Synchrotron Radiation μ‑XRF Imaging Reveals Mn Zoning in Freshwater Pearls

Chemical zoning is commonly seen in inorganic minerals, and it holds implications for magmatic processes, hydrothermal evolution, or metal mineralization. However, few studies are available on oscillatory zoning in biominerals, which carries the most direct and unique information on the biomineralization mechanism. This study investigates spatial and temporal resolution of trace element distributions in pearls that were cultivated in the Hyriopsis cumingii mantle (non-nucleated pearls and nucleated Akoya pearls) or visceral mass (nucleated Edison pearls) for 1–5 years. Using synchrotron radiation micro-X-ray fluorescence imaging, we find a variety of trace elements such as Sc, Cr, Mn, Cu, Zn, Ge, and Ba. The types of trace elements are slightly different for individuals. For the first time, submillimeter-scale Mn zoning is identified ubiquitously, concentric with the pearl, and exhibits increased concentrations toward the pearl margin. In non-nucleated pearls and nucleated Akoya pearls, the Mn zones are superposed with a spatially damped pattern with a decrease in the interzones. In contrast, no damped trends are observed in the Mn zones in nucleated Edison pearls. This difference may be due to different cultivation sites within mollusks that have different requirements for Mn during pearl growth. We suggest a growth model of dissipative structure for the Mn zoning in pearls, which depends upon the coupling between the interface kinetics and the diffusion of chemical species in the environment. The trace elements (including Mn) substitute Ca in aragonite isomorphically, based on Raman imaging. The scanning electron microscopy images show a periodic structure of aragonite platelets and organic matter of pearls. Locally in the Mn zones, there are minor defects on platelets, which may arise from the enrichment of trace elements. This study would develop a new research field for chemical zoning in minerals and introduce a new angle in understanding trace element incorporation in biominerals and the biomineralization processes

AGEs impair voltage-gated K⁺ (K_v) current and expression via interacting with receptor of advanced glycation products (RAGE).

<p>A: Sample traces of whole cell K⁺ currents recorded before and after incubation with 3 mmol/L 4-aminopyridine (4-AP). K⁺ currents were generated by 10-mV incremental depolarizing steps from -60 to +60 mV. B: I-V relationships of K_v current density in vascular smooth muscle cells. <i>n</i> = 6 for independent cells in each group. C and D: After treatment with AGEs alone or AGEs plus anti-RAGE, expression of K_v1.2 and K_v1.5 at the gene and protein level was evaluated by quantitative real-time-PCR (C) and western blot analysis (D). * <i>P</i> < 0.05 <i>vs</i>. Control.</p

Role of AGEs in impaired K_v channels-mediated coronary vasodilation in diabetic rats.

<p>Control and Diabetic rats were treated with aminoguanidine (AG) or vehicle for 10 weeks. Rat small coronary arteries (RSCAs) were isolated from different rat groups. A: K_v current density in vascular smooth muscle cells isolated from different rat groups. <i>n</i> = 6 for independent cells in each group. B and C: Expression of K_v1.2 and K_v1.5 at the gene and protein level was evaluated by quantitative real-time-PCR (B) and western blot analysis (C). D: Dose-dependent dilation to forskolin in RSCAs was measured using a pressurized myograph. E: After incubation of RSCAs with 3 mmol/L K_v inhibitor 4-aminopyridine (4-AP) for 20 min, dilations to forskolin in all rat groups were significantly reduced. K_v channels-mediated vasodilation was defined as the difference between dilations measured before and after incubation with 4-AP. <i>n</i> = 8 for independent arterial rings in each group. * <i>P</i> < 0.05 <i>vs</i>. Control. # <i>P</i> < 0.05 <i>vs</i>. diabetic group (DM).</p

Clinical characteristics of control and diabetic rats.

<p>Values are presented as mean ± SD. <i>n</i> = 8 for each group. BP, blood pressure. AGEs, advanced glycation end products. AG, aminoguanidine.</p><p>* <i>P</i> < 0.05 <i>vs</i>. control.</p><p>^#<i>P</i> < 0.05 <i>vs</i>. diabetic group (DM).</p><p>Clinical characteristics of control and diabetic rats.</p

The role of AGEs in high glucose-induced voltage-gated K⁺ (K_v) channels dysfunction in vascular smooth muscle cells (VSMCs).

