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Increased oceanic heat transport plays a key role in the accelerated mass loss of Greenland’s marine-terminating glaciers. The melt rate of major glaciers in Northeast Greenland (NEG) is controlled by ocean variability, in particular warm Atlantic Intermediate Water (AIW), on the continental shelf. A high-resolution configuration of the ocean sea-ice model FESOM2.1 is validated at local and regional scales, and used to investigate the drivers of AIW temperature variability on the NEG shelf. The seasonal to decadal variability of the AIW is characterised, featuring both pronounced interannual fluctuations and a long-term warming trend. A major source of AIW is Atlantic Water (AW) originating from the West Spitsbergen Current that recirculates in Fram Strait. AW anomalies are advected westwards and partly control the AIW temperatures on the shelf. Increased AIW temperatures are also connected to more pronounced northern and middle branches of recirculating AW in Fram Strait, and enhanced AW temperatures more regionally. This strengthening of the pathways brings more and warmer AIW onto the northern part of the NEG shelf. There, it circulates anti-cyclonically and results in shelf-wide warming. Regional atmospheric forcing is connected to the changes in the AW circulation regime. The strengthening of the northern AW branches is likely caused by anticyclonic wind anomalies over the Barents Sea that drive an enhanced northwards AW transport in Fram Strait. Thus, controlled by a combination of both upstream and regionally forced circulation conditions, the changes in local AIW temperatures may also affect the oceanic heat transport reaching the Arctic Ocean.

An along-channel momentum budget is quantified in the near-field plume region of a controlled river flow entering Doubtful Sound, New Zealand. Observations include highly resolved density, velocity and turbulence, enabling a momentum budget to be constructed over a control volume. Estimates of internal stress (τ) were made from direct measurements of turbulence dissipation rates (ϵ) using vertical microstructure profiles. High flow speeds of the surface plume over 2 m s−1 and strong stratification (N2∼10-1 s−2) resulted in enhanced turbulence dissipation rates (ϵ>10-3 W kg−1) and internal stress (τ>10-2 m2 s−2) at the base of the surface layer. Internal waves were observed propagating along the base of the plume, potentially released subsequent to a hydraulic jump in the initial 1 km downstream of the plume discharge point. The momentum flux divergence of these internal waves suggests that almost 15 % of the total plume momentum can be transported out of the system by wave radiation, therefore playing a crucial role in the redistribution of momentum within the near-field plume. Observations illustrate that the evolution of the momentum budget components vary between the distinct surface plume layer and the turbulent, shear-stratified interfacial layer. Within the surface plume, a momentum balance was achieved. The dynamical balance demonstrates that the deceleration of the plume, driven by along-channel advection, is controlled by turbulence stress from the plume discharge point to as far as 3 km downstream. In the interfacial layer, however, the momentum equation was dominated by the turbulence stress term and the balance was not closed. The redistribution of momentum within the shear-stratified layer by internal wave radiation and other hydraulic features could account for the discrepancy in the budget.

Arctic microbial communities (i.e., protists and bacteria) are increasingly subjected to an intrusion of new species via Atlantification and an uncertain degree of ocean warming. As species differ in adaptive traits, these oceanic conditions may lead to compositional changes with functional implications for the ecosystem. In June 2021, we incubated water from the western Fram Strait at three temperatures (2 °C, 6 °C, and 9 °C), mimicking the current and potential future properties of the Arctic Ocean. Our results show that increasing the temperature to 6 °C only minorly affects the community, while an increase to 9 °C significantly lowers the diversity and shifts the composition. A higher relative abundance of large hetero- and mixotrophic protists was observed at 2 °C and 6 °C compared to a higher abundance of intermediate-sized temperate diatoms at 9 °C. The compositional differences at 9 °C led to a higher chlorophyll a:POC ratio, but the C:N ratio remained similar. Our results contradict the common assumption that smaller organisms and heterotrophs are favored under warming and strongly indicate a thermal limit between 6 °C and 9 °C for many Arctic species. Consequently, the magnitude of temperature increase is a crucial factor for microbial community reorganization and the ensuing ecological consequences in the future Arctic Ocean.

