Trends in Isolated Mitral Valve Repair or Replacement Surgery in Australia: A Statewide Cohort Linkage Study.

BACKGROUND: Global trends in mitral valve surgery (MVSx) suggest increasing repair compared with replacement, especially in the United States and European countries. The relative use, and outcomes of, MV repair and replacement in Australia are unknown. METHODS: New South Wales residents who underwent isolated MVSx between 2001 and 2017 were identified from the Admitted-Patient-Data-Collection database. Mortality outcomes were tracked to 31 Dec 2018 and adjusted based on age, sex, urgency of operation, and comorbidity status. RESULTS: The study cohort comprised 5,693 patients: 2020 (35%) underwent repair (MVr), 1,656 (29%) underwent mechanical replacement (mech.MVR), and 2017 (35%) underwent bioprosthetic replacement (bio.MVR). Respective median ages [interquartile range] were 67 yo [59-75 yo], 64 yo [55-71 yo], and 75 yo [68-80 yo] (p<0.001 across groups). Between 2001 and 2017, total MVSx increased steadily with population growth. Whereas the relative use of MVr remained static (34% to 38%), that for bio.MVR (22% to 50%) and mech.MVR (45% to 13%) changed significantly. MVr had the best outcome with 1.2% in-hospital, 2.5% 1-year, and 21.6% total cumulative mortality during a median follow-up of 6.5 years. Compared to MVr, the adjusted hazard ratio (aHR) for mech.MVR and bio.MVR for long-term mortality were 1.41 (95% confidence interval [CI]=1.24-1.61) and 1.73 (95% CI=1.53-1.95), respectively. Heart failure and sepsis were the main cardiovascular and noncardiovascular causes of death in all groups. CONCLUSION: In this statewide Australian cohort examined over 17 years, MVr is potentially underutilised despite having superior outcomes to MVR. Access to quality dataset which provides the indication for MVSx and quantitative clinical factors is critical to further improve MVr coverage and outcome MVSx.

Genome-Wide Association Studies for Albuminuria of Nondiabetic Taiwanese Population.

INTRODUCTION: Chronic kidney disease, which is defined by a reduced estimated glomerular filtration rate and albuminuria, imposes a large health burden worldwide. Ethnicity-specific associations are frequently observed in genome-wide association studies (GWAS). This study conducts a GWAS of albuminuria in the nondiabetic population of Taiwan. METHODS: Nondiabetic individuals aged 30-70 years without a history of cancer were enrolled from the Taiwan Biobank. A total of 6,768 subjects were subjected to a spot urine examination. After quality control using PLINK and imputation using SHAPEIT and IMPUTE2, a total of 3,638,350 single-nucleotide polymorphisms (SNPs) remained for testing. SNPs with a minor allele frequency of less than 0.1% were excluded. Linear regression was used to determine the relationship between SNPs and log urine albumin-to-creatinine ratio. RESULTS: Six suggestive loci are identified in or near the FCRL3 (p = 2.56 × 10-6), TMEM161 (p = 4.43 × 10-6), EFCAB1 (p = 2.03 × 10-6), ELMOD1 (p = 2.97 × 10-6), RYR3 (p = 1.34 × 10-6), and PIEZO2 (p = 2.19 × 10-7). Genetic variants in the FCRL3 gene that encode a secretory IgA receptor are found to be associated with IgA nephropathy, which can manifest as proteinuria. The PIEZO2 gene encodes a sensor for mechanical forces in mesangial cells and renin-producing cells. Five SNPs with a p-value between 5 × 10-6 and 5 × 10-5 are also identified in five genes that may have a biological role in the development of albuminuria. CONCLUSION: Five new loci and one known suggestive locus for albuminuria are identified in the nondiabetic Taiwanese population.

ER ribosomal-binding protein 1 regulates blood pressure and potassium homeostasis by modulating intracellular renin trafficking.

