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Article ; Online: Peripheral nitric oxide signaling directly blocks inflammatory pain.

Gomes, Francisco Isaac F / Cunha, Fernando Q / Cunha, Thiago M

2020 Volume 176, Page(s) 113862

Abstract: Pain is a classical sign of inflammation, and sensitization of primary sensory neurons (PSN) is the most important mediating mechanism. This mechanism involves direct action of inflammatory mediators such as prostaglandins and sympathetic amines. ... ...

Abstract	Pain is a classical sign of inflammation, and sensitization of primary sensory neurons (PSN) is the most important mediating mechanism. This mechanism involves direct action of inflammatory mediators such as prostaglandins and sympathetic amines. Pharmacologic control of inflammatory pain is based on two principal strategies: (i) non-steroidal anti-inflammatory drugs targeting inhibition of prostaglandin production by cyclooxygenases and preventing nociceptor sensitization in humans and animals; (ii) opioids and dipyrone that directly block nociceptor sensitization via activation of the NO signaling pathway. This review summarizes basic concepts of inflammatory pain that are necessary to understand the mechanisms of peripheral NO signaling that promote peripheral analgesia; we also discuss therapeutic perspectives based on the modulation of the NO pathway.
MeSH term(s)	Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Dipyrone/pharmacology ; Humans ; Inflammation/complications ; Inflammation/metabolism ; Inflammation/prevention & control ; Nitric Oxide/metabolism ; Pain/etiology ; Pain/metabolism ; Pain/prevention & control ; Prostaglandins/metabolism ; Sensory Receptor Cells/drug effects ; Sensory Receptor Cells/metabolism ; Signal Transduction/drug effects
Chemical Substances	Anti-Inflammatory Agents, Non-Steroidal ; Prostaglandins ; Nitric Oxide (31C4KY9ESH) ; Dipyrone (6429L0L52Y)
Language	English
Publishing date	2020-02-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2020.113862
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Zs.A 19: Show issues

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Article ; Online: C5a and pain development: An old molecule, a new target.

Quadros, Andreza U / Cunha, Thiago M

Pharmacological research

2016 Volume 112, Page(s) 58–67

Abstract: Pain is a distressing sensation, resulting from real or potential tissue damage. It is crucial to protect our body, but it can be so intense that it requires treatment. Furthermore, in some circumstances, pain can become persistent/chronic, such as that ... ...

Abstract	Pain is a distressing sensation, resulting from real or potential tissue damage. It is crucial to protect our body, but it can be so intense that it requires treatment. Furthermore, in some circumstances, pain can become persistent/chronic, such as that triggered by inflammatory disease or neuropathy. Treatments for pain are still a clinical challenge. An advance in the knowledge of the neurobiological mechanisms involved in the genesis of acute and chronic pain might be the fundamental approach for developing novel classes of analgesic drugs. In this context, there is emerging evidence indicating that C5a, a component of the complement system, and its cell membrane receptor, C5aR, play a critical role in the genesis of acute and chronic pain states. Thus, this review will describe the mechanisms by which C5a/C5aR signaling participates in the cascade of events involved in the pathophysiology of acute (postoperative), inflammatory and neuropathic pain states. Furthermore, it will also highlight the current possibilities for the development of a novel class of analgesic drugs that target C5a/C5aR signaling.
MeSH term(s)	Acute Pain/drug therapy ; Acute Pain/physiopathology ; Analgesics/immunology ; Analgesics/pharmacology ; Analgesics/therapeutic use ; Animals ; Cell Membrane/drug effects ; Chronic Pain/drug therapy ; Chronic Pain/physiopathology ; Complement Activation/drug effects ; Complement C5a/antagonists & inhibitors ; Complement C5a/immunology ; Complement C5a/metabolism ; Complement C5a/pharmacology ; Drug Discovery ; Humans ; Inflammation/drug therapy ; Molecular Targeted Therapy ; Neuralgia/drug therapy ; Neuralgia/physiopathology ; Pain, Postoperative/drug therapy ; Pain, Postoperative/physiopathology ; Receptor, Anaphylatoxin C5a/antagonists & inhibitors ; Receptor, Anaphylatoxin C5a/immunology ; Receptor, Anaphylatoxin C5a/metabolism ; Signal Transduction/drug effects
Chemical Substances	Analgesics ; Receptor, Anaphylatoxin C5a ; Complement C5a (80295-54-1)
Language	English
Publishing date	2016-10
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2016.02.004
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Zs.A 721: Show issues

