No description available.

Six primiparous Holstein cows were assigned to a half udder design (n=6) 40 days prior to parturition. Beginning at parturition, one udder half was milked once daily (24hr interval) and the other four times daily (6hr interval). Udder halves were biopsied at days 15, 60, 120, and 230 of lactation for mammary tissue to perform mitochondrial staining and apoptosis studies. Increasing the milking frequency from 1x to 4x elevated the 4x udder half milk yield at early (d1-45) (P<0.0001), mid (d46-150) (P<0.0001) and late (d151-230) (P<0.0001) lactation. Milk protein percent (P= 0.013), lactose percent (P=0.004) and SNF percent (P=0.006), were elevated in milk from 4x udder halves over milk from 1x udder halves. We did not detect an effect of increased milking frequency on milk fat percent (P=0.25); however, yield of all components was increased. Increased milking frequency also increased mitochondrial numbers in mammary cells from 4x udder half (P=0.002) compared to 1x. We did not detect an effect of increased milking frequency on mammary apoptosis percentage. We also did not detect a difference in the abundance of gene transcripts for SOCS1, SOCS2, SOCS3 and CIS in milk; but could find an increase in alpha-lactalbumin (P=0.04) and beta-casein (P=0.001) 4x udder half gene transcripts.

Efficacy of a sustained-release formulation of bST was evaluated for two consecutive lactations. Response in milk and milk component yield was positive and very consistent for multiparous cows between lactations. Average responses in milk production for the first lactation and for the 320-, 640-, and 960-mg$ cdot$28d$ sp{-1}$ doses of bST were 4.3, 5.2 and 5.9 kg$ cdot$d$ sp{-1}$, respectively. Response was 4.9 kg$ cdot$d$ sp{-1}$ for the average of the second lactation with 640 mg bST$ cdot$28d$ sp{-1}$. Primiparous cows responded with the same numerical magnitude as multiparous cows but with higher variability. BST caused a response in milk yield irrespective of the stage of lactation when injections commenced, but the magnitude of response was greater at latter stages of lactation. No adverse effect of treatment on final body condition score and achievement of proper condition for a subsequent lactation was found. No effect of treatment was observed on health parameters in either lactation. Trends towards longer days open and more breedings per conception were apparent for both lactations. Total milk protein, caseins and whey proteins were not changed at any stage of lactation and for the average of the full lactation. BST did not significantly change proportions of $ alpha sb{s}$-, $ beta$- and K-caseins. Milk fat percentage and milk fatty acid profiles were not different between control and any dose level of bST for a complete lactation. Maximum response in milk yield for the different doses of bST was from d8 to 12 of the 28d cycle and was almost eliminated by d22 to 24. A 3.1 and 3.6 kg$ cdot$d$ sp{-1}$ milk augmentation with bST was estimated in cows infused for 6d with glucose and saline, respectively during peak lactation. There was no apparent milk yield response when cows were infused with insulin + glucose but cows exhibited positive energy balance, weight gain and only 5% less milk. Insulin + glucose infusion increased milk protein 11% and 14% compa

Clonal cell lines were isolated from mammary gland tissue epithelial cell cultures of lactating cows. Early passage clonal bovine mammary epithelial cells (clone LMH17) gave rise to several established cell lines (MAC-T lines) after being cotransfected with plasmids containing the temperature sensitive mutant SV40 large T antigen gene (pBAPSV40TtsA58) and the bacterial phosphotransferase gene (pSV2-neo). Unlike other cell types which were transformed after being transfected with SV40, MAC-T cells maintained many characteristics of non-transformed cells: MAC-T cells were serum and anchorage dependent, showed contact inhibition, and were not tumorigenic in immunodeficient mice. However, Southern transfer analysis revealed an integrated SV40 gene and cells showed no senescence after 50 passages. These cells are morphologically indistinguishable from parental LMH17 cells and retain the typical morphology of mammary epithelial cells. Positive cytokeratin immunostaining and the absence of vimentin staining indicated that these cells were epithelial in origin. / MAC-T cells grew rapidly on plastic substratum with a doubling time of approximately 17 hours and became differentiated when grown on floating collagen gels in the presence of prolactin. The differentiated phenotype was characterized to include (1) the ability to form secretory domes with a lumen from a pavement of columnar cells; (2) increased casein mRNA abundance; (3) increased alpha S and beta casein secretion; (4) increased number and size of casein secretory vesicles; and (5) increased lactose synthesis and secretion.