BACKGROUND: Genome-wide association studies (GWASs) have linked RRBP1 (ribosomal-binding protein 1) genetic variants to atherosclerotic cardiovascular diseases and serum lipoprotein levels. However, how RRBP1 regulates blood pressure is unknown. METHODS: To identify genetic variants associated with blood pressure, we performed a genome-wide linkage analysis with regional fine mapping in the Stanford Asia-Pacific Program for Hypertension and Insulin Resistance (SAPPHIRe) cohort. We further investigated the role of the RRBP1 gene using a transgenic mouse model and a human cell model. RESULTS: In the SAPPHIRe cohort, we discovered that genetic variants of the RRBP1 gene were associated with blood pressure variation, which was confirmed by other GWASs for blood pressure. Rrbp1- knockout (KO) mice had lower blood pressure and were more likely to die suddenly from severe hyperkalemia caused by phenotypically hyporeninemic hypoaldosteronism than wild-type controls. The survival of Rrbp1-KO mice significantly decreased under high potassium intake due to lethal hyperkalemia-induced arrhythmia and persistent hypoaldosteronism, which could be rescued by fludrocortisone. An immunohistochemical study revealed renin accumulation in the juxtaglomerular cells of Rrbp1-KO mice. In the RRBP1-knockdown Calu-6 cells, a human renin-producing cell line, transmission electron and confocal microscopy revealed that renin was primarily retained in the endoplasmic reticulum and was unable to efficiently target the Golgi apparatus for secretion. CONCLUSIONS: RRBP1 deficiency in mice caused hyporeninemic hypoaldosteronism, resulting in lower blood pressure, severe hyperkalemia, and sudden cardiac death. In juxtaglomerular cells, deficiency of RRBP1 reduced renin intracellular trafficking from ER to Golgi apparatus. RRBP1 is a brand-new regulator of blood pressure and potassium homeostasis discovered in this study.

Polarized evanescent waves reveal trochoidal dichroism.

Matter's sensitivity to light polarization is characterized by linear and circular polarization effects, corresponding to the system's anisotropy and handedness, respectively. Recent investigations into the near-field properties of evanescent waves have revealed polarization states with out-of-phase transverse and longitudinal oscillations, resulting in trochoidal, or cartwheeling, field motion. Here, we demonstrate matter's inherent sensitivity to the direction of the trochoidal field and name this property trochoidal dichroism. We observe trochoidal dichroism in the differential excitation of bonding and antibonding plasmon modes for a system composed of two coupled dipole scatterers. Trochoidal dichroism constitutes the observation of a geometric basis for polarization sensitivity that fundamentally differs from linear and circular dichroism. It could also be used to characterize molecular systems, such as certain light-harvesting antennas, with cartwheeling charge motion upon excitation.

Microvascular reactivity using laser Doppler measurement in type 2 diabetes with subclinical atherosclerosis.

Microangiopathy should be noted in diabetes with subclinical vascular diseases. Little is known about whether various surrogate markers of systemic arterial trees exacerbate simultaneously in preclinical atherosclerosis. To clarify the association of skin microvascular reactivity with arterial stiffness is essential to elucidating early atherosclerotic changes. The post-occlusive reactive hyperemia of skin microcirculation was evaluated in 27 control and 65 type 2 diabetic subjects, including 31 microalbuminuria (MAU) and 34 normoalbuminuria (NAU) patients. The laser Doppler skin perfusion signals were transformed into three frequency intervals for the investigation of endothelial, neurogenic, and myogenic effects on basal and reactive flow motion changes. The analysis of spectral intensity and distribution provided insight into potential significance of microvascular regulation in subclinical atherosclerotic diseases. Systemic arterial stiffness was studied by the brachial ankle pulse wave velocity (baPWV). Following occlusive ischemia, the percent change of endothelial flow motion was lower in MAU than in NAU and control groups. The MAU group revealed a relative increase in myogenic activity and a decrease in endothelial activity in normalized spectra. The baPWV showed more significant associations with reactive endothelial change (r = - 0.48, P < 0.01) and normalized myogenic value (r = - 0.37, P < 0.05) than diabetes duration and HbA1c. By multivariate regression analysis, only endothelial vasomotor changes independently contributed to the decreased baPWV (OR 3.47, 95% CI 1.63-7.42, P < 0.05). Impaired microcirculatory control is associated with increased arterial stiffness in preclinical atherosclerosis. To identify the early manifestations is necessary for at-risk patients to prevent from further vascular damage.

