Editorial: Global excellence in inflammation pharmacology

In our day-to-day life, acute inflammation occurs commonly as a part of the body’s regular healing process post an injury or infection and is usually short term in nature. The problem arises when this inflammation becomes chronic, due to the failure in resolving itself, leading to a spectrum of diseases which explicitly contributes to more than 50% of worldwide mortality (GBD, 2017 Causes of Death Collaborators, 2018; Furman et al., 2019) Thus, prolonged inflammation is emerging as a serious threat to the global population and socioeconomic sustainability. Advancements in effective anti-inflammatory therapies have been significantly evolving, but challenges persist (Netea et al., 2017). Hence, scientists globally or in global alliance, with varied scientific perspectives, are actively working on finding out pharmacological interventions against inflammation associated pathogenesis and diseases. A major part of the research is also focused on scientific advancements of evolving therapeutic strategies by identifying the central signaling molecules or cascades involved in the onset and progression of chronic inflammation. This special edition Research Topic Global Excellence in Inflammation Pharmacology aims in emphasizing on the recent progress made in these fields, highlighting the diversified research performed across the entire breadth of Inflammation Pharmacology and providing insights to it. This Research Topic comprises of four extensive literature reviews discussing the potential pharmacological interventions and their allied risk in inflammation associated diseases

Visualizing museums through the visitors’ eye: An n-gram model-based text analysis approach

21-32    All over the world Museums are developing a Customer Service mindset characteristic of large businesses. Part of this shift can be seen in the rapid adoption of museum visitor surveys that gather feedback about a visitor’s experience in relation to their demographic characteristics — such as likes, dislikes, etc. as per their age, gender and income. The concept of listening to the visitor through such census data collection is not new, it was there from the very beginning, but in certain aspects, it appears to be deficient. For example, it becomes arduous and difficult to identify if the visitors find the place “memorable”. Did they feel “welcome” from the beginning? Do they think “science” is given a due share in that science museum? Can we build an at-a-glance graphical representation of the museum’s image in the visitor’s mental map?     Census type data collection is very manpower intensive and is often biased as the visitors feel righteous to answer the questionnaire more “correctly” than “frankly”. They are not generally considered “easy in-person survey tools”. In this paper, we will discuss a very new way of listening to the visitors and reconstructing their free and fair post-visit overall mental map of the museum. In this new effort, we have tried to construct an automated AI-based word-cloud image from visitors’ feedback offered voluntarily in social networks like, say, in Google review. This image is helpful in summarizing and analysing a large amount of feedback data on a single page by focusing on the keywords and phrases adopted by the visitor in describing her experience. This approach is especially useful for centralized analysis of feedback data on museums having a large number of branches.     Hence, we have applied this method to process feedback on the National Council of Science Museums, the largest body of science museums in India managing twenty-five centres all over the country. For the very first time applying this method, we have been able to visualize our museums through the visitor’s eye rendering the analytic result in the form of a word-cloud that reflects what the visitors fancy most when they recall the museum experience after the visit

Visualizing museums through the visitors’ eye: An n-gram model-based text analysis approach

All over the world Museums are developing a Customer Service mindset characteristic of large businesses. Part of this shift can be seen in the rapid adoption of museum visitor surveys that gather feedback about a visitor’s experience in relation to their demographic characteristics — such as likes, dislikes, etc. as per their age, gender and income. The concept of listening to the visitor through such census data collection is not new, it was there from the very beginning, but in certain aspects, it appears to be deficient. For example, it becomes arduous and difficult to identify if the visitors find the place “memorable”. Did they feel “welcome” from the beginning? Do they think “science” is given a due share in that science museum? Can we build an at-a-glance graphical representation of the museum’s image in the visitor’s mental map? Census type data collection is very manpower intensive and is often biased as the visitors feel righteous to answer the questionnaire more “correctly” than “frankly”. They are not generally considered “easy in-person survey tools”. In this paper, we will discuss a very new way of listening to the visitors and reconstructing their free and fair post-visit overall mental map of the museum. In this new effort, we have tried to construct an automated AI-based word-cloud image from visitors’ feedback offered voluntarily in social networks like, say, in Google review. This image is helpful in summarizing and analysing a large amount of feedback data on a single page by focusing on the keywords and phrases adopted by the visitor in describing her experience. This approach is especially useful for centralized analysis of feedback data on museums having a large number of branches. Hence, we have applied this method to process feedback on the National Council of Science Museums, the largest body of science museums in India managing twenty-five centres all over the country. For the very first time applying this method, we have been able to visualize our museums through the visitor’s eye rendering the analytic result in the form of a word-cloud that reflects what the visitors fancy most when they recall the museum experience after the visit

