDMARK}, author={Smoak, IW}, year={2002}, month={Jan}, pages={D307–D318} }
 @article{smoak_2002, title={Tolbutamide alters glucose transport and metabolism in the embryonic mouse heart}, volume={65}, ISSN={["0040-3709"]}, DOI={10.1002/tera.1094}, abstractNote={Tolbutamide is a sulfonylurea oral hypoglycemic agent widely used for the treatment of non insulin-dependent diabetes mellitus. Tolbutamide produces dysmorphogenesis in rodent embryos and becomes concentrated in the embryonic heart after maternal oral dosing. Tolbutamide increases glucose metabolism in extra-pancreatic adult tissues, but this has not previously been examined in embryonic heart.CD-1 mouse embryos were exposed on GD 9.5 to tolbutamide (0, 100, 250, or 500 microg/ml) for 6, 12, or 24 hr in whole-embryo culture. Isolated hearts were evaluated for (3)H-2DG uptake and conversion of (14)C-glucose to (14)C-lactate. Glut-1, HKI, and GRP78 protein levels were determined by Western analysis, and Glut-1 mRNA was measured by RT-PCR.Cardiac (3)H-2DG uptake increased after exposure to 500 microg/ml tolbutamide for 6 hr, and 100, 250, or 500 microg/ml tolbutamide for 24 hr, compared to controls. Glycolysis increased after exposure to 500 microg/ml tolbutamide for 6 or 24 hr compared to controls. Glut-1 protein levels increased in hearts exposed to 500 microg/ml tolbutamide for 12 or 24 hr, and Glut-1 mRNA increased in hearts exposed to 500 microg/ml tolbutamide for 24 hr compared to controls. HKI protein levels increased in hearts exposed to 500 microg/ml tolbutamide for 6 hr, but not 12 or 24 hr. There was no effect on GRP78 protein levels in hearts exposed to tolbutamide for 6, 12, or 24 hr.Tolbutamide stimulates glucose uptake and metabolism in the embryonic heart, as occurs in adult extra-pancreatic tissues. Glut-1 and HKI, but not GRP78, are likely involved in tolbutamide-induced cardiac dysmorphogenesis.}, number={1}, journal={TERATOLOGY}, author={Smoak, IW}, year={2002}, month={Jan}, pages={19–25} }
 @article{barnes_smoak_2000, title={Glucose-regulated protein 78 (GRP78) is elevated in embryonic mouse heart and induced following hypoglycemic stress}, volume={202}, ISSN={["0340-2061"]}, DOI={10.1007/s004290000090}, number={1}, journal={ANATOMY AND EMBRYOLOGY}, author={Barnes, JA and Smoak, IW}, year={2000}, month={Jul}, pages={67–74} }
 @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}, number={5}, journal={ANATOMY AND EMBRYOLOGY}, author={Smoak, IW and Branch, S}, year={2000}, month={May}, pages={327–333} }
 @book{smoak_2000, title={Veterinary embryology and teratology}, ISBN={0966683250}, publisher={Weybridge, VT: Cherry Tree Books}, author={Smoak, I. W.}, year={2000} }
 @article{smoak_1999, title={Cromakalim: Embryonic effects and reduction of tolbutamide-induced dysmorphogenesis in vitro}, volume={60}, ISSN={["0040-3709"]}, DOI={10.1002/(SICI)1096-9926(199911)60:5<260::AID-TERA6>3.0.CO;2-P}, abstractNote={Cromakalim is a K+ channel opener that causes smooth muscle relaxation by activating ATP-sensitive K+ (KATP) channels and producing membrane hyperpolarization. Cromakalim counteracts sulfonylurea-induced KATP channel inhibition in adult cells, but little is known regarding its embryonic effects, alone or in combination with sulfonylureas. KATP channels have been demonstrated in the embryo, but their role in normal and abnormal development is unknown. Early-somite mouse embryos were exposed for 24 hr in vitro to cromakalim at concentrations of 0 (Cntl), 1, 10, 100, 200, or 500 μM in 0.125% DMSO. Embryos were also exposed for 24 hr in vitro to a dysmorphogenic tolbutamide concentration (110 μg/ml) combined with a subdysmorphogenic concentration of cromakalim (1 μM). Embryos were evaluated for somite number, heart rate, malformations, and embryonic and yolk sac protein content. Embryos exposed to 1 μM cromakalim were similar to controls. Cromakalim exposure increased malformation rates at concentrations ≥200 μM, decreased heart rates at ≥10 μM, and decreased somite and protein values at 500 μM. Defects involved cranial neural tube, optic vesicle, heart, and somites. A malformation rate of 59% in embryos exposed to 110 μg/ml tolbutamide was reduced to 13% by adding 1 μM cromakalim to the culture medium. Heart rate, somite number, and protein values were also improved by combined exposure to cromakalim and tolbutamide compared with exposure to tolbutamide alone. These results support previous findings with diazoxide (K+ channel opener) and chlorpropamide (sulfonylurea) and further suggest a potential role for KATP channel effects in sulfonylurea-induced dysmorphogenesis. Teratology 60:260–264, 1999. © 1999 Wiley-Liss, Inc.}, number={5}, journal={TERATOLOGY}, author={Smoak, IW}, year={1999}, month={Nov}, pages={260–264} }
