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Do Politics Matter to the Market? The Long-Term View
Posted by: Tad Weiss on October 5, 2020, Market Update
In our last blog post we explored stock market performance based on who is in the Oval Office, a Republican or Democrat. Surprisingly, the average annual returns over the past 82 years turned out to be very similar. We came across another graph that emphasizes this point and shows the advantage of staying invested in the stock market over the long-term.
Despite economic setbacks, history shows that the stock market trends upward. The attached chart from AllianceBerstein illustrates the growth of $10,000 invested in the Dow Jones Industrial average since 1937. The blue line represents an investor who kept their money in the market exclusively during Democratic presidencies while the red line shows one who stayed invested only during the Republican terms. The teal line represents someone fully invested during all presidencies, Democratic and Republican. While the red and blue lines trend upward, it's clearly visible that the teal line dwarfs them over time.
Trying to "time the market" by moving money out of stocks is tempting, especially during times of high uncertainty. The stock market has had fantastic years when Democrats control the White House, and when Republicans are in charge. It is important to be invested when these years occur. We recommend that our clients focus on "time in the markets" versus moving in and out based on political or other factors.
If you have any questions about the economic impact of this year's election or any other topic, please don't hesitate to contact us at Modus Advisors.
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The commentary on this website reflects the personal opinions, viewpoints and analyses of the Modus Advisors, LLC employees providing such comments, and should not be regarded as a description of advisory services provided by Modus Advisors, LLC or performance returns of any Modus Advisors, LLC client. The views reflected in the commentary are subject to change at any time without notice. Nothing on this website constitutes investment advice, performance data or any recommendation that any particular security, portfolio of securities, transaction or investment strategy is suitable for any specific person. Any mention of a particular security and related performance data is not a recommendation to buy or sell that security. Modus Advisors, LLC manages its clients' accounts using a variety of investment techniques and strategies, which are not necessarily discussed in the commentary. Investments in securities involve the risk of loss. Past performance is no guarantee of future results.


text: The committee is a academic platform which include the summary and communication of majority of workers in defense science and technology management, promotion of domestic and foreign modern defense science and technology management theory, with advanced experience and the innovation of management. Since the special committees was prepared in 2005, it has held six consecutive annual seminar. During these years, it totally exchanged more than 500 academic papers, published over 300 articles, and nearly 100 articles were retrieved by EI , it has achieved very good results in the industry .

subset: commoncrawl


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In this report, we describe the case of a 17-year-old boy with progressive respiratory failure requiring extracorporeal support who met clinical criteria for a presumptive diagnosis of electronic cigarette or vaping-associated acute lung injury (EVALI), with clinical, pathologic, and laboratory evidence of hemophagocytic lymphohistiocytosis (HLH) and macrophage activation syndrome (MAS). The patient in our report had a history of tetrahydrocannabinol and nicotine electronic cigarette use for months leading up to his presentation of fever, headache, emesis, and weight loss with respiratory distress. Multiple potential diagnoses were explored, and the patient's respiratory status improved, and he was initially discharged from the hospital. Roughly one week later, the patient was readmitted for worsening respiratory distress. The patient then met sufficient criteria for a potential diagnosis of HLH and MAS (elevated ferritin level, inflammatory markers, and cytopenia) to warrant a bone marrow aspirate, which revealed rare hemophagocytic cells. Given the severity of his symptoms and laboratory evidence of HLH and MAS, the patient was started on a course of steroids and anakinra. Although laboratory markers improved after treatment, the patient's respiratory failure worsened, ultimately progressing to a need for mechanical ventilation and extracorporeal support and leading to worsening multiorgan system failure and, ultimately, death. To the best of our knowledge, this is the first report of a patient with a presumptive diagnosis of EVALI with evidence of HLH and MAS, raising the possibility that macrophage activation may play a role in the pathogenesis of EVALI.
AssuntosLesão Pulmonar Aguda/induzido quimicamente , Sistemas Eletrônicos de Liberação de Nicotina , Linfo-Histiocitose Hemofagocítica/induzido quimicamente , Vaping/efeitos adversos , Adolescente , Evolução Fatal , Humanos , Síndrome de Ativação Macrofágica/induzido quimicamente , Masculino , Insuficiência de Múltiplos Órgãos/etiologia
Paraquat (PQ) as a non-selective heterocyclic herbicide, has been applied worldwide for over a few decades. But PQ is very harmful to humans and rodents. The lung is the main target organ of PQ poisoning. It is an important event that lung epithelial cells are injured during PQ-induced acute lung injury and pulmonary fibrosis. As a regulator of mRNA expression, microRNA (miRNA) may play an important role in the progress. Our study was to investigate the mechanisms of PQ-induced injury of pulmonary epithelial cells through analyzing the profiling of miRNAs and their target genes. As a result, 11 differentially expressed miRNAs were screened, including 1 upregulated miRNA and 10 downregulated miRNAs in PQ-treated murine lung alveolar epithelial cells (MLE-12 cells). The bioinformatic analyses suggested that the target genes of these miRNAs were involved in mitochondrial apoptosis pathway and DNA methylation, and participated in the regulation of PI3K-Akt, mTOR, RAS, TNF, MAPK and other signal pathways which related to oxidative stress and apoptosis. This indicated that miRNAs were an important regulator of oxidative stress and apoptosis during PQ-induced injury of murine lung alveolar epithelial cells. The findings would deepen our understanding of the mechanisms of PQ-induced pulmonary injury and might provide new treatment targets for this disease.
AssuntosLesão Pulmonar Aguda/induzido quimicamente , Lesão Pulmonar Aguda/genética , Apoptose/genética , Células Epiteliais/efeitos dos fármacos , Perfilação da Expressão Gênica , Expressão Gênica , Herbicidas/toxicidade , MicroRNAs/genética , MicroRNAs/metabolismo , Estresse Oxidativo/genética , Paraquat/toxicidade , Alvéolos Pulmonares/citologia , Lesão Pulmonar Aguda/patologia , Animais , Células Cultivadas , Metilação de DNA/genética , Camundongos , MicroRNAs/fisiologia , Mitocôndrias/patologia
Acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome (ARDS) are common lung disorders characterized by alveolar-capillary barrier disruption and dyspnea, which can cause substantial morbidity and mortality. Currently, a cluster of acute respiratory illnesses, known as novel coronavirus (2019-nCoV)-infected pneumonia (NCIP), which allegedly originally occurred in Wuhan, China, has increased rapidly worldwide. The critically ill patients with ARDS have high mortality in subjects with comorbidities. Previously, the excessive recruitment and activation of neutrophils (polymorphonuclear leukocytes [PMNs]), accompanied by neutrophil extracellular traps (NETs) formation were reported being implicated in the pathogenesis of ALI/ARDS. However, the direct visualization of lung epithelial injuries caused by NETs, and the qualitative and quantitative evaluations of this damage are still lacking. Additionally, those already reported methods are limited for their neglect of the pathological role exerted by NETs and focusing only on the morphological features of NETosis. Therefore, we established a cell-based assay for detecting NETs during lung epithelial cells-neutrophils co-culture using the xCELLigence system, a recognized real-time, dynamic, label-free, sensitive, and high-throughput apparatus. Our results demonstrated that lung epithelial injuries, reflected by declines in cell index (CI) values, could be induced by lipopolysaccharide (LPS)-activated PMNs, or NETs in a time and dose-dependent manner. NETs generation was verified to be the major contributor to the cytotoxicity of activated PMNs; protein components of NETs were the prevailing cytotoxic mediators. Moreover, this cell-based assay identified that PMNs from severe pneumonia patients had a high NETs formative potential. Additionally, acetylsalicylic acid (ASA) and acetaminophen (APAP) were discovered alleviating NETs formation. Thus, this study not only presents a new methodology for detecting the pathophysiologic role of NETs but also lays down a foundation for exploring therapeutic interventions in an effort to cure ALI/ARDS in the clinical setting of severe pneumonia, including the emerging of NCIP.