An along-channel momentum budget is quantified in the near-field plume region of a controlled river flow entering Doubtful Sound, New Zealand. Observations include highly resolved density, velocity and turbulence, enabling a momentum budget to be constructed over a control volume. Estimates of internal stress (τ) were made from direct measurements of turbulence dissipation rates (ε) using vertical microstructure profiles. High flow speeds of the surface plume over 2 m s−1 and strong stratification (N2 ~ 10−1 s−2) resulted in enhanced turbulence dissipation rates (ε > 10−3 W kg−1) and internal stress (τ > 10−2 m2 s−2) at the base of surface layer. An observed transition from a supercritical to sub-critical flow regime in the initial 1 km indicates the presence of an internal hydraulic jump and the subsequent release of internal gravity waves. The momentum flux divergence of these internal waves suggests that almost 15 % of the total plume momentum can be transported out of the system by wave radiation, therefore playing a crucial role in the redistribution of momentum within the near-field plume. Observations illustrate that the evolution of the momentum budget components vary between the distinct surface plume layer and the turbulent, shear-stratified interfacial layer. Within the surface plume, a momentum balance was achieved. The dynamical balance demonstrates that the deceleration of the plume, driven by along-channel advection, is controlled by turbulence stress from the plume discharge point to as far as 3 km downstream. In the interfacial layer however, the momentum equation was dominated by the turbulence stress term and the balance was not closed. The redistribution of momentum within the shear-stratified layer by the observed hydraulic jump and internal wave radiation could account for the discrepancy in the budget.

Age-associated central arterial stiffening contributes to both cerebral arterial fibrosis and to cognitive impairment. Accelerated aging, accompanied by a gradual increase in blood pressure (BP) and aortic remodeling, occurs in Dahl-S rats (DSS) vs. normotensive Sprague-Dawley rats (S-D) counterparts even in the absence of a high salt intake. A novel pro-hypertensive factor marinobufagenin (MBG) is implicated in DSS hypertension. Here we determined whether an increase in MBG is also implicated in age-associated arterial remodeling in DSS. Methods: Life span was measured in 60 S-D and 78 DSS. BP, pulse wave velocity (PWV), behavioral water maze test, ANGII, MBG and aortic collagen were assessed in 3 and 9-mo S-D and DSS on a normal 0.5% NaCl intake. Results: Median life span in DSS is reduced by 50% vs. S-D (12±1 vs. 24±2 mo, p Conclusions: In DSS high MBG occurred concurrently with fibrosis of aorta and large cerebral arteries and numerically impaired spatial memory. With advancing age of DSS further increase in BP, aortic stiffness and spatial learning/motor deficit occurred in context with an increase in MBG, which suggested an implication of MBG in these declines.

Motor output capabilities of the forelimb representation of dorsal motor area (PMd) and ventral motor area (PMv) were compared with primary motor cortex (M1) in terms of latency, strength, sign, and distribution of effects. Stimulus-triggered averages (60 microA) of electromyographic activity collected from 24 forelimb muscles were computed at 314 tracks in 2 monkeys trained to perform a reach-to-grasp task. The onset latency and magnitude of facilitation effects from PMd and PMv were significantly longer and 7- to 9-fold weaker than those from M1. Proximal muscles were predominantly represented in PMd and PMv. A joint-dependent flexor or extensor preference was also present. Distal and proximal muscle representations were intermingled in PMd and PMv. A gradual increase in latency and decrease in magnitude of effects were observed in moving from M1 surface sites toward more anterior sites in PMd. For many muscles, segregated areas producing suppression effects were found along the medial portion of PMd and adjacent M1. Although some facilitation effects from PMd and PMv had onset latencies as short as those from M1 in the same muscle, suggesting equal direct linkage, the vast majority had properties consistent with a more indirect linkage to motoneurons either through corticocortical connections with M1 and/or interneuronal linkages in the spinal cord.

Three hundred twenty fetuses were obtained from 33 pregnant gilts (Camborough-22, Pig Improvement Co.) to determine rates of nutrient deposition in fetal tissues and to estimate nutrient requirements for fetal growth. Pregnant gilts were fed an equal amount of a gestation diet (2.0 kg/d; as-fed basis), and were slaughtered at d 0, 45, 60, 75, 90, 102, or 110 of gestation (n = 3 to 6 per day). Fetuses were dissected into carcass and individual tissues (including gastrointestinal tract, liver, lung, heart, kidney, spleen [> or = d 75]), and partial placental collection was made for chemical analysis. Fetal tissues were weighed and analyzed for DM, ash, CP, and crude fat. Regression equations were obtained to explain the weight and compositional changes of individual tissues during gestation. Weights of the fetus, carcass, gastrointestinal tract, liver, heart, lung, and kidney increased cubically (P < 0.001), whereas brain weight increased linearly (P < 0.001) as gestation progressed. Fetal protein and fat contents increased quadratically (P < 0.001) as gestation progressed (R2 = 0.906 and 0.904, respectively). Changes in fetal protein and fat contents fit a multiphasic regression that consisted of two linear equations (P < 0.001, R2 = 0.988 and P < 0.001, R2 = 0.983, respectively), indicating that protein and fat growth accelerated after d 69 of gestation. Fetal protein and fat accretions were 0.25 and 0.06 g/d (P < 0.001) before d 69 of gestation, and increased to 4.63 and 1.09 g/d (P < 0.001) after d 69 of gestation. Protein needs for tissue protein gains increased 19-fold after d 69 of gestation. Results of this study indicate that the growth of the fetus and fetal tissues occurs at different rates during gestation and support the practice of a two-phase feeding strategy (before and after approximately d 70 of gestation) for pregnant gilts.