Problématique. Basée sur les constats effectués lors d’un essai clinique randomisé qui visait à évaluer les effets du lait maternel de fin d’expression sur la croissance et le développement de nouveau-nés prématurés et qui s’est soldé par un recrutement infructueux, une intervention de soutien à la lactation chez les mères de nouveau-nés prématurés a été développée. La mère d’un nouveau-né prématuré est en effet trois fois plus à risque qu’une autre de présenter une production lactée insuffisante. Il est donc crucial de soutenir ces mères dans l’établissement et le maintien d’une production lactée adéquate. Le but de cette étude pilote est d’estimer les effets d’une intervention de soutien à la lactation sur l’expression de lait maternel et la production lactée de mères ayant donné naissance prématurément ainsi que d’évaluer les aspects d’acceptabilité et de faisabilité de l’intervention, de l’étude et de ses procédures. Hypothèse de recherche. Les mères de nouveau-nés prématurés qui reçoivent une intervention de soutien à la lactation expriment leur lait significativement plus longtemps et plus fréquemment et produisent significativement un plus grand volume de lait à plus grande concentration lipidique sur une base quotidienne que celles qui reçoivent les soins usuels. Méthode. Devis : Projet-pilote de type essai clinique randomisé. Échantillon: Quarante mères de nouveau-nés prématurés de <30 semaines de gestation admis à une unité de soins intensifs néonatals. Procédures: Les mères du groupe témoin reçoivent les soins usuels alors que celles du groupe expérimental reçoivent une intervention de soutien à la lactation. Cette dernière comporte quatre volets: une séance d’enseignement portant sur l’établissement et le maintien d’une production lactée suffisante, un suivi téléphonique, une ligne d’aide téléphonique et le prêt d’un tire-lait électrique double pompage. Dans les deux groupes, les mères sont amenées à tenir un journal de bord de leurs séances d’expression et du volume de lait maternel exprimé. Résultats. L’étude et ses procédures de même que l’intervention de soutien sont acceptables et faisables. Les résultats observés en lien avec l’hypothèse de recherche sont orientés dans la même direction que cette dernière à l’exception de la concentration lipidique du lait maternel. Recommandations. Une étude à plus grande échelle doit être réalisée afin d’évaluer les effets de l’intervention de soutien à la lactation sur la production lactée de mères de nouveau-nés prématurés. Quant à la clinique, des actions concertées doivent être menées afin de créer un contexte propice et des conditions favorables à l’expression de lait maternel chez les mères de nouveau-nés prématurés. / Problem statement. Based on observations from an unsuccessful randomized clinical trial that aimed to evaluate the effects of hindmilk on the short-term growth and development of preterm infants, a lactation support intervention for mothers of preterm infants has been developed. Mothers who give birth prematurely are three times more likely to have an insufficient milk output compared to those who give birth at term. It is therefore crucial to support these mothers in order to facilitate the establishment and maintenance of their milk supply. The aim of this pilot study is to estimate the effects of a lactation support intervention on the expression of breast milk and milk output of mothers who gave birth prematurely and assess the acceptability and feasibility of the intervention, study and its procedures. Research hypothesis. A lactation support intervention in mothers who deliver prematurely enables them to express their milk significantly longer and more frequently, and produce a greater milk output with a higher lipid concentration compared to mothers who deliver prematurely and receive usual care. Method. Design: A pilot study of a randomized clinical trial. Sample: Forty mothers of preterm infants born at <30 weeks of gestation and admitted to a neonatal intensive care unit. Procedures: The mothers in the control group receive usual care while those in the experimental group receive a lactation support intervention. The intervention has four components: an education session on the establishment and maintenance of an adequate milk supply, a telephone follow-up, a telephone helpline and the loan of a double electric breast pump. In both the intervention and control groups, mothers kept a logbook of the frequency, duration and volume of their breast milk expressions. Results. Both the study design and the intervention are feasible and acceptable to mothers of preterm infants. With the exception of milk lipid concentration, the results are oriented in the same direction as the research hypothesis. Recommendations. A larger scale study should be conducted to evaluate the effects of the lactation support intervention on the frequency, duration, and volume of breast milk expression among mothers of premature infants. As for the clinical practice, concerted interprofessional actions must be undertaken to create the environment and conditions conducive to breast milk expression in these mothers.

No description available.

No description available.