AssuntosLesão Pulmonar Aguda/sangue , Infecções por Coronavirus/sangue , Armadilhas Extracelulares/diagnóstico por imagem , Neutrófilos/metabolismo , Pneumonia Viral/sangue , Síndrome do Desconforto Respiratório do Adulto/sangue , Lesão Pulmonar Aguda/induzido quimicamente , Lesão Pulmonar Aguda/diagnóstico por imagem , Lesão Pulmonar Aguda/virologia , Animais , Betacoronavirus/patogenicidade , Infecções por Coronavirus/diagnóstico por imagem , Infecções por Coronavirus/virologia , Células Epiteliais/patologia , Células Epiteliais/virologia , Armadilhas Extracelulares/virologia , Humanos , Lipopolissacarídeos/toxicidade , Pulmão/diagnóstico por imagem , Pulmão/virologia , Masculino , Neutrófilos/virologia , Pandemias , Pneumonia/sangue , Pneumonia/diagnóstico por imagem , Pneumonia/virologia , Pneumonia Viral/diagnóstico por imagem , Pneumonia Viral/virologia , Síndrome do Desconforto Respiratório do Adulto/patologia , Síndrome do Desconforto Respiratório do Adulto/virologia
Acute exposure to hydrogen sulfide (H2S) can cause fatal acute lung injury (ALI). However, the mechanisms of H2S-induced ALI are still not fully understood. This study aims to investigate the role of the tight junction protein claudin-5 in H2S-induced ALI. In our study, Sprague-Dawley (SD) rats were exposed to H2S to establish the ALI model, and in parallel, human pulmonary microvascular endothelial cells (HPMECs) were incubated with NaHS (a H2S donor) to establish a cell model. Lung immunohistochemistry and electron microscopy assays were used to identify H2S-induced ALI, and the expression of claudin-5, p-AKT/t-AKT and p-FoxO1/t-FoxO1 was detected. Our results show that H2S promoted the formation of ALI by morphological investigation and decreased claudin-5 expression. Dexamethasone (Dex) could partly attenuate NaHS-mediated claudin-5 downregulation, and the protective effects of Dex could be partially blocked by LY294002, a PI3K/AKT/FoxO1 pathway antagonist. Moreover, as a consequence of the altered phosphorylation of AKT and FoxO1, a change in claudin-5 with the same trend was observed. Therefore, the tight junction protein claudin-5 might be considered a therapeutic target for the treatment of ALI induced by H2S and other hazardous gases.
AssuntosLesão Pulmonar Aguda/induzido quimicamente , Lesão Pulmonar Aguda/metabolismo , Claudina-5/metabolismo , Claudina-5/fisiologia , Sulfeto de Hidrogênio/toxicidade , Lesão Pulmonar Aguda/tratamento farmacológico , Lesão Pulmonar Aguda/genética , Animais , Células Cultivadas , Claudina-5/genética , Dexametasona/farmacologia , Dexametasona/uso terapêutico , Modelos Animais de Doenças , Regulação para Baixo/efeitos dos fármacos , Expressão Gênica/efeitos dos fármacos , Humanos , Pulmão/metabolismo , Pulmão/patologia , Masculino , Terapia de Alvo Molecular , Ratos Sprague-Dawley
OBJECTIVE: To investigate the changes in phagocytic function of alveolar macrophages (AMs) in mice with lipopolysaccharide (LPS)-induced acute lung injury (ALI) and explore the possible mechanism. METHODS: Kunming mice were randomly divided into normal control group and ALI (induced by LPS instillation in the airway) model group. AMs were obtained from bronchoalveolar lavage fluid in both groups, and phagocytosis of the AMs was observed using flow cytometry and fluorescence microscopy. Western blotting and ELISA were used to detect the expression and secretion of IL-33 in the lung tissue of the mice. We also detected the secretion of IL-33 by an alveolar epithelial cell line MLE-12 in response to stimulation with different concentrations of LPS. The AMs from the normal control mice were treated with different concentrations of LPS and IL-33, and the changes in the phagocytic activity of the cells were observed. RESULTS: Compared with those in normal control group, the percentage of AMs phagocytosing fluorescent microspheres was significantly decreased, and the expression of IL-33 in lung tissue and IL-33 level in the bronchoalveolar lavage fluid were significantly increased in ALI mice (P < 0.01). LPS (100-1000 ng/mL) obviously promoted the secretion of IL-33 in cultured MLE-12 cells (P < 0.01). Both LPS (10-500 ng/mL) and IL-33 (100 ng/mL) significantly inhibited the phagocytic activity of the AMs from normal control mice (P < 0.01). CONCLUSIONS: The phagocytic activity of AMs is weakened in ALI mice possibly due to direct LPS stimulation and the inhibitory effect of the alarmin IL-33 produced by LPS-stimulated alveolar epithelial cells.
AssuntosLesão Pulmonar Aguda , Macrófagos Alveolares , Lesão Pulmonar Aguda/induzido quimicamente , Animais , Lipopolissacarídeos , Pulmão , Camundongos , Fagocitose
Objective: To investigate the CT features of lung injury induced by paraquat poisoning and its relationship with prognosis, and to provide reference for the judgment of the condition and prognosis of paraquat poisoning. Methods: 146 cases of paraquat poisoning patients were treated in the Third People's Hospital of Xuzhou City from January 2013 to April 2016. The cases were divided into mild group, moderate-severe group and fulminant group according to the concentration of paraquat in urine. The clinical data and CT imaging findings were analyzed and reconstructed in three-dimensional reconstruction. The extent of the lesion was observed and the relationship between CT and prognosis was explored. Results: Paraquat lung injury has many manifestations on CT images, and it's performance can be intersecting at the same time. Early lesions lighter cases, late CT imaging lesions can be completely absorbed or residual fibrosis, the prognosis was good; the early lesion was pulmonary consolidation, pleural effusion cases, the late CT image was usually pleural thickening and bronchiectasis, the prognosis was relatively good; early lesions were large patches of ground glass opacity cases, finally, pulmonary fibrosis was common, the mortality rate of 56.57%. There were significant differences in the extent of lung injury between different groups (P<0.001) , and the difference in mortality was statistically significant when the lung injury was different (P<0.001) . Multivariate stepwise Logistic regression analysis showed that ground-glass opacity (OR value=2.013) , interstitial lung fibrosis (OR=3.779) and mediastinal emphysema (OR=33.118) were risk factors for death of lung injury caused by paraquat poisoning (P<0.05) . Conclusion: There were many manifestations on CT images of paraquat lung injury, and the manifestations of paraquat lung injury can be intersecting at the same time. The pulmonary manifestations and outcomes of different paraquat types were different. The CT manifestations of lung injury in paraquat poisoning were mainly exudative changes at early stage, and can be gradually absorbed or evolved into interstitial changes at later stage. The cumulative damage range can be used as a reference for evaluating the prognosis. Ground-glass opacity, interstitial pulmonary fibrosis and mediastinal emphysema are the risk factors for death of lung injury caused by paraquat poisoning.
AssuntosLesão Pulmonar Aguda/diagnóstico por imagem , Paraquat/envenenamento , Lesão Pulmonar Aguda/induzido quimicamente , Humanos , Pulmão/diagnóstico por imagem , Pulmão/patologia , Prognóstico , Tomografia Computadorizada por Raios X
Background: Mitochondrial dysfunction played a vital role in the pathogenesis of various diseases, including acute lung injury (ALI). However, few strategies targeting mitochondria were developed in treating ALI. Recently, we fabricated a porous Se@SiO2 nanoparticles (NPs) with antioxidant properties. Methods: The protective effect of Se@SiO2 NPs was assessed using confocal imaging, immunoblotting, RNA-seq, mitochondrial respiratory chain (MRC) activity assay, and transmission electron microscopy (TEM) in airway epithelial cell line (Beas-2B). The in vivo efficacy of Se@SiO2 NPs was evaluated in a lipopolysaccharide (LPS)-induced ALI mouse model. Results: This study demonstrated that Se@SiO2 NPs significantly increased the resistance of airway epithelial cells under oxidative injury and shifted lipopolysaccharide-induced gene expression profile closer to the untreated controls. The cytoprotection of Se@SiO2 was found to be achieved by maintaining mitochondrial function, activity, and dynamics. In an animal model of ALI, pretreated with the NPs improved mitochondrial dysfunction, thus reducing inflammatory responses and diffuse damage in lung tissues. Additionally, RNA-seq analysis provided evidence for the broad modulatory activity of our Se@SiO2 NPs in various metabolic disorders and inflammatory diseases. Conclusion: This study brought new insights into mitochondria-targeting bioactive NPs, with application potential in curing ALI or other human mitochondria-related disorders.
