Adipose-derived stem cell exosomes loaded with icariin alleviates rheumatoid arthritis by modulating macrophage polarization in rats.

Rheumatoid arthritis (RA) is a chronic autoimmune disease marked by synovitis and cartilage destruction. The active compound, icariin (ICA), derived from the herb Epimedium, exhibits potent anti-inflammatory properties. However, its clinical utility is limited by its water insolubility, poor permeability, and low bioavailability. To address these challenges, we developed a multifunctional drug delivery system-adipose-derived stem cells-exosomes (ADSCs-EXO)-ICA to target active macrophages in synovial tissue and modulate macrophage polarization from M1 to M2. High-performance liquid chromatography analysis confirmed a 92.4 ± 0.008% loading efficiency for ADSCs-EXO-ICA. In vitro studies utilizing cellular immunofluorescence (IF) and flow cytometry demonstrated significant inhibition of M1 macrophage proliferation by ADSCs-EXO-ICA. Enzyme-linked immunosorbent assay, cellular transcriptomics, and real-time quantitative PCR indicated that ADSCs-EXO-ICA promotes an M1-to-M2 phenotypic transition by reducing glycolysis through the inhibition of the ERK/HIF-1α/GLUT1 pathway. In vivo, ADSCs-EXO-ICA effectively accumulated in the joints. Pharmacodynamic assessments revealed that ADSCs-EXO-ICA decreased cytokine levels and mitigated arthritis symptoms in collagen-induced arthritis (CIA) rats. Histological analysis and micro computed tomography confirmed that ADSCs-EXO-ICA markedly ameliorated synovitis and preserved cartilage. Further in vivo studies indicated that ADSCs-EXO-ICA suppresses arthritis by promoting an M1-to-M2 switch and suppressing glycolysis. Western blotting supported the therapeutic efficacy of ADSCs-EXO-ICA in RA, confirming its role in modulating macrophage function through energy metabolism regulation. Thus, this study not only introduces a drug delivery system that significantly enhances the anti-RA efficacy of ADSCs-EXO-ICA but also elucidates its mechanism of action in macrophage function inhibition.

Adipose-derived stem cell exosomes loaded with icariin attenuated M1 polarization of macrophages via inhibiting the TLR4/Myd88/NF-κB signaling pathway.

Abnormal macrophage polarization is one of the common pathological bases of various inflammatory diseases. The current research focus involves targeting macrophages to remodel their phenotype as a treatment approach for inflammatory diseases. Notably, exosomes can be delivered to specific types of cells or tissues or inflammatory area to realize targeted drug delivery. Although icariin (ICA) exhibits regulatory potential in macrophage polarization, the practical application of ICA is impeded by its water insolubility, poor permeability, and low bioavailability. Exploiting the inherent advantages of exosomes as natural drug carriers, we introduce a novel drug delivery system-adipose-derived stem cells-exosomes (ADSCs-EXO)-ICA. High-performance liquid chromatography analysis confirmed a loading rate of 92.7 ± 0.01 % for ADSCs-EXO-ICA, indicating the successful incorporation of ICA. As demonstrated by cell counting kit-8 assays, ADSCs-EXO exerted a significantly higher promotion effect on macrophage proliferation. The subsequent experimental results revealed the superior anti-inflammatory effect of ADSCs-EXO-ICA compared to individual treatments with EXO or ICA in the lipopolysaccharide + interferon-gamma-induced M1 inflammation model. Additionally, results from enzyme-linked immunosorbent assay, quantitative polymerase chain reaction, and western blot analyses revealed that ADSCs-EXO-ICA effectively inhibited macrophage polarization toward the M1-type and concurrently promoted polarization toward the M2-type. The underlying mechanism involved the modulation of macrophage polarization through inhibition of the Toll-like receptor 4/myeloid differentiation factor 88/nuclear transcription factor-kappa B signaling pathway, thereby mitigating inflammation. These findings underscore the potential therapeutic value of ADSCs-EXO-ICA as a novel intervention for inflammatory diseases.

Combination of fractional carbon dioxide laser with recombinant human collagen in periocular skin rejuvenation.

