Thirteen abortuses with a known chromosomal complement of 45 (XO) were collected. Of these, eight contained an embryo or fetus ranging in age from five weeks to four months. Various gross anatomical abnormalities were evident in the four larger specimens and these included horseshoe kidney, unicornate uterus, single umbilical artery and cystic hygroma. One specimen had bilateral cystic hygromata. In all specimens, the gross anatomical appearance of the gonad was normal and, when examined histologically, the presence of primordial germ cells could be demonstrated.Histological sections of the XO gonads were compared with sections of gonads from known XX specimens of similar ages. There was no significant difference between the XO and XX gonads up to the third intrauterine month. In the older fetuses there was a relative increase in the connective tissue of the XO gonad.The finding of germ cells in the gonads of the XO fetuses is in contrast to the findings in XO adults who usually do not have germ cells in the gonads.

Thyroxine replacement therapy for 21 adult patients with primary hypothyroidism was adjusted to the dosage at which each patient had a normal thyrotrophin (TSH) response to thyrotrophin releasing hormone (TRH). Clinical assessment and measurement of TSH (by sensitive immunoradiometric assay), free thyroxine (FT4) and free tri-iodothyronine (FT3) were made at this dosage and at higher and lower doses of thyroxine. Clinical observations, FT3 and FT4 assays were relatively insensitive to small alterations of thyroxine dosage, in contrast to which basal TSH measurements correlated well with TRH responsiveness and were sensitive to fine adjustments of thyroxine dosage.

Twenty-four crossbred pigs of 15 kg initial bodyweight were fed four semi-synthetic diets for 10 days according to a completely randomised design. The study aimed to determine the effects of state of body nitrogen balance and the presence of dietary peptides and protein in the digestive tract on the excretion of endogenous amino acids from the ileum of the pig. Endogenous lysine excretion was determined for pigs given a protein-free (PF) diet, an enzymically hydrolysed casein-(EHC), a zein-(ZN) or a synthetic amino acid-(SAA) based diet. Digesta from the EHC-fed animals were centrifuged and ultrafiltered after collection and the precipitate plus retentate fraction was used to determine the endogenous flows. Such processing excludes unabsorbed dietary amino acids from the measure of endogenous loss. ZN is naturally deficient in lysine and tryptophan and these two amino acids were omitted from the synthetic amino acid-based diet to allow direct measurement of endogenous lysine flow. Pigs given the ZN and SAA diets received free lysine and tryptophan orally throughout the study except for the final 2 days of the study, when these amino acids were infused intravenously. Endogenous flows for amino acids other than lysine were determined for pigs given the PF and EHC diets. On the final day of the study the pigs were given their daily dietary allowance hourly and killed 10 h after the start of feeding. Digesta were collected from the terminal ileum (20 cm anterior to the ileo-caecal junction) and endogenous flows were determined by reference to the marker chromic oxide. The mean endogenous ileal lysine flows for the ZN-and EHC-fed pigs were not significantly different (overall mean, 419 mg kg-' dry matter intake), but were higher (P < 005) than those for the PF-and SAA-fed pigs (overall mean, 268 mg kg-' dry matter intake) whose mean flows were not significantly different from each other. The mean endogenous ileal flows for amino acids other than lysine were higher (P < 0.05) for the EHC-fed pigs compared to the animals on the PF diet, except for proline, glycine and arginine. The similar endogenous ileal lysine excretion for pigs receiving a SAA-based diet and in positive body nitrogen balance, and PF-fed pigs in negative body nitrogen balance, indicates that negative body nitrogen balance per se does not lead to a lowered endogenous ileal excretion. It would appear, however, that the presence of dietary peptides or protein in the gut increases amino acid excretion at the terminal ileum above that found with PF or SAA alimentation. Consequently, endogenous ileal amino acid flow in the pig may be underestimated when determined by the traditional PF method.