<p>A: Overproduction of AGEs in high glucose was blunted by treatment with aminoguanidine (AG). B: I-V relationships of K_v current density in VSMCs. <i>n</i> = 6 for independent cells in each group. C: Sample traces of whole cell K⁺ currents recorded before and after incubation with 3 mmol/L 4-aminopyridine (4-AP). K⁺ currents were generated by 10-mV incremental depolarizing steps from -60 to +60 mV. D: Expression of receptor of advanced glycation products (RAGE) was determined by western blotting. Pretreatment with anti-RAGE decreased available RAGE for AGEs to bind. * <i>P</i> < 0.05 <i>vs</i>. normal glucose (NG). # <i>P</i> < 0.05 <i>vs</i>. high glucose (HG).</p

The role of AGEs in high glucose-induced downregulation of voltage-gated K⁺ (K_v) channels expression in vascular smooth muscle cells (VSMCs).

<p>VSMCs were incubated with Aminoguanidine (AG) or anti-receptor of advanced glycation products (RAGE) for 30 min, followed by high glucose treatment, and expression of K_v1.2 and K_v1.5 at the gene and protein level was evaluated by quantitative real-time-PCR (A and B) and western blot analysis (C). * <i>P</i> < 0.05 <i>vs</i>. normal glucose (NG). # <i>P</i> < 0.05 <i>vs</i>. high glucose (HG).</p

Comparison of Conscious and Anesthetized Blood Pressures.

<p><i>Left Panels-</i> Scatterplot comparison of systolic (top) and pulse (bottom) arterial pressure measurements via implanted telemetry under conscious (blue) and anesthetized (red) conditions. Horizontal bars represent the measurement mean. <i>Right panels-</i> Scatterplot of the differences between conscious and anesthetized measurements on a subject-by-subject basis. Circles denote subjects infused with AngII while ‘x’s denote controls. Horizontal bars represent the measurement mean.</p

Telemetric Blood Pressure Assessment in Angiotensin II-Infused ApoE^-/- Mice: 28 Day Natural History and Comparison to Tail-Cuff Measurements

<div><p>Abdominal aortic aneurysm (AAA) is a disease of the aortic wall, which can progress to catastrophic rupture. Assessment of mechanical characteristics of AAA, such as aortic distensibility, may provide important insights to help identify at-risk patients and understand disease progression. While the majority of studies on this topic have focused on retrospective patient data, recent studies have used mouse models of AAA to prospectively evaluate the evolution of aortic mechanics. Quantification of aortic distensibility requires accurate measurement of arterial blood pressure, particularly pulse pressure, which is challenging to perform accurately in murine models. We hypothesized that volume/pressure tail-cuff measurements of arterial pulse pressure in anesthetized mice would have sufficient accuracy to enable calculations of aortic distensibility with minimal error. Telemetry devices and osmotic mini-pumps filled with saline or angiotensin-II were surgically implanted in male apolipoprotein-E deficient (ApoE^-/-) mice. Blood pressure in the aortic arch was measured continuously via telemetry. In addition, simultaneous blood pressure measurements with a volume/pressure tail-cuff system were performed under anesthesia at specific intervals to assess agreement between techniques. Compared to controls, mice infused with angiotensin-II had an overall statistically significant increase in systolic pressure, with no overall difference in pulse pressure; however, pulse pressure did increase significantly with time. Systolic measurements agreed well between telemetry and tail-cuff (coefficient of variation = 10%), but agreement of pulse pressure was weak (20%). In fact, group-averaged pulse pressure from telemetry was a better predictor of a subject’s pulse pressure on a given day than a simultaneous tail-cuff measurement. Furthermore, these approximations introduced acceptable errors (15.1 ± 12.8%) into the calculation of aortic distensibility. Contrary to our hypothesis, we conclude that tail-cuff measures of arterial pulse pressure have limited accuracy. Future studies of aneurysm mechanics using the ApoE^-/-/angiotensin-II model would be better in assuming pulse pressure profiles consistent with our telemetry findings instead of attempting to measure pulse pressure in individual mice.</p></div

Comparison of Simultaneous Measurements of Implanted Telemetry and Non-Invasive Tail-cuff.

<p>Bland-Altman plot comparing telemetry and tail-cuff measurements of systolic (top) and pulse (bottom) blood pressures. Circles denote subjects infused with AngII while ‘x’s denote controls. Overlaid numbers represent the measurement bias (adjacent to the dotted lines) and 95% limits of agreement (adjacent to solid lines). The mean coefficient of variation (CoV) is also reported.</p

Error Analysis of Pulse Pressure Estimation for Distensibility Calculations by Group.

<p>Mean group errors for the calculation of aortic distensibility introduced by the group-averaged estimation of arterial pulse pressure as a function of the time (days) with continuous infusion of AngII (after removal of statistical outlier) or saline (‘Control’).</p