AssuntosLesão Pulmonar Aguda/tratamento farmacológico , Mitocôndrias/efeitos dos fármacos , Nanopartículas/química , Selênio/farmacologia , Dióxido de Silício/farmacologia , Lesão Pulmonar Aguda/induzido quimicamente , Lesão Pulmonar Aguda/patologia , Animais , Antioxidantes/química , Antioxidantes/farmacologia , Linhagem Celular , Citoproteção , Modelos Animais de Doenças , Células Epiteliais/metabolismo , Humanos , Lipopolissacarídeos/toxicidade , Pulmão/efeitos dos fármacos , Pulmão/patologia , Camundongos , Mitocôndrias/metabolismo , Nanopartículas/uso terapêutico , Oxirredução , Estresse Oxidativo/efeitos dos fármacos , Porosidade , Selênio/química , Dióxido de Silício/química
MECP2 (Methyl-CpG-binding protein 2) has been shown to have a critical role in regulating DNA methylation against smoke exposed lung injury. However, the biological function of MECP2 and the underlying molecular mechanism remains elusive. Human bronchial epithelial (16HBE) and alveolar type II epithelial cells (AECII) were exposed to increasing concentrations of cigarette smoke extracts (CSE) solution to establish CSE-induced lung epithelial cell injury models. Our findings revealed that MECP2 was down-regulated, while CYP1B1 was up-regulated in CSE-induced lung epithelial cell injury models by quantitative real time PCR, western blotting and immunoï¬uorescence staining. Down-regulated CYP1B1 was ascribed to the demethylation of its promoter by methylation-specific PCR (MSP). The in vitro experiments further showed that MECP2 overexpression significantly attenuated CSE-triggered cell growth attenuation, cell cycle arrest, apoptosis and ROS generation in lung epithelial cells by CCK-8 and flow cytometry assays. In molecular level, we further demonstrated that MECP2 overexpression obviously suppressed the expression of CYP1B1 through enhancing DNA methylation. Therefore, our data suggest that MECP2 protects against CSE-induced lung epithelial cell injury possibly through down-regulating CYP1B1 expression via elevating its methylation status.
AssuntosLesão Pulmonar Aguda/induzido quimicamente , Lesão Pulmonar Aguda/genética , Fumar Cigarros/efeitos adversos , Citocromo P-450 CYP1B1/metabolismo , Metilação de DNA , Células Epiteliais/efeitos dos fármacos , Células Epiteliais/patologia , Expressão Gênica , Pulmão/citologia , Proteína 2 de Ligação a Metil-CpG/genética , Proteína 2 de Ligação a Metil-CpG/metabolismo , Extratos Vegetais/efeitos adversos , Tabaco/química , Lesão Pulmonar Aguda/patologia , Células Cultivadas , Citocromo P-450 CYP1B1/genética , Humanos , Extratos Vegetais/isolamento & purificação
Clinical studies have established that the capacity of removing excess fluid from alveoli is impaired in most patients with acute respiratory distress syndrome. Impaired alveolar fluid clearance (AFC) correlates with poor outcomes. Adenosine A2B receptor (A2BAR) has the lowest affinity with adenosine among four adenosine receptors. It is documented that A2BAR can activate adenylyl cyclase (AC) resulting in elevated cAMP. Based on the understanding that cAMP is a key regulator of epithelial sodium channel (ENaC), which is the limited step in sodium transport, we hypothesized that A2BAR signaling may affect AFC in acute lung injury (ALI) through regulating ENaC via cAMP, thus attenuating pulmonary edema. To address this, we utilized pharmacological approaches to determine the role of A2BAR in AFC in rats with endotoxin-induced lung injury and further focused on the mechanisms in vitro. We observed elevated pulmonary A2BAR level in rats with ALI and the similar upregulation in alveolar epithelial cells exposed to LPS. A2BAR stimulation significantly attenuated pulmonary edema during ALI, an effect that was associated with enhanced AFC and increased ENaC expression. The regulatory effects of A2BAR on ENaC-α expression were further verified in cultured alveolar epithelial type II (ATII) cells. More importantly, activation of A2BAR dramatically increased amiloride-sensitive Na+ currents in ATII cells. Moreover, we observed that A2BAR activation stimulated cAMP accumulation, whereas the cAMP inhibitor abolished the regulatory effect of A2BAR on ENaC-α expression, suggesting that A2BAR activation regulates ENaC-α expression via cAMP-dependent mechanism. Together, these findings suggest that signaling through alveolar epithelial A2BAR promotes alveolar fluid balance during endotoxin-induced ALI by regulating ENaC via cAMP pathway, raising the hopes for treatment of pulmonary edema due to ALI.
AssuntosLesão Pulmonar Aguda/metabolismo , Células Epiteliais Alveolares/metabolismo , AMP Cíclico/metabolismo , Alvéolos Pulmonares/metabolismo , Receptor A2B de Adenosina/metabolismo , Transdução de Sinais/fisiologia , Lesão Pulmonar Aguda/induzido quimicamente , Adenosina/metabolismo , Células Epiteliais Alveolares/efeitos dos fármacos , Animais , Endotoxinas/farmacologia , Canais Epiteliais de Sódio/metabolismo , Lipopolissacarídeos/farmacologia , Pulmão/efeitos dos fármacos , Pulmão/metabolismo , Masculino , Alvéolos Pulmonares/efeitos dos fármacos , Edema Pulmonar/induzido quimicamente , Edema Pulmonar/metabolismo , Ratos , Ratos Sprague-Dawley , Transdução de Sinais/efeitos dos fármacos
Mitophagy is involved in sepsis-induced acute lung injury (ALI). Bcl-2 family proteins play an important role in mitochondrial homeostasis. However, whether targeting Bcl-2 proteins (Bcl-2 and Bad) could influence mitophagy in ALI remains unclear. In this study, lipopolysaccharide (LPS) was used to induce injury in A549 cells and ALI in mice. LPS treatment resulted in elevated cell apoptosis, enhanced mitophagy, decreased Bcl-2 expression, increased Bad expression, and activation of PINK1/Parkin signaling in cells and lung tissues. Both Bcl-2 overexpression and Bad knockdown attenuated LPS-induced injury, inhibited cell apoptosis and mitophagy, and improved survival. Atg5 knockout (KO) inhibited LPS-induced cell apoptosis. Furthermore, Bcl-2 proteins regulated mitophagy by modulating the recruitment of Parkin from the cytoplasm to mitochondria via direct protein-protein interactions. These results were further confirmed in Park2 KO cells and Park2-/- mice. This is the first study to demonstrate that Bcl-2 proteins regulated mitophagy in LPS-induced ALI via modulating the PINK1/Parkin signaling pathway, promoting new insights into the mechanisms and investigation of therapeutic strategies for a septic patient with ALI.
AssuntosLesão Pulmonar Aguda/induzido quimicamente , Lipopolissacarídeos/efeitos adversos , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Ubiquitina-Proteína Ligases/genética , Animais , Modelos Animais de Doenças , Humanos , Camundongos , Mitofagia , Transdução de Sinais , Ubiquitina-Proteína Ligases/metabolismo
AssuntosLesão Pulmonar Aguda/metabolismo , Betacoronavirus/efeitos dos fármacos , Peptidil Dipeptidase A/metabolismo , Peptidil Dipeptidase A/farmacologia , Lesão Pulmonar Aguda/induzido quimicamente , Lesão Pulmonar Aguda/virologia , Animais , Infecções por Coronavirus/tratamento farmacológico , Infecções por Coronavirus/metabolismo , Infecções por Coronavirus/virologia , Modelos Animais de Doenças , Interações Hospedeiro-Patógeno , Humanos , Pulmão/efeitos dos fármacos , Pulmão/metabolismo , Camundongos , Pandemias , Pneumonia Viral/tratamento farmacológico , Pneumonia Viral/metabolismo , Pneumonia Viral/virologia , Receptor Tipo 1 de Angiotensina/metabolismo , Receptor Tipo 2 de Angiotensina/metabolismo , Receptores de Angiotensina/metabolismo
Beginning in April of 2019, the US saw >â2,000 cases of hospitalized, often young, patients with severe acute lung injury, of which over 40 died, and the only existing connection between patients was their use of electronic cigarettes (e-cigarettes). The acronym EVALI ("e-cigarette, or vaping, product use associated lung injury") has since been established for the condition. This review article is intended to provide an overview of recent, mainly US literature on EVALI, including the case definition, epidemiology, clinical presentation, typical disease progression, as well as potential triggers. Ancillary to this, the review further provides a general overview of the basic function of e-cigarettes, the ingredients of the liquids used in these (e-liquids), as well as a brief description of the associated potential inhalation risks.