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Article ; Online: The PI3Kγ/AKT signaling pathway mediates peripheral antinociceptive action of dipyrone.

Cecílio, Nerry T / Souza, Guilherme R / Alves-Filho, Jose C / Cunha, Fernando Q / Cunha, Thiago M

Fundamental & clinical pharmacology

2020 Volume 35, Issue 2, Page(s) 364–370

Abstract: Dipyrone (DIP), also known as metamizole, is an over-the-counter analgesic used in Europe and Latin America. Evidence suggesting that inflammatory pain attenuation by DIP is associated with a direct impact on peripheral primary nociceptive neurons ... ...

Abstract	Dipyrone (DIP), also known as metamizole, is an over-the-counter analgesic used in Europe and Latin America. Evidence suggesting that inflammatory pain attenuation by DIP is associated with a direct impact on peripheral primary nociceptive neurons through the stimulation of nitric oxide signaling pathway. However, the molecular mechanism by which DIP activates this pathway remains unknown. The PI3Kγ/AKT signaling cascade activation is one of the well-known molecular mechanisms that promote nitric oxide production in sensory neurons. Herein, we investigated the role of the PI3Kγ/AKT signaling cascade in the context of peripheral analgesic effect of DIP. DIP was administered into PGE2 pre-sensitized paws of rats and mechanical hyperalgesia was determined using electronic von Frey test after 1 h. Nonselective or selective pharmacological inhibitors of PI3Kγ and AKT were also administered in DIP-treated rats under paws sensitized with PGE2. Intraplantar injection of DIP attenuated PGE2-induced hyperalgesia in a dose-dependent manner. Treatment with nonselective (wortmannin or LY294002) or selective (AS605240) pharmacological inhibitors of PI3Kγ reduced the peripheral antihypernociceptive effect of DIP. Consistently, AKT selective inhibitor also reversed analgesic DIP effects. Corroborating these data, we found that DIP induced AKT phosphorylation in cultured dorsal root ganglion neurons, which was prevented in the presence of PI3Kγ selective inhibitor. Taken together, these findings provide evidence that peripheral analgesic effect of DIP is dependent on the activation of PI3Kγ/AKT signaling pathway.
MeSH term(s)	Analgesics/pharmacology ; Animals ; Class Ib Phosphatidylinositol 3-Kinase/metabolism ; Dipyrone/pharmacology ; Male ; Nociceptors/drug effects ; Pain/prevention & control ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Rats, Wistar
Chemical Substances	Analgesics ; Dipyrone (6429L0L52Y) ; Class Ib Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; PIK3CG protein, human (EC 2.7.1.137) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2020-10-10
Publishing country	England
Document type	Journal Article
ZDB-ID	639134-5
ISSN	1472-8206 ; 0767-3981
ISSN (online)	1472-8206
ISSN	0767-3981
DOI	10.1111/fcp.12606
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Zs.A 2247: Show issues

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Article ; Online: Inhibition of Pro-Inflammatory Microglia with Minocycline Improves Cognitive and Sleep-Wake Dysfunction Under Respiratory Stress in a Sporadic Model for Alzheimer's Disease.

