Multi-organ involvement caused by Scedosporium apiospermum infection after near drowning: a case report and literature review.

BACKGROUND: Scedosporium apiospermum (S. apiospermum) is a rare fungal pathogen that causes disseminated infections. It rarely affects immunocompetent individuals and has a poor prognosis. CASE PRESENTATION: A 37-year-old woman presented with multiple lesions in the lungs, brain, and eyes, shortly after near drowning in a car accident. The primary symptoms were chest tightness, limb weakness, headache, and poor vision in the left eye. S. apiospermum infection was confirmed by metagenomic next-generation sequencing (mNGS) of intracranial abscess drainage fluid, although intracranial metastases were initially considered. After systemic treatment with voriconazole, her symptoms improved significantly; however, she lost vision in her left eye due to delayed diagnosis. CONCLUSION: While S. apiospermum infection is rare, it should be considered even in immunocompetent patients. Prompt diagnosis and treatment are essential. Voriconazole may be an effective treatment option.

The bacterial pathogen Pseudomonas plecoglossicida, its epidemiology, virulence factors, vaccine development, and host-pathogen interactions.

OBJECTIVE: Pseudomoans plecoglossicida has been identified as a fish pathogen since 2000 and has caused serious infections in cultured Large Yellow Croakers Larimiththys crocea in coastal eastern China during recent years. METHODS: Published literatures of this pathogen have been reviewed. RESULT: Several strains with high genomic similarity have been isolated and identified; the bacteria induce natural infection at lower water temperatures (12.0-25.5°C) and induce numerous granulomas and nodules in the visceral organs of croakers. Researchers have investigated the epidemiology of P. plecoglossicida infection, identified major virulence factors, searched for pathogenic genes, analyzed host-pathogen interactions, and endeavored to develop efficient vaccines. CONCLUSION: This paper provides an overview of these research advances to elucidate the virulence mechanisms of the pathogen and to promote vaccine development against infection.

MicroRNA-218-5p-Ddx41 axis restrains microglia-mediated neuroinflammation through downregulating type I interferon response in a mouse model of Parkinson's disease.

BACKGROUND: Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic (DA) neurons in the substantia nigra (SN). Microglia-mediated neuroinflammation has been largely considered one of main factors to the PD pathology. MicroRNA-218-5p (miR-218-5p) is a microRNA that plays a role in neurodevelopment and function, while its potential function in PD and neuroinflammation remains unclear. METHODS: We explore the involvement of miR-218-5p in the PD in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model. The miR-218-5p agomir used for overexpression was delivered into the substantia nigra (SN) by bilateral stereotaxic infusions. The loss of dopaminergic (DA) neurons and microglial inflammation in the SN was determined using Western blotting and immunofluorescence. Motor function was assessed using the rotarod test. RNA sequencing (RNA-seq) was performed to explore the pathways regulated by miR-218-5p. The target genes of miR-218-5p were predicted using TargetScan and confirmed using dual luciferase reporter assays. The effects of miR-218-5p on microglial inflammation and related pathways were verified in murine microglia-like BV2 cells. To stimulate BV2 cells, SH-SY5Y cells were treated with 1-methyl-4-phenylpyridinium (MPP+) and the conditioned media (CM) were collected. RESULTS: MiR-218-5p expression was reduced in both the SN of MPTP-induced mice and MPP+-treated BV2 cells. MiR-218-5p overexpression significantly alleviated MPTP-induced microglial inflammation, loss of DA neurons, and motor dysfunction. RNA sequence and gene set enrichment analysis showed that type I interferon (IFN-I) pathways were upregulated in MPTP-induced mice, while this upregulation was reversed by miR-218-5p overexpression. A luciferase reporter assay verified that Ddx41 was a target gene of miR-218-5p. In vitro, miR-218-5p overexpression or Ddx41 knockdown inhibited the IFN-I response and expression of inflammatory cytokines in BV2 cells stimulated with MPP+-CM. CONCLUSIONS: MiR-218-5p suppresses microglia-mediated neuroinflammation and preserves DA neurons via Ddx41/IFN-I. Hence, miR-218-5p-Ddx41 is a promising therapeutic target for PD.

