Inhibition of cytosolic Phospholipase A2 prevents prion peptide-induced neuronal damage and co-localisation with Beta III Tubulin

ABSTRACT: BACKGROUND: Activation of phospholipase A2 (PLA2) and the subsequent metabolism of arachidonic acid (AA) to prostaglandins have been shown to play an important role in neuronal death in neurodegenerative disease. Here we report the effects of the prion peptide fragment HuPrP106-126 on the PLA2 cascade in primary cortical neurons and translocation of cPLA2 to neurites. RESULTS: Exposure of primary cortical neurons to HuPrP106-126 increased the levels of phosphorylated cPLA2 and caused phosphorylated cPLA2 to relocate from the cell body to the cellular neurite in a PrP-dependent manner, a previously unreported observation. HuPrP106-126 also induced significant AA release, an indicator of cPLA2 activation; this preceded synapse damage and subsequent cellular death. The novel translocation of p-cPLA2 postulated the potential for exposure to HuPrP106-126 to result in a re-arrangement of the cellular cytoskeleton. However p-cPLA2 did not colocalise significantly with F-actin, intermediate filaments, or microtubule-associated proteins. Conversely, p-cPLA2 did significantly colocalise with the cytoskeletal protein beta III tubulin. Pre-treatment with the PLA2 inhibitor, palmitoyl trifluoromethyl ketone (PACOCF3) reduced cPLA2 activation, AA release and damage to the neuronal synapse. Furthermore, PACOCF3 reduced expression of p-cPLA2 in neurites and inhibited colocalisation with beta III tubulin, resulting in protection against PrP-induced cell death. CONCLUSIONS: Collectively, these findings suggest that cPLA2 plays a vital role in the action of HuPrP106-126 and that the colocalisation of p-cPLA2 with beta III tubulin could be central to the progress of neurodegeneration caused by prion peptides. Further work is needed to define exactly how PLA2 inhibitors protect neurons from peptide-induced toxicity and how this relates to intracellular structural changes occurring in neurodegeneration.     

大鼠脑组织含磷代谢物随年龄变化的NMR研究

随着人口老龄化的不断加剧,衰老相关疾病已成为全球关注的问题.神经系统功能的退行性改变居于衰老相关疾病的首位,其机制尚不明了.该文旨在通过核磁共振磷谱(~(31)P NMR)检测不同月龄大鼠脑组织中小分子物质的改变,明确能量相关的含磷化合物随大鼠年龄增长的变化,从而揭示脑组织中年龄相关代谢物的变化规律.该研究萃取了不同年龄(幼年、中年及老年)Sprague-Dawley(SD)大鼠脑组织中的小分子物质,进行了~(31)P NMR检测分析.结果显示:老年大鼠脑组织中能量代谢相关物质——磷酸肌酸的含量显著升高,而磷脂酰胆碱及磷酸肌醇含量显著降低,并且出现了磷酸化葡萄糖.这一发现有助于理解衰老相关的脑结构和功能下调,为神经退行性疾病的发生提供依据.     

乌头碱对大鼠尿样代谢产物影响的

将NMR谱和主成分分析(principal component analysis, PCA)相结合用于研究不同剂量下乌头碱（aconitine, AC）急性毒性作用后大鼠尿样的代谢特征. 结果表明灌胃给药后代表能量代谢的柠檬酸（citrate）,2-酮戊二酸（2-oxoglutarate）和顺乌火酸（cis-aconitate）,反应肠道菌群代谢状况的马尿酸盐（hippurate）和苯乙尿酸（phenylacetylglycine）出现异常,并且这些变化在给药后0~8 h达到最大,16 h后基本恢复正常. 且给药剂量越大代谢物异常越明显,需要的恢复时间也越长. 实验中发现2-oxoglutarate的异常增加可能与AC的神经毒性有关,或与2-oxoglutarate的代谢异常有关. 这些信息为进一步阐明AC的毒理学机制和临床毒性监测都会有一定的帮助.     