Curcumin protects rat liver from streptozotocin-induced diabetic pathophysiology by counteracting reactive oxygen species and inhibiting the activation of p53 and MAPKs mediated stress response pathways

Curcumin (CUR) is a highly pleiotropic molecule and possesses anti-inflammatory, hypoglycemic, antioxidative, wound-healing and antimicrobial activities. The present study was carried out to investigate whether CUR plays any beneficial role in streptozotocin (STZ) induced hepatic pathophysiology in diabetic rats. STZ exposure increased hepatic damage associated serum markers (ALT, ALP and LDH) as well as NO production in the liver tissue. Moreover, the same exposure enhanced ROS generation and lipid peroxidation; reduced GSH levels and antioxidant enzyme activities. Hyperglycemia induced hepatic pathophysiology also activated stress response pathways (involving phosphorylation of p38, ERK1/2 MAPKs and p53) and reduced mitochondrial membrane potential which in turn led to cellular apoptosis as evidenced from increased hepatic DNA fragmentation as well as FACS analysis. However, treatment with CUR effectively counteracts diabetes-induced, oxidative stress mediated hepatic damage and could act as a therapeutic in lessening liver dysfunction in diabetic subjects

Silymarin protects mouse liver and kidney from thioacetamide induced toxicity by scavenging reactive oxygen species and activating PI3K-Akt pathway

Abstract:Silymarin (SMN) has been shown to possess a wide range of biological and pharmacological effects. Besides, SMN has antioxidant and free radical scavenging activities. Thioacetamide (TAA) is a well-documented liver toxin that requires oxidative bioactivation to elicit its hepatotoxic effect which ultimately modifies amine-lipids and proteins. Our study has been designed in a TAA exposed mouse model to investigate whether silymarin could protect TAA-induced oxidative stress mediated hepatic and renal damage. Results suggest that TAA generated reactive oxygen species (ROS), caused oxidative stress and induced apoptosis in the liver and kidney cells via JNK as well as PKC and MAPKs signalling. All these detrimental effects of TAA could, however, be suppressed by SMN which not only scavenged ROS but also induced PI3K-Akt cell survival pathway in the liver and prevented apoptotic pathways in both the organs. Histological studies, collagen staining and DNA fragmentation analysis also supported our results. Combining, we say that SMN possess beneficial role against TAA mediated hepatic and renal pathophysiology

Studies on histological assessments.

<p><b>Panel A.</b> Haematoxylin and eosin stained liver section of (A) normal mice liver (x 100),(B) ASA intoxicated liver section (x 100), (C) PNP treated liver section (x 100) and (D) PNP treated after ASA intoxicated liver section (x 100). Arrows indicate apoptosis in the liver tissue compared to the normal liver section. <b>Panel B.</b> Haematoxylin and eosin stained spleen section of (A) normal mice spleen (x 100), (B) ASA intoxicated spleen section (x 100), (C) PNP treated spleen section (x 100) and (D) PNP treated after ASA intoxicated spleen section (x 100). Arrows indicate apoptosis in the spleen tissue compared to the normal spleen section.</p

Schematic representation of aspirin overdose induced toxicity to hepatic and spleen tissue along with the protective mechanism by PNP treatment.