Third ventricular width by transcranial sonography is associated with cognitive impairment in Parkinson's disease.

BACKGROUND: One-fourth of Parkinson's disease (PD) patients suffer from cognitive impairment. However, few neuroimaging markers have been identified regarding cognitive impairment in PD. OBJECTIVE: This study aimed to explore the association between third ventricular width by transcranial sonography (TCS) and cognitive decline in PD. METHOD: Participants with PD were recruited from one medical center in China. Third ventricular width was assessed by TCS, and cognitive function was analyzed by the Mini-Mental State Examination (MMSE). Receiver operating characteristic (ROC) analysis and Cox model analysis were utilized to determine the diagnostic and predictive accuracy of third ventricular width by TCS for cognitive decline in PD patients. RESULT: A total of 174 PD patients were recruited. Third ventricular width was negatively correlated with MMSE scores. ROC analysis suggested that the optimal cutoff point for third ventricular width in screening for cognitive impairment in PD was 4.75 mm (sensitivity 62.7%; specificity 75.6%). After 21.5 (18.0, 26.0) months of follow-up in PD patients without cognitive impairment, it was found that those with a third ventricular width greater than 4.75 mm exhibited a 7.975 times higher risk of developing cognitive impairment [hazard ratio = 7.975, 95% CI 1.609, 39.532, p = 0.011] compared with patients with a third ventricular width less than 4.75 mm. CONCLUSION: Third ventricular width based on TCS emerged as an independent predictor of developing cognitive impairment in PD patients.

CCL5 promotes LFA-1 expression in Th17 cells and induces LCK and ZAP70 activation in a mouse model of Parkinson's disease.

Background: Parkinson's disease (PD), which is associated to autoimmune disorders, is characterized by the pathological deposition of alpha-synuclein (α-Syn) and loss of dopaminergic (DA) neurons. Th17 cells are thought to be responsible for the direct loss of DA neurons. C-C chemokine ligand 5 (CCL5) specifically induces Th17 cell infiltration into the SN. However, the specific effect of CCL5 on Th17 cells in PD and the relationship between CCL5 and lymphocyte function-associated antigen-1 (LFA-1) expression in Th17 cells are unknown. Methods: We evaluated the effects of CCL5 on LFA-1 expression in Th17 cells in mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and examined Th17 cell differentiation upon CCL5 stimulation in vitro. Furthermore, we assessed the effects of CCL5 on tyrosine kinase zeta-chain-associated protein kinase 70 (ZAP70) and lymphocyte-specific protein tyrosine kinase (LCK) activity in CCL5-stimulated Th17 cells in vivo and in vitro. Results: CCL5 increased the proportion of peripheral Th17 cells in MPTP-treated mice, LFA-1 expression on Th17 cells, and Th17 cell levels in the SN of MPTP-treated mice. CCL5 promoted Th17 cell differentiation and LFA-1 expression in naive T cells in vitro. Moreover, CCL5 increased Th17 cell differentiation and LFA-1 expression by stimulating LCK and ZAP70 activation in naive CD4+ T cells. Inhibiting LCK and ZAP70 activation reduced the proportion of peripheral Th17 cells and LFA-1 surface expression in MPTP-treated mice, and Th17 cell levels in the SN also significantly decreased. Conclusion: CCL5, which increased Th17 cell differentiation and LFA-1 protein expression by activating LCK and ZAP70, could increase the Th17 cell number in the SN, induce DA neuron death and aggravate PD.

Estimated glomerular filtration rate is a biomarker of cognitive impairment in Parkinson's disease.