Testosterone regulation of sex steroid-related mRNAs and dopamine-related mRNAs in adolescent male rat substantia nigra

ABSTRACT: BACKGROUND: Increased risk of schizophrenia in adolescent males indicates that a link between the development of dopamine-related psychopathology and testosterone-driven brain changes may exist. However, contradictions as to whether testosterone increases or decreases dopamine neurotransmission are found and most studies address this question in adult animals. Testosterone-dependent actions in neurons are direct via activation of androgen receptors (AR) or indirect by conversion to 17beta-estradiol and activation of estrogen receptors (ER). How midbrain dopamine neurons respond to sex steroids depends on the presence of sex steroid receptor(s) and the level of steroid conversion enzymes (aromatase and 5alpha-reductase). We investigated whether gonadectomy and sex steroid replacement could influence dopamine levels by changing tyrosine hydroxylase (TH) protein and mRNA and/or dopamine breakdown enzyme mRNA levels [catechol-O-methyl transferase (COMT) and monoamine oxygenase (MAO) A and B] in the adolescent male rat substantia nigra. We hypothesized that adolescent testosterone would regulate sex steroid signaling through regulation of ER and AR mRNAs and through modulation of aromatase and 5alpha-reductase mRNA levels. RESULTS: We find ERalpha and AR in midbrain dopamine neurons in adolescent male rats, indicating that dopamine neurons are poised to respond to circulating sex steroids. We report that androgens increase TH protein and increase COMT, MAOA and MAOB mRNAs in the adolescent male rat substantia nigra. We report that all three sex steroids increase AR mRNA. Differential action on ER pathways, with ERalpha mRNA down-regulation and ERbeta mRNA up-regulation by testosterone was found. 5alpha reductase-1 mRNA was increased by AR activation, and aromatase mRNA was decreased by gonadectomy. CONCLUSIONS: We conclude that increased testosterone at adolescence can shift the balance of sex steroid signaling to favor androgenic responses through promoting conversion of T to DHT and increasing AR mRNA. Further, testosterone may increase local dopamine synthesis and metabolism, thereby changing dopamine regulation within the substantia nigra. We show that testosterone action through both AR and ERs modulates synthesis of sex steroid receptor by altering AR and ER mRNA levels in normal adolescent male substantia nigra. Increased sex steroids in the brain at adolescence may alter substantia nigra dopamine pathways, increasing vulnerability for the development of psychopathology.     

Effects of cocaine on blood flow and oxygen metabolism in the rat brain: implications for phMRI

The effects of cocaine on cerebral blood flow and tissue oxygen levels in the rat brain were investigated with concurrent laser Doppler flowmetry and fluorescence quenching spectroscopy. Responses elicited by mild hypercapnia were used as calibration to assess the effects of cocaine on oxidative metabolism. Intravenous cocaine challenge of 0.5 mg/kg induced significant increases in tissular oxygenation and perfusion in all regions investigated (primary motor cortex, medial prefrontal cortex and dorsal striatum). Mild hypercapnia, a challenge that affects haemodynamics but not metabolism, elicited comparable changes in blood flow but substantially larger changes in tissue oxygen levels. These differences in tissue oxygen build-up suggest that increased oxidative metabolism is a significant component of the cerebral metabolic response to acute cocaine challenge. The implications for the interpretation of pharmacological MRI data are discussed.     

急性低氧大鼠脑31P核磁共振波谱研究

³¹P磁共振波谱是目前唯一可以用作在体无损伤的检测细胞水平能量代谢变化的非侵入性技术,可测得脑内多种能量代谢产物.目的：急性低氧大鼠脑组织的³¹P MRS检测.方法：(1)20只成年SD大鼠分为4组：低氧0min(对照),5min,10min,15min后,迅速液氮冷冻;(2)将脑组织研碎后,加入高氯酸(PCA),冷冻干燥;(3)将提取物用0.5mL D\-2O溶解后进行MRS检测.结果：(1)急性低氧早期即引起³¹P MRS中PCr和ATP峰降低,ADP和Pi峰增高,PCr/Pi和ATP/Pi降低,而ADP/ATP增高.可交换磷池(EPP)中PCr的正常值为42.4%,低氧5min后降到28.9%, ATP从33.8%降到19.2%,Pi从17.7%升到42.0%.(2)急性低氧时³¹P MRS中脑内磷酯分解代谢产物GPC、GPE含量增加,说明低氧早期脑内即有膜磷酯的分解增加.结论：³¹P磁共振波谱可用于脑低氧性疾病的诊断,我们波谱中最敏感的指标是PCr/Pi和ATP/Pi,尤其早期降低更为显著.     

