Understanding the margin squeeze: differentiation in fitness-related traits between central and trailing edge populations of Corallina officinalis

Assessing population responses to climate-related environmental change is key to understanding the adaptive potential of the species as a whole. Coralline algae are critical components of marine shallow water ecosystems where they function as important ecosystem engineers. Populations of the calcifying algae Corallina officinalis from the center (southern UK) and periphery (northern Spain) of the North Atlantic species natural distribution were selected to test for functional differentiation in thermal stress response. Physiological measurements of calcification, photosynthesis, respiration, growth rates, oxygen, and calcification evolution curves were performed using closed cell respirometry methods. Species identity was genetically confirmed via DNA barcoding. Through a common garden approach, we identified distinct vulnerability to thermal stress of central and peripheral populations. Southern populations showed a decrease in photosynthetic rate under environmental conditions of central locations, and central populations showed a decline in calcification rates under southern conditions. This shows that the two processes of calcification and photosynthesis are not as tightly coupled as previously assumed. How the species as whole will react to future climatic changes will be determined by the interplay of local environmental conditions and these distinct population adaptive traits.South African Research Chairs Initiative (SARChI) IF/01413/2014/CP1217/CT0004 University of Portsmouthinfo:eu-repo/semantics/publishedVersio

Understanding the margin squeeze: Differentiation in fitness-related traits between central and trailing edge populations of Corallina officinalis

Assessing population responses to climate‐related environmental change is key to understanding the adaptive potential of the species as a whole. Coralline algae are critical components of marine shallow water ecosystems where they function as important ecosystem engineers. Populations of the calcifying algae Corallina officinalis from the centre (southern UK) and periphery (northern Spain) of the North Atlantic species natural distribution were selected to test for functional differentiation in thermal stress response. Physiological measurements of calcification, photosynthesis, respiration, growth rates, oxygen and calcification evolution curves were performed using closed cell respirometry methods. Species identity was genetically confirmed via DNA barcoding. Through a common garden approach, we identified distinct vulnerability to thermal stress of central and peripheral populations. Southern populations showed a decrease in photosynthetic rate under environmental conditions of central locations and central populations showed a decline in calcification rates under southern conditions. This shows that the two processes of calcification and photosynthesis are not as tightly coupled as previously assumed. How the species as whole will react to future climatic changes will be determined by the interplay of local environmental conditions and these distinct population adaptive traits

HELP LDL apheresis reduces plasma pentraxin 3 in familial hypercholesterolemia.

BACKGROUND:Pentraxin 3 (PTX3), a key component of the humoral arm of innate immunity, is secreted by vascular cells in response to injury, possibly aiming at tuning arterial activation associated with vascular damage. Severe hypercholesterolemia as in familial hypercholesterolemia (FH) promotes vascular inflammation and atherosclerosis; low-density lipoprotein (LDL) apheresis is currently the treatment of choice to reduce plasma lipids in FH. HELP LDL apheresis affects pro- and antiinflammatory biomarkers, however its effects on PTX3 levels are unknown. We assessed the impact of FH and of LDL removal by HELP apheresis on PTX3. METHODS:Plasma lipids, PTX3, and CRP were measured in 19 patients with FH undergoing chronic HELP LDL apheresis before and after treatment and in 20 control subjects. In the patients assessment of inflammation and oxidative stress markers included also plasma TNFα, fibrinogen and TBARS. RESULTS:At baseline, FH patients had higher (p = 0.0002) plasma PTX3 than matched control subjects. In FH PTX3 correlated positively (p≤0.05) with age, gender and CRP and negatively (p = 0.01) with HELP LDL apheresis vintage. The latter association was confirmed after correction for age, gender and CRP. HELP LDL apheresis acutely reduced (p≤0.04) plasma PTX3, CRP, fibrinogen, TBARS and lipids, but not TNFα. No association was observed between mean decrease in PTX3 and in LDL cholesterol. PTX3 paralleled lipids, oxidative stress and inflammation markers in time-course study. CONCLUSION:FH is associated with increased plasma PTX3, which is acutely reduced by HELP LDL apheresis independently of LDL cholesterol, as reflected by the lack of association between change in PTX3 and in LDL levels. These results, together with the finding of a negative relationship between PTX3 and duration of treatment suggest that HELP LDL apheresis may influence both acutely and chronically cardiovascular outcomes in FH by modulating PTX3

Plasma levels of PTX3 in control (n = 20) and FH patients (n = 19).

<p>P = 0.0002.</p

Fourteen-days trend analysis of pre- and post-treatment A) PTX3, CRP and TBARS plasma levels and B) LDL-cholesterol (LDL-CT) and fibrinogen in nine patients on chronic HELP LDL-apheresis.

<p>Within each curve, values sharing the same superscript letter do not differ significantly (P<0.05).</p

Multiple regression model predicting LDL apheresis vintage in FH patients.

<p>PTX3: pentraxin 3, CRP: C reactive protein.</p

Anthropometric and clinical characteristics of study subjects.

<p>FH: familial hypercholesterolemia. Data are means±SEM. SBP: systolic blood pressure; DBP: diastolic arterial pressure; CAD: coronary artery disease.</p

Plasma concentrations of inflammatory proteins A) CRP, B) PTX3, C) fibrinogen, D) TNFα in study patients.

<p>n = 19 both before and after HELP LDL-apheresis. *P≤0.04; **P≤0.003.</p