Backgrounds: The relationship between kidney function and cognitive impairment in Parkinson's disease (PD) is poorly understood and underexplored. This study aims to explore whether renal indices can serve as indicators to monitor the cognitive impairment of PD. Methods: A total of 508 PD patients and 168 healthy controls from the Parkinson's Progression Markers Initiative (PPMI) were recruited, and 486 (95.7%) PD patients underwent longitudinal measurements. The renal indicators including serum creatinine (Scr), uric acid (UA), and urea nitrogen, as well as UA/Scr ratio and estimated glomerular filtration rate (eGFR), were measured. Cross-sectional and longitudinal associations between kidney function and cognitive impairment were evaluated using multivariable-adjusted models. Results: eGFR was associated with lower levels of cerebrospinal fluid (CSF) Aß1-42 (p = 0.0156) and α-synuclein (p = 0.0151) and higher serum NfL (p = 0.0215) in PD patients at baseline. Longitudinal results showed that decreased eGFR predicted a higher risk of cognitive impairment (HR = 0.7382, 95% CI = 0.6329-0.8610). Additionally, eGFR decline was significantly associated with higher rates of increase in CSF T-tau (p = 0.0096), P-tau (p = 0.0250), and serum NfL (p = 0.0189), as well as global cognition and various cognitive domains (p < 0.0500). The reduced UA/Scr ratio was also linked to higher NfL levels (p = 0.0282) and greater accumulation of T-tau (p = 0.0282) and P-tau (p = 0.0317). However, no significant associations were found between other renal indices and cognition. Conclusion: eGFR is altered in PD subjects with cognitive impairment, and predict larger progression of cognitive decline. It may assist identifying patients with PD at risk of rapid cognitive decline and have the potential to monitoring responses to therapy in future clinical practice.

Diagnostic Performance of Putaminal Hypointensity on Susceptibility MRI in Distinguishing Parkinson Disease from Progressive Supranuclear Palsy: A Meta-Analysis.

Background: Idiopathic Parkinson's disease (IPD) and progressive supranuclear palsy (PSP) have similar clinical signs and symptoms, making accurate clinical diagnosis difficult. T2* gradient echo (T2* GRE), susceptibility-weighted imaging (SWI), and quantitative susceptibility mapping (QSM) are susceptibility MR imaging sequences that provide more information about brain iron levels than other conventional MR imaging. Objective: This study aimed to evaluate the diagnostic power of putaminal hypointensity on T2* GRE, SWI, and QSM in distinguishing PSP from IPD. Methods: Eligible studies were identified via systematic searches of PubMed and Clarivate Analytics® Web of Science® Core Collection. Studies that satisfied the inclusion and exclusion criteria were reviewed. A meta-analysis was conducted using the hierarchical summary receiver operating characteristic curve approach. Results: Our literature search of the two databases yielded 562 primary articles, 10 of which were deemed relevant and only six were eligible for further analyses. We performed a meta-analysis of putaminal hypointensity measurements: 438 patients with IPD and 109 patients with PSP were enrolled in the quantitative synthesis. The meta-analysis of six studies with 547 patients revealed a sensitivity of 69% (95% confidence interval (CI): 33%-90%) and specificity of 91% (95% CI: 80%-96%) for putaminal hypointensity on T2* GRE, SWI, or QSM distinguishing PSP from IPD. Conclusions: Putaminal hypointensity on T2* GRE, SWI, or QSM is able to distinguish patients with PSP from those with IPD with high specificity. Further multicenter prospective studies on patients are needed to verify our results.

A systematic review and meta-analysis of inflammatory biomarkers in Parkinson's disease.