BACKGROUND: The most visible sign of facial aging is often seen in the periocular area. However, periocular rejuvenation remains challenging due to the particularity of periocular anatomic locations. AIMS: We aimed to evaluate the efficacy and safety of the fractional-ablative CO2 laser-facilitated recombinant human collagen permeation in periocular rejuvenation. PATIENTS/METHODS: This 3-month prospective single-blinded and self-controlled trial enrolled 26 patients with periocular aging who underwent the treatments of fractional-ablative CO2 laser along with laser-facilitated recombinant human collagen permeation. Following the treatments, the patients were quantitatively assessed by various periocular skin aging indices before and after the treatment and monitored for any related adverse events. RESULTS: The patients showed significant improvements with the periocular skin aging indices 3 months after the treatments, which were detailed with a 47.3% decrease in lower eyelid skin rhytids, a 41.4% decrease in the lower eyelid skin texture, a 35.0% decrease in the static crow's feet, a 29.3% decrease in the amount of upper eyelid laxity, and a 20.2% increase in the MRD1 as compared with baseline (p < 0.05). Moreover, total skin thickness under ultrasound was increased in both upper and lower eyelids (5.6% and 3.3%, p < 0.05, respectively). Moreover, six patients (23.1%, 6/26) had erythema for 2 weeks, and two (2/26, 7.7%) had mild hyperpigmentation for 3 months. CONCLUSIONS: Fractional-ablative CO2 laser combined with laser-facilitated recombinant human collagen permeation can be a safe and effective treatment for periocular rejuvenation.

The relationship between serum creatinine/cystatin C ratio and mortality in hypertensive patients.

BACKGROUND AND AIMS: Sarcopenia is a disease characterized by loss of skeletal muscle mass and function that is closely associated with cardiovascular disease. The serum creatinine/cystatin C (Cr/CysC) ratio has been shown to be a simplified indicator for identifying low muscle mass (LMM) or sarcopenia. The aim of this study was to investigate whether the Cr/CysC ratio helps to predict prognostic information in hypertensive patients. METHODS AND RESULTS: This cohort study included 2509 patients with hypertension from the National Health and Nutrition Survey 1999-2002. To evaluate the association between Cr/CysC ratio and mortality, we used Kaplan Meier estimates to calculate cumulative survival probabilities for all-cause mortality and cardiovascular mortality, Cox regression analyses, and hazard ratio (HR) and 95% confidence interval (CI) were calculated. Over a median follow-up of 11.76 years, lower Cr/CysC ratio was associated with lower risk of all-cause mortality (per 0.1 increase, HR:0.81, 95% CI: 0.77-0.85, P < 0.001) and cardiovascular mortality (per 0.1 increase, HR:0.80, 95% CI: 0.72-0.89, P < 0.001). Compared with patients with normal muscle mass, all-cause mortality, and cardiovascular mortality HR for patients with LMM diagnosed by Cr/CysC ratio were 1.57 (95% CI: 1.36-1.82, P < 0.001) and 1.64 (95% CI: 1.12-2.42, P = 0.012), respectively. CONCLUSION: We found that low muscle mass shown by lower Cr/CysC ratio was an independent risk factor for poor prognosis in hypertensive patients. We recommend routine screening of Cr/CysC ratio in hypertensive patients and early intervention for low muscle mass or sarcopenia.

Influence of Various Nanomaterials on the Rheology and Hydration Kinetics of Oil Well Cement.

Nanomaterials have great potential to influence the properties of cement-based materials due to their small particle size and large specific surface area. The influences of Nano-SiO2 (NS), gamma-nano-Al2O3 (GNA), alpha-nano-Al2O3 (ANA), and nano-TiO2 (NT) on the rheology and hydration kinetics of class G cement at 30 °C were investigated in this study. The nanomaterials were added in dry powder form at dosages of 1, 2, 3, 5, and 7% by weight of cement (bwoc), and their dispersion was accomplished using polycarboxylate superplasticizer (PCE) at a dosage of 1.6% bwoc. PCE provides a uniform dispersion of nanoparticles in the cement matrix, enhancing the efficiency of nanomaterials. The w/c ratio varied between 0.718 and 0.78 to form a constant-density slurry of 1.65 g/cm3. Our test results showed that NS and GNA caused significant increases in the rheology of the cement slurry, with this effect increasing with dosage, while ANA and NT tended to reduce the rheology of the slurry. Compared to a well-suspended and well-dispersed cement slurry generated by the use of PCE and diutan gum, all nanomaterials can accelerate early hydration by reducing the induction time, with GNA having the strongest influence, while NS was the only nanomaterial that further increased the long-term hydration heat release at 7 days. The stronger effect of NS and GNA on the cement slurry properties can be attributed to their higher chemical reactivity. The dosage effect on total hydration extent was relatively strong for ANA, NT, and NS from 3% to 5% but weak for GNA in the range from 3% to 7%.