AssuntosLesão Pulmonar Aguda/induzido quimicamente , Dronabinol/efeitos adversos , Sistemas Eletrônicos de Liberação de Nicotina , Vaping/efeitos adversos , Lesão Pulmonar Aguda/epidemiologia , Canabidiol/administração & dosagem , Canabidiol/efeitos adversos , Surtos de Doenças , Dronabinol/administração & dosagem , Humanos , Nicotina/administração & dosagem , Nicotina/efeitos adversos , Fatores de Risco
The adaptive immune response could play a major role in the resolution of lung injury. Although regulatory T cells (Tregs) have been implicated in promoting the resolution of lung injury, therapeutic strategies to enhance Treg quantity and activity at the site of injury need further exploration. In the current study, Akt inhibition using triciribine (TCBN), given 48 h after lipopolysaccharide (LPS) administration, increased Tregs-promoted resolution of acute lung injury (ALI). TCBN treatment enhanced the resolution of LPS-induced ALI on day 7 by reducing pulmonary edema and neutrophil activity associated with an increased number of CD4+/FoxP3+/CD103+ and CTLA4+ effector Tregs, specifically in the injured lungs and not in the spleen. Treatment of EL-4 T-lymphocytes with two Akt inhibitors (TCBN and MK-2206) for 72 h resulted in increased FoxP3 expression in vitro. On the other end, Treg-specific PTEN knockout (PTENTreg KO) mice that have a higher Akt activity in its Tregs exhibited a significant impairment in ALI resolution, increased edema, and neutrophil activity associated with a reduced number of CD4+/FoxP3+/CD103+ and CTLA4+ effector Tregs as compared with the control group. In conclusion, our study identifies a potential target for the treatment of late-stage ALI by promoting resolution through effector Treg-mediated suppression of inflammation.
AssuntosLesão Pulmonar Aguda/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Linfócitos T Reguladores/metabolismo , Lesão Pulmonar Aguda/induzido quimicamente , Transferência Adotiva/métodos , Animais , Antígenos CD/metabolismo , Antígenos CD4/metabolismo , Modelos Animais de Doenças , Feminino , Fatores de Transcrição Forkhead/metabolismo , Cadeias alfa de Integrinas/metabolismo , Lipopolissacarídeos/farmacologia , Pulmão/efeitos dos fármacos , Pulmão/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Neutrófilos/efeitos dos fármacos , Neutrófilos/metabolismo , Edema Pulmonar/induzido quimicamente , Edema Pulmonar/metabolismo , Baço , Linfócitos T Reguladores/efeitos dos fármacos
OBJECTIVE: To investigate the impact of death-associated protein kinase 1 (Dapk1) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) via p38MAPK/NF-κB pathway. METHODS: Dapk1+/+ and Dapk1-/- mice were randomized into Control, LPS, SB203580 (a p38MAPK pathway inhibitor) + LPS, and PDTC (a NF-κB pathway inhibitor) + LPS groups. Cell counts, lung wet to dry weight ratio (W/D weight ratio), as well as indicators of oxidative stress were determined followed by the detection with HE staining, ELISA, qRT-PCR, Western blotting and Immunofluorescence. Besides, to explore whether the effect of Dapk1 on ALI directly mediated via p38MAPK/NF-κB pathway, mice were injected with TC-DAPK 6 (a Dapk1 inhibitor) with or without SB203580/PDTC before LPS administration. RESULTS: LPS induced lung injury with increased lung W/D weight ratio, which could be partly reversed by SB203580 and PDTC in LPS-induced mice with activated p38MAPK/NF-κB pathway in lung tissues, especially in Dapk1-/- mice. SB203580 and PDTC reduced total cells and neutrophils in BALF in LPS-induced mice, accompanying with decreased levels of TNF-α, IL-6, MPO, LPO and MDA and the expressions of beclin-1, Atg5 and LC3II, but with the up-regulated activities of SOD and GSH-Px, as well as p62 protein expression. Besides, TC-DAPK 6 aggravated the pathologic injury in LPS-induced ALI with more serious inflammatory response, oxidative stress and autophagy as well as the activated p38MAPK/NF-κB pathway, which were reversed by SB203580 or PDTC. CONCLUSION: Dapk1 improved oxidative stress, inhibited autophagy, and reduce inflammatory response of LPS-induced ALI mice by inhibiting p38MAPK/NF-κB pathway.
AssuntosLesão Pulmonar Aguda/metabolismo , Proteínas Quinases Associadas com Morte Celular/metabolismo , Lesão Pulmonar Aguda/induzido quimicamente , Lesão Pulmonar Aguda/patologia , Animais , Autofagia , Proteínas Quinases Associadas com Morte Celular/deficiência , Proteínas Quinases Associadas com Morte Celular/genética , Imidazóis/farmacologia , Inflamação/metabolismo , Inflamação/patologia , Lipopolissacarídeos/toxicidade , Pulmão/efeitos dos fármacos , Pulmão/metabolismo , Pulmão/patologia , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , NF-kappa B/antagonistas & inibidores , NF-kappa B/metabolismo , Estresse Oxidativo , Piridinas/farmacologia , Pirrolidinas/farmacologia , Transdução de Sinais/efeitos dos fármacos , Tiocarbamatos/farmacologia , Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
Acute respiratory distress syndrome (ARDS) is a common cause of death in the intensive care unit, with mortality rates of ~30-40%. To reduce invasive diagnostics such as bronchoalveolar lavage and time-consuming in-hospital transports for imaging diagnostics, we hypothesized that particle flow rate (PFR) pattern from the airways could be an early detection method and contribute to improving diagnostics and optimizing personalized therapies. Porcine models were ventilated mechanically. Lipopolysaccharide (LPS) was administered endotracheally and in the pulmonary artery to induce ARDS. PFR was measured using a customized particles in exhaled air (PExA 2.0) device. In contrast to control animals undergoing mechanical ventilation and receiving saline administration, animals who received LPS developed ARDS according to clinical guidelines and histologic assessment. Plasma levels of TNF-α and IL-6 increased significantly compared with baseline after 120 and 180 min, respectively. On the other hand, the PFR significantly increased and peaked 60 min after LPS administration, i.e., ~30 min before any ARDS stage was observed with other well-established outcome measurements such as hypoxemia, increased inspiratory pressure, and lower tidal volumes or plasma cytokine levels. The present results imply that PFR could be used to detect early biomarkers or as a clinical indicator for the onset of ARDS.
AssuntosLesão Pulmonar Aguda/patologia , Modelos Animais de Doenças , Lipopolissacarídeos/toxicidade , Troca Gasosa Pulmonar , Síndrome do Desconforto Respiratório do Adulto/patologia , Lesão Pulmonar Aguda/induzido quimicamente , Lesão Pulmonar Aguda/metabolismo , Animais , Gasometria , Citocinas/metabolismo , Hemodinâmica , Tamanho da Partícula , Reologia , Suínos , Volume de Ventilação Pulmonar
Acute lung injury (ALI) is characterized by neutrophilic infiltration, uncontrolled oxidative stress and inflammatory processes. Despite various therapeutic regimes having been performed, there remains no effective pharmacotherapy available to treat ALI. Halofuginone (HF), a ketone isolated from Dichroa febrifuga, exhibits significant antiinflammatory and antifibrotic effects. Dexamethasone (DEX), a synthetic glucocorticoid, has been routinely used as an adjuvant therapy in treating inflammatory diseases, including ALI. The present study aimed to investigate the effects of the combination of HF and DEX in the treatment of ALI. The present results suggested that the simultaneous administration of HF and DEX markedly decreased the level of proinflammatory cytokines and increased the level of antiinflammatory cytokines, as assessed by western blot analysis. In addition, HF and DEX effectively decreased nuclear factorκB activity via suppressing the phosphorylation of P65 in lipopolysaccharide (LPS)induced human pulmonary alveolar epithelial cells (HPAEpiC) and lung tissues extracted from ALI rats, as determined by immunofluorescence. Furthermore, in vivo experiments demonstrated that the combination of HF and DEX in LPSinduced ALI rats defended against lung fibrosis, perivascular inflammation, congestion and edema of pulmonary alveoli, as assessed by histopathological analysis, TUNEL staining and immunohistochemistry assay. Taken together, the present study indicated the synergistic effect of HF and DEX on LPSinduced ALI in HPAEpiC cells and a rat model. These results offer a novel therapeutic approach for the treatment of ALI.