This study was conducted to determine the effect of dietary arginine supplementation on the growth of artificially reared piglets. The pigs (n = 24; 7 d old) were removed from sows to a nursery facility and assigned randomly to 1 of the 3 treatments representing diets supplemented with 0, 0.2, or 0.4% L-arginine (on the basis of milk replacer powder). Each milk feeder was assigned to 1 dietary treatment. Fresh liquid milk replacer (18.6% dry matter) was provided daily ( approximately 0800 h) to piglets. Body weights of piglets were measured and jugular venous blood samples were obtained for metabolite analysis at d 7, 14, and 21 of age. Food intake did not differ between control and arginine-supplemented piglets [66.7 vs. 69.5 g dry matter/(kg body wt. d)]. Compared with control piglets, dietary supplementation with 0.2 and 0.4% L-arginine dose dependently increased (P < 0.05) plasma concentrations of arginine by 30 and 61%, and decreased (P < 0.05) plasma concentrations of ammonia by 20 and 35%, and those of urea by 19 and 33%, respectively. Dietary supplementation with 0.4% L-arginine also increased (P < 0.05) plasma concentrations of insulin and growth hormone by 24-27% in piglets, compared with controls. Between 7 and 21 d of age, the supplementation of 0.2 and 0.4% L-arginine to piglets enhanced (P < 0.05) average daily weight gain by 28 and 66%, and body weight by 15 and 32%, respectively, compared with control piglets. Collectively, both the metabolic and growth data demonstrate unequivocally that arginine is deficient in milk-fed young pigs and that this arginine deficiency represents a major obstacle to maximal growth in piglets.

Transforming growth factor alpha (TGF-a) and beta 2 (TGF-s2) are present in human milk and are involved in growth differentiation and repair of neonatal intestinal epithelia. Heat treatment at 56°C has been shown effective for providing safe banked donor milk, with good retention of other biologically active factors. The purpose of our study was to determine the effect of heat sterilization on TGF-a and TGF-s2 concentrations in human milk. Twenty milk samples were collected from 20 lactating mothers in polypropylene containers and frozen at -20°C for transport or storage. Before heat treatment by holder pasteurization, the frozen milk was thawed and divided into 1-mL aliquots. All samples were heated in an accurately regulated water bath until a holding temperature was achieved, then held for 30 minutes using constant agitation. Holding temperature ranged from 56.5°C to 56.9°C. The milk was then stored at 4°C overnight for analysis the following day. The concentration of TGF-a was measured by radioimmunoassay. Mean concentration ± SD of TGF-a in raw milk samples was 119 ± 50 pg/mL, range 57 to 234. The mean concentration ± SD of TGF-a in heat treated samples was 113 ± 50 pg/mL, range 51 to 227. TGF-a concentration was minimally affected by pasteurization, with an overall loss of 6.1%. Of 19 samples, 4 had increased and 15 had decreased concentrations after pasteurization (mean percent ± SEM: 94% ± 7% of raw milk, range 72%-107%). The concentration of acid-activated TGF- 32 was measured by enzyme-linked immunosorbent assay. Mean concentration ± SD of TGF- 32 in raw milk samples was 5624 ± 5038 pg/mL, range 195 to 15480. The mean concentration ± SD of TGF-s2 in heat-treated samples was 5073 ± 4646pg/mL, range 181 to 15140. TGF-s2 survived with relatively little loss (0.6%): of 18 samples, 11 had increased and 7 had decreased concentrations after pasteurization (mean percent ± SEM: 99.4 ± 6.7% of raw milk, range 79%-120%). In conclusion, both TGF-a and TGF-132 were well-preserved in whole milk after holder pasteurization at 56.5°C. The relative increase in growth factor concentration in some of the samples may be attributable to the release of that factor from the cellular and/or fat compartments into the aqueous fraction of human milk These findings have implications regarding use of donor milk as an alternate source of growth factors and cytokines for the newborn gut when mother’s milk is unavailable.