<p>Schematic representation of aspirin overdose induced toxicity to hepatic and spleen tissue along with the protective mechanism by PNP treatment.</p

Effects of aspirin and PNP on the liver weight to body weight ratio and oxidative stress related parameters.

<p><b>Panel A.</b> Measurement of liver weight to body weight ratio. <b>Panel B.</b> Measurement of the ferric reducing antioxidant Power (FRAP). CONT: normal mice group, PNP: mice treated with only PNP, ASA: mice administrated with aspirin, ASA+PNP: mice treated with PNP after aspirin intoxication. <b>Panel C.</b> Effect of Aspirin and PNP on Glutathione (GSH & GSSG) activities in liver tissue. GSH to GSSG ratio. <b>Panel D.</b> Effect of Aspirin and PNP on Glutathione (GSH & GSSG) activities in spleen tissue. GSH to GSSG ratio. Cont: normal mice, PNP: mice treated with only PNP, ASA: mice intoxicated with aspirin, ASA+PNP: mice treated with PNP after aspirin intoxication. ASA+VitC: mice treated with vitamin C after aspirin intoxication. “a” indicates the significant difference between the normal control and ASA intoxicated groups, and “b” indicates the significant difference between ASA intoxicated (toxin) and PNP post-treated groups. Each column represents mean ± SD, n = 6; (P^a<0.05, P^b<0.05).</p

Effect of PNP on aspirin induced ROS production.

<p><b>Panel A.</b> Impact on ROS production in liver tissue. The intracellular ROS production was detected by FACS using DCF-DA. Normal: normal mice, PNP: mice treated with only PNP_, ASA: mice intoxicated with aspirin, ASA+PNP: mice treated with PNP after aspirin intoxication. <b>Panel B.</b> Impact on ROS production in spleen tissue. The intracellular ROS production was measured by spectroflurimeter. Normal: normal mice, PNP: mice treated with only PNP_, ASA: mice administrated with aspirin, ASA+PNP: mice treated with PNP after aspirin intoxication. <b>Panel C.</b> Impact on ROS production in hepatocytes. The intracellular ROS production was detected by FACS using DCF-DA. Normal: normal mice, PNP: mice treated with only PNP_, ASA: mice intoxicated with aspirin, ASA+PNP: mice treated with PNP after aspirin intoxication. “a” indicates the significant difference between the normal control and ASA intoxicated groups, and “b” indicates the significant difference between ASA intoxicated (toxin) and PNP treated groups. Each column represents mean ± SD, n = 6; (P^a<0.05, P^b<0.05).</p

Amelioration of Aspirin Induced Oxidative Impairment and Apoptotic Cell Death by a Novel Antioxidant Protein Molecule Isolated from the Herb <i>Phyllanthus niruri</i>

<div><p>Aspirin has been used for a long time as an analgesic and anti-pyretic drug. Limitations of its use, however, remain for the gastro-intestinal side effects and erosions. Although the role of aspirin on gastro-intestinal injury has been extensively studied, the molecular mechanisms underlying aspirin<b>-</b>induced liver and spleen pathophysiology are poorly defined. The present study has been conducted to investigate whether phyllanthus niruri protein (PNP) possesses any protective role against aspirin mediated liver and spleen tissue toxicity, and if so, what signaling pathways it utilizes to convey its protective action. Aspirin administration in mice enhanced serum marker (ALP) levels, reactive oxygen species (ROS) generation, reduced antioxidant power and altered oxidative stress related biochemical parameters in liver and spleen tissues. Moreover, we observed that aspirin intoxication activated both the extrinsic and intrinsic apoptotic pathways, as well as down regulated NF-κB activation and the phosphorylation of p38 and JNK MAPKs. Histological assessments and TUNEL assay also supported that aspirin induced tissue damages are apoptotic in nature. PNP treatment after aspirin exposure effectively neutralizes all these abnormalities via the activation of survival PI3k/Akt pathways. Combining all results suggest that PNP could be a potential protective agent to protect liver and spleen from the detrimental effects of aspirin.</p></div