Outcomes after arthroscopic treatment for scaphoid nonunion using ipsilateral radius bone graft and a headless compression screw: a comparison between the patients with and without avascular necrosis.

PURPOSE: To determine whether avascular necrosis can affect clinical outcomes or the union incidence after arthroscopic bone grafting for the treatment of scaphoid nonunion. METHODS: This retrospective comparative study included thirty-four patients with scaphoid nonunion that underwent arthroscopic bone graft from the ipsilateral radius and internal fixation. The patients were divided into two cohorts (group A, with avascular necrosis, n = 15; group B, without avascular necrosis, n = 19) based on pre-operative magnetic resonance imaging findings. Additionally, the patients were grouped in accordance with the location of nonunion (waist, n = 27; proximal pole, n = 7). The mean follow-up was 20.7 months (range 12.0-40.0 months). Clinical outcomes, including the visual analog scale (VAS) pain score, grip strength, range of motion (ROM), Mayo Wrist Score (MWS), and Disabilities of the Arm, Shoulder, and Hand (DASH) score, were evaluated. Radiographic measurements for carpal bone alignment were assessed as well. RESULTS: Union rates did not differ between groups (group A, 93.3%; group B, 94.7%: p = 0.863), and the post-operative VAS pain score, ROM, and MWS were similar at follow-up for a minimum of one year. DASH and grip strength were significantly better in group B, but the intergroup differences were minimal (mean DASH 11.9 versus 9.6; mean grip strength 77.5% versus 95.4% of contralateral side). There was no significant intergroup difference in mean time to achieving union (group A, 14.9 weeks; group B, 14.6 weeks; p = 0.900). In post-operative radiographic assessments, no significant intergroup differences were noted in any of the parameters. Subgroup analysis regarding the location of nonunion showed there were no significant intergroup differences in union rates, mean time to achieving union, and clinical outcome measures at the last post-operative follow-up. CONCLUSIONS: Arthroscopic bone grafting and internal fixation in the treatment of scaphoid nonunion provided good union rates and satisfactory outcomes regardless of vascularity status.

Voice banking to support individuals who use speech-generating devices: development and evaluation of Singaporean-accented English synthetic voices and a Singapore Colloquial English recording inventory.

Voice banking involves recording an inventory of sentences produced via natural speech. The recordings are used to create a synthetic text-to-speech voice that can be installed on speech-generating devices. This study highlights a minimally researched, clinically relevant issue surrounding the development and evaluation of Singaporean-accented English synthetic voices that were created using readily available voice banking software and hardware. Processes used to create seven unique synthetic voices that produce Singaporean-accented English, and the development of a custom Singaporean Colloquial English (SCE) recording inventory, are reviewed. The perspectives of adults who spoke SCE and banked their voices for this project are summarized and were generally positive. Finally, 100 adults familiar with SCE participated in an experiment that evaluated the intelligibility and naturalness of the Singaporean-accented synthetic voices, as well as the effect of the SCE custom inventory on listener preferences. The addition of the custom SCE inventory did not affect intelligibility or naturalness of the synthetic speech, and listeners tended to prefer the voice created with the SCE inventory when the stimulus was an SCE passage. The procedures used in this project may be helpful for interventionists who wish to create synthetic voices with accents that are not commercially available.

Predator Scent-Induced Sensitization of Hypertension and Anxiety-like Behaviors.

Post-traumatic stress disorder (PTSD), an anxiety-related syndrome, is associated with increased risk for cardiovascular diseases. The present study investigated whether predator scent (PS) stress, a model of PTSD, induces sensitization of hypertension and anxiety-like behaviors and underlying mechanisms related to renin-angiotensin systems (RAS) and inflammation. Coyote urine, as a PS stressor, was used to model PTSD. After PS exposures, separate cohorts of rats were studied for hypertensive response sensitization (HTRS), anxiety-like behaviors, and changes in plasma levels and mRNA expression of several components of the RAS and proinflammatory cytokines (PICs) in the lamina terminalis (LT), paraventricular nucleus (PVN), and amygdala (AMY). Rats exposed to PS as compared to control animals exhibited (1) a significantly greater hypertensive response (i.e., HTRS) when challenged with a slow-pressor dose of angiotensin (ANG) II, (2) significant decrease in locomotor activity and increase in time spent in the closed arms of a plus maze as well as general immobility (i.e., behavioral signs of increased anxiety), (3) upregulated plasma levels of ANG II and interleukin-6, and (4) increased expression of message for components of the RAS and PICs in key brain nuclei. All the PS-induced adverse effects were blocked by pretreatment with either an angiotensin-converting enzyme antagonist or a tumor necrosis factor-α inhibitor. The results suggest that PS, used as an experimental model of PTSD, sensitizes ANG II-induced hypertension and produces behavioral signs of anxiety, probably through upregulation of RAS components and inflammatory markers in plasma and brain areas associated with anxiety and blood pressure control.