Association of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and acute kidney disease in patients undergoing coronary angiography: a cohort study.

BACKGROUND: Acute kidney disease (AKD) following coronary angiography (CAG) indicates a higher risk of chronic kidney disease and follow-up cardiovascular comorbidities. However, the predictive risk factor of AKD is not clear. We sought to verify whether preoperative N-terminal pro-B-type natriuretic peptide (NT-proBNP) level was associated with AKD in patients undergoing CAG. METHOD: We analyzed 7602 patients underwent CAG in this multi-center registry cohort study. Cardiorenal ImprovemeNt II (CIN-II) in five Chinese tertiary hospitals from 2007 to 2020. The primary outcome was AKD, defined as a ≥ 50% increase of serum creatinine within 7-90 days. Multivariable logistic regressions were used to assess the association between NT-proBNP and AKD. RESULT: 1009 patients (13.27%) eventually developed AKD, who were more likely to be female, older, and with comorbidities of chronic heart failure and anemia. After adjusting to the potential confounders, the NT-proBNP level remained an independent predictor of AKD (lnNT-proBNP OR: 1.20, 95% CI 1.13-1.28, p < 0.005). Restricted cubic spline analysis demonstrated a linear relationship between elevated NT-proBNP and AKD (p for trend < 0.001). In the subgroup analysis, elevated NT-proBNP level in patients with percutaneous coronary intervention (p for interaction < 0.001) or without previous congestive heart failure (p for interaction = 0.0346) has a more significant value of AKD prediction. CONCLUSION: Pre-operative NT-proBNP level was independently associated with the risk of AKD in patients following CAG. Perioperative strategies are warranted to prevent AKD in patients with elevated NT-proBNP levels.

Red blood cell distribution width predicts gastrointestinal bleeding after coronary artery bypass grafting.

BACKGROUND: Red blood cell distribution width (RDW) is highly associated with adverse clinical outcomes in many diseases. The present study aimed to evaluate the relationship between RDW and gastrointestinal bleeding (GIB) after isolated coronary artery bypass grafting (CABG). METHODS: This was a retrospective observational study that included 4473 patients who received CABG, and all the data were extracted from the Medical Information Mart for Intensive Care III database. Data collected included patient demographics, associated comorbid illnesses, laboratory parameters, and medications. The receiver operating characteristic (ROC) curve was used to determine the best cutoff value of RDW for the diagnosis of GIB. Multivariable logistic regression analysis was used to analyze the relationship between RDW and GIB. RESULTS: The incidence of GIB in patients receiving CABG was 1.1%. Quartile analyses showed a significant increase in GIB incidence at the fourth RDW quartile (> 14.3%; P < 0.001). The ROC curve analysis revealed that an RDW level > 14.1% measured on admission had 59.6% sensitivity and 69.4% specificity in predicting GIB after CABG. After adjustment for confounders, high RDW was still associated with an increased risk of GIB in patients with CABG (odds ratio = 2.83, 95% confidence interval 1.46-5.51, P = 0.002). CONCLUSIONS: Our study indicates that the elevated RDW level is associated with an increased risk of GIB after CABG, and it can be an independent predictor of GIB. The introduction of RDW to study GIB enriches the diagnosis method of GIB and ensures the rapid and accurate diagnosis of GIB.

Case Report: An Unusual Case of Pheochromocytoma.

Pheochromocytoma is a benign catecholamine secreting tumor, which is rare and originates from the adrenal gland. It has been known for a wide range of clinical manifestations and can mimic other difficult-to-diagnose diseases. Here, we report a female patient with acquired long QT syndrome, which is a rare complication of pheochromocytoma. Although relatively rare, the presence of pheochromocytoma should be considered in the case of malignant arrhythmias and electrocardiographic changes in patients.

Global knowledge mapping and emerging trends in research between spasmolytic polypeptide-expressing metaplasia and gastric carcinogenesis: A bibliometric analysis from 2002 to 2022.