Vicente, Mariane C / Paneghini, Julia L / Stabile, Angelita M / Amorim, Mateus / Anibal Silva, Conceição E / Patrone, Luis Gustavo A / Cunha, Thiago M / Bícego, Kênia C / Almeida, Maria C / Carrettiero, Daniel C / Gargaglioni, Luciane H

Journal of Alzheimer's disease : JAD

2023 Volume 95, Issue 1, Page(s) 317–337

Abstract: Background: Neuroinflammation in Alzheimer's disease (AD) can occur due to excessive activation of microglia in response to the accumulation of amyloid-β peptide (Aβ). Previously, we demonstrated an increased expression of this peptide in the locus ... ...

Abstract	Background: Neuroinflammation in Alzheimer's disease (AD) can occur due to excessive activation of microglia in response to the accumulation of amyloid-β peptide (Aβ). Previously, we demonstrated an increased expression of this peptide in the locus coeruleus (LC) in a sporadic model for AD (streptozotocin, STZ; 2 mg/kg, ICV). We hypothesized that the STZ-AD model exhibits neuroinflammation, and treatment with an inhibitor of microglia (minocycline) can reverse the cognitive, respiratory, sleep, and molecular disorders of this model. Objective: To evaluate the effect of minocycline treatment in STZ model disorders. Methods: We treated control and STZ-treated rats for five days with minocycline (30 mg/kg, IP) and evaluated cognitive performance, chemoreflex response to hypercapnia and hypoxia, and total sleep time. Additionally, quantification of Aβ, microglia analyses, and relative expression of cytokines in the LC were performed. Results: Minocycline treatment improved learning and memory, which was concomitant with a decrease in microglial cell density and re-establishment of morphological changes induced by STZ in the LC region. Minocycline did not reverse the STZ-induced increase in CO2 sensitivity during wakefulness. However, it restored the daytime sleep-wake cycle in STZ-treated animals to the same levels as those observed in control animals. In the LC, levels of A and expression of Il10, Il1b, and Mcp1 mRNA remained unaffected by minocycline, but we found a strong trend of minocycline effect on Tnf- α. Conclusion: Our findings suggest that minocycline effectively reduces microglial recruitment and the inflammatory morphological profile in the LC, while it recovers cognitive performance and restores the sleep-wake pattern impaired by STZ.
MeSH term(s)	Rats ; Animals ; Alzheimer Disease/metabolism ; Microglia/metabolism ; Minocycline/adverse effects ; Neuroinflammatory Diseases ; Streptozocin ; Sleep Wake Disorders/complications ; Sleep ; Cognition/physiology ; Disease Models, Animal ; Maze Learning ; Cognitive Dysfunction/metabolism
Chemical Substances	Minocycline (FYY3R43WGO) ; Streptozocin (5W494URQ81)
Language	English
Publishing date	2023-07-31
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-230151
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Article ; Online: Paediatric sepsis survivors are resistant to sepsis-induced long-term immune dysfunction.

Colón, David F / Wanderley, Carlos W / Turato, Walter M / Borges, Vanessa F / Franchin, Marcelo / Castanheira, Fernanda V S / Nascimento, Daniele / Prado, Douglas / Haruo Fernandes de Lima, Mikhael / Volpon, Leila C / Kavaguti, Silvia K / Carlotti, Ana P / Carmona, Fabio / Franklin, Bernardo S / Cunha, Thiago M / Alves-Filho, Jose Carlos / Cunha, Fernando Q

British journal of pharmacology

2024 Volume 181, Issue 8, Page(s) 1308–1323

Abstract: Background and purpose: Sepsis-surviving adult individuals commonly develop immunosuppression and increased susceptibility to secondary infections, an outcome mediated by the axis IL-33/ILC2s/M2 macrophages/Tregs. Nonetheless, the long-term immune ... ...