Neuroinflammation plays a crucial role in the pathogenesis of Parkinson's disease (PD), but controversies persist. Studies reporting concentrations of blood or cerebrospinal fluid (CSF) markers for patients with PD and controls were included and extracted. Pooled Hedges'g was adopted to illustrate comparisons, and covariates were used to explore sources of heterogeneity. Finally, 152 studies were included. Increased IL-6, TNF-α, IL-1ß, STNFR1, CRP, CCL2, CX3CL1, and CXCL12 levels and decreased INF-γ and IL-4 levels were noted in the PD group. In addition, increased CSF levels of IL-6, TNF-α, IL-1ß, CRP and CCL2 were revealed in patients with PD compared to controls. Consequently, significantly altered levels of inflammatory markers were verified between PD group and control, suggesting that PD is accompanied by inflammatory responses in both the peripheral blood and CSF. This study was registered with PROSPERO, CRD42022349182.

α-Synuclein induces Th17 differentiation and impairs the function and stability of Tregs by promoting RORC transcription in Parkinson's disease.

BACKGROUND: Parkinson's disease (PD) is characterized by the loss of dopaminergic neurons (DA) and the accumulation of Lewy body deposits composed of alpha-Synuclein (α-Syn), which act as antigenic epitopes to drive cytotoxic T-cell responses in PD. Increased T helper 17 (Th17) cells and dysfunctional regulatory T cells (Tregs) have been reported to be associated with the loss of DA in PD. However, the mechanism underlying the Th17/Treg imbalance remains unknown. METHODS: Here, we examined the percentage of Th17 cells, the percentage of Tregs and the α-Syn level and analysed their correlations in the peripheral blood of PD patients and in the substantia nigra pars compacta (SNpc) and spleen of MPTP-treated mice and A53 transgenic mice. We assessed the effect of α-Syn on the stability and function of Tregs and the differentiation of Th17 cells and evaluated the role of retinoid-related orphan nuclear receptor (RORγt) upregulation in α-Syn stimulation in vivo and in vitro. RESULTS: We found that the α-Syn level and severity of motor symptoms were positively correlated with the increase in Th17 cells and decrease in Tregs in PD patients. Moreover, α-Syn stimulation led to the loss of Forkhead box protein P3 (FOXP3) expression in Tregs, accompanied by the acquisition of IL-17A expression. Increased Th17 differentiation was detected upon α-Syn stimulation when naïve CD4+ T cells were cultured under Th17-polarizing conditions. Mechanistically, α-Syn promotes the transcription of RORC, encoding RORγt, in Tregs and Th17 cells, leading to increased Th17 differentiation and loss of Treg function. Intriguingly, the increase in Th17 cells, decrease in Tregs and apoptosis of DA were suppressed by a RORγt inhibitor (GSK805) in MPTP-treated mice. CONCLUSION: Together, our data suggest that α-Syn promotes the transcription of RORC in circulating CD4+ T cells, including Tregs and Th17 cells, to impair the stability of Tregs and promote the differentiation of Th17 cells in PD. Inhibition of RORγt attenuated the apoptosis of DA and alleviated the increase in Th17 cells and decrease in Tregs in PD.

Freezing of gait is a risk factor for cognitive decline in Parkinson's disease.

BACKGROUNDS: Freezing of gait (FOG) and cognitive impairment are serious symptoms of Parkinson's disease (PD). Understanding the association between FOG and cognition may help formulate specific interventions for PD individuals. OBJECTIVES: We aimed to investigate the associations of cognitive impairment in different domains with FOG status using multiple neuropsychological tests. METHODS: Two cohorts including 691 and 104 participants were recruited from Parkinson's progression markers initiative (PPMI) and central China, respectively. All participants underwent FOG assessment and neuropsychological tests, and 595 individuals from PPMI and 51 from central China were enrolled for longitudinal observation. Cross-sectional and longitudinal associations between cognition and FOG status were evaluated using multivariable-adjusted models. RESULTS: Worse cognitive performances were observed in patients with FOG compared to those without FOG in both cohorts (ß = - 0.020, p < 0.001) using multivariate-adjusted models. Moreover, patients with progressive FOG during follow-up manifested more serious cognitive declines (HR = 1.40, 95% CI = 1.07-1.80). The FOG was mainly associated with the decline of executive, attention, and orientation. Furthermore, FOG was associated with higher levels of cognition-related biomarkers including T-tau, P-tau, and NfL in cerebrospinal fluid (p < 0.050). CONCLUSIONS: FOG is a risk factor for cognitive decline in PD, which emphasizes the need for early detection and monitoring of cognitive changes and interventions on cognitive impairments in PD patients with FOG.