Human milk fortifiers (HMF) are commonly added to human milk to increase caloric density and nutrient delivery to preterm infants. TGFβ2 is present in human milk, has immunoregulatory properties, and is involved in growth, differentiation, and repair of neonatal gut epithelia. The effect of HMF on TGFβ2 concentration is unknown. We sought to measure the concentration of TGFβ2 in whole milk following the addition of a commercially available powdered HMF. Human milk samples (N=23) were collected and stored at -20°C. For analysis, milk samples were thawed and divided into two aliquots. HMF was added at a concentration of 0.0384 g/mL (or one 0.96 g packet per 25 mL) to the 2nd aliquot of each pair. Controls included:(1) HMF at a concentration of 0.0384 g/mL in calibrator diluent (CD) and (2) HMF 0.0384 g/mL in CD with recombinant TGFβ2 at 2000 and 500 pg/mL. The concentration of the 25 kD acid-activated TGFβ2 isoform was measured using an ELISA (R&D Systems). The mean±SD concentration of TGFβ2 in unfortified milk was 5554±5345 (range 143-17640) pg/mL human milk. The mean±SD concentration of TGFβ2 in fortified milk was 7135±4774 (range 1641-17390) pg/mL. The mean relative increase in milk TGFβ2 concentration after the addition of HMF was 3.4 times that of unfortified milk. The mean TGFβ2 concentration in HMF control was 2518 pg/mL. HMF doubled the concentration of TGFTGFβ2 standards. In summary, with the addition of HMF to whole milk samples, TGFβ2 concentration decreased 2-to-10% in 4 samples but increased 1-to- 3174% in 19 samples. It appears that HMF is an additional source of TGFβ2 when added to human milk. What effect this alteration in human milk TGFβ2 concentration has on neonatal immune and gut function remains unknown.

The Effect of Antenatal Steroids on Transforming Growth Factor β-2(TGFβ 2 ) Concentrations in Human Milk ♦ 588

Human milk contains transforming growth factor-beta isoforms(TGFβ1 and β2). TGFβ affects growth and differentiation of neonatal intestinal epithelia, and modulates restitution of the gut epithilium following injury. A differential distribution of some bioactive factors in milk fat and aqueous fractions has been shown, which could affect bioavailability. It is unknown if TGF-β2 shares similar distribution properties. We sought to determine if there is a differential concentration of TGFβ2 in human milk aqueous and fat compartments. Eighteen milk samples were collected from 15 lactating mothers on postpartum day 2 to 27; gestational age of their infants at delivery ranged from 24 to 40 weeks. Whole milk was centrifuged at 2500g × 20 min at 4°C to achieve separation and isolation of its fat, aqueous and cellular components. Sodium taurcholate(STC) was added to the fat for emulsion. The concentration of acid-activated TGFβ2 in the aqueous and fat components of human milk was measured by ELISA (RD sensitivity 55 pg/ml sample; cross-reactivity with other TGFβ species/receptors is not significant; standard curve unaffected by STC). TGFβ2 was detected in all aqueous samples (6214 ± 5083 pg/mL; range 1619 to 20686); and all fat samples (6987 ± 5344 pg/mL; range 1736 to 20576). Similac Special Care formula and Enfamil Premature formula, also tested, did not have detectable levels of TGFβ2. In conclusion TGFβ2 is found in high concentrations in both the aqueous and fat compartments of human milk. These findings may be of significance for differential distribution and bioavailability of TGFβ2 in the newborn gut. Results of this study are important to future research, as fat is often discarded during human milk investigations.

Human milk contains many cytokines, including transforming growth factor-beta isoforms (TGFβ1 and β2). TGFβ appears to control growth and differentiation of neonatal intestinal epithelia, and to act in the repair of the gut following injury. It is thought that the bioavailability of these factors can be affected by their compartmentalization in milk. While an increase of certain bioactive factors within the fat compartment of milk has been shown, it is unknown if TGFβ1 shares similar distribution properties. We sought to determine if there is a differential concentration of TGFβ1 in the human milk fat layer compared with whole milk and its aqueous fraction. Thirty-six whole milk samples and an additional 13 milk fat samples were collected from 35 lactating mothers on postpartum day 3 to 6 mo.; gestational age of their infants at delivery ranged from 32 to 42 weeks. Whole milk was centrifuged at 1000g× 20 min at 4°C to achieve separation and isolation of its fat, aqueous and cellular components. Tris buffered saline (TBS; 200 μL) with 10μL Tween-20 was added to the fat for emulsion. The concentration of acid-activated TGFβ1 in whole milk, and its aqueous and fat components was measured by ELISA (Promega; sensitivity 25 pg/ml sample; cross-reactivity with other TGFβ species of