Physiological responses of king penguins during simulated diving to 136 m depth

1999 ◽  
Vol 202 (20) ◽  
pp. 2819-2822 ◽  
Author(s):  
P.J. Ponganis ◽  
G.L. Kooyman ◽  
R. van Dam ◽  
Y. LeMaho

To evaluate blood N(2) uptake and the role of the respiratory volume (air sacs/lungs) as a N(2) and O(2) reservoir in deep-diving penguins, diving respiratory volume (Vdr), heart rate (fh), venous P(N)(sum), blood volume (V(b)) and hemoglobin (Hb) concentration were measured in king penguins (Aptenodytes patagonicus) during forced submersions and compressions equivalent to depths up to 136 m. Vdr was 69+/−18 ml kg(−)(1) (mean +/− s.d.) in 62 submersions ranging from 4.4 atmospheres absolute (ATA; 1 ATA=101 kPa) (34 m) to 14.6 ATA (136 m). Submersion fh averaged 30+/−7 beats min(−)(1) (N=18), approximately 20 % of pre- and post-submersion values. Venous P(N)(sum) values during and after submersions as deep as 11.2 ATA (102 m) were all less than 2.8 atmospheres N(2) (283 kPa) above ambient pressure, a previously measured threshold for symptomatic bubble formation. Mean V(b) was 83+/−8 ml kg(−)(1) (N=6); [Hb] was 17.6+/−0.7 g dl(−)(1) (N=7). On a mass-specific basis, mean Vdr, and therefore total available N(2), is 41 % of that in shallow-diving penguin species. Total body O(2) stores, calculated from measured Vdr, V(b), [Hb], muscle mass and myoglobin concentration, are 45 ml kg(−)(1), with 23 % in the respiratory system. This small respiratory fraction in comparison with that in shallow-diving penguins suggests a lesser reliance on the respiratory oxygen store for extended breath-holding and also a reduced uptake of nitrogen at depth.

2018 ◽  
Vol 239 (3) ◽  
pp. 303-312 ◽  
Author(s):  
H H Farman ◽  
K L Gustafsson ◽  
P Henning ◽  
L Grahnemo ◽  
V Lionikaite ◽  
...  

The importance of estrogen receptor α (ERα) for the regulation of bone mass in males is well established. ERα mediates estrogenic effects both via nuclear and membrane-initiated ERα (mERα) signaling. The role of mERα signaling for the effects of estrogen on bone in male mice is unknown. To investigate the role of mERα signaling, we have used mice (Nuclear-Only-ER; NOER) with a point mutation (C451A), which results in inhibited trafficking of ERα to the plasma membrane. Gonadal-intact male NOER mice had a significantly decreased total body areal bone mineral density (aBMD) compared to WT littermates at 3, 6 and 9 months of age as measured by dual-energy X-ray absorptiometry (DEXA). High-resolution microcomputed tomography (µCT) analysis of tibia in 3-month-old males demonstrated a decrease in cortical and trabecular thickness in NOER mice compared to WT littermates. As expected, estradiol (E2) treatment of orchidectomized (ORX) WT mice increased total body aBMD, trabecular BV/TV and cortical thickness in tibia compared to placebo treatment. E2 treatment increased these skeletal parameters also in ORX NOER mice. However, the estrogenic responses were significantly decreased in ORX NOER mice compared with ORX WT mice. In conclusion, mERα is essential for normal estrogen signaling in both trabecular and cortical bone in male mice. Increased knowledge of estrogen signaling mechanisms in the regulation of the male skeleton may aid in the development of new treatment options for male osteoporosis.


2019 ◽  
Vol 28 (4) ◽  
pp. 1016-1036
Author(s):  
Mengyu Miranda Gao ◽  
Aryanne D. de Silva ◽  
E. Mark Cummings ◽  
Patrick T. Davies

2017 ◽  
Vol 30 (4) ◽  
pp. 379-395 ◽  
Author(s):  
Alia J. Crum ◽  
Modupe Akinola ◽  
Ashley Martin ◽  
Sean Fath

2006 ◽  
Vol 13 (1) ◽  
pp. 257-269 ◽  
Author(s):  
G Riesco-Eizaguirre ◽  
P Gutiérrez-Martínez ◽  
M A García-Cabezas ◽  
M Nistal ◽  
P Santisteban

The oncogene BRAFV600E is the most frequent genetic event in papillary thyroid carcinoma (PTC) but its prognostic impact still remains to be elucidated. We evaluated a representative series of 67 individuals with PTC who underwent total thyroidectomy. BRAF-positive tumours correlated with early recurrences (32% vs 7.6%; P=0.02) during a median postoperative follow-up period of 3 years. Interestingly, within the recurrences, a significant majority had negative radioiodine (131I) total body scans, predicting a poorer outcome as treatment with 131I is not effective. This last observation led us to investigate the role of BRAFV600E and the MEK-ERK pathway in thyroid dedifferentiation, particularly in Na+/I− symporter (NIS) impairment, as this thyroid-specific plasma membrane glycoprotein mediates active transport of I− into the thyroid follicular cells. A subset of 60 PTC samples was evaluated for NIS immunoreactivity and, accordingly, we confirmed a significant low NIS expression and impaired targeting to membranes in BRAF-positive samples (3.5% vs 30%; P=0.005). Furthermore, experiments with differentiated PCCl3 thyroid cells demonstrated that transient expression of BRAFV600E sharply impaired both NIS expression and targeting to membrane and, surprisingly, this impairment was not totally dependent on the MEK-ERK pathway. We have concluded that BRAFV600E is a new prognostic factor in PTC that correlates with a high risk of recurrences and less differentiated tumours due to the loss of NIS-mediated 131I uptake.


