scholarly journals Air pollution and childhood obesity

2020 ◽  
Vol 63 (10) ◽  
pp. 382-388
Author(s):  
Moon Young Seo ◽  
Shin-Hye Kim ◽  
Mi Jung Park

Childhood obesity is a global health concern. Air pollution is also a crucial health threat, especially in developing countries. Over the past decade, a number of epidemiologic and animal studies have suggested a possible role of pre- or postnatal exposure to air pollutants on childhood obesity. Although no clear mechanism has been elucidated, physical inactivity, oxidative stress, and epigenetic modifications have been suggested as possible mechanisms by which obesity develops due to air pollution. In this review, we summarize and review previous epidemiologic studies linking air pollution and childhood obesity and discuss the possible mechanisms underlying air pollution-induced obesity based on in vivo and in vitro evidence.


1992 ◽  
Vol 3 (4) ◽  
pp. 193-201 ◽  
Author(s):  
George G Zhanel ◽  
Daryl J Hoban ◽  
Godfrey KM Harding

Antimicrobial activity is not an ‘all or none’ effect. An increase in the rate and extent of antimicrobial action is usually observed over a wide range of antimicrobial concentrations. Subinhibitory antimicrobial concentrations are well known to produce significant antibacterial effects, and various antimicrobials at subinhibitory concentrations have been reported to inhibit the rate of bacterial growth. Bacterial virulence may be increased or decreased by subinhibitory antimicrobial concentrations by changes in the ability of bacteria to adhere to epithelial cells or by alterations in bacterial susceptibility to host immune defences. Animal studies performed in rats, hamsters and rabbits demonstrate decreased bacterial adherence, reduced infectivity and increased survival of animals treated with subinhibitory antimicrobial concentrations compared to untreated controls. The major future role of investigation of subinhibitory antimicrobial concentrations will be to define more fully, at a molecular level, how antimicrobials exert their antibacterial effects.



2020 ◽  
Vol 2020 ◽  
pp. 1-14 ◽  
Author(s):  
Iwona Zwolak

Vanadium (V) in its inorganic forms is a toxic metal and a potent environmental and occupational pollutant and has been reported to induce toxic effects in animals and people. In vivo and in vitro data show that high levels of reactive oxygen species are often implicated in vanadium deleterious effects. Since many dietary (exogenous) antioxidants are known to upregulate the intrinsic antioxidant system and ameliorate oxidative stress-related disorders, this review evaluates their effectiveness in the treatment of vanadium-induced toxicity. Collected data, mostly from animal studies, suggest that dietary antioxidants including ascorbic acid, vitamin E, polyphenols, phytosterols, and extracts from medicinal plants can bring a beneficial effect in vanadium toxicity. These findings show potential preventive effects of dietary antioxidants on vanadium-induced oxidative stress, DNA damage, neurotoxicity, testicular toxicity, and kidney damage. The relevant mechanistic insights of these events are discussed. In summary, the results of studies on the role of dietary antioxidants in vanadium toxicology appear encouraging enough to merit further investigations.



2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Shengyang Qiu ◽  
Gianluca Pellino ◽  
Francesca Fiorentino ◽  
Shahnawaz Rasheed ◽  
Ara Darzi ◽  
...  

Neurotensin (NTS) is a physiologically occurring hormone which affects the function of the gastrointestinal (GI) tract. In recent years, NTS, acting through its cellular receptors (NTSR), has been implicated in the carcinogenesis of several cancers. In colorectal cancer (CRC), a significant body of evidence, from in vitro and in vivo studies, is available which elucidates the molecular biology of NTS/NTSR signalling and the resultant growth of CRC cells. There is growing clinical data from human studies which corroborate the role NTS/NTSR plays in the development of human CRC. Furthermore, blockade and modulation of the NTS/NTSR signalling pathways appears to reduce CRC growth in cell cultures and animal studies. Lastly, NTS/NTSR also shows potential of being utilised as a diagnostic biomarker for cancers as well as targets for functional imaging. We summarise the existing evidence and understanding of the role of NTS and its receptors in CRC.