Characterization of 4 deletion mutants of Pseudomonas plecoglossicida and their potential for live attenuated vaccines in large yellow croaker (Larimichthys crocea).

To search for live attenuated vaccines (LAV) candidates against Pseudomonas plecoglossicida, the causative agent of the visceral granulomas disease in farmed large yellow croaker (Larimichthys crocea), two type Ⅵ secretion systems (T6SS) and a predicted α/ß fold family hydrolase encoding gene, ORF4885 were targeted to construct deletion mutants. The biological profiles of 4 mutants were characterized; LD50 to the croakers detected, in vivo survival post-infection investigated， relative percent of survival (RPS) of the croakers 28d post-vaccination determined, and transcription of five immunity-related genes of the treated fish was quantified. On comparison to the WT, the mutants revealed similar growth curves in 11h; swarming motility of Δ4885 declined significantly at 72h post-incubation (P < 0.05); ΔS1Δ4885 showed significantly poor biofilm formation and weak resistance to fish serum bactericidal activity (P < 0.05). LD50 of the mutants were much higher than the WT, indication of strong virulence attenuation; in vivo survival test showed the mutant ΔS1Δ4885 and ΔS1ΔS3 were eliminated by the host 10d post-infection, demonstration of the safety and potentiality to be LAV candidates. Immunization with the mutant ΔS1Δ4885 provided higher RPS than ΔS1ΔS3. Transcription of IgT was significant in all immunized groups while IgM increased only in intraperitoneally injected groups. This study successfully searched a quite safe and strong immunogenic LAV candidate to defeat P. plecoglossicida infection.

Upregulated hexokinase 2 expression induces the apoptosis of dopaminergic neurons by promoting lactate production in Parkinson's disease.

Parkinson's disease (PD) is characterized by impaired mitochondrial function and decreased ATP levels. Aerobic glycolysis and lactate production have been shown to be upregulated in dopaminergic neurons to sustain ATP levels, but the effect of upregulated glycolysis on dopaminergic neurons remains unknown. Since lactate promotes apoptosis and α-synuclein accumulation in neurons, we hypothesized that the lactate produced upon upregulated glycolysis is involved in the apoptosis of dopaminergic neurons in PD. In this study, we examined the expression of hexokinase 2 (HK2) and lactate dehydrogenase (LDH), the key enzymes in glycolysis, and lactate levels in the substantia nigra pars compacta (SNpc) of a MPTP-induced mouse model of PD and in MPP+-treated SH-SY5Y cells. We found that the expression of HK2 and LDHA and the lactate levels were markedly increased in the SNpc of MPTP-treated mice and in MPP+-treated SH-SY5Y cells. Exogenous lactate treatment led to the apoptosis of SH-SY5Y cells. Intriguingly, lactate production and the apoptosis of dopaminergic neurons were suppressed by the application of 3-bromopyruvic acid (3-Brpa), a HK2 inhibitor, or siRNA both in vivo and in vitro. 3-Brpa treatment markedly improved the motor behaviour of MPTP-treated mice in pole test and rotarod test. Mechanistically, lactate increases the activity of adenosine monophosphate-activated protein kinase (AMPK) and suppresses the phosphorylation of serine/threonine kinase 1 (Akt) and mammalian target of rapamycin (mTOR). Together, our data suggest that upregulated HK2 and LDHA and increased lactate levels prompt the apoptosis of dopaminergic neurons in PD. Inhibition of HK2 expression attenuated the apoptosis of dopaminergic neurons by downregulating lactate production and AMPK/Akt/mTOR pathway in PD.