Activation of Erk and JNK MAPK pathways by acute swim stress in rat brain regions

Background

The mitogen-activated protein kinases (MAPKs) have been shown to participate in a wide array of cellular functions. A role for some MAPKs (e.g., extracellular signal-regulated kinase, Erk1/2) has been documented in response to certain physiological stimuli, such as ischemia, visceral pain and electroconvulsive shock. We recently demonstrated that restraint stress activates the Erk MAPK pathway, but not c-Jun-N-terminal kinase/stress-activated protein kinase (JNK/SAPK) or p38MAPK, in several rat brain regions. In the present study, we investigated the effects of a different stressor, acute forced swim stress, on the phosphorylation (P) state of these MAPKs in the hippocampus, neocortex, prefrontal cortex, amygdala and striatum. In addition, effects on the phosphorylation state of the upstream activators of the MAPKs, their respective MAPK kinases (MAPKKs; P-MEK1/2, P-MKK4 and P-MKK3/6), were determined. Finally, because the Erk pathway can activate c-AMP response element (CRE) binding (CREB) protein, and swim stress has recently been reported to enhance CREB phosphorylation, changes in P-CREB were also examined.

Results

A single 15 min session of forced swimming increased P-Erk2 levels 2–3-fold in the neocortex, prefrontal cortex and striatum, but not in the hippocampus or amygdala. P-JNK levels (P-JNK1 and/or P-JNK2/3) were increased in all brain regions about 2–5-fold, whereas P-p38MAPK levels remained essentially unchanged. Surprisingly, levels of the phosphorylated MAPKKs, P-MEK1/2 and P-MKK4 (activators of the Erk and JNK pathways, respectively) were increased in all five brain regions, and much more dramatically (P-MEK1/2, 4.5 to > 100-fold; P-MKK4, 12 to ~300-fold). Consistent with the lack of forced swim on phosphorylation of p38MAPK, there appeared to be no change in levels of its activator, P-MKK3/6. P-CREB was increased in all but cortical (prefrontal, neocortex) areas.

Conclusions

Swim stress specifically and markedly enhanced the phosphorylation of the MAPKKs P-MEK1/2 and P-MKK4 in all brain regions tested without apparent alteration in the phosphorylation of P-MKK3/6. Curiously, phosphorylation of their cognate substrates (Erk and JNK) was increased to a much more modest extent, and in some brain regions was not altered. Similarly, there was a region-specific discrepancy between Erk and CREB phosphorylation. Possible explanations for these findings and comparison with the effects of restraint stress will be discussed.

     

Protein fingerprints of cultured CA3-CA1 hippocampal neurons: comparative analysis of the distribution of synaptosomal and cytosolic proteins

Background  

All studies aimed at understanding complex molecular changes occurring at synapses face the problem of how a complete view of the synaptic proteome and of its changes can be efficiently met. This is highly desirable when synaptic plasticity processes are analyzed since the structure and the biochemistry of neurons and synapses get completely reshaped. Because most molecular studies of synapses are nowadays mainly or at least in part based on protein extracts from neuronal cultures, this is not a feasible option: these simplified versions of the brain tissue on one hand provide an homogeneous pure population of neurons but on the other yield only tiny amounts of proteins, many orders of magnitude smaller than conventional brain tissue. As a way to overcome this limitation and to find a simple way to screen for protein changes at cultured synapses, we have produced and characterized two dimensional electrophoresis (2DE) maps of the synaptic proteome of CA3-CA1 hippocampal neurons in culture.     

Heterogeneity of regional cerebral glucose metabolism demonstrated in situ in rat brain by 19F NMR rotating frame zeugmatography: one dimensional chemical shift imaging of normal and gliosarcoma implanted brain

Using 19-fluorine (19F) as nuclear magnetic resonance (NMR) signal probe and 2-fluoro-2-deoxy-D-glucose (2-FDG) as metabolic probe, one dimensional "imaging" (metabolite mapping) of pathway specific glucose metabolism in the pentose monophosphate shunt (PMS) and aldose reductase sorbitol (ARS) pathways were performed in situ in rat brain utilizing one dimensional rotating frame zeugmatography. Normal brain showed highest PMS activities in the brainstem consonant with known spatially heterogeneous concentration of glucose-6-phosphate dehydrogenase, the rate limiting enzyme for the PMS. The brain harboring sufficiently large gliosarcoma in the cerebrum showed a higher PMS/ARS area ratio indicating higher PMS activities in tumor which was localized by zeugmatography. The present study demonstrated the feasibility of studying regional glucose metabolism in the PMS and ARS utilizing 2-FDG.     