AssuntosLesão Pulmonar Aguda/patologia , Células Epiteliais Alveolares/patologia , Dexametasona/farmacologia , Piperidinas/farmacologia , Quinazolinonas/farmacologia , Lesão Pulmonar Aguda/induzido quimicamente , Células Epiteliais Alveolares/efeitos dos fármacos , Animais , Sobrevivência Celular/efeitos dos fármacos , Modelos Animais de Doenças , Sinergismo Farmacológico , Humanos , Inflamação/patologia , Lipopolissacarídeos , NF-kappa B/metabolismo , Fosforilação/efeitos dos fármacos , Ratos Sprague-Dawley , Transdução de Sinais/efeitos dos fármacos
INTRODUCTION: Zinc is well known for its anti-inflammatory effects, including regulation of migration and activity of polymorphonuclear neutrophils (PMN). Zinc deficiency is associated with inflammatory diseases such as acute lung injury (ALI). As deregulated neutrophil recruitment and their hyper-activation are hallmarks of ALI, benefits of zinc supplementation on the development of lipopolysaccharides (LPS)-induced ALI were tested. METHODS: 64 C57Bl/6 mice, split into eight groups, were injected with 30 µg zinc 24 hours before exposure to aerosolised LPS for 4 hours. Zinc homoeostasis was characterised measuring serum and lung zinc concentrations as well as metallothionein-1 expression. Recruitment of neutrophils to alveolar, interstitial and intravascular space was assessed using flow cytometry. To determine the extent of lung damage, permeability and histological changes and the influx of protein into the bronchoalveolar lavage fluid were measured. Inflammatory status and PMN activity were evaluated via tumour necrosis factor α levels and formation of neutrophil extracellular traps. The effects of zinc supplementation prior to LPS stimulation on activation of primary human granulocytes and integrity of human lung cell monolayers were assessed as well. RESULTS: Injecting zinc 24 hours prior to LPS-induced ALI indeed significantly decreased the recruitment of neutrophils to the lungs and prevented their hyperactivity and thus lung damage was decreased. Results from in vitro investigations using human cells suggest the transferability of the finding to human disease, which remains to be tested in more detail. CONCLUSION: Zinc supplementation attenuated LPS-induced lung injury in a murine ALI model. Thus, the usage of zinc-based strategies should be considered to prevent detrimental consequences of respiratory infection and lung damage in risk groups.
AssuntosLesão Pulmonar Aguda/metabolismo , Lesão Pulmonar Aguda/prevenção & controle , Infiltração de Neutrófilos/efeitos dos fármacos , Neutrófilos/fisiologia , Zinco/farmacologia , Lesão Pulmonar Aguda/induzido quimicamente , Lesão Pulmonar Aguda/patologia , Animais , Líquido da Lavagem Broncoalveolar/química , Proteínas de Transporte de Cátions/genética , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Quimiocina CXCL1/metabolismo , Modelos Animais de Doenças , Expressão Gênica/efeitos dos fármacos , Fator Estimulador de Colônias de Granulócitos/genética , Homeostase , Humanos , Selectina L/metabolismo , Lipopolissacarídeos , Masculino , Metalotioneína/genética , Metalotioneína/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , RNA Mensageiro , Receptores de Complemento 3b/metabolismo , Fator de Transcrição STAT3/metabolismo , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismo , Zinco/metabolismo , Zinco/uso terapêutico
The purpose of this paper is to observe the protective action and its effective mechanism of eriodictyol on lipopolysaccharide (LPS)-induced acute lung injury (ALI). In this study, our results indicated that eriodictyol could dramatically suppress the inflammatory mediators, including interleukin-6 (IL-6), IL-1ß, prostaglandin E2, and tumor necrosis factor-α in bronchoalveolar lavage fluid of LPS-challenged mice. Eriodictyol also alleviated the wet/dry ratio and improved pathological changes of the lung. In addition, eriodictyol significantly decreased myeloperoxidase activity and malondialdehyde content as well as increased superoxide dismutase activity. Moreover, eriodictyol inhibited the COX-2/NLRP3/NF-κB signaling pathway in the lung tissues of ALI mice. In conclusion, our observations validated that eriodictyol processed the protective effects on ALI mice, which was related to the regulation of the COX-2/NLRP3/NF-κB signaling pathway.
AssuntosLesão Pulmonar Aguda , Ciclo-Oxigenase 2/metabolismo , Flavanonas/farmacologia , Lipopolissacarídeos/toxicidade , NF-kappa B/metabolismo , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Transdução de Sinais/efeitos dos fármacos , Lesão Pulmonar Aguda/induzido quimicamente , Lesão Pulmonar Aguda/tratamento farmacológico , Lesão Pulmonar Aguda/metabolismo , Lesão Pulmonar Aguda/patologia , Animais , Inflamação/induzido quimicamente , Inflamação/tratamento farmacológico , Inflamação/metabolismo , Inflamação/patologia , Masculino , Camundongos , Camundongos Endogâmicos BALB C
Organosulfur compounds, such as L-cysteine, allicin and other sulfur-containing organic compounds in Allium species, have been proposed to possess many important physiological and pharmacological functions. A novel L-cysteine derivative, t-Butyl S-allylthio-L-cysteinate (5P39), was designed and synthesized by combining L-cysteine derivative and allicin pharmacophore through a disulfide bond. This study aimed to explore the effects and mechanisms of 5P39 on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. At the experimental concentration (5, 10 and 20 µM), 5P39 suppressed the excessive secretion of nitric oxide (NO) and interleukin-6 (IL-6) in mice peritoneal macrophages stimulated by LPS. A mouse model of ALI was established by tracheal instillation of LPS for 2 h before 5P39 (30 and 60 mg/kg) administration. The results showed that 5P39 treatment down-regulated the wet/dry weight ratio (W/D ratio) of lungs and reduced the protein concentration, the number of total cells as well as the myeloperoxidase (MPO) activity in bronchoalveolar lavage fluid (BALF). 5P39 administration improved the histopathological changes of lungs in ALI mice with the decreased levels of pro-inflammatory cytokines in BALF. The inhibitory effects of 5P39 on the toll-like receptor 4 (TLR4) expression and macrophages accumulation in lung tissues were observed by immunohistochemistry. Additionally, 5P39 significantly attenuated the LPS-activated high expression of key proteins in TLR4/MyD88 signaling pathway. Taken together, the present study showed that 5P39 effectively alleviate the severity of ALI, and its mechanism might relate to the inhibition of LPS-activated TLR4/MyD88 signaling pathway, demonstrating a promising potential for further development into an anti-inflammatory drug candidate.


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11 Pinoy scientists and researchers, among Asia's top 100 best scientists
- Eleven Filipinos, constisting of scientists and researchers, made it to this year's top 100 list made by the Asian Scientist magazine
- To be added to this list means the honoree must have received a national or international prize for his or her research, or have made a significant scientific discovery
- Since 2017, the Asian Scientist magazine has been compiling a list of Asia's most outstanding scientists and researchers
To recognize their pivotal studies and research in the scientific department, 11 Filipinos, consist of researchers and scientists, have joined the prestigious list of top 100 scientists in Asia for this year's edition of Asian Scientist magazine.
"Every year since 2017, Asian Scientist magazine compiles a list of Asia's most outstanding researchers. Now on its fourth edition, the Asian Scientist 100 list celebrates the success of the region's best and brightest; highlighting their achievements across a range of scientific disciplines," the publication said.
Among the 11 Filipino scientists and researchers, is the head of research and development institutes of the Department of Science and Technology (DOST): Dr. Raul Destura of the National Institutes of Health (NIH) of University of the Philippines (UP) Manila.