Comparative cardiovascular effectiveness of glucagon-like peptide-1 receptor agonists versus sodium-glucose cotransporter-2 inhibitors in patients with type 2 diabetes: A population-based cohort study.

AIMS: To examine the comparative effectiveness of glucagon-like peptide-1 receptor agonists (GLP-1RAs) and sodium-glucose cotransporter-2 (SGLT2) inhibitors for select cardiovascular outcomes and to examine whether the relative risks varied across different patient subgroups in patients with type 2 diabetes. MATERIALS AND METHODS: We conducted a nationwide cohort study of patients with type 2 diabetes who initiated GLP-1RAs or SGLT2 inhibitors between 2012 and 2018 in Taiwan. The study outcomes included myocardial infarction and total stroke, further classified into ischaemic or haemorrhagic stroke. We estimated the hazard ratios (HRs) and 95% confidence intervals (CIs) for each outcome, comparing GLP-1RAs with SGLT2 inhibitors using Cox proportional hazards models after 1:1 propensity-score (PS) matching. We also examined if there was effect modification by age, underlying chronic kidney disease, or coexisting cardiovascular disease in prespecified subgroup analyses. RESULTS: Among 26 032 PS-matched patients, GLP-1RA initiators and SGLT2 inhibitor initiators showed similar risks of myocardial infarction (HR 0.99, 95% CI 0.65-1.52), total stroke (HR 0.90, 95% CI 0.69-1.17), ischaemic stroke (HR 0.86, 95% CI 0.65-1.14) and haemorrhagic stroke (HR 0.88, 95% CI 0.63-1.25). However, GLP-1RA treatment was associated with an increased risk of total stroke (HR 1.76, 95% CI 1.06-2.94) and ischaemic stroke (HR 1.88, 95% CI 1.09-3.23) among patients with chronic kidney disease, but not among patients without chronic kidney disease. GLP-1RA therapy seemed to have a lower risk of haemorrhagic stroke among patients with cardiovascular disease (HR 0.64, 95% CI 0.43-0.97), but not in patients without cardiovascular disease. CONCLUSIONS: Glucagon-like peptide-1 receptor agonists and SGLT2 inhibitors appeared to have comparable effectiveness with regard to several cardiovascular outcomes overall, but their comparative effectiveness may vary in certain patient subgroups.

Estrogen deficiency aggravates fluoride-induced small intestinal mucosa damage and junctional complexes proteins expression disorder in rats.

To investigate the effect of estrogen deficiency on the small intestinal mucosal barrier induced by fluoride (F), F exposure models of ovariectomy (OVX) rats (surgically removed ovaries) and non-OVX rats (normal condition) were established by adding sodium fluoride (NaF) (0, 25, 50, and 100 mg/L, calculated by F ion) in drinking water for 90 days. The intestinal mucosal histomorphology, mucosal barrier function, and protein expression levels of tight junctions (TJs), adhesion junctions (AJs), and desmosomes were evaluated in the duodenum, jejunum, and ileum. Hematoxylin-eosin (HE) staining and 5-Bromo-2-deoxyUridine (BrdU) measurement showed that excessive F-induced damage to intestinal epithelial cells and inhibited the proliferation of intestinal epithelial cells, eventually decreasing the number of goblet cells and decreasing glycoprotein secretion, as indicated by Alcian blue and periodic acid-Schiff (AB-PAS) and periodic acid-Schiff (PAS) staining. Further immunofluorescence analysis demonstrated that excessive F decreased the protein expression levels of occludin, zonula occludens-1 (ZO-1), E-cadherin, and desmoplakin (P < 0.05, P < 0.01) and enhanced the expression of claudin-2 (P < 0.01), suggesting that cell-to-cell junctions were disrupted. Collectively, F exposure impaired the small intestinal mucosal barrier by inducing damage to intestinal epithelial cells and inhibiting intestinal epithelial cell proliferation. Disorders in the junctional complex protein expression blocked the synergy between intercellular communication and aggravated mucosal injury. In particular, estrogen deficiency exacerbated F-induced enterotoxicity, which provides new explanations for the development and severity of intestinal disease in postmenopausal women with high-F areas.