No abstract

Fetal growth restriction (FGR) occurs in ∼8% of pregnancies and is a major cause of perinatal mortality and morbidity. There is no effective treatment. FGR is characterized by reduced uterine blood flow (UBF). In normal sheep pregnancies, local uterine artery (UtA) adenovirus (Ad)-mediated overexpression of vascular endothelial growth factor (VEGF) increases UBF. Herein we evaluated Ad.VEGF therapy in the overnourished adolescent ewe, an experimental paradigm in which reduced UBF from midgestation correlates with reduced lamb birthweight near term. Singleton pregnancies were established using embryo transfer in adolescent ewes subsequently offered a high intake (n=45) or control intake (n=12) of a complete diet to generate FGR or normal fetoplacental growth, respectively. High-intake ewes were randomized midgestation to receive bilateral UtA injections of 5×10¹¹ particles Ad.VEGF-A165 (n=18), control vector Ad.LacZ (n=14), or control saline (n=13). Fetal growth/well-being were evaluated using serial ultrasound. UBF was monitored using indwelling flowprobes until necropsy at 0.9 gestation. Vasorelaxation, neovascularization within the perivascular adventitia, and placental mRNA expression of angiogenic factors/receptors were examined using organ bath analysis, anti-vWF immunohistochemistry, and qRT-PCR, respectively. Ad.VEGF significantly increased ultrasonographic fetal growth velocity at 3-4 weeks postinjection (p=0.016-0.047). At 0.9 gestation fewer fetuses were markedly growth-restricted (birthweight >2SD below contemporaneous control-intake mean) after Ad.VEGF therapy. There was also evidence of mitigated fetal brain sparing (lower biparietal diameter-to-abdominal circumference and brain-to-liver weight ratios). No effects were observed on UBF or neovascularization; however, Ad.VEGF-transduced vessels demonstrated strikingly enhanced vasorelaxation. Placental efficiency (fetal-to-placental weight ratio) and FLT1/KDR mRNA expression were increased in the maternal but not fetal placental compartments, suggesting downstream effects on placental function. Ad.VEGF gene therapy improves fetal growth in a sheep model of FGR, although the precise mechanism of action remains unclear.

SummaryA new understanding of leaf starch degradation has emerged in the last 10 years. It has been shown that starch phosphorylation and dephosphorylation are critical components of this process. Glucan, water dikinase (GWD) (and phosphoglucan, water dikinase) adds phosphate to starch, and phosphoglucan phosphatase (SEX4) removes these phosphates. To explore the use of this metabolism to manipulate starch accumulation, Arabidopsis (Arabidopsis thaliana) plants were engineered by introducing RNAi constructs designed to reduce expression of AtGWD and AtSEX4. The timing of starch build-up was altered with ethanol-inducible and senescence-induced gene promoters. Ethanol induction of RNAi lines reduced transcript for AtGWD and AtSEX4 by 50%. The transgenic lines had seven times more starch than wild type at the end of the dark period but similar growth rates and total biomass. Elevated leaf starch content in maize leaves was engineered by making an RNAi construct against a gene in maize that appeared to be homologous to AtGWD. The RNAi construct was expressed using the constitutive ubiquitin promoter. Leaf starch content at the end of a night period in engineered maize plants was 20-fold higher than in untransformed plants with no impact on total plant biomass. We conclude that plants can be engineered to accumulate starch in the leaves with little impact on vegetative biomass.

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A B S T R A~. Cells derived from cultures of bone marrow or leucocytes were treated with hypotonic citrate solution, squashed in 45% acetic acid frozen with COz to allow removal of the cover glass without disturbing the smear, and stained by the following schedule: abm lute alcohol, 5 min; coat with 0.2% parlodion and air dry; 70% alcohol, 5 min; distilled water, 5 min; stain 2-5 min in a mixture of 45 ml of a 0.3% solution of basic fuchsin in 5% phenol, 6 ml of glacial acetic acid, and 6 ml of 37% formaldehyde. Differentiate and dehydrate in a b solute alcohol, clear in xylene and cover. The stain is durable for several weeks if slides are stored in darkness when not in use. Results resemble those obtained by Feulgen or acetoorcein methods.Pvcn, T. T., CIECIIJRA, S. J., and ROBINSON, A. 108, 949-55.Biotech Histochem Downloaded from informahealthcare.com by University of Newcastle on 12/28/14For personal use only.