Abstract	Background and purpose: Sepsis-surviving adult individuals commonly develop immunosuppression and increased susceptibility to secondary infections, an outcome mediated by the axis IL-33/ILC2s/M2 macrophages/Tregs. Nonetheless, the long-term immune consequences of paediatric sepsis are indeterminate. We sought to investigate the role of age in the genesis of immunosuppression following sepsis. Experimental approach: Here, we compared the frequency of Tregs, the activation of the IL-33/ILC2s axis in M2 macrophages and the DNA methylation of epithelial lung cells from post-septic infant and adult mice. Likewise, sepsis-surviving mice were inoculated intranasally with Pseudomonas aeruginosa or by subcutaneous inoculation of the B16 melanoma cell line. Finally, blood samples from sepsis-surviving patients were collected and the concentration of IL-33 and Tregs frequency were assessed. Key results: In contrast to 6-week-old mice, 2-week-old mice were resistant to secondary infection and did not show impairment in tumour controls upon melanoma challenge. Mechanistically, increased IL-33 levels, Tregs expansion, and activation of ILC2s and M2-macrophages were observed in 6-week-old but not 2-week-old post-septic mice. Moreover, impaired IL-33 production in 2-week-old post-septic mice was associated with increased DNA methylation in lung epithelial cells. Notably, IL-33 treatment boosted the expansion of Tregs and induced immunosuppression in 2-week-old mice. Clinically, adults but not paediatric post-septic patients exhibited higher counts of Tregs and seral IL-33 levels. Conclusion and implications: These findings demonstrate a crucial and age-dependent role for IL-33 in post-sepsis immunosuppression. Thus, a better understanding of this process may lead to differential treatments for adult and paediatric sepsis.
MeSH term(s)	Humans ; Mice ; Animals ; Child ; Interleukin-33 ; Immunity, Innate ; Lymphocytes/metabolism ; Lymphocytes/pathology ; Sepsis ; Immunosuppression Therapy
Chemical Substances	Interleukin-33
Language	English
Publishing date	2024-01-11
Publishing country	England
Document type	Journal Article
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.16286
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Article: Brief research report: Repurposing pentoxifylline to treat intense acute swimming-Induced delayed-onset muscle soreness in mice: Targeting peripheral and spinal cord nociceptive mechanisms.

Borghi, Sergio M / Zaninelli, Tiago H / Saraiva-Santos, Telma / Bertozzi, Mariana M / Cardoso, Renato D R / Carvalho, Thacyana T / Ferraz, Camila R / Camilios-Neto, Doumit / Cunha, Fernando Q / Cunha, Thiago M / Pinho-Ribeiro, Felipe A / Casagrande, Rubia / Verri, Waldiceu A

Frontiers in pharmacology

2023 Volume 13, Page(s) 950314

Abstract: In this study, we pursue determining the effect of pentoxifylline (Ptx) in delayed-onset muscle soreness (DOMS) triggered by exposing untrained mice to intense acute swimming exercise (120 min), which, to our knowledge, has not been investigated. Ptx ... ...

Abstract	In this study, we pursue determining the effect of pentoxifylline (Ptx) in delayed-onset muscle soreness (DOMS) triggered by exposing untrained mice to intense acute swimming exercise (120 min), which, to our knowledge, has not been investigated. Ptx treatment (1.5, 4.5, and 13.5 mg/kg; i.p., 30 min before and 12 h after the session) reduced intense acute swimming-induced mechanical hyperalgesia in a dose-dependent manner. The selected dose of Ptx (4.5 mg/kg) inhibited recruitment of neutrophils to the muscle tissue, oxidative stress, and both pro- and anti-inflammatory cytokine production in the soleus muscle and spinal cord. Furthermore, Ptx treatment also reduced spinal cord glial cell activation. In conclusion, Ptx reduces pain by targeting peripheral and spinal cord mechanisms of DOMS.
Language	English
Publishing date	2023-01-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2022.950314
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Article ; Online: Neuron-associated macrophage proliferation in the sensory ganglia is associated with peripheral nerve injury-induced neuropathic pain involving CX3CR1 signaling.