Twelve competitive male swimmers were studied for a comparison of lactate/velocity profiles to heart rate/velocity profiles during a season of swim training. Lactate concentration (mM) and post-exercise heart rate (sum of three) after a 200-yard submaximal swim (approximately 90% of maximal attainable velocity) and a maximal swim were determined three times during the season: at the beginning (T1), after two months of training (T2) and after four months of training (T3). Both profiles demonstrated a significant rightward shift at T2 and a smaller, further shift at T3. Both lactate and heart rate significantly decreased at an absolute and relative exercise intensity in response to training. It is concluded that either parameter can be useful in monitoring training progress and for determining optimal training intensities. Because of the expense and difficulty of blood lactate measurements, heart rate/ velocity profiles can provide a practical and non-invasive alternative to blood lactate testing.

[Truncated abstract] Mastitis during lactation is a severe illness and approximately one in five breastfeeding women in Australia suffer at least one episode in the first 3-6 months post partum. Despite this, there is little understanding of the physiological and pathological processes occurring before, during and following mastitis. In this study 26 women who, on the basis of my previous research, were assessed to be at risk for developing mastitis, were recruited during the first week post partum and followed prospectively throughout the course of their lactation. Breastmilk, and 24 hour urine samples were collected at Days 5, 14, 30, 60 and 90 post partum and blood was collected at Days 5 and 14 post partum. If participants experienced inflammation of the breast at any time, either during the 90 day reference sampling period or later in their lactation, samples were then collected daily for the duration of symptoms and then, as a follow up, again one week following resolution of symptoms. Breastmilk samples were analysed for a range of biochemical components that reflect immunological (sIgA, lactoferrin) and acute phase (C-reactive protein) response, synthetic activity (lactose, glucose), and permeability of the paracellular pathway (sodium, chloride, lactose and serum albumin) within the breast. Blood and 24 hour urine samples were analysed for lactose, and blood was also analysed for C-reactive protein (CRP). Bacteriological examination of milk samples was undertaken where clinical mastitis was present. Results from these analyses were compared to the severity of breast and systemic symptoms experienced. Twenty-two episodes of mastitis and 13 episodes of blocked duct(s) were identified during the study period. When adjusted for co-existing breast pathology milk composition in the breast affected by blocked duct(s) was generally not different from that of healthy breasts. One mother, who was IgA deficient, experienced six of the 13 episodes of blocked duct(s). It is possible that the absence of sIgA in the milk of this mother increased her susceptibility to inflammation of the breast. During mastitis there was a significant increase in sodium, chloride, and serum albumin to a median concentration of 23 mmol⁄l; (p<0.001); 30 mmol⁄l; (p<0.001) and 0.8g⁄l; (p<0.001) respectively, and a decrease in the median concentration of lactose in milk to 152mmol⁄l; (p<0.016) from the mastitis breast when compared to the contralateral asymptomatic breast. Increased permeability of the paracellular pathway was confirmed by a significant increase in the median daily excretion of lactose in urine to 7.5 mmol⁄24hour (p<0.001). The rate of excretion of lactose in urine over a 24 hour period proved to be, not only a reliable means of assessing breast permeability, but also allowed the researcher to discern whether milk sampled from the breast affected was representative of milk at the site of the inflammation. The changes in lactose in urine were generally consistent with the changes in sodium, chloride and lactose in milk confirming milk expressed for sample analysis was representative of milk from the site of the inflammation

[Truncated abstract] There is a large body of evidence describing the benefits and risks, to the human fetus, of antenatal glucocorticoid treatment, but no published research on the effects on lactation. The withdrawal of progesterone, in the presence of high levels of endogenous glucocorticoids and prolactin, triggers the onset of copious milk secretion (lactogenesis II) at the end of pregnancy. The alteration of lactogenesis II by exogenous glucocorticoids could potentially have adverse impacts on postnatal nutrition in both term and preterm infants. I aimed to determine the effects of maternal antenatal glucocorticoid treatment on lactogenesis II in both ewes and women. I found profound adverse effects on lactation in ewes, and similar but more subtle effects on lactation in women . . . This thesis represents the first investigation of the effects of antenatal glucocorticoid treatment on lactogenesis II in both ewes and women. I found that, in ewes, antenatal glucocorticoid treatment stimulated premature lactogenesis II, and this was caused by disruptions to hormonal regulation during pregnancy. This event was followed by profound delays in lactogenesis II after term parturition. More subtle effects in women suggest that antenatal glucocorticoid treatment did not have a major, prolonged impact on postnatal lactogenesis II. Very preterm gestational age strongly predicted delays in lactogenesis II stressing the importance of assistance for these mothers when they are establishing lactation.