2014 ◽  
Vol 222 (1) ◽  
pp. R11-R24 ◽  
Author(s):  
Syed Jalal Khundmiri

Cardiotonic steroids have been used for the past 200 years in the treatment of congestive heart failure. As specific inhibitors of membrane-bound Na+/K+ATPase, they enhance cardiac contractility through increasing myocardial cell calcium concentration in response to the resulting increase in intracellular Na concentration. The half-minimal concentrations of cardiotonic steroids required to inhibit Na+/K+ATPase range from nanomolar to micromolar concentrations. In contrast, the circulating levels of cardiotonic steroids under physiological conditions are in the low picomolar concentration range in healthy subjects, increasing to high picomolar levels under pathophysiological conditions including chronic kidney disease and heart failure. Little is known about the physiological function of low picomolar concentrations of cardiotonic steroids. Recent studies have indicated that physiological concentrations of cardiotonic steroids acutely stimulate the activity of Na+/K+ATPase and activate an intracellular signaling pathway that regulates a variety of intracellular functions including cell growth and hypertrophy. The effects of circulating cardiotonic steroids on renal salt handling and total body sodium homeostasis are unknown. This review will focus on the role of low picomolar concentrations of cardiotonic steroids in renal Na+/K+ATPase activity, cell signaling, and blood pressure regulation.


Blood ◽  
2006 ◽  
Vol 107 (2) ◽  
pp. 835-840 ◽  
Author(s):  
Daniel E. Cramer ◽  
Daniel J. Allendorf ◽  
Jarek T. Baran ◽  
Richard Hansen ◽  
Jose Marroquin ◽  
...  

AbstractMyelotoxic injury in the bone marrow (BM) as a consequence of total body irradiation (TBI) or granulocyte colony-stimulating factor (G-CSF) mobilization results in the deposition of iC3b on BM stroma (stroma-iC3b). In the present study, we have examined how stroma-iC3b interacts with hematopoietic progenitor cells (HPCs) and the role of complement (C) and complement receptor 3 (CR3) in BM injury/repair. We demonstrate here that stroma-iC3b tethers HPCs via the inserted (I) domain of HPC complement receptor 3 (CR3, CD11b/CD18, Mac-1). Following irradiation, stroma-iC3b was observed in the presence of purified IgM and normal mouse serum (NMS), but not serum from Rag-2-/- mice, implicating a role for antibody (Ab) and the classic pathway of C activation. Furthermore, a novel role for soluble yeast β-glucan, a ligand for the CR3 lectin-like domain (LLD), in the priming of CR3+ HPC is suggested. Soluble yeast β-glucan could enhance the proliferation of tethered HPCs, promote leukocyte recovery following sublethal irradiation, and increase the survival of lethally irradiated animals following allogeneic HPC transplantation in a CR3-dependent manner. Taken together, these observations suggest a novel role for C, CR3, and β-glucan in the restoration of hematopoiesis following injury. (Blood. 2006;107:835-840)


2018 ◽  
Vol 51 (3) ◽  
pp. 349-361
Author(s):  
Fernanda Patricia Gottardi ◽  
Tairon Pannunzio Dias e Silva ◽  
Patrick Elves Paraguaio ◽  
Jacira Neves da Costa Torreão ◽  
Carlo Aldrovandi Torreão Marques ◽  
...  

2016 ◽  
Vol 800 ◽  
pp. 180-212 ◽  
Author(s):  
Pablo Peñas-López ◽  
Miguel A. Parrales ◽  
Javier Rodríguez-Rodríguez ◽  
Devaraj van der Meer

The term ‘history effect’ refers to the contribution of any past mass transfer events between a gas bubble and its liquid surroundings towards the current diffusion-driven growth or dissolution dynamics of that same bubble. The history effect arises from the (non-instantaneous) development of the dissolved gas concentration boundary layer in the liquid in response to changes in the concentration at the bubble interface caused, for instance, by variations of the ambient pressure in time. Essentially, the history effect amounts to the acknowledgement that at any given time the mass flux across the bubble is conditioned by the preceding time history of the concentration at the bubble boundary. Considering the canonical problem of an isolated spherical bubble at rest, we show that the contribution of the history effect in the current interfacial concentration gradient is fully contained within a memory integral of the interface concentration. Retaining this integral term, we formulate a governing differential equation for the bubble dynamics, analogous to the well-known Epstein–Plesset solution. Our equation does not make use of the quasi-static radius approximation. An analytical solution is presented for the case of multiple step-like jumps in pressure. The nature and relevance of the history effect is then assessed through illustrative examples. Finally, we investigate the role of the history effect in rectified diffusion for a bubble that pulsates under harmonic pressure forcing in the non-inertial, isothermal regime.


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