Dr. Destura headed a team of UP Manila researchers that developed an affordable rapid dengue diagnostic kit. He also heads a health tech startup called Marikina City-based Manila HealthTek, Inc. which is responsible for developing and producing the country's first and only locally produced real time-polymerase chain reaction swab test for COVID-19.
The other honorees are Carlos Arcilla, the executive director of the DOST-Philippine Nuclear Research Institute, engineer Robert Dizon, the executive director of the DOST-Metals Industry Research and Development Center, and National Scientist Emil Javier.
Also included in the list are Alicia Aguinaldo of the University of Santo Tomas; Emma Sales of the University of Southern Mindanao; Cleotilde Hidalgo How of UP Manila; the late Alonzo Gabriel of UP Diliman; Raymond Tan and Susan Gallardo, both of the De La Salle University.
According to the Asian Scientist magazine, "to be acknowledged in this list, the honoree must have received a national or international prize in the preceding year for his or her research. Alternatively, he or she must have made a significant scientific discovery or provided leadership in academia or industry."
Also inculded in the top 100 are prestigious scientists in Asia, which also featured past Nobel Prize winners. View the complete list of the Asian Scientist 100 at this link: https://www.asianscientist.com/as100/


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by David Lamb ‧ RELEASE DATE: March 30, 1987
A refreshing, insightful portrait of the Arab people, by a reporter with a flair for his craft. Lamb (The Africans) uses his personal experiences as a Middle Eastern correspondent for the Los Angeles Times as a background for this fascinating study of a region torn between regressive religious fundamentalism and the inescapable pull of the modern world. In the tradition of Hedrick Smith's The Russians, the book is really an anecdotal travel narrative with historical, social and political analyses thrown in; it is well-written, intelligent, often amusing, and hard to put down. The Islamic religion and the Arabic language are the only real unifiers of this huge region whose per capita income ranges from $42,000 (Qatar--oil) to $310 (South Yemen--cotton) and where attitudes toward change range from cautiously enthusiastic (Oman) to openly negative (Libya). Most Arabs, Lamb says, are not extremists, but feel caught in the middle of conflicting views, and are hurt by the ethnic stereotyping they often receive in the Western press; they are hospitable and friendly to individual travelers, and have an infectious sense of humor. Lamb does, too, and in detailing the ironies of Middle Eastern life--the behaviour of Egyptians in traffic jams, the difficulty of bringing western women into Saudi restaurants where signs read ""women must behave in a modest and bashful manner at all times""--he manages to present his subject with both sympathy and quiet criticism. He discusses politics and international relations with sultans, visits peasants in their roofless homes, and devotes many pages to the Palestinian view of the Arab-Israeli conflict. Still, even for a reporter as well-traveled as Lamb, the culture remains very difficult for non-Arabs to penetrate. ""The Middle East,"" he writes at one point, ""was the most inherently alien place I ever encountered. . .to survive the Arab world, you have to yield. Fight it and you lose. Move with its rhythms or be jarred into mental exhaustion."" An enlightening and enjoyable book--a must for anybody with an interest in the Middle East.
Pub Date: March 30, 1987
Page Count: -
Publisher: Random House
Review Posted Online: N/A
Kirkus Reviews Issue: Feb. 15, 1987
Categories: NONFICTION
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More Show Me How: Everything We Couldn't Fit in the First Book Instructions for Life from the Everyday to the Exotic
A new collection of fun, practical, and outrageous projects from the genius minds of the original Show Me How.
Volume two of the Show Me How series contains brand-new instructions that show readers how to amaze, trick, create, style, and love, among other endeavors. Ideas range from the practical (hang a ceiling fixture; hem a pair of pants) to the outrageous (boobytrap a bathroom; forge an antiquity) to the romantic (ace a school crush; send a saucy cell phone pic.) So go ahead and learn some killer pool moves. Or stage your own impromptu gallery show. Style you hair in a fauxhawk. More Show Me How is the indispensable real-life resource that helps readers live life to the fullest and be the star of the party.
The following ISBNs are associated with this title:
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Security-focused and diligent guard, protecting personnel and premises. Respond and act appropriately depending on situational assessments, including criminal acts, fire and medical emergencies. Anticipate trouble and take steps to intervene, diffusing situations. Keen eye for detail, alert, attentive and vigilant at all times.
Companies Worked For:
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© 2020, Bold Limited. All rights reserved.


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davit simikyanSend Message
How do you serve precious pets?
- Pet Transport
At what level do you transport furry/fleecy/spiky travelers?
- Locally (Local Pet Taxi Service)
- Regionally (Regional Pet Transport)
What part of the animal kingdom do you serve?
- Birds
- Cats
- Chinchillas
- Dogs
- Hamsters
- Hedgehogs
- Mice
- Parrots
- Rabbits
- Turtles
Are you registered with the Department of Agriculture?
- No
Cat-astrophes happen! What is your cancellation policy?
- 24 hours notice required
Which part of the country do you serve pets?
What year did you begin serving pets?


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In late August, payments juggernaut PayPal announced their new product 'Pay-in-4'. The Buy Now, Pay Later (BNPL) adoption was unexpected for many and sent the ASX BNPL 7 into shock. Afterpay's share price dropped over 20% in the two weeks following.
But is PayPal's entry into the already crowded BNPL space detrimental to the current leaders? History suggests not, as recognised by our experts. PayPal's experience in the BNPL arena has previously fallen short, which is unknown to many. Further, PayPal's entry may just give its smaller counterparts the push they have been waiting for. In part two of this Collection, I asked our three experts what effect PayPal's entry will have on Buy Now, Pay Later.
Responses come from:
- Emanuel Datt, Datt Capital
- Jun Bei Liu, Tribeca Investment Management
- Dushko Bajic, First Sentier Investors
They've failed once, will they fail again?
Emanuel Datt, Datt Capital
We don't expect that the dynamic of the BNPL space will change a great deal given the entrance of Paypal into the sector. What is not commonly known is that Paypal have previously attempted to break into the space on numerous occasions, first rolling out a BNPL product called Paypal Later in 2010. This product was not successful and was withdrawn after a short period. In 2016, Paypal tried entering BNPL once again with an instalment extension to a product known as Paypal Credit, which was effectively a short-term lending facility. This was again withdrawn after a short period, but was resurrected in September 2020; no doubt attracted by the roaring success of Afterpay.
Paypal is best known as a payment processor. We do note that there are vast differences in competencies between payment processing and the BNPL sector. For example, credit risk management in the payment processing field is fairly broad brush when it comes to the transaction level; whilst in the BNPL sectors each transaction is generally assessed at a relatively granular level. This has historically been Paypal's downfall in their past experiences and it will be interesting to see if they are agile enough to compete in the space.
The benefits of PayPal
Jun Bei Liu, Tribeca Investment Partners
PayPal has certainly had an impact on the share price of the sector. First of all, PayPal is a very large payment system and it's certainly not something to be dismissed, but last year, PayPal released another version of Buy Now, Pay Later, but it didn't quite work out. Now they have relaunched another one, which is at a significantly lower cost, and hopefully it can capture some of the market share.
If you take a step back, Buy Now, Pay Later is a very new industry. Afterpay only moved in 18 months or two years ago. The penetration of this service is very, very low. If anything, PayPal's offering is going to drive more awareness and adoption of this service.
The large players who have already signed up a lot of retailers and have consumers using their platforms will be the ones who benefit. Yes, it is a threat, but it is just a demonstration of the proliferation of this space and it, in turn, will drive traffic back into the market leaders.
PayPal brings great validation
Dushko Bajic, First Sentier Investors
For a payments juggernaut like PayPal to enter, we think it brings great validation to the BNPL industry. This is not PayPal's first foray into instalments. However this time around, the proposed product ('Pay in 4') is more akin to the key BNPL players, which really validates this particular model that has been doubted by many.
PayPal boasts over 320 million active customers and 26 million merchant relationships and should not be dismissed as a competitor.
PayPal charges anywhere between 2.6-2.9% for the service, and the 'Pay in 4' product will be offered to merchants with no additional costs. Given BNPL fees average around 4%, PayPal's entry may stimulate more discussions around price. However, intensive pricing discussions are not new to the BNPL industry given the number of new players. We believe retailers are more focused on partnering with a BNPL provider that can offer a valuable customer network rather than squeezing out a couple basis points of fees.