A nomogram based on iron metabolism can help identify apathy in patients with Parkinson's disease.

Backgrounds: Apathy is common in Parkinson's disease (PD) but difficult to identify. Growing evidence suggests that abnormal iron metabolism is associated with apathy in PD. We aimed to investigate the clinical features and iron metabolism of apathetic patients with PD, and construct a nomogram for predicting apathy in PD. Methods: Data of 201 patients with PD were analyzed. Demographic data, Apathy Scale (AS) assessments, and serum iron metabolism parameters were obtained. Spearman correlations were used to assess relationships between AS scores and iron metabolism parameters, separately for male and female patients. Additionally, a nomograph for detecting apathetic patients with PD was built based on the results of logistic regression analysis. Results: The serum transferrin (TRF, p < 0.0024) concentration and total iron binding capacity (TIBC, p < 0.0024) were lower in the apathetic group after Bonferroni correction, and they were negatively associated with AS scores in male participants with PD (TRF, r = -0.27, p = 0.010; TIBC, r = -0.259, p = 0.014). The nomogram was developed by incorporating the following five parameters: age, sex, serum iron concentration, TIBC and Hamilton Depression Rating Scale (HAMD) scores, which showed good discrimination and calibration, with a consistency index of 0.799 (95% confidence interval = 0.732-0.865). Conclusion: Abnormal iron metabolism may contribute to apathy in PD, especially among men. TIBC levels in combination with HAMD scores can be effectively used for the prediction of apathetic patients with PD.

Generation of an induced pluripotent stem cell line HUSTTJi001-A from a Moyamoya disease patient with RNF213 gene mutation.

Moyamoya disease (MMD) is an idiopathic and chronic steno-occlusive cerebrovascular disease. Genetic studies identified RNF213 as a principal susceptibility gene of MMD. In this study, peripheral blood mononuclear cells (PBMCs) were obtained from an MMD patient with RNF213 p. R4810K mutations, and the PBMCs were then reprogrammed to induced pluripotent stem cells (iPSCs) by the transfection of non-integrated episomal vectors. The iPSC line shows pluripotency markers and has the potential for in vitro differentiation into three germ layers, and will be valuable for elucidating the underlying cellular mechanisms of MMD, selecting therapeutic targets, and developing drugs.

Preliminary studies on the different roles of T6SSs in pathogenicity of Pseudomonas plecoglossicida NB2011.

Pseudomonas plecoglossicida, the causative agent of visceral granulomas in the large yellow croaker (Larimichthys crocea) in China, encodes three sets of type Ⅵ secretion systems (T6SS1-3). The purpose of this study was to characterize the different roles of T6SSs involved in infection. In-frame deletion of T6SSs was constructed, which resulted in 8 mutants. Competition against E. coli DH5α, virulence against the croaker and in vivo survival ability of the mutants were tested. The expression and secretion of Hcp by P. plecoglossicida NB2011 were investigated. The results showed T6SS2 mutant failed to inhibit the growth of E. coli, which is an indication of T6SS2 acting against environmental bacteria. The LD50 value of T6SS1 mutant strongly increased; T6SS2 and T6SS3 mutants were similar to that of the wild type; and the virulence of double deletion or triple deletion mutant was drastically alleviated, indicating that T6SS1 being one of the major virulence factors, and T6SS2 and T6SS3 directly or indirectly being involved in the pathogenicity. T6SS1 mutant disappeared in the fish spleen in 3 days, while other strains kept increasing, indicating the T6SS1 stimulation bacteria replication in vivo. Hcp1 secreted at 12-28°C and Hcp2 secreted at 12-35°C, while Hcp3 secretion not detected in vitro. This study has thrown some insights on the understanding of pathogenicity mechanisms of this pathogen.

Hydrodynamic cavitation: A feasible approach to intensify the emulsion cross-linking process for chitosan nanoparticle synthesis.