Measurement of regional cerebral glucose uptake by magnetic resonance spin-lock imaging

Purpose

The regional uptake of glucose in rat brain in vivo was measured at high resolution using spin-lock magnetic resonance imaging after infusion of the glucose analogue 2-deoxy-d-glucose (2DG). Previous studies of glucose metabolism have used ¹³C-labeled 2DG and NMR spectroscopy, ¹⁸F-labeled fluorodeoxyglucose (FDG) and PET, or chemical exchange saturation transfer (CEST) MRI, all of which have practical limitations. Our goal was to explore the ability of spin-lock sequences to detect specific chemically-exchanging species in vivo and to compare the effects of 2DG in brain tissue on CEST images.

Methods

Numerical simulations of R_1p and CEST contrasts for a variety of sample parameters were performed to evaluate the potential specificity of each method for detecting the exchange contributions of 2DG. Experimental measurements were made in tissue phantoms and in rat brain in vivo which demonstrated the ability of spin-lock sequences for detecting 2DG.

Results

R_1p contrast acquired with appropriate spin-lock sequences can isolate the contribution of exchanging protons in 2DG in vivo and appears to have better sensitivity and more specificity to 2DG–water exchange effects than CEST.

Conclusion

Spin-lock imaging provides a novel approach to the detection and measurement of glucose uptake in brain in vivo.     

Effects of genetic deficiency of cyclooxygenase-1 or cyclooxygenase-2 on functional and histological outcomes following traumatic brain injury in mice

Background  

Neuroinflammation contributes to the pathophysiology of acute CNS injury, including traumatic brain injury (TBI). Although prostaglandin lipid mediators of inflammation contribute to a variety of inflammatory responses, their importance in neuroinflammation is not clear. There are conflicting reports as to the efficacy of inhibiting the enzymes required for prostaglandin formation, cyclooxygenase (COX) -1 and COX-2, for improving outcomes following TBI. The purpose of the current study was to determine the role of the COX isoforms in contributing to pathological processes resulting from TBI by utilizing mice deficient in COX-1 or COX-2.     

The Influence of Feeding Frequency on Nitrogen Turnover and Whole Body Protein Synthesis in Adult Rats (Estimation using [14C]- and [15N]- Labelled Leucine)

Abstract

Male Wistar rats (17 wks. old, body weight ～400 g), fitted with an intra gastric cannula and with a catheter in the vena jugularis were divided into 3 groups and given a marginal ration of the feeding solution Nutrison Standard (1g protein and 350 kJ ME per day). Group 1 had ad lib. access to the drinking bottle, the groups 2 and 3 were pair fed by gastric infusion, splitted up into 2 greater meals for group 2 respectively into 6 smaller meals for group 3. After adaptation all animals get an i.p. injection of doubly labelled tracer solution (200μl) containing 2.5mg L-[¹⁵N]leucine (72 atom% ¹⁵N) combined with either [1-¹⁴C]- or [U-¹⁴C] leucine (37 kBq).

The course of ¹⁴CO₂ expiration was estimated by breath test over 4h in intervals of 15 min and the course of urinary ¹⁵N excretion over 24h in intervals of 45 resp. 90 min. An infusion of saline (0.9% 5ml/h) into the vena jugularis was used to provoke sustained urine production of the animals during the experiment.

From the parameters of the excretion curves of breath ¹⁴CO₂ resp. urine ¹⁵N (cumulative end value) and from the N balance the portions of leucine-C and leucine-N used for protein synthesis, transamination decarboxylation and total oxidation as well as the kinetic parameters for whole body protein metabolism were computed.

The following conclusions were drawn:

6 x feeding regime produces a small but measurable amino acid economy effect in comparison to 2 x feeding regime.

