Decreased Serum Hepcidin Concentration Correlates with Brain Iron Deposition in Patients with HBV-Related Cirrhosis

Purpose

Excessive brain iron accumulation contributes to cognitive impairments in hepatitis B virus (HBV)-related cirrhotic patients. The underlying mechanism remains unclear. Hepcidin, a liver-produced, 25-aminoacid peptide, is the major regulator of systemic iron metabolism. Abnormal hepcidin level is a key factor in some body iron accumulation or deficiency disorders, especially in those associated with liver diseases. Our study was aimed to explore the relationship between brain iron content in patients with HBV-related cirrhosis and serum hepcidin level.

Methods

Seventy HBV-related cirrhotic patients and forty age- sex-matched healthy controls were enrolled. Brain iron content was quantified by susceptibility weighted phase imaging technique. Serum hepcidin as well as serum iron, serum transferrin, ferritin, soluble transferrin receptor, total iron binding capacity, and transferrin saturation were tested in thirty cirrhotic patients and nineteen healthy controls. Pearson correlation analysis was performed to investigate correlation between brain iron concentrations and serum hepcidin, or other iron parameters.

Results

Cirrhotic patients had increased brain iron accumulation compared to controls in the left red nuclear, the bilateral substantia nigra, the bilateral thalamus, the right caudate, and the right putamen. Cirrhotic patients had significantly decreased serum hepcidin concentration, as well as lower serum transferring level, lower total iron binding capacity and higher transferrin saturation, compared to controls. Serum hepcidin level negatively correlated with the iron content in the right caudate, while serum ferritin level positively correlated with the iron content in the bilateral putamen in cirrhotic patients.

Conclusions

Decreased serum hepcidin level correlated with excessive iron accumulation in the basal ganglia in HBV-related cirrhotic patients. Our results indicated that systemic iron overload underlined regional brain iron repletion. Serum hepcidin may be a clinical biomarker for brain iron deposition in cirrhotic patients, which may have therapeutic potential.     

Mechanisms Involved in Calcium Deficiency Development in Tomato Fruit in Response to Gibberellins

Although gibberellins (GAs) have been shown to induce development of the physiological disorder blossom-end rot (BER) in tomato fruit (Solanum lycopersicum), the mechanisms involved remain largely unexplored. BER is believed to result from calcium (Ca) deficiency, but the relationship between Ca content and BER incidence is not strong. Our objectives were to better understand how GAs and a GA biosynthesis inhibitor affect BER development in tomato fruit. Tomato plants of two BER-susceptible cultivars, ‘Ace 55 (Vf)’ and ‘AB2,’ were grown in a greenhouse environment and subjected to Ca-deficiency conditions. Plants were treated weekly during fruit growth and development with 300 mg L^?1 GA₄₊₇, 300 mg L^?1 prohexadione-calcium (Apogee^®, a GA biosynthesis inhibitor), or water beginning 1 day after flower pollination. GA₄₊₇ treatment induced an increase in BER incidence in both cultivars up to 100%, whereas ‘Ace 55 (Vf)’ and ‘AB2’ plants treated with Apogee did not show BER incidence. The number of functional xylem vessels was higher in the placental and pericarp tissue of tomato fruit treated with Apogee at the early stages of fruit growth. Treatment with Apogee also increased fruit pericarp Ca concentration. GA₄₊₇ treatment enhanced the expression of the putative CAX and Ca-ATPase genes, that code for proteins involved in Ca movement into storage organelles. The lowest water-soluble apoplastic Ca concentration and the highest membrane leakage values were observed in the pericarp of GA₄₊₇-treated fruit. These results suggest that GAs consistently reduced fruit Ca uptake and water-soluble apoplastic Ca concentration, leading to leakier plasma membranes and an increase in BER development in fruit tissue of both tomato cultivars.     

用于全眼段成像和视轴参数测量的四焦点开关光学相干断层扫描

本文演示了四焦点开关傅里叶域光学相干断层扫描系统用于全眼段成像和体内视轴参数(VAP)测量的可行性.使用包括不同厚度平行玻璃板的两个同步转盘来将探测光束的焦点位置从角膜以及晶状体的前部和后部切换到视网膜.该过程同时增加了参考光束的深度范围.这种多级聚焦的方法可以使探测光束完全聚焦在人眼的每个部分.初步实验表明,该方法可...     

Regulation of photosynthesis in developing leaves of soybean chlorophyll-deficient mutants

In this report we examine the factors that regulate photosynthesis during leaf ontogeny in y3y3 and Y11y11, two chlorophyll-deficient mutants of soybean. Photosynthetic rates were similar during wild type and Y11y11 leaf development, but the senescence decline in photosynthesis was accelerated in y3y3. Photosynthetic rates fell more rapidly than chlorophyll concentrations during senescence in wild type leaves, indicating that light harvesting is not strongly limiting for photosynthesis during this phase of leaf development. Chlorophyll concentrations in Y11y11, though significantly lower than normal, were able to support normal photosynthetic rates throughout leaf ontogeny. Chlorophyll a/b ratios were constant during leaf development in the wild type, but in the mutants they progressively increased (y3y3) or decreased (Y11y11). In all three sets of plants, photosynthetic rates were directly proportional to Rubisco contents and activities, suggesting that Rubisco plays a dominant role in regulating photosynthesis throughout leaf ontogeny in these plants. The expression of some photosynthetic proteins, such as Rubisco activase, was coordinately regulated with that of Rubisco in all three genotypes, i.e. an early increase, coincident with leaf expansion, followed by a senescence decline in the fully-expanded leaf. On the other hand, the light harvesting chlorophyll a/b-binding proteins of PS II (the CAB proteins), while they showed a profile similar to that of Rubisco in the wild type and y3y3, progressively increased in amount during Y11y11 leaf development. We conclude that Y11y11 may be defective in the accumulation of a component required for LHC II assembly or function, while y3y3 has more global effects and may be a regulatory factor that controls the duration of senescence.     

Antisense RNA inhibition of Rubisco activase expression

Ribulose bisphosphate carboxylase (Rubisco) activase catalyzes the activation of Rubisco in vivo. Activase antisense DNA mutants of tobacco have been generated to explore the control that activase exerts on the photosynthetic process. These mutants have up to 90% reductions in activase protein levels as a consequence of an inhibition of activase mRNA accumulation. It is shown that photosynthesis, measured as the rate of CO₂ exchange (CER), is modestly decreased in plants exposed to high irradiances. The decreases in CER in the transgenic plants are accompanied by corresponding decreases in Rubisco activation, indicating that activase has a direct effect on photosynthetic rates in the antisense plants by influencing the activation state of Rubisco. It is concluded that in high light conditions, control of photosynthesis is largely shared between Rubisco and activase. Plant growth is also impaired in mutant plants that have severe reductions in activase. The inhibition of activase in the antisense plants does not have an impact on the accumulation of Rubisco large subunit or small subunit mRNAs or proteins. This indicates that the concerted expression of the genes for activase (Rca) and Rubisco (rbcL and rbcS) in response to light, developmental factors and circadian controls is not due to feedback regulation of rbcL or rbcS by the amount of activase protein.