Chitosan nanoparticles (NPs) exhibit great potential in drug-controlled release systems. A controlled hydrodynamic cavitation (HC) technique was developed to intensify the emulsion crosslinking process for the synthesis of chitosan NPs. Experiments were performed using a circular venturi and under varying operating conditions, i.e., types of oil, addition mode of glutaraldehyde (Glu) solution, inlet pressure (Pin), and rheological properties of chitosan solution. Palm oil was more appropriate for use as the oil phase for the HC-intensified process than the other oil types. The addition mode of water-in-oil (W/O) emulsion containing Glu (with Span 80) was more favorable than the other modes for obtaining a narrow distribution of chitosan NPs. The minimum size of NPs with polydispersity index of 0.342 was 286.5 nm, and the maximum production yield (Py) could reach 47.26%. A positive correlation was found between the size of NPs and the droplet size of W/O emulsion containing chitosan at increasing Pin. Particle size, size distribution, and the formation of NPs were greatly dependent on the rheological properties of the chitosan solution. Fourier transform infrared spectroscopy (FTIR) analysis indicated that the molecular structure of palm oil was unaffected by HC-induced effects. Compared with ultrasonic horn, stirring-based, and conventional drop-by-drop processes, the application of HC to intensify the emulsion crosslinking process allowed the preparation of a finer and a narrower distribution of chitosan NPs in a more energy-efficient manner. The novel route developed in this work is a viable option for chitosan NP synthesis.

Lead ion adsorption on functionalized sugarcane bagasse prepared by concerted oxidation and deprotonation.

Targeting the removal of Pb2+ in wastewater, sugarcane bagasse was treated with nitric acid and an alkaline solution to prepare adsorbents. On a typical adsorbent, the adsorption isotherms agreed well with the Langmuir expression, and the maximum adsorption capacity reached 200.3 mg/g. In the presence of 150 ppm Ca2+, a common cation in natural water, the Pb2+ adsorption capacity slightly declined. In contrast, Mg2+ obviously prohibited the adsorption for Pb2+. The spent adsorbent could be regenerated at least five times through elution with an EDTA solution. EDS and XPS results demonstrated that nitric acid functioned as an oxidant instead of nitrification agent in the treatment of bagasse. The adsorption process was consistent with quasi-second-order kinetics. Based on thermodynamic studies, the changes in enthalpy and Gibbs free energy were calculated to be - 33.3 and ca. - 18 kJ/mol, indicating that the adsorption process was exothermic and spontaneous. The equilibrium Pb2+ adsorption amounts were proportional to the numbers of carboxylate groups on different adsorbents. The binding energies of Pd 4f5/2 and Pd 4f7/2 XPS spectra of Pb2+ adsorbed were 0.6-0.7 eV lower than those of free Pb(NO3)2, indicating the transfer of electrons during adsorption. The conversion of hydroxymethyl groups in sugarcane bagasse into carboxylate groups, as well as the chelation between Pb2+ ions and carboxylate groups, was validated in this work, which is beneficial for the treatment of wastewater polluted by lead ions.

Fast and reversible adsorption for dibenzothiophene in fuel oils with metallic nano-copper supported on mesoporous silica.

Dibenzothiophene (DBT) in fuel oils causes the release of toxic sulfur oxide gases, and it is necessary to remove DBT in fuels. Herein, metallic copper was loaded on SBA-15 mesoporous silica through simple reduction reactions for the preparation of DBT adsorbents. On an adsorbent with a copper loading of 0.3 wt%, adsorption equilibrium was achieved within 5 min, and a DBT removal rate of 90.4% was achieved. The adsorption isotherm agreed with a linear Freundlich model and adsorption capacity was 12.1 mg sulfur/g. Nano-sized copper particles were observed by TEM, indicating the size effect of copper particles in DBT adsorption. A broad band, corresponding to copper-sulfur coordination bonds, was observed at 300-600 cm-1 in the Raman spectrum of DBT-doped adsorbent. Meanwhile, the band at 1233 cm-1 corresponding to C = C (-S) bonds in DBT was shifted to 1229 cm-1 in DBT adsorbed. XPS and Cu LMM XPS spectra proved that Cu(0) was oxidized by DBT sulfur during adsorption. Furthermore, Auger spectra verified that the adsorption of DBT on Cu(0) involved the formation of Cu(I) and Cu(II) species through coordination bonds. The adsorption capacity could be completely recovered via elution. This work sheds light on the removal of DBT in fuel oils with cost-effective efficient adsorbents.