TNF-α-induced sympathetic excitation requires EGFR and ERK1/2 signaling in cardiovascular regulatory regions of the forebrain.

Peripherally or centrally administered TNF-α elicits a prolonged sympathetically mediated pressor response, but the underlying molecular mechanisms are unknown. Activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in cardiovascular regions of the brain has recently been recognized as a key mediator of sympathetic excitation, and ERK1/2 signaling is induced by activation of epidermal growth factor receptor (EGFR) tyrosine kinase activity. The present study examined the role of EGFR and ERK1/2 signaling in the sympathetic response to TNF-α. In urethane-anesthetized rats, intracarotid artery injection of TNF-α increased phosphorylation of EGFR and ERK1/2 in the subfornical organ (SFO) and the hypothalamic paraventricular nucleus (PVN); upregulated the gene expression of excitatory mediators in SFO and PVN; and increased blood pressure (BP), heart rate (HR), and renal sympathetic nerve activity (RSNA). A continuous intracerebroventricular infusion of the selective EGFR tyrosine kinase inhibitor AG1478 or the ERK1/2 inhibitor PD98059 significantly attenuated these responses. Bilateral PVN microinjections of TNF-α also increased phosphorylated ERK1/2 and the gene expression of excitatory mediators in PVN, along with increases in BP, HR, and RSNA, and these responses were substantially reduced by prior bilateral PVN microinjections of AG1478. These results identify activation of EGFR in cardiovascular regulatory regions of the forebrain as an important molecular mediator of TNF-α-driven sympatho-excitatory responses and suggest that EGFR activation of the ERK1/2 signaling pathway plays an essential role. These mechanisms likely contribute to sympathetic excitation in pathophysiological states like heart failure and hypertension, in which circulating and brain TNF-α levels are increased.NEW & NOTEWORTHY Proinflammatory cytokines contribute to the augmented sympathetic nerve activity in hypertension and heart failure, but the central mechanisms involved are largely unknown. The present study reveals that TNF-α transactivates EGFR in the subfornical organ and the hypothalamic paraventricular nucleus to initiate ERK1/2 signaling, upregulate the gene expression of excitatory mediators, and increase sympathetic nerve activity. These findings identify EGFR as a gateway to sympathetic excitation and a potential target for intervention in cardiovascular disease states.

iTRAQ-based quantitative proteomic analysis of low molybdenum inducing thymus atrophy and participating in immune deficiency-related diseases.

Molybdenum is a trace element with extremely uneven distribution in the environment. It constitutes the active sites of molybdenum enzymes that can catalyze redox reactions in almost all organisms. In this study, a mouse model with a low molybdenum diet was established to investigate the differential protein expressions in the thymus and the mechanism of molybdenum regulating thymocyte development. Results showed that the thymus evidently atrophied, and the weight and organ index of the thymus substantially decreased under the condition of low molybdenum (P < 0.01). A total of 274 differentially expressed proteins (DEPs) were screened through isobaric tag for relative and absolute quantification; amongst them, ribosomal proteins (38) were the most abundant. Bioinformatics analysis revealed that DEPs were mainly involved in protein metabolism (18%), nucleus (15%) and nucleic acid binding activity (17%), corresponding to biological process, cellular component and molecular function, respectively. Moreover, DEPs induced by low molybdenum were enriched in 94 pathways, of which typical maps including ribosome, oxidative phosphorylation and systemic lupus erythematosus. Flow cytometry analysis indicated the prominent imbalances of CD4+ and CD8+ cell ratios (P < 0.05, P < 0.01), suggesting the disordered development of T cell subsets. Overall, low molybdenum resulted in thymus atrophy by interfering with ribosomal protein expression and protein metabolism. This study provides a data platform for revealing the linkage between molybdenum and thymus-dependent immunity.