Protein gain for 2 x feeding group was significant smaller than for 6 x feeding group, though protein synthesis rate was higher, but was overcompensated by a greater increase of protein breakdown rate for the 2 x feeding group. Energy storage in form of fat and glycogen built from decarboxylation was unaffected by feeding frequency. The amount of leucine oxidized for heat production was 4% higher for the 6 x feeding group. Transamination rate for leucine was estimated to 8–15%. Absolute values for protein flux, protein synthesis and protein breakdown may be overestimated or underestimated because the metabolism of [¹⁵N] leucine does not exactly agree with that of total N; but the proportions of them and therefore also the conclusions will be true. Better results for absolute values will be obtained using a mixture of ¹⁵N labelled AA, ¹⁵N labelled protein or hydrolysate of ¹⁵N labelled protein (yeast) as the tracer source.     

Early raise of BDNF in hippocampus suggests induction of posttranscriptional mechanisms by antidepressants

Background  

The neurotrophin BDNF has been implicated in the regulation of neuroplasticity, gene expression, and synaptic function in the adult brain, as well as in the pathophysiology of neuropsychiatric disorders and the mechanism of action of antidepressants. Antidepressant treatments have been shown to increase the expression of BDNF mRNA, although the changes measured were found to be different depending on various factors. A few studies only have measured levels of BDNF protein after antidepressant treatments, and poor correlation was found between mRNA and protein changes. We studied the time course of expression of BDNF mRNA and protein during drug treatments, in order to elucidate the temporal profile of regulation of this effector and whether mRNA and protein levels correlate. Rat groups were treated for 1, 2 or 3 weeks with fluoxetine or reboxetine; in additional groups drug treatment was followed by a washout week (3+1). Total BDNF mRNA was measured by Real Time PCR, pro- and mature BDNF proteins were measured by Western blot.     

BDNF Val66Met polymorphism and protein levels in Amniotic Fluid

Background

Brain-Derived Neurotrophic Factor (BDNF) is a neurotrophin which plays survival- and growth-promoting activity in neuronal cells and it is involved in cellular plasticity mechanisms as it controls activity dependent synaptic transmission. A functional polymorphism (Val66Met) in the pro-region of BDNF, which affects the intracellular trafficking of proBDNF has been associated with memory and cognitive deficits as well as to an increased susceptibility for several psychiatric disorders especially those with a neurodevelopmental origin. To date, no study has evaluated the influence of the Val66Met polymorphism on BDNF levels in a peripheral system that may reflect fetal neurodevelopment. Therefore we investigated in amniotic fluids (AF) obtained from 139 healthy women during 15-17 week of pregnancy, BDNF protein levels in correlation with the Val66Met polymorphism.

Results

Interestingly we found a significant BDNF protein levels reduction in 55 Met carriers (Val/Met and Met/Met) (p = 0.002) as compared to 84 non carriers (Val/Val), and no effect of fetus gender, maternal age or gestation week on BDNF levels has been observed.

Conclusion

These results, although explorative, indicate that during fetal life the Val66Met genotype might influences BDNF protein levels in AF supporting the involvement of this polymorphism in behavioral and functional brain individual differences in the adulthood.     

The role of mammalian autophagy in protein metabolism

Autophagy is in principle a non-selective degradation system within cells, which is conserved in all eukaryotic cells. Autophagy is usually suppressed at low levels but can be upregulated during periods of nutrient starvation, which facilitates cell survival. In addition to this fundamental role, basal autophagy was recently revealed to be important for constitutive turnover of intracellular proteins and organelles. Autophagy has been considered to be involved also in presentation of endogenous antigens, degradation of invasive bacteria, tumor suppression, cell death and development. This review will discuss the biological significance of autophagy, particularly focusing on its implications in protein metabolism in mammals.     

The neuroprotective effect of post ischemic brief mild hypothermic treatment correlates with apoptosis, but not with gliosis in endothelin-1 treated rats