Background: Spasmolytic polypeptide expression metaplasia (SPEM) occurs in the corpus of the stomach and is closely related to inflammations caused by H. pylori infection. Recently, SPEM was suggested as one of the dubious precancerous lesions of gastric cancer (GC). Thus, further research on SPEM cell transdifferentiation and its underlying mechanisms could facilitate the development of new molecular targets improving the therapeutics of GC. Using bibliometrics, we analyzed publications, summarized the research hotspots and provided references for scientific researchers engaged in related research fields. Methods: We searched the Web of Science Core Collection (WoSCC) for publications related to SPEM-GC from 2002 to 2022. The VOSviewer, SCImago, CiteSpace and R software were used to visualize and analyze the data. Gene targets identified in the keyword list were analyzed for functional enrichment using the KEGG and GO databases. Results: Of the 292 articles identified in the initial search, we observed a stable trend in SPEM-GC research but rapid growth in the number of citations. The United States was the leader in terms of quality publications and international cooperation among them. The total number of articles published by Chinese scholars was second to the United States. Additionally, despite its low centrality and average citation frequency, China has become one of the world's most dynamic countries in academics. In terms of productivity, Vanderbilt University was identified as the most productive institution. Further, we also observed that Gastroenterology was the highest co-cited journal, and Goldenring Jr. was the most prolific author with the largest centrality. Conclusion: SPEM could serve as an initial step in diagnosing gastric precancerous lesions. Current hotspots and frontiers of research include SPEM cell lineage differentiation, interaction with H. pylori, disturbances of the mucosal microenvironment, biomarkers, clinical diagnosis and outcomes of SPEM, as well as the development of proliferative SPEM animal models. However, further research and collaboration are still required. The findings presented in this study can be used as reference for the research status of SPEM-GC and determine new directions for future studies.

Development of bacterial biosensor for sensitive and selective detection of acetaldehyde.

Acetaldehyde is a human carcinogen and widely existed in alcoholic beverages and polluted air. In this study, a simple, fast, convenient and sensitive acetaldehyde biosensor was developed based on an acetaldehyde dehydrogenase (AldDH) bacteria surface display system. The whole-cell catalyst facilitated the dehydrogenation of acetaldehyde, while coenzyme NAD+ was reduced and the resultant NADH can be detected spectrometrically at 340 nm. The correct location of AldDH on the bacteria surface was confirmed by the subcellular fraction and immunofluorescence analysis. By comparing the fusion protein expression level and whole-cell activity, the proper display system for anchoring AldDH on the cell surface was obtained. The results of kinetics analysis towards both surface-displayed AldDH and intracellular expressed AldDH demonstrated that the mass-transport resistance was dramatically alleviated by cell-surface display strategy. Under optimal conditions, AldDH-surface display strain with the highest whole-cell activity (3.41 ± 0.3 mU/OD600) was applied to spectrophotometry acetaldehyde detection system. An excellent linear relationship between the increases of absorbance at 340 nm and acetaldehyde concentration over the range from 1 µM to 300 µM was reached. The proposed approach offered adequate sensitivity for the detection of acetaldehyde at 0.33 µM. Most importantly, the developed biosensor showed the narrowest substrate specificity towards acetaldehyde, which has been employed for quick determination of acetaldehyde in real samples with good accuracy. The total detection time was within 20 min. The method reported here provided a simple, rapid, and low-cost strategy for the sensitive and selective measurement of acetaldehyde. Therefore, genetically engineered cells may find broad application in biosensors and biocatalysts.

Thalidomide Improves Psoriasis-like Lesions and Inhibits Cutaneous VEGF Expression without Alteration of Microvessel Density in Imiquimod- induced Psoriatic Mouse Model.