2021 ◽  
Author(s):  
Soma Chattopadhyay ◽  
Prabhudutta Mamidi ◽  
Tapas Kumar Nayak ◽  
Abhishek Kumar ◽  
Sameer Kumar ◽  
...  

Chikungunya virus (CHIKV) epidemics around the world have created public health concern with the unavailability of effective drugs and vaccines. This emphasizes the need for molecular understanding of host-virus interactions for developing effective targeted antivirals. Microarray analysis was carried out using CHIKV strain (Prototype and Indian) infected Vero cells and two host isozymes, MK2 and MK3 were selected for further analysis. Gene silencing and drug treatment were performed in vitro and in vivo to unravel the role of MK2/MK3 in CHIKV infection. Gene silencing of MK2 and MK3 abrogated around 58% CHIKV progeny release from the host cell and a MK2 activation (a) inhibitor (CMPD1) treatment demonstrated 68% inhibition of viral infection suggesting a major role of MAPKAPKs during the late phase of CHIKV infection in vitro. Further, it was observed that the inhibition in viral infection is primarily due to the abrogation of lamellipodium formation through modulation of factors involved in the actin cytoskeleton remodeling pathway that is responsible for releasing the virus from the infected cells.  Moreover, CHIKV-infected C57BL/6 mice demonstrated reduction in the viral copy number, lessened disease score and better survivability after CMPD1 treatment. In addition, reduction in expression of key pro-inflammatory mediators such as CXCL13, RAGE, FGF, MMP9 and increase in HGF (a CHIKV infection recovery marker) was observed indicating the effectiveness of this drug against CHIKV. Additionally, CMPD1 also inhibited HSV1 and SARS CoV2-19 infection in vitro. Taken together it can be proposed that MK2 and MK3 are crucial host factors for CHIKV infection and can be considered as key targets for developing effective anti-CHIKV strategies in future.



2021 ◽  
Vol 14 ◽  
Author(s):  
Klaus Lange ◽  
Yukiko Nakamura

Entomophagy (consumption of insects) is an issue of global nutritional and environmental interest. The nutritional value of insects appears to be high, since they are rich in protein and fat and provide a range of vitamins and minerals. Edible insects contain similar amounts of protein to conventional meat and higher levels of polyunsaturated fatty acids. Due to their high content of protein, micronutrients and fiber, insects could become a valuable alternative to food derived from other animals. The findings of various in vitro and in vivo animal studies suggest beneficial effects of entomophagy with respect to cardiovascular, gastrointestinal and non-communicable diseases as well as immune functions and carcinogenesis. Edible insects appear to be a promising and insufficiently explored source of macronutrients, micronutrients and food bioactives. In the course of time, some edible insects may meet the criteria of functional food ingredients. However, there is a significant lack of research investigating health outcomes in humans. The available evidence in humans, derived from randomized controlled trials, suggests a role of edible insects in the promotion of mineral status and the modulation of gut microbiota, with some prebiotic effects. High-quality clinical studies assessing efficacy, oral intake safety and allergy risk are needed.



Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4312-4312 ◽  
Author(s):  
Melissa Woelfel ◽  
Simon De Meyer ◽  
Patricia Wagner ◽  
Kathleen E McGinness ◽  
Denisa D. Wagner ◽  
...  