Concentrations, sizes distributions, and seasonal variations of ambient air pollutants (particulates, trace metals) in Daya/Xitun District, Taichung, Central Taiwan: a case study at Taichung Science Park.

Taichung Science Park in central Taiwan releases ambient air pollutants to the atmosphere. This issue has attracted much attention over the past few years. This study concerns seasonal concentrations of atmospheric particles and metallic elements and particle size distributions. A M.O.U.D.I sampler is used at a Taichung Science Park sampling site to obtain relevant data. Fe, followed by Al, had the highest average metallic element concentrations in particles of various sizes (PM18, PM10, PM2.5, PM1 and PM<1(0.3)); Cd had the lowest. The average concentrations of metallic elements in particles of various sizes were lowest in the summer. Fe, Al and Cr had the three highest concentrations among all metallic elements for all particles sizes in all seasons. Ambient air particulate pollutants (crustal and anthropogenic metallic elements) were released from a single emission source at Taichung Science Park site.

Feasibility and effectiveness of interactive stepping exercise on community-dwelling older adults: A pilot randomized controlled trial.

Recently, the interactive stepping exercise (ISE) was developed on the basis of square stepping exercise. The aim of this study was to examine the feasibility and effectiveness of ISE on executive function and gait variability among community-dwelling older adults. Fourteen participants were recruited and randomly assigned to the experimental group (n=7) or control group (n=7) and received ISE or home exercise program, respectively, three times a week for 12 weeks. The outcomes included retention rate, attendance rate, Trail Making Test, and dual-task walking. The results showed that participants had high retention and attendance rate for the ISE intervention. Moreover, significant improvement in the part A of Trail Making Test and stride length variability during cognitive dual-task walking after 12-week ISE intervention. The current results suggested that ISE is a feasible and effective intervention on executive function and gait variability in community-dwelling older adults.

An Injectable Microparticle Formulation Provides Long-Term Inhibition of Hypothalamic ERK1/2 Activity and Sympathetic Excitation in Rats with Heart Failure.

Sympathetic excitation contributes to clinical deterioration in systolic heart failure (HF). Significant inhibition of hypothalamic paraventricular nucleus (PVN) ERK1/2 signaling and a subsequent reduction of plasma norepinephrine (NE) levels in HF rats were achieved 2 weeks after a single subcutaneous injection of PD98059-loaded polymeric microparticles, without apparent adverse events, while blank microparticles had no effect. Similar reductions in plasma NE, a general indicator of sympathetic excitation, were previously achieved in HF rats by intracerebroventricular infusion of PD98059 or genetic knockdown of PVN ERK1/2 expression. This study presents a clinically feasible therapeutic approach to the central abnormalities contributing to HF progression.

Acoustic Vibrations of Al Nanocrystals: Size, Shape, and Crystallinity Revealed by Single-Particle Transient Extinction Spectroscopy.

Acoustic vibrations in plasmonic nanoparticles, monitored by an all-optical means, have attracted significant increasing interest because they provide unique insight into the mechanical properties of these metallic nanostructures. Al nanostructures are a recently emerging alternative to noble metal nanoparticles, because their broad wavelength tunability and high natural abundance make them ideal for many potential applications. Here, we investigate the acoustic vibrations of individual Al nanocrystals using a combination of electron microscopy and single-particle transient extinction spectroscopy, made possible with a low-pulse energy, high sensitivity, and probe-wavelength-tunable, single-particle transient extinction microscope. For chemically synthesized, faceted Al nanocrystals, the observed vibration frequency scales with the inverse particle diameter. In contrast, triangularly shaped Al nanocrystals support two distinct frequencies, corresponding to their in- and out-of-plane breathing modes. Unlike ensemble measurements, which measure average properties, measuring the damping time of the acoustic vibrations for individual particles enables us to investigate variations of the quality factor on the particle-to-particle level. Surprisingly, we find a large variation in quality factors even for nanocrystals of similar size and shape. This observed heterogeneity appears to result from substantially varying degrees of nanoparticle crystallinity even for chemically synthesized nanocrystals.