On that note, we think PayPal faces several hurdles in its BNPL product launch. Firstly, customer engagement will be crucial. PayPal has generally been an 'after-thought' in a consumer's purchase cycle – a means to an end – which will need to be improved in order to invigorate better spending metrics in its customer base. Secondly, a great proportion of retailers will demand an omni-channel solution to enhance customer engagement from online to in-store. PayPal has historically been an online offering and is yet to bring a greater presence offline. Lastly, it will be interesting to see the route PayPal takes in financing the product and managing credit risk as it will dictate the adoption of the product and impact the customer experience.
It seems like PayPal's past may be haunting them. Regardless of the impact of the juggernaut on the Aussie BNPL stocks, one thing these fundies can agree upon is that the effect will not be detrimental. With Afterpay's share price starting to rally, some might argue that the worst is behind us... but if we've learnt one thing from BNPL, it's that you never know what's around the corner.
In the next instalment of this collection, I ask the experts what they're looking for in a BNPL company, and what is critical to a company's success. Ensure you're following my profile by clicking FOLLOW to be updated when this wire is posted.
You can access part 1 of this Collection, Is there still opportunity in the BNPL space? here
Not already a Livewire member? Sign up today to get free access to investment ideas and strategies from Australia's leading investors. Enjoy this wire? Hit the 'like' button to let us know.
Jack Liang
Excellent article on a sector specific topic. Look forward to more like this.
Justin Brooks
Would be helpful to note if any of the experts are current holders of BNPL stock...
Geoffrey W McRae
This article misses the point. Paypal has invested heavily in Mercardolibre, which is the most popular platform of its type in South America and now entering Europe. One of the offshoots of Mercadolibre is Mercadopago which is a fintech which is the payment platform so feared by mainstream banking and companies like as it offers quotas as well as interest-bearing accounts. Afterpay and similar platforms could well be toast as Paypal roles out this Mercadolibre technology.
Jonathan Free
Sounds like it was written with a certain degree of bias? I agree with Geoffrey's comments below. It would be incredibly unwise to play down PayPal's entry into the BNPL space. They have incredibly deep pockets, a huge customer and merchant base, as well as a long established reputation and great team to back all that up. On the other hand, I'm not sure it will necessarily spell the end for ZIP, Afterpay, Humm, Laybuy and so on... However it seems a large enough threat to severely impact important growth markets, which are much larger than the ASIA Pacific region. BNPL is merely a stepping stone for the fintech sector.
Japan already offers BNPL at the point of transaction on credit card purchases, both online and in store. Has done so for decades now. Have you not heard of this? Or just ignoring? Once Visa and Mastercard enter the market it's game over for Zip/Afterpay/etc.
Bella Kidman
Thanks Jack! Glad you enjoyed it.
Bella Kidman
Thanks Justin, the experts will be talking about their analysis of specific BNPL stocks in the next upcoming wire in this collection.
Cat Marriott
The path to success is through failure, I see other contributors note the size of Paypal. I wouldn't write off their past failures so quickly. A good outcome would be that it expands the whole BNPL market and erodes credit card spending.
Evan Yang
It's kind of funny to see people saying Mastercard and Visa will end the BNPL. Clearly you you don't understand the user demographics of the service.
Rus Watson
Nice work Bella. Just what I was looking for!
Patrick Poke
Spot on Evan. Most BNPL users don't even have a credit card. Paypal is an interesting one though, it's definitely widely used by younger people, but more out of necessity than love of the service. I've never heard someone gush about how good Paypal is, but plenty of Afterpay users will sing its praise.


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Moses Lake Startup Attorneys & Lawyers
How it Works
Steven Stark
Joshua Garber
Richard Gora
David S. Rubenstein
Yuan "Ruth" Qi
Joey Myers
John Graham
Gregory Wilson
Kenneth Mitchell-Phillips
Marcus Harjani
Useful Resources
- S Corporation in NYC: Everything You Need to Know
- IRS S Corporation Election Form: Everything You Need to Know
- Difference Between Articles and Bylaws
- How To Write a Terms of Service Agreement
- Additional Section 263A Costs Attach Schedule
- Dissolving an S Corp: Everything You Need to Know
- Demand Promissory Note
- Release of Liability
- Clinical Trial Agreement Definition: What You Need to Know
- Corporate Resolution
More Moses Lake Attorneys
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- Moses Lake Immigration Attorneys
Nearby Attorneys
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TV Series
Really fantastic TV Show tv show, with deep message carried on. North Woods Law - Season 15 has literally no weak scenes. North Woods Law - Season 15 stands out above all other films I've seen at least for last 5 years. When I saw North Woods Law - Season 15 online for the first time, I was really surprised. Like always, directing by Nicole Page was marvelous. Artistry of actors are just magnificent, no one give bad performance. North Woods Law - Season 15 will live with us forever. No matter how many years passed. It's a modern classic tv show, 2020 year is all yours North Woods Law - Season 15. In 2020 you have to watch North Woods Law - Season 15 online on 123Movies.... Show more
Risks and dramas are on every corner in Maine foresters Elite, then in this series because navigate employs the rugged terrain in the state and filled with the risk of the hunting season.
Watch North Woods Law - Season 15 (2020) on 123movies. North Woods Law - Season 15 is one of the best TV Shows to stream online with English and Hindi Subtitles. TV series that is starring: Charles Parnell, Glen Annis, Dan Carroll and others. Directed by Nicole Page in United States. North Woods Law - Season 15 is one of the most rated TV Show TV Series Episodes.
60 min
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Retrieve data from Excel file then connect to website SQL database and push updated data into 4 tables
Budget $30-250 USD
Hi there,
I'm looking for someone to set up PHP on my office PC and create a PHP script that runs every X minutes (probably X = 5) , connects to my website's SQL server with a given IP and credentials, and pushes only data that has been updated in the last X minutes.
The data source on the office PC is 2 Excel files consisting of 5 spreadsheets. On the website, Table 1 has 20 fields, Table 2 has 2 fields, Table 3 has 4 fields, Table 4 has 5 fields.
Thank you.
- jt
Décerné à:
Hello, Is the database in ms sql server or MySQL? As you will run the program in local computer in schedule, i think php would not be the right choice. If you prefer, i can develop a program based on .Net. Let's discu Plus
30 freelances font une offre moyenne de 166 $ pour ce travail
Hi i can Retrieve data from Excel file then connect to website SQL database and push updated data into 4 tables i am good at Php , Excel , SQL , MySql so lets do talk more about it Thanks
Hi, I am interested in your project and like to handle it. But I have question about the project. Why you like to use PHP scripts while you can have it as windows desktop application or as windows service that work in Plus
Hello sir, I already gone through the all information or description which is detailed by you. You are looking for Retrieve data from Excel file then connect to website SQL database and push updated data into 4 tables Plus
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WatTMDb Library
WatTMDb Library is a .NET library for accessing The Movie DB API. In order to use the library, developers will need to get an API key from The Movie DB.
September 19, 2014
Single purpose API
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Hollywood studios haven't released their good fall movies yet. TV shows like Game of Thrones, Mad Men and the like are months away from their next seasons. You need something to watch, preferably right now. Don't worry, the ProgrammableWeb community is here to help you out. Movie mashups are always a popular submission to our directory and last year we took a look at a few of them. Today we'll look at some recent movie mashups that should help all but the most picky viewers find something worth checking out.
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GU-Q: IPOL387: the European Union and the GCC in Comparative Perspective
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Successful transformation processes toward democracy based on the rule of law and a market economy flanked by sociopolitical safeguards are happening all around the world. The project aims to help improve the political management of these processes by analyzing strengths and weaknesses and facilitating the knowledge transfer of good practices.
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Access analysis on over 200 countries worldwide with the Economist Intelligence Unit. The Economist.
Human Development Index
U.N. According to the index, three parameters govern human development and quality of life: wealth, health and education. The wealth of a nation is measured this year by Gross National Income (it used to be measured by Gross National Product), health is quantified by citizens' longevity (life expectancy at birth) and years of schooling indicate education.
Social Justice in the OECD
A cross-national comparison of social justice in the OECD shows considerable variation in the extent to which this principle is developed in these market-based democracies.