 @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{smoak_1999, title={Glucose metabolism in mouse embryos exposed to metformin in vitro}, volume={13}, ISSN={["0887-2333"]}, DOI={10.1016/S0887-2333(98)00061-7}, abstractNote={Metformin is an oral hypoglycaemic agent used to treat patients with non-insulin-dependent diabetes mellitus, but its effect on embryonic tissues has not been well studied. Early-somite mouse embryos were exposed in whole embryo culture to metformin (0-2000mug/ml) and assayed for glucose uptake and glycolysis at 6, 12 and 24 hours. Embryos exposed to metformin for 6 hours were also evaluated for glucose uptake in the presence of 0 or 100 mum cytochalasin B. Glucose uptake was increased in embryos exposed to metformin at 2000mug/ml for 6 hours and 1000mug/ml or more for 12 hours. Glycolysis was increased in embryos exposed to metformin at 2000mug/ml for 6 or 24 hours and 1000mug/ml or more for 12 hours, producing lactate concentrations up to six times higher than controls. Glut-1 was increased in embryos exposed to 1000mug/ml or more for 6 hours, and metformin-stimulated glucose uptake was significantly decreased by cytochalasin B. Thus, glucose uptake and glycolytic metabolism are increased in early-somite mouse embryos in response to high concentrations of metformin in vitro, and the mechanism of increased glucose uptake appears to involve a cytochalasin B-sensitive glucose transporter.}, number={1}, journal={TOXICOLOGY IN VITRO}, author={Smoak, IW}, year={1999}, month={Feb}, pages={27–33} }
 @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}, number={5}, journal={HISTOCHEMISTRY AND CELL BIOLOGY}, author={Fritz, HL and Smoak, IW and Branch, S}, year={1999}, month={Nov}, pages={359–365} }
 @article{smoak_emanuel_1998, title={Tolbutamide: Placental transfer, tissue distribution, and metabolic effects in murine embryos}, volume={82}, number={4}, journal={Pharmacology and Toxicology}, author={Smoak, I. W. and Emanuel, A. N.}, year={1998}, pages={203–208} }
 @article{smoak_1997, title={Brief hypoglycemia alters morphology, function, and metabolism of the embryonic mouse heart}, volume={11}, number={4}, journal={Reproductive Toxicology (Elmsford, N.Y.)}, author={Smoak, I. W.}, year={1997}, pages={495–502} }
 @article{smoak_amiss_1997, title={Chlorobutanol: maternal serum levels and placental transfer in the mouse}, volume={39}, number={5}, journal={Veterinary and Human Toxicology}, author={Smoak, I. W. and Amiss, T. J.}, year={1997}, pages={287–290} }
 @article{piscopo_smoak_1997, title={Comparison of effects of albendazole sulfoxide on in vitro produced bovine embryos and rat embryos}, volume={58}, number={9}, journal={American Journal of Veterinary Research}, author={Piscopo, S. E. and Smoak, I. W.}, year={1997}, pages={1038–1042} }
 @article{barnes_smoak_1997, title={Immunolocalization and heart levels of GRP94 in the mouse during post-implantation development}, volume={196}, ISSN={["0340-2061"]}, DOI={10.1007/s004290050102}, number={4}, journal={ANATOMY AND EMBRYOLOGY}, author={Barnes, JA and Smoak, IW}, year={1997}, month={Oct}, pages={335–341} }
 @article{smoak_hudson_1996, title={Persistent oropharyngeal membrane in a Hereford calf}, volume={33}, ISSN={["0300-9858"]}, DOI={10.1177/030098589603300110}, abstractNote={Persistent oropharyngeal membrane was found in a 6-day-old Hereford calf. The calf was unable to nurse and had not passed feces since birth. Physical examination revealed a fold of tissue spanning the caudal oral cavity, and a barium study demonstrated that food remained within the oral cavity despite a swallowing reflex. A thickened epiglottis was demonstrated radiographically but was not confirmed on necropsy. Necropsy revealed a complete soft-tissue partition between oral cavity and oropharynx with a central blind-ended diverticulum. Only a few cases of persistent oropharyngeal membrane have been reported previously, all in humans. This is the first report of this defect in domestic animals. Possible similarities to the more common persistent anal membrane are discussed.}, number={1}, journal={VETERINARY PATHOLOGY}, author={Smoak, IW and Hudson, LC}, year={1996}, month={Jan}, pages={80–82} }