BACKGROUND: Psoriasis is a chronic inflammatory skin disorder of unknown etiology. Increasing evidence suggests that psoriasis is probably an angiogenesis-dependent disease. Thalidomide has been reported being able to inhibit the effects of fibroblast growth factor 2 and vascular endothelial growth factor (VEGF), and inhibit tumour necrosis factor-alpha synthesis, and suppress tumour necrosis factor-induced nuclear factor-kappa B activation in Jurkat cells, resulting in suppression of proliferation inflammation, angiogenesis, and the immune system, which are related to the pathogenesis of psoriasis. OBJECTIVE: Our study evaluated the influence of thalidomide on the lesional alterations, VEGF expressions and angiogenesis in imiquimod-induced mouse model. METHODS: Balb/c female mice (n=48) 8-12 weeks of age were randomly divided into 6 groups including negative control (vaseline cream), positive control (5% imiquimod cream), and experimental groups including low-dose (10 mg/kg.d), moderate-dose (30 mg/kg.d) and high-dose thalidomide (85 mg/kg.d), and acitretin group (6 mg/kg.d). Serum levels of VEGF-A were quantified by enzyme-linked immunosorbent assay. VEGF protein expression was measured by western blotting and the microvessel density by immunohistochemical staining. RESULTS: The total psoriasis area and severity index scores in the moderate- and high-dose thalidomide and acitretin groups decreased significantly (p<0.001 for each), and so were the total Baker's scores in the high-dose thalidomide (p=0.008) and acitretin groups (p=0.021). The mean thickness of the epidermis in the experimental and acitretin groups decreased significantly, respectively (p<0.001 for all); the acitretin group was the thinnest. The cutaneous VEGF protein levels down-expressed significantly in the moderate- and high-dose thalidomide groups (p<0.05 for both), while those in the low-dose thalidomide and acitretin did not (p>0.05 for both). There were no differences for serum VEGF-A levels and the density of microvessels among the positive and experimental groups. CONCLUSION: Thalidomide can improve the psoriasis-like lesions and inhibit the expression of cutaneous VEGF in imiquimod-induced psoriatic model with dose-dependence, however, it does not alter circulating VEGF-A levels and microvessel density in dermis.

Redesigning of Microbial Cell Surface and Its Application to Whole-Cell Biocatalysis and Biosensors.

Microbial cell surface display technology can redesign cell surfaces with functional proteins and peptides to endow cells some unique features. Foreign peptides or proteins are transported out of cells and immobilized on cell surface by fusing with anchoring proteins, which is an effective solution to avoid substance transfer limitation, enzyme purification, and enzyme instability. As the most frequently used prokaryotic and eukaryotic protein surface display system, bacterial and yeast surface display systems have been widely applied in vaccine, biocatalysis, biosensor, bioadsorption, and polypeptide library screening. In this review of bacterial and yeast surface display systems, different cell surface display mechanisms and their applications in biocatalysis as well as biosensors are described with their strengths and shortcomings. In addition to single enzyme display systems, multi-enzyme co-display systems are presented here. Finally, future developments based on our and other previous reports are discussed.

Protective Effect of Norcantharidin on Collagen-Induced Arthritis Rats.

OBJECTIVE: To observe the effect of norcantharidin (NCTD) on collagen-induced arthritis (CIA) rats. METHODS: Sixty Sprague-Dawley(SD) rats were randomly divided into 6 groups (n=10): normal group, CIA model group(model group), NCTD low-dose group [1.35 mg/(kg•d)], NCTD middle-dose group [2.7 mg/(kg•d)], NCTD high-dose group [5.4 mg/(kg•d)] and methotrexate (MTX) group [1.8 mg/(kg/w)]. Anesthetized rats were sacrificed by luxation of cervical vertebra after 4 weeks of administration. The arthritis scores were evaluated twice a week. The pathological changes in the ankle joints of rats were observed by hematoxylin-eosin (H&E) staining. The serum levels of interleukin (IL) 1ß, IL-6, tumor necrosis factor (TNF)-α, vascular endothelial growth factor (VEGF), IL-17 and transform growth factor (TGF) ß were detected by enzyme linked immunosorbent assay (ELISA). The mRNA expression of retinoid-related orphan nuclear receptorγt (RORγt) and forkhead box P3 (Foxp3) in peripheral blood lymphocytes were confirmed by real-time polymerase chain reaction. RESULTS: MTX and high-dose NCTD not only decreased the arthritis scores but also alleviated the pathological changes in CIA rats' ankle joints compared with the model group (P<0.05 or P<0.01). All doses of NCTD significantly inhibited the serum levels of IL-6, IL-17 and TNF-α in CIA rats (P<0.05). Only middle- and high-dose of NCTD prominently decreased serum IL-1ß and TGF-ß levels of CIA rats (P<0.05). However, NCTD has no effect on vascular endothelial growth factor (VEGF) level in CIA rats. The Foxp3 mRNA expression in all NCTD groups were increased significantly than in the model group (P<0.05). The mRNA expression of RORγt in NCTD high-dose group was decreased apparently in comparison with the model group (P<0.05). CONCLUSIONS: NCTD showed therapeutic effect on CIA rats by inhibition of cytokines and regulation of Th17/Treg cells.