Abstract Abstract 4312 Venous thromboembolism (VTE) is a national health concern, with an occurrence of over 900,000 cases per year and over 300,000 deaths per year. The total number of cases of VTE and the incidence of VTE-related deaths exceeds those related to both myocardial infarction and stroke. With an aging population, the incidence of VTE has also been increasing. Current treatment of venous thromboembolism with anti-coagulation is not optimal. There is a risk of bleeding, thrombus extension, pain and swelling as well as a recurrence rate of 3–9%. A significant inflammatory response occurs with venous thromboembolism. This inflammation can influence the extent of thrombosis, vein wall fibrosis and valve damage in the thrombosed vein. In a high percentage of VTE patients a condition of venous insufficiency known as post-thrombotic syndrome (PTS) can develop. PTS is associated with stasis ulceration, dermatitis and edema. Venous thrombogenesis is influenced by platelet (PLT) and leukocyte (WBC) adhesion as well as interactions between these cells. There is growing evidence to suggest that VWF interactions with PLT GPIbα can mediate some of these early events. This is evidenced by the reduction in PLT/WBC recruitment and reduced thrombus growth seen in either VWF or GPIbα deficient mice. These data point to a role for VWF in VTE. We sought to develop an aptamer to mouse VWF that would inhibit its interactions with platelet GPIbα. The availability of this tool would support investigations into the role of VWF in mouse models of VTE. Aptamers are oligonucleotides that fold into three-dimensional structures and specifically bind to ligands with high affinity. Aptamers bound to proteins can modify and/or inhibit protein-protein interactions. Using an in vitro selection method known as Systematic Evolution of Ligands by EXponential enrichment (SELEX), we generated aptamers that bind to murine VWF (mVWF) from a modified RNA pool. Nine of these aptamers bind to mVWF with single-digit or sub- nanomolar affinity. A subset of these aptamers also binds to human VWF (hVWF). The aptamers that bind to hVWF inhibit platelet adhesion/aggregation in human whole blood. Further in vitro characterization has demonstrated that five of these aptamers specifically inhibit the interaction between mVWF and recombinant human GPIbα, but do not interfere with the binding of mVWF to collagen. These five aptamers were also active in vivo in a FeCl3-induced thrombosis model in mice. Intravenous injection of the anti-mVWF aptamers prolonged time to occlusion from a baseline of 10–15 minutes to either 25–35 minutes or >40 minutes in this model, depending on the aptamer. These results demonstrate that we have identified high affinity aptamers to mVWF that specifically disrupt mVWF binding to platelets and have an antithrombotic effect in an in vivo mouse model of thrombosis. These aptamers will allow us to investigate the role of VWF in murine models of venous thrombosis. This project was supported by Award Number R01HL095091 from the National Heart, Lung, And Blood Institute. Disclosures: Woelfel: Archemix Corporation: Employment. Wagner:Archemix Corporation: Employment. McGinness:Archemix Corporation: Employment. Schaub:Archemix Corporation: Employment.



2021 ◽  
Vol 17 (11) ◽  
pp. e1009667
Author(s):  
Prabhudutta Mamidi ◽  
Tapas Kumar Nayak ◽  
Abhishek Kumar ◽  
Sameer Kumar ◽  
Sanchari Chatterjee ◽  
...  

Chikungunya virus (CHIKV) epidemics around the world have created public health concern with the unavailability of effective drugs and vaccines. This emphasizes the need for molecular understanding of host-virus interactions for developing effective targeted antivirals. Microarray analysis was carried out using CHIKV strain (Prototype and Indian) infected Vero cells and two host isozymes, MAPK activated protein kinase 2 (MK2) and MAPK activated protein kinase 3 (MK3) were selected for further analysis. The substrate spectrum of both enzymes is indistinguishable and covers proteins involved in cytokines production, endocytosis, reorganization of the cytoskeleton, cell migration, cell cycle control, chromatin remodeling and transcriptional regulation. Gene silencing and drug treatment were performed in vitro and in vivo to unravel the role of MK2/MK3 in CHIKV infection. Gene silencing of MK2 and MK3 abrogated around 58% CHIKV progeny release from the host cell and a MK2 activation inhibitor (CMPD1) treatment demonstrated 68% inhibition of viral infection suggesting a major role of MAPKAPKs during late CHIKV infection in vitro. Further, it was observed that the inhibition in viral infection is primarily due to the abrogation of lamellipodium formation through modulation of factors involved in the actin cytoskeleton remodeling pathway. Moreover, CHIKV-infected C57BL/6 mice demonstrated reduction in the viral copy number, lessened disease score and better survivability after CMPD1 treatment. In addition, reduction in expression of key pro-inflammatory mediators such as CXCL13, RAGE, FGF, MMP9 and increase in HGF (a CHIKV infection recovery marker) was observed indicating the effectiveness of the drug against CHIKV. Taken together it can be proposed that MK2 and MK3 are crucial host factors for CHIKV infection and can be considered as important target for developing effective anti-CHIKV strategies.