Essential tremor vs idiopathic Parkinson disease: Utility of transcranial sonography.

Substantia nigra (SN) hyperechogenicity measured by transcranial sonography (TCS) is a promising biomarker for Parkinson disease (PD). The aim of this study was to explore the diagnostic accuracy of SN hyperechogenicity (SN) for differentiating PD from essential tremor (ET). A total of 119 patients with PD, 106 ET patients and 112 healthy controls that underwent TCS from November 2016 to February 2019 were included in this single-center retrospective case-control study. Two reviewers who were blinded to clinical information independently measured the SN by TCS imaging. The diagnostic sensitivity, specificity, and accuracy of TCS imaging were evaluated between the PD and healthy controls and between patients with PD and ET. Interrater agreement was assessed with the Cohen κ statistic. TCS imaging of the SN allowed to differentiate between patients with PD and ET with a sensitivity (91.6% and 90.8%) and specificity (91.5% and 89.6%) for readers 1 and 2, respectively. Interobserver agreement was excellent (к = 0.87). In addition, measurement of the SN allowed to differentiate between patients with PD and healthy subjects with a sensitivity (91.6% and 90.8%) and specificity (88.4% and 89.3%) for readers 1 and 2, respectively. Interobserver agreement was excellent (к = 0.91). Measurement of SN on TCS images could be a useful tool to distinguishing patients with PD from those with ET.

Ultrasonic assisted water-in-oil emulsions encapsulating macro-molecular polysaccharide chitosan: Influence of molecular properties, emulsion viscosity and their stability.

An ultrasonic technique was applied to formulation of two-phase water-in-paraffin oil emulsions loading a high-molecular polysaccharide chitosan (CS) and stabilized by an oil-soluble surfactant (Span80) at different operational conditions. The influence of chitosan molecular properties, phase volume ratio (φw), Span80 volume fraction (φs) and ultrasonic processing parameters were systemically investigated on the basis of mean droplet diameter (MDD) and polydispersity index (PDI) of emulsions. It was observed that the molecular weight (Mw) of CS was an important influential factor to MDD due to the non-Newtonian properties of CS solution varying with Mw. The minimum MDD of 198.5 nm with PDI of 0.326 was obtained with ultrasonic amplitude of 32% for 15 min at an optimum φw of 35%, φs of 8%, probe position of 2.2 cm to the top of emulsion, while CS with Mw of 400 kDa and deacetylation degree of 84.6% was used. The rise of emulsion viscosity and the reduction of negative zeta potential at φw increasing from 5% to 35% were beneficial to obtain finer droplets and more uniform distribution of emulsions, and emulsion viscosity could be represented as a monotonically-decreasing power function of MDD at the same φw. FTIR analysis indicated that the molecular structure of paraffin oil was unaffected during ultrasonication. Moreover, the emulsions exhibited a good stability at 4 °C with a slight phase separation at 25 °C after 24 h of storage. By analyzing the evolution of MDD, PDI and sedimentation index (SI) with time, coalescence model showed better fitting results as comparison to Ostwald ripening model, which demonstrated that the coalescence or flocculation was the dominant destabilizing mechanism for such W/O emulsions encapsulating CS. This study may provide a valuable contribution for the application of a non-Newtonian macromolecule solution as dispersed phase to generate nano-size W/O emulsions via ultrasound, and widen knowledge and interest of such emulsions in the functional biomaterial field.