THE EFFECTS OF 5-AZA-2'-DEOXYCYTIDINE (D-AZA) ON SONIC HEDGEHOG EXPRESSION IN MOUSE EMBRYONIC LIMB BUDS.

5-Aza-2'-deoxycytidine (d-AZA) causes temporally-related defects in the mouse. At 1.0 mg/kg on gestational day (GD) 10, d-AZA causes hindlimb phocomelia.

Host and bacterial factors in listeriosis pathogenesis.

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.

Pathology of end-stage remodeling in a family of cats with hypertrophic cardiomyopathy.

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.

Hyperglycemia-induced TGFbeta and fibronectin expression in embryonic mouse heart.

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 (TGF beta1) likely mediates this effect. The objective of this study was to characterize TGF beta expression in the organogenesis-stage mouse heart and to evaluate TGF beta and fibronectin expression in embryonic mouse heart exposed to hyperglycemia.

In vivo hyperglycemia and its effect on Glut-1 expression in the embryonic heart.

Background: 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.

Methods: Pregnant mice were exposed to 6 or 12 hr hyperglycemia during organogenesis using intraperitoneal (IP) injections of D-glucose on gestational day (GD) 9.

Hypoglycemia induced changes in cell death and cell proliferation in the organogenesis stage embryonic mouse heart.

Background: Hypoglycemia is a side effect of diabetes therapy and causes abnormal heart development. Embryonic heart cells are largely resistant to teratogen-induced apoptosis.

Methods: Hypoglycemia was tested for effects on cell death and cell proliferation in embryonic heart cells by exposing mouse embryos on embryonic day (E) 9.

Influence of pregnancy on the pathogenesis of listeriosis in mice inoculated intragastrically.

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).

13C-NMR study of hypoglycemia-induced glycolytic changes in embryonic mouse heart.

Background: 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.

Methods: In this study, CD-1 mice were mated and embryos excised on gestational day (GD) 10.

Fgf8 is required for pharyngeal arch and cardiovascular development in the mouse.

We present here an analysis of cardiovascular and pharyngeal arch development in mouse embryos hypomorphic for Fgf8. Previously, we have described the generation of Fgf8 compound heterozygous (Fgf8(neo/-)) embryos. Although early analysis demonstrated that some of these embryos have abnormal left-right (LR) axis specification and cardiac looping reversals, the number and type of cardiac defects present at term suggested an additional role for Fgf8 in cardiovascular development.

Embryotoxicity of the pesticide mirex in vitro.

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.

Tolbutamide alters glucose transport and metabolism in the embryonic mouse heart.

Background: 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.

Hypoglycemia and embryonic heart development.

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.

Glucose-regulated protein 78 (GRP78) is elevated in embryonic mouse heart and induced following hypoglycemic stress.

This study investigates the distribution and heart levels of glucose regulated protein (GRP) 78 during normal development and in response to hypoglycemia in the mouse. Results demonstrate that GRP78 is strongly expressed with in the heart, neural tube, gut endoderm, somites, and surface ectoderm of mouse embryos during early organogenesis, and GRP78 staining remains prominent in the heart from gestational days 9.5 through 13.

Glut-1 expression and its response to hypoglycemia in the embryonic mouse heart.

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.

Hexokinase I expression and activity in embryonic mouse heart during early and late organogenesis.

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.

Expression of glucose-regulated proteins (GRP78 and GRP94) in hearts and fore-limb buds of mouse embryos exposed to hypoglycemia in vitro.

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.

Cromakalim: embryonic effects and reduction of tolbutamide-induced dysmorphogenesis in vitro.

Cromakalim is a K(+) channel opener that causes smooth muscle relaxation by activating ATP-sensitive K(+) (K(ATP)) channels and producing membrane hyperpolarization. Cromakalim counteracts sulfonylurea-induced K(ATP) channel inhibition in adult cells, but little is known regarding its embryonic effects, alone or in combination with sulfonylureas. K(ATP) channels have been demonstrated in the embryo, but their role in normal and abnormal development is unknown.

Glucose metabolism in mouse embryos exposed to metformin in vitro.

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.

Tolbutamide: placental transfer, tissue distribution, and metabolic effects in murine embryos.

Tolbutamide is a sulfonylurea oral hypoglycaemic agent with suspected teratogenicity in humans and demonstrated teratogenicity in laboratory animals, but the underlying mechanism is unknown. This study examined maternal-to-conceptus tolbutamide transfer on gestational days 9.5 and 10.

Immunolocalization and heart levels of GRP94 in the mouse during post-implantation development.

Glucose-regulated proteins (GRPs), which belong to the highly conserved family of stress proteins, are resident to the endoplasmic reticulum and function as molecular chaperones. Heat shock proteins have been shown to be developmentally regulated, but little work has been done to investigate the expression of GRPs during embryogenesis. Therefore, this study examined the distribution of GRP94 within mouse embryos during the period of organogenesis and characterized levels of GRP94 within the developing heart during organogenesis and late fetal stages.

Chlorobutanol: maternal serum levels and placental transfer in the mouse.

Chlorobutanol (CB) is a pharmaceutical preservative and the active ingredient in certain sedatives and anesthetics and produces adverse effects in adult tissues and mouse embryos in vitro. Chlorobutanol is slowly eliminated in humans, but little is known about its serum levels in other species or placental transfer in any species. Pregnant mice gavaged with 80 mg CB/kg on gestational day (gd) 9.

Comparison of effects of albendazole sulfoxide on in vitro produced bovine embryos and rat embryos.

Objective: To evaluate and compare effects of albendazole sulfoxide (ABZSO) on rat embryos and bovine embryos produced in vitro.

Animals: In vitro produced bovine embryos. Rat embryos recovered from naturally bred Sprague-Dawley rats.

Brief hypoglycemia alters morphology, function, and metabolism of the embryonic mouse heart.

This study examined effects of brief embryonic exposure to hypoglycemia on the developing mouse heart during organogenesis. Mouse embryos were exposed in whole-embryo culture to brief periods (2, 4, or 6 h) of hypoglycemia (20, 40, or 80 mg/dL glucose) at three developmental stages (10, 20, or 30 somites), and hearts were examined for morphologic, functional, and metabolic effects. Hypoglycemia produced abnormal cardiac structure and expansion and pericardial edema, and it disrupted histologic integrity and growth of the heart, particularly at 20 somites.

Persistent oropharyngeal membrane in a Hereford calf.

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.

Determination of chlorobutanol in mouse serum, urine and embryos by capillary gas chromatography with electron capture detection.

A sensitive and specific method for the determination of chlorobutanol (1,1,1-trichloro-2-methyl-2-propanol) in mouse serum, urine, and embryos by capillary gas chromatography with electron capture detection is described. For sample preparation n-hexane was used to extract chlorobutanol and the internal standard 2,2,2-trichloroethanol (TCE) from each matrix. Following extraction chromatographic separation of the samples was achieved with a fused-silica capillary column (30 m x 0.