Trends in culprit drugs and clinical entities in cutaneous adverse drug reactions: a retrospective study.

PURPOSE: Morbidity due to cutaneous adverse drug reactions (CADRs) is quite common. The specific culprit drugs change over time and clinicians must be kept informed with updated knowledge, thus preventing potential CADRs. This retrospective study is a survey of CADRs encountered in a hospital-based population in Southern China during three time intervals, from 1984 to 2015. MATERIALS AND METHODS: The clinical records were review of 306 patients with CADRs who were admitted to our hospital from 2011 to 2015. These data were compared with patients visiting our hospital during 1984-1994 and 2003-2010. RESULTS: From 2011 to 2015, the most common CADRs were exanthematous reactions (40.8%) and Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN; 17.0%). There were eight cases (2.6%) of CADRs related to targeted therapy in oncology. In the 205 CADR cases that were due to single medications, the most common offending drugs were allopurinol (21.5%), cephalosporins (10.7%) and carbamazepine (10.2%). The percentages of CADR cases due to allopurinol, carbamazepine, or epidermal growth factor receptor inhibitors were significantly higher from 2011 to 2015 compared with 1984-1994 or 2003-2010. The rate of SJS/TEN occurrence was significantly higher in the two recent periods compared with 1984-1994. CONCLUSIONS: Changes in drug prescriptions are a major factor that affects the CADRs seen in clinical records. Newer drugs can be culpable for CADRs, and more CADRs are now documented with increased severity at clinical presentation. Reliable screening tests for specific drugs are urgently required to eliminate possible fatalities.

Bufei Huoxue Capsule Attenuates PM2.5-Induced Pulmonary Inflammation in Mice.

Atmospheric fine particulate matter 2.5 (PM 2.5) may carry many toxic substances on its surface and this may pose a public health threat. Epidemiological research indicates that cumulative ambient PM2.5 is correlated to morbidity and mortality due to pulmonary and cardiovascular diseases and cancer. Mitigating the toxic effects of PM2.5 is therefore highly desired. Bufei Huoxue (BFHX) capsules have been used in China to treat pulmonary heart disease (cor pulmonale). Thus, we assessed the effects of BFHX capsules on PM2.5-induced pulmonary inflammation and the underlying mechanisms of action. Using Polysearch and Cytoscape 3.2.1 software, pharmacological targets of BFHX capsules in atmospheric PM2.5-related respiratory disorders were predicted and found to be related to biological pathways of inflammation and immune function. In a mouse model of PM2.5-induced inflammation established with intranasal instillation of PM2.5 suspension, BFHX significantly reduced pathological response and inflammatory mediators including IL-4, IL-6, IL-10, IL-8, TNF-α, and IL-1ß. BFHX also reduced keratinocyte growth factor (KGF), secretory immunoglobulin A (sIgA), and collagen fibers deposition in lung and improved lung function. Thus, BFHX reduced pathological responses induced by PM2.5, possibly via regulation of inflammatory mediators in mouse lungs.

Iron-cobalt bimetal oxide nanorods as efficient and robust water oxidation catalysts.

Cobalt-based oxides are considered as potential water oxidation catalysts for future artificial photosynthetic systems because of their high abundance, strong stability and efficient performance. Herein, a series of cobalt-based oxides, MnCo3-nO4 (M = Mn, Fe, Co) samples, were synthesized through changing the metal sources by a low-temperature coprecipitation method. These catalysts were investigated under photochemical and electrochemical water oxidation conditions. And they all exhibited efficient activity for water oxidation under alkaline, acidic and neutral conditions under visible light irradiation. An excellent O2 yield of 90.4% for Fe-Co bimetal oxide (Fe1.1Co1.9O4) nanorods was obtained under optimal conditions (photoirradiation at λ ≥ 420 nm, [Ru(bpy)3](ClO4)2 as the photosensitizer, Na2S2O8 as the oxidant in borate buffer at pH = 9.0, bpy = 2,2-bipyridine). Among MnCo3-nO4 samples, Fe1.1Co1.9O4 nanorods were proved to be the optimal electrocatalytic water oxidation catalyst as well. Multiple experiments (SEM, FT-IR, XRD, XPS, Bulk electrolysis) were used to test the stability of Fe1.1CO1.9O4 and these results indicate that Fe1.1CO1.9O4 nanorods are highly stable. Furthermore, based on Mott-Schottky and cyclic voltammetry analysis, the best balanced flat-band potential of Fe1.1CO1.9O4 nanorods is just located at the middle position between the oxidation potential of O2/H2O and the half-wave potential of [Ru(bpy)3]3+/2+, which was probably responsible for their superior photocatalytic water oxidation performance.