ABSTRACT: BACKGROUND: Stroke remains one of the most common diseases with a serious impact on quality of life but few effective treatments exist. Mild hypothermia (33[DEGREE SIGN]C) is a promising neuroprotective therapy in stroke management. This study investigated whether a delayed short mild hypothermic treatment is still beneficial as neuroprotective strategy in the endothelin-1 (Et-1) rat model for a transient focal cerebral ischemia. Two hours of mild hypothermia (33[DEGREE SIGN]C) was induced 20, 60 or 120 minutes after Et-1 infusion. During the experiment the cerebral blood flow (CBF) was measured via Laser Doppler Flowmetry in the striatum, which represents the core of the infarct. Functional outcome and infarct volume were assessed 24 hours after the insult. In this sub-acute phase following stroke induction, the effects of the hypothermic treatment on apoptosis, phagocytosis and astrogliosis were assessed as well. Apoptosis was determined using caspase-3 immunohistochemistry, phagocytic cells were visualized by CD-68 expression and astrogliosis was studied by glial fibrillary acidic protein (GFAP) staining. RESULTS: Cooling could be postponed up to 1 hour after the onset of the insult without losing its positive effects on neurological deficit and infarct volume. These results correlated with the caspase-3 staining. In contrast, the increased CD-68 expression post-stroke was reduced in the core of the insult with all treatment protocols. Hypothermia also reduced the increased levels of GFAP staining, even when it was delayed up to 2 hours after the insult. The study confirmed that the induction of the hypothermia treatment in the Et-1 model does not affect the CBF. CONCLUSIONS: These data indicate that in the Et-1 rat model, a short mild hypothermic treatment delayed for 1 hour is still neuroprotective and correlates with apoptosis. At the same time, hypothermia also establishes a lasting inhibitory effect on the activation of astrogliosis.     

PA28αβ overexpression enhances learning and memory of female mice without inducing 20S proteasome activity

Background

The proteasome system plays an important role in synaptic plasticity. Induction and maintenance of long term potentiation is directly dependent on selective targeting of proteins for proteasomal degradation. The 20S proteasome activator PA28αβ activates hydrolysis of small nonubiquitinated peptides and possesses protective functions upon oxidative stress and proteinopathy. The effect of PA28αβ activity on behavior and memory function is, however, not known. We generated a mouse model that overexpresses PA28α (PA28αOE) to understand PA28αβ function during healthy adult homeostasis via assessment of physiological and behavioral profiles, focusing on female mice.

Results

PA28α and PA28β protein levels were markedly increased in all PA28αOE tissues analyzed. PA28αOE displayed reduced depressive-like behavior in the forced swim test and improved memory/learning function assessed by intersession habituation in activity box and shuttle box passive avoidance test, with no significant differences in anxiety or general locomotor activity. Nor were there any differences found when compared to WT for body composition or immuno-profile. The cognitive effects of PA28αOE were female specific, but could not be explained by alterations in estrogen serum levels or hippocampal regulation of estrogen receptor β. Further, there were no differences in hippocampal protein expression of neuronal or synaptic markers between PA28αOE and WT. Biochemical analysis of hippocampal extracts demonstrated that PA28α overexpression did not increase PA28–20S peptidase activity or decrease K48-polyubiquitin levels. Instead, PA28αOE exhibited elevated efficiency in preventing aggregation in the hippocampus.

Conclusions

This study reveals, for the first time, a connection between PA28αβ and neuronal function. We found that PA28α overexpressing female mice displayed reduced depressive-like behavior and enhanced learning and memory. Since the positive effects of PA28α overexpression arose without an activation of 20S proteasome capacity, they are likely independent of PA28αβ’s role as a 20S proteasome activator and instead depend on a recognized chaperone-like function. These findings suggest that proteostasis in synaptic plasticity is more diverse than previously reported, and demonstrates a novel function of PA28αβ in the brain.

     

Core–corona PSt/P(BA–AA) composite particles by two-stage emulsion polymerization

Raspberry-shaped composite particles with polystyrene (PSt) as core and poly(n-butyl acrylate-co-acrylic acid) (P(BA–AA)) as corona were synthesized via emulsion polymerization. The random copolymer, P(BA–AA), was pre-prepared and used as a polymeric surfactant, its emulsifying properties adjusted by changing the mass ratio of BA and AA. The morphology of the resulting core–corona composite particles, P(St/P(BA–AA)), could be regulated and controlled by varying the concentrations of P(BA–AA) or the mass ratio of BA:AA in P(BA–AA). The experimental results indicate that 3.0–6.0 wt% of P(BA–AA) is required to obtain stable composite emulsions, and P(BA–AA) with a mass ratio of BA:AA = 1:2 is able to generate distinct core–corona structures. A mechanism of composite particle formation is proposed based on the high affinity between the PSt core and the hydrophobic segments of P(BA–A). The regular morphology of the colloidal film is expected to facilitate potential application of core–corona particles in the field of light scattering. Furthermore, the diversity of core–corona particles can be expanded by replacing P(BA–AA) corona particles with other amphiphilic particles.