Guimarães, Rafaela M / Aníbal-Silva, Conceição E / Davoli-Ferreira, Marcela / Gomes, Francisco Isaac F / Mendes, Atlante / Cavallini, Maria C M / Fonseca, Miriam M / Damasceno, Samara / Andrade, Larissa P / Colonna, Marco / Rivat, Cyril / Cunha, Fernando Q / Alves-Filho, José C / Cunha, Thiago M

eLife

2023 Volume 12

Abstract: Resident macrophages are distributed across all tissues and are highly heterogeneous due to adaptation to different tissue-specific environments. The resident macrophages of the sensory ganglia (sensory neuron-associated macrophages, sNAMs) are in close ... ...

Abstract	Resident macrophages are distributed across all tissues and are highly heterogeneous due to adaptation to different tissue-specific environments. The resident macrophages of the sensory ganglia (sensory neuron-associated macrophages, sNAMs) are in close contact with the cell body of primary sensory neurons and might play physiological and pathophysiological roles. After peripheral nerve injury, there is an increase in the population of macrophages in the sensory ganglia, which have been implicated in different conditions, including neuropathic pain development. However, it is still under debate whether macrophage accumulation in the sensory ganglia after peripheral nerve injury is due to the local proliferation of resident macrophages or a result of blood monocyte infiltration. Here, we confirmed that the number of macrophages increased in the sensory ganglia after the spared nerve injury (SNI) model in mice. Using different approaches, we found that the increase in the number of macrophages in the sensory ganglia after SNI is a consequence of the proliferation of resident CX3CR1
MeSH term(s)	Mice ; Animals ; Peripheral Nerve Injuries/complications ; Ganglia, Spinal ; Neuralgia ; Macrophages ; Ganglia, Sensory ; Sensory Receptor Cells ; Cell Proliferation ; Hyperalgesia
Language	English
Publishing date	2023-05-31
Publishing country	England
Document type	Journal Article
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.78515
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Article ; Online: CXCL1/CXCR2 signaling in pathological pain: Role in peripheral and central sensitization.

Silva, Rangel L / Lopes, Alexandre H / Guimarães, Rafaela M / Cunha, Thiago M

Neurobiology of disease

2017 Volume 105, Page(s) 109–116

Abstract: Pathological pain conditions can be triggered after peripheral nerve injury and/or inflammation. It is associated with plasticity of nociceptive pathway in which pain is prolonged even after healing of the injured tissue. Generally combinations of ... ...

Abstract	Pathological pain conditions can be triggered after peripheral nerve injury and/or inflammation. It is associated with plasticity of nociceptive pathway in which pain is prolonged even after healing of the injured tissue. Generally combinations of analgesic drugs are not sufficient to achieve selective palliation from chronic pain, besides causing a greater number of side effects. In order to identify novel alternatives for more effective treatments, it is necessary to clarify the underlying mechanisms of pathological pain. It is well established that there are two main components in pathological pain development and maintenance: (i) primary sensory neuron sensitization (peripheral sensitization), and (ii) central sensitization. In both components cytokines and chemokines act as key mediators in pain modulation. CXCL1 is a chemokine that promote both nociceptor and central sensitization via its main receptor CXCR2, which is a promising target for novel analgesic drugs. Here, we reviewed and discussed the role of the CXCL1/CXCR2 signaling axis in pathological pain conditions triggered by either peripheral inflammation or nerve injury.
Language	English
Publishing date	2017-09
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2017.06.001
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Article ; Online: Clinical-like cryotherapy in acute knee arthritis of the knee improves inflammation signs, pain, joint swelling, and motor performance in mice.

Castro, Paula A T S / Barbosa, Germanna M / Machanocker, Dafiner H / Peres, Raphael S / Cunha, Thiago M / Cunha, Jonathan E / Oliveira, Francisco F B / Ramalho, Fernando Silva / Russo, Thiago L / Cunha, Fernando Q / Salvini, Tania F

PloS one

2022 Volume 17, Issue 1, Page(s) e0261667

Abstract: To assess the effects of clinical-like cryotherapy on inflammatory signs (in vivo neutrophil migration, cytokines, and joint inflammation), pain, joint swelling, balance, and motor coordination in mice with knee arthritis. Young C57BL/6 mice were ... ...