Interferon-gamma-induced local leukocytoclastic vasculitis at the subcutaneous injection site

Abstract Cutaneous reactions associated with interferons (IFNs) treatment are either localized or generalized. The most common presentation of localized reactions at IFNs injection site is usually an erythematous patch or plaque. Local leukocytoclastic vasculitis presenting with cutaneous necrosis is extremely rare. We report a 19-year-old man with hepatitis B who had local leukocytoclastic vasculitis induced by interferon-gama injection at the injection site. After changing the injection sites and using the combined treatment of prednisone and colchicine, the previous lesion healed and no other cutaneous lesion occurred. We also made a mini review of such cases.

Lupus Panniculitis as an Initial Manifestation of Systemic Lupus Erythematosus: A Case Report.

Lupus erythematosus panniculitis (LEP) is a variant of chronic cutaneous lupus erythematosus (CCLE). Reported cases of LEP lesions before the diagnosis of systemic lupus erythematosus (SLE) were very rare; only 9 cases have been reported, to the best of our knowledge. We now describe the case of a 19-year-old male patient, with an overall review of the English literature. In the earliest stage of the present case, nodules and ulcers involved his left leg and face, with no other accompanied symptoms. The skin lesions disappeared after treatment with methylprednisolone, 16 mg/d for 1 month. Seven months after discontinuing methylprednisolone, the cutaneous nodules and ulcers on his back recurred and were accompanied by fever, hair loss, and polyarthritis. Blood tests revealed leucopenia, positive antinuclear antibody and Smith antibody, and proteinuria. Histopathological findings were most consistent with LEP. This was followed sequentially by the diagnosis of SLE. The patient improved again after treatment with methylprednisolone and cyclophosphamide.Patients with LEP should have regular follow-ups because the development of SLE is possible. Early diagnosis and proper treatment is pivotal to improve the prognosis of such patients.

Triptolide Modulates TREM-1 Signal Pathway to Inhibit the Inflammatory Response in Rheumatoid Arthritis.

Triptolide (TP), an active component isolated from Tripterygiumwilfordii Hook F, has therapeutic potential against rheumatoid arthritis (RA). However, the underlying molecular mechanism has not been fully elucidated. The aim of this study is to investigate the mechanisms of TP acting on RA by combining bioinformatics analysis with experiment validation. The human protein targets of TP and the human genes of RA were found in the PubChem database and NCBI, respectively. These two dataset were then imported into Ingenuity Pathway Analysis (IPA) software online, and then the molecular network of TP on RA could be set up and analyzed. After that, both in vitro and in vivo experiments were done to further verify the prediction. The results indicated that the main canonical signal pathways of TP protein targets networks were mainly centered on cytokine and cellular immune signaling, and triggering receptors expressed on myeloid cells (TREM)-1 signaling was searched to be the top one shared signaling pathway and involved in the cytokine and cellular immune signaling. Further in vitro experiments indicated that TP not only remarkably lowered the levels of TREM-1 and DNAX-associated protein (DAP)12, but also significantly suppressed the activation of janus activating kinase (JAK)2 and signal transducers and activators of transcription (STAT)3. The expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1ß and IL-6 in lipopolysaccharides (LPS)-stimulated U937 cells also decreased after treatment with TP. Furthermore, TREM-1 knockdown was able to interfere with the inhibition effects of TP on these cytokines production. In vivo experiments showed that TP not only significantly inhibited the TREM-1 mRNA and DAP12 mRNA expression, and activation of JAK2 and STAT3 in ankle of rats with collagen-induced arthritis (CIA), but also remarkably decreased production of TNF-α, IL-1ß and IL-6 in serum and joint. These findings demonstrated that TP could modulate the TREM1 signal pathway to inhibit the inflammatory response in RA.