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2020-10-19 20:48:00
NEW DELHI: The National Highways Authority of India (NHAI) has received upfront consideration of ₹5,011 crore on Monday from Cube Highways, under the third bundle of the toll-operate-transfer (TOT) model.
The award ceremony was conducted via video conferencing and was chaired by road transport and highways minister Nitin Gadkari, minister of state General VK Singh and NHAI chairman Sukhbir Singh Sandhu.
Last year, the highway authority had put up nine stretches of roads, totalling 566 km across, and comprising nine toll plaza across Uttar Pradesh, Jharkhand, Bihar and Tamil Nadu, in the third round of TOT.
TOT is part of the government's initiative to monetize public infrastructure and build new assets. Under this model, the highest bidder wins the right to operate and maintain highway assets for 30 years. The one who wins the bid garners toll revenue during that time period.
"The concession period is 30 years and the concessionaire shall operate, maintain and collect the toll during the concession period," an official statement said.
The first round of TOT in February, 2018 was a success. The winning bidder Macquarie offered ₹9,691 crore for 700 km highways. However, NHAI cancelled the second bundle that was spread over 584 km over four states as the bids that were received were far below the expectation.
Currently, NHAI is in the process of awarding more stretches under TOT for monetization of its public funded projects. Last month, it invited bids for the fifth set of projects, while cancelling the fourth bundle.


text: tag:blogger.com,1999:blog-5686500107282182587.post7652990652009770128..comments2020-03-20T21:06:53.834-07:00Comments on 22C+: Vanity, Thy Name is FreakMarcus T. Anthonyhttp://email@example.com:blogger.com,1999:blog-5686500107282182587.post-40129618026886428142010-05-20T08:46:00.997-07:002010-05-20T08:46:00.997-07:00Nancy, I suspect it must be harder for a woman, in...Nancy, I suspect it must be harder for a woman, in just about any culture, to grow old. A woman's value is often associated with her capacity to perform sexually, and reproduce, and any look at advertising confirms this. There are, of course, equal constrictions upon men - to be powerful, in control, successful, brave and so on. The idea of the "soft" male is rejected by numerous cultures (but not all).Marcus T. Anthonyhttps://firstname.lastname@example.com:blogger.com,1999:blog-5686500107282182587.post-53888136247138812172010-05-20T07:57:10.163-07:002010-05-20T07:57:10.163-07:00As a woman, it is difficult to age in a culture th...As a woman, it is difficult to age in a culture that does not respect the process. However, I refuse to bow to that mindset. I am a woman in her 50's, I had my time of looking young, and I'm happy to move on. I love the pictures of your teachers. There is wisdom in wrinkles.Nancyhttps://email@example.com


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By Vidthug Pte Ltd
Insta Pressure Cooker Recipes app is the complete guide for you to learn Pressure Cooker, Instant Pot and Air Fryer recipes. Insta Pressure Cooker Recipes app is most comprehensive, easiest and very useful recipes information for Pressure Cookers and we have over 1000+ recipes in our database. We have recipes for : - Breakfast - Lunch - Dinner - Dessert - Appetizer So What Are you Waiting For? Download the "Insta Pressure Cooker Recipes" App Now!
Just downloaded this app and paid (like an idiot!) to unlock "without ads" but when you click on a recipe, it gives you ingredients but no instructions for preparation without being bombarded with ads!!!! I want a refund!!
I downloaded the app and couldn't even begin to look at the first recipe before I was blocked by ads. I finally got into the second recipe and it crashed because the ad it ran only showed a black screen and wouldn't let me go forward or back. I stopped the app and retried with the same results...deleted app.
All the preparation instructions are a link to advert laden internet pages. Wasted my money.
Deceiving and less than a dozen recipes for Air Fryer. Want my money back.
While the design looks good, whenever you click on a recipe it takes you to another website. You're better off just googling stuff wince that's free. And some recipe websites don't even work. 👎🏽
Where are the air fryer recipes that I was promised?
I don't want the pressure cooker recipes. I paid the $3.99 thinking it would open recipes for the Air Fryer..... NOT!!! Very disappointed.
Wish I'd read the reviews first. The recipes don't even load.
No recipes. Zero. Zilch nada. And that after paying $4. I want my money back
Can find these recipes online for free but this app wants to charge. It isn't worth the money.


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Pattern reads: cast on 4sts, slide sts to opposite end of needle, pulling yarn across back of work, k4. Beg at center back of heel with RS facing, pick up and knit 1 st along edge of slipper-- 5 sts.
Work applied I-cord as follows:
K3, k2tog (last st on needle an picked up st), pick up and knit another st from edge of slipper; rep from around top edge, skipping a row of slipper when picking up sts as needed to keep edge flat.:
Okay this is like a foreign language to me. If I do what the first paragraph asks, then pick up and knit picked up, when I move to the second paragraph the last 2 sts do not include my picked up st. This leads me to assume I'm doing it wrong… Plz help me someone!


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The title "legend" is thrown around far too casually in entertainment circles, but it's the perfect description for Carol Burnett, whose weekly variety show won 23 Emmys in the 11 years it ruled the airwaves on Saturday nights. She redefined comedy for woman on television.
These days, Burnett makes occasional cameos on TV and in movies. She's a voice in the Disney animated film"The Secret World of Arrietty" and also tours the country doing Q-and-A shows. Tickets are available for her May 8 show at the Rialto Square Theater in Joliet.
Q: Does it get exhausting having people heap praise on you, telling you what an influence you were?
A: No, not really. It's not that it's exhausting or not, it's just that people don't do it all of the time ... so, when they don't, I just look in the mirror and do it myself (laughs).
Q: Last year has been called the year of the "women in comedy" with the success of Tina Fey, Amy Poehler and the cast of "Bridesmaids," Kristen Wiig, Melissa McCarthy and Maya Rudolph. Wiig reminds me of you with all of her characters, but I'm sure it was quite different when you were first getting started.
A: Definitely. That's a big compliment because I think that Kristen Wiig is phenomenal. She's a phenomenal actress. When I started, there was Lucy (Lucille Ball) and Martha Raye and that's about it. Women had to have zany personas so, of course, I started developing mine. I hopefully got rid of it after about three years on my show. I wanted to change away from it because I became a grown-up.
One time, what was very interesting, we were rehearsing a "Mama's Family" sketch, and Maggie Smith was a guest on our show. Eunice, Mama and Ed were called into a schoolroom. Maggie was the teacher and was talking to us about our son, Bubba, who was a bully. Well, of course, it all comes out that no wonder why he's a bully with this family and so forth, but someone had the idea to just try to do the sketch "straight," without the comedy and those accents. It was amazingly profound. There wasn't one joke. ... It was great but we did it the regular way and got all of the laughs instead.
Q: How do we get Carol Burnett to host "Saturday Night Live" the way Betty White did? Do we need to start a Facebook campaign for you?
A: I'd probably be scared to death.
Q: It's not the way you used to do your old show?
A: Well, yes but I was so used to it. We were a family, so it wasn't new every week. It was comfortable and we could just go with it. And when (Tim) Conway went off with whatever he'd be up to, we'd just sit back and enjoy it. We were loose. ... We'd do one version of the show, a dress rehearsal, and tape that with an audience exactly the way it was written on the page. We'd make sure that the director had gotten all the shots he needed but when it came time to tape the "real" show with a different audience, then we went wild.
Q: What do you remember about your time in Chicago when "Hollywood Arms" played at the Goodman Theatre?
A: I loved doing it, and I loved (director) Hal Prince. He is aptly named. The whole project was quite a thing for me because my daughter, Carrie, who passed away, and I started working on this together. She never lived to see it finished.
Q: Was it cathartic for you to finish it or difficult?
A: It saved my life to finish it. We had some rewrite things and some stuff to finish right after she had died. I didn't want to get out of bed but my husband said, "You've got to do this ... and you have to do it for Carrie and for Hal and for yourself" and so forth. Having to finish it and go to Chicago really saved my sanity. Now, I'm writing my third book. It's based on the letters and emails I shared with Carrie.
Travel expenses paid for by Walt Disney Pictures and WGN-TV. Watch my interviews from 4 to 9 a.m. Monday through Friday on WGN-Ch. 9 Morning News. My radio show airs 9 a.m. to 1 p.m. Sundays on WGN-AM 720 and wgnradio.com. You can also go to wgntv.com/deanslist.