Abstract	To assess the effects of clinical-like cryotherapy on inflammatory signs (in vivo neutrophil migration, cytokines, and joint inflammation), pain, joint swelling, balance, and motor coordination in mice with knee arthritis. Young C57BL/6 mice were randomly divided into three groups (8 to 10 mice per group): Control group: mice with no intervention; antigen-induced arthritis (AIA) group: mice sensitized and immunized with intra-articular (i.a.) injection of methylated bovine serum albumin (mBSA); and AIA + cryotherapy group: mice sensitized, immunized with i.a. injection of mBSA, and submitted to a clinical-like cryotherapy protocol. After 21 days of sensitization, AIA and AIA + cryotherapy groups received i.a. injection of mBSA (100 μg/joint) to induce joint inflammation, and a clinical-like cryotherapy protocol was applied to AIA + cryotherapy group (crushed ice bag, two cryotherapy sessions of 20 min every two hours). Experimental analysis was conducted in the initial (immediately after i.a. injection of mBSA) and final periods (two hours after the second cryotherapy session). The number of synovial fluid neutrophils, cytokine levels, joint histology, pain, joint swelling, and motor performance were also analyzed. Our results showed that clinical-like cryotherapy in mice with acute knee arthritis reduced inflammatory signs, pain, and joint swelling, and improved balance and motor coordination.
MeSH term(s)	Inflammation
Language	English
Publishing date	2022-01-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0261667
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Article ; Online: Clinical-Like Cryotherapy in Acute Knee Arthritis Protects Neuromuscular Junctions of Quadriceps and Reduces Joint Inflammation in Mice.

Castro, Paula A T S / Machanocker, Dafiner H / Luna, Genoveva F / Barbosa, Germanna M / Cunha, Jonathan E / Cunha, Thiago M / Cunha, Fernando Q / Russo, Thiago L / Salvini, Tania F

BioMed research international

2022 Volume 2022, Page(s) 7442289

Abstract: Rheumatoid arthritis is an autoimmune and inflammatory disease that affects synovial joint tissues and skeletal muscle. Clinical-like cryotherapy benefits signs of joint inflammation in knee osteoarthritis after 60 days of anterior cruciate ligament ... ...

Abstract	Rheumatoid arthritis is an autoimmune and inflammatory disease that affects synovial joint tissues and skeletal muscle. Clinical-like cryotherapy benefits signs of joint inflammation in knee osteoarthritis after 60 days of anterior cruciate ligament transection surgery. However, it is unknown whether it also benefits acute knee arthritis (e.g., reduces inflammatory process and protects neuromuscular junction [NMJ] and muscle fibers). We aimed to analyze the effects of clinical-like cryotherapy on NMJ and quadriceps muscle fibers in a model of acute knee arthritis. Twenty-four male C57BL/6 mice (20 to 25 g) were randomly allocated into three groups: control (mice with no intervention), antigen-induced arthritis (AIA; mice sensitized and immunized with intra-articular [i.a.] injection of methylated bovine serum albumin [mBSA]), and AIA+cryotherapy (mice sensitized, immunized with i.a. injection of mBSA, and submitted to a clinical-like cryotherapy protocol). Twenty-one days after sensitization, arthritis was induced in immunized mice via i.a. injection of mBSA (100
MeSH term(s)	Acute Disease ; Animals ; Arthritis, Experimental/therapy ; Arthritis, Rheumatoid/therapy ; Cell Movement ; Cryotherapy/methods ; Inflammation/prevention & control ; Knee Joint ; Male ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Neuromuscular Junction ; Quadriceps Muscle/innervation ; Thermography
Language	English
Publishing date	2022-01-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2698540-8
ISSN	2314-6141 ; 2314-6133
ISSN (online)	2314-6141
ISSN	2314-6133
DOI	10.1155/2022/7442289
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