Vibrational coupling in plasmonic molecules.

Plasmon hybridization theory, inspired by molecular orbital theory, has been extremely successful in describing the near-field coupling in clusters of plasmonic nanoparticles, also known as plasmonic molecules. However, the vibrational modes of plasmonic molecules have been virtually unexplored. By designing precisely configured plasmonic molecules of varying complexity and probing them at the individual plasmonic molecule level, intramolecular coupling of acoustic modes, mediated by the underlying substrate, is observed. The strength of this coupling can be manipulated through the configuration of the plasmonic molecules. Surprisingly, classical continuum elastic theory fails to account for the experimental trends, which are well described by a simple coupled oscillator picture that assumes the vibrational coupling is mediated by coherent phonons with low energies. These findings provide a route to the systematic optical control of the gigahertz response of metallic nanostructures, opening the door to new optomechanical device strategies.

Anti-Stokes Emission from Hot Carriers in Gold Nanorods.

The origin of light emission from plasmonic nanoparticles has been strongly debated lately. It is present as the background of surface-enhanced Raman scattering and, despite the low yield, has been used for novel sensing and imaging applications because of its photostability. Although the role of surface plasmons as an enhancing antenna is widely accepted, the main controversy regarding the mechanism of the emission is its assignment to either radiative recombination of hot carriers (photoluminescence) or electronic Raman scattering (inelastic light scattering). We have previously interpreted the Stokes-shifted emission from gold nanorods as the Purcell effect enhanced radiative recombination of hot carriers. Here we specifically focused on the anti-Stokes emission from single gold nanorods of varying aspect ratios with excitation wavelengths below and above the interband transition threshold while still employing continuous wave lasers. Analysis of the intensity ratios between Stokes and anti-Stokes emission yields temperatures that can only be interpreted as originating from the excited electron distribution and not a thermally equilibrated phonon population despite not using pulsed laser excitation. Consistent with this result as well as previous emission studies using ultrafast lasers, the power-dependence of the upconverted emission is nonlinear and gives the average number of participating photons as a function of emission wavelength. Our findings thus show that hot carriers and photoluminescence play a major role in the upconverted emission.

Hot Holes Assist Plasmonic Nanoelectrode Dissolution.

Strong light-absorbing properties allow plasmonic metal nanoparticles to serve as antennas for other catalysts to function as photocatalysts. To achieve plasmonic photocatalysis, the hot charge carriers created when light is absorbed must be harnessed before they decay through internal relaxation pathways. We demonstrate the role of photogenerated hot holes in the oxidative dissolution of individual gold nanorods with millisecond time resolution while tuning charge-carrier density and photon energy using snapshot hyperspectral imaging. We show that light-induced hot charge carriers enhance the rate of gold oxidation and subsequent electrodissolution. Importantly, we distinguish how hot holes generated from interband transitions versus hot holes around the Fermi level contribute to photooxidative dissolution. The results provide new insights into hot-hole-driven processes with relevance to photocatalysis while emphasizing the need for statistical descriptions of nonequilibrium processes on innately heterogeneous nanoparticle supports.

Ultrafast Electron Dynamics in Single Aluminum Nanostructures.

Aluminum nanostructures are a promising alternative material to noble metal nanostructures for several photonic and catalytic applications, but their ultrafast electron dynamics remain elusive. Here, we combine single-particle transient extinction spectroscopy and parameter-free first-principles calculations to investigate the non-equilibrium carrier dynamics in aluminum nanostructures. Unlike gold nanostructures, we find the sub-picosecond optical response of lithographically fabricated aluminum nanodisks to be more sensitive to the lattice temperature than the electron temperature. We assign the rise in the transient transmission to electron-phonon coupling with a pump-power-independent lifetime of 500 ± 100 fs and theoretically confirm this strong electron-phonon coupling behavior. We also measure electron-phonon lifetimes in chemically synthesized aluminum nanocrystals and find them to be even longer (1.0 ± 0.1 ps) than for the nanodisks. We also observe a rise and decay in the transient transmissions with amplitudes that scale with the surface-to-volume ratio of the aluminum nanodisks, implying a possible hot carrier trapping and detrapping at the native oxide shell-metal core interface.