2021 ◽  
Vol 22 (7) ◽  
pp. 3415
Author(s):  
Chung-Kuan Wu ◽  
Ji-Fan Lin ◽  
Tzong-Shyuan Lee ◽  
Yu Ru Kou ◽  
Der-Cherng Tarng

TRPA1, a nonselective cation channel, is expressed in sensory afferent that innervates peripheral targets. Neuronal TRPA1 can promote tissue repair, remove harmful stimuli and induce protective responses via the release of neuropeptides after the activation of the channel by chemical, exogenous, or endogenous irritants in the injured tissue. However, chronic inflammation after repeated noxious stimuli may result in the development of several diseases. In addition to sensory neurons, TRPA1, activated by inflammatory agents from some non-neuronal cells in the injured area or disease, might promote or protect disease progression. Therefore, TRPA1 works as a molecular sentinel of tissue damage or as an inflammation gatekeeper. Most kidney damage cases are associated with inflammation. In this review, we summarised the role of TRPA1 in neurogenic or non-neurogenic inflammation and in kidney disease, especially the non-neuronal TRPA1. In in vivo animal studies, TRPA1 prevented sepsis-induced or Ang-II-induced and ischemia-reperfusion renal injury by maintaining mitochondrial haemostasis or via the downregulation of macrophage-mediated inflammation, respectively. Renal tubular epithelial TRPA1 acts as an oxidative stress sensor to mediate hypoxia–reoxygenation injury in vitro and ischaemia–reperfusion-induced kidney injury in vivo through MAPKs/NF-kB signalling. Acute kidney injury (AKI) patients with high renal tubular TRPA1 expression had low complete renal function recovery. In renal disease, TPRA1 plays different roles in different cell types accordingly. These findings depict the important role of TRPA1 and warrant further investigation.



2004 ◽  
Vol 16 (7) ◽  
pp. 719 ◽  
Author(s):  
Barry Bavister

Although average success rates of human IVF have increased progressively during the past two decades, the efficiency of this technique, based on each embryo produced or transferred, is still low. High success rates are usually achieved by transferring several embryos to the patient, which is often associated with multiple pregnancies. The quality of in vitro produced embryos is a major area that needs attention. Because there is no in vivo database for human embryos, the properties of normal embryos are not known, and so it is difficult to know how to improve quality and viability. In addition, selection of the most viable embryos for transfer is a rather subjective process. The origins of human assisted reproductive technology (ART) are based on animal ART; however, the two areas of research (animal and human ART) appear to have become disconnected. Re-examination of progress in animal ART could help improve human embryo quality and thereby assist efforts to sustain high pregnancy rates with only one or two embryos transferred. Some key areas in which animal ART can help guide progress in human ART are discussed.



Author(s):  
Bharat Kwatra

The present review is based mainly on papers published between 2000 and 2011 and gives information about the properties of the carotenoid lycopene in chemical and biological systems and its possible role in preventing cardiovascular diseases (CVD). The main aim of this report is to highlight its role as an antioxidant, also reported are bioactive properties that may influence the development of foam cells and protection against endothelial cell damage. The paper will also examine recent observations that lycopene may improve blood flow and reduce inflammatory responses. Lycopene possesses antioxidant properties in vitro, and some epidemiological studies have reported protective effects against the progression of CVD. The oxidation of human low density lipoproteins (LDL) is a fundamental mechanism in the initiation of atherosclerosis. A beneficial role of lycopene as antioxidant in the prevention of CVD is suggested but the data are still controversial. Lycopene is believed to be the most potent carotenoid antioxidant in vitro. Tissue culture experiments and animal studies support potential cardioprotective effects for lycopene and other carotenoids in the blood. Most studies showed beneficial effects of lycopene to individuals who are antioxidant-deficient like elderly patients, or humans exposed to higher levels of oxidative stress like smokers, diabetics, hemodialysis patients and acute myocardial infarction patients. By defining the right population and combining antioxidant potentials of lycopene with vitamins and other bioactive plant compounds, the beneficial role of lycopene in CVD can be clarified in future studies. Keywords: Atherosclerosis, isomerization, in vitro, in vivo, LDL oxidatin



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