inflammation

Aim: To compare the anatomical and functional outcomes of cataract surgery with manual small incision cataract surgery (MSICS) to those of extracapsular cataract extraction (ECCE) in Lome. Patients and Methods: A prospective study involved two groups of patients who underwent ECCE (group 1) and MSICS (group 2) by the same surgeon in the same conditions in different periods. Complications and visual results to the 45th postoperative day were compared. Results: At the 45th postoperative day, 60% of operated eyes of the ECCE group (G1) and 83.9% in the group of MSICS (G2) had uncorrected visual acuity greater than or equal to 3/10. Through the pinhole, these proportions increased to 73.3% for G1 and 92.2% for G2. Visual acuity was less than 1/10 in 4.4% for G1 and 1.1% for G2. The vitreous loss was observed in proportions of 3.8% for G1 and 3.3% for G2. During follow-up, the three main early postoperative complications were inflammation (13.9%), corneal edema (13.3%), and the pigment dispersion (7.2%) in G1 and corneal edema (9.4%), pigment dispersion (8.3%) and hypertonia (6.6%) in G 2. Conclusion: Two cataract extraction techniques offer the same level of safety in intraoperative period. However, MSICS has certain advantages over the ECCE and would be an alternative technique in developing countries.

Cystoid macular edema is a common cause for unexplained painless vision loss after cataract surgery. Even the pathogenesis of pseudophakic cystoid macular edema (PCME) still remains undefined, it can most frequently occur in eyes with high vasoactive profile, had complicated cataract surgery such as posterior capsule rupture and risk of inflammation. Increased inflammation, ultimately leading to the breakdown of the blood-retinal barrier and cystic accumulation of extracellular intraretinal fluid. The natural history of PCME is spontaneous resolution without any treatment in most of patient, but it may take weeks or months, in addition permanent visual morbidity may occur in some cases. Therefore there is lack of consensus regarding treatment approach for this common ocular condition. In this review treatment alternatives of PCME and its relation with underlying patho-physiologic mechanism are evaluated.

Introduction: The HRMT (Human Resting Myofasial Tone) factor plays an important role to initiate the trigger the inflammation at the disease site in Ankylosing spondylitis (AS) as in all spondyloarthropathies. The incidence of fibromyalgia is higher in AS and a limiting factor to undergo the exercise program. Aim of the study: To know the effectiveness of soft tissue mobilisation in patients with Ankylosing Spondylitis when it used as an adjuncts to the conventional exercises. Methodology: 40 subjects were randomly assigned in to experimental and conventional group. Experimental group (n=20) received conventional exercises along with soft tissue mobilisation and the conventional group (n=20) received only conventional exercises (flexibility exercises, aerobic exercise and breathing exercise) for a period of 4 weeks, 5days/week. Results: The result of the study showed that both the conventional and experimental groups improved significantly in stiffness, pain and physical function aspects after treatment. However the experimental group had a greater change as compared to conventional group. Conclusion: The study demonstrates that soft tissue mobilisation has an effect when it used before the conventional exercise in patients with ankylosing spondylitis.

Background: Adipose tissue is one of the main sites of energy homeostasis that regulates whole body metabolism with the help of adipokines. Disruption in its proper functioning results in adipose tissue remodeling (primarily hypertrophy and hyperplasia) which directly influences the secretion of said adipokines. Obesity characterized as chronic low-grade inflammation of the adipose tissue is one such condition that has far reaching effects on whole body metabolism. Inflammation in turn results in immune cells infiltrating into the tissue and further promoting adipocyte dysfunction. Purpose: In our study we explored this adipose tissue-innate immunity axis by differentiating adipose tissue derived stem cells (ADSCs) into white and beige adipocytes. We further stimulated our cultures with lipopolysaccharide (LPS), flagellin, or meteorin-like, glial cell differentiation regulator (METRNL) to trigger an inflammatory response. We then evaluated Toll-like receptor (TLR) mRNA expression and secretion of interleukin (IL-6), interleukin-8 (IL-8), brain-derived neurotrophic factor (BDNF), and nerve growth factor (NGF) in these cultures. Results: We found that TLR2 is the highest expressed receptor in adipocytes. Further, LPS and METRNL are strong activators of TLR2 in white and beigeBMP7(-) adipocytes. TLR4 was not significantly expressed in any of our cultures despite LPS stimulation. TLR9 expression is upregulated in ADSCs upon LPS and METRNL stimulation. IL-6 and IL-8 secretion is increased upon LPS stimulation in white adipocytes. METRNL activates both IL-6 and IL-8 expression in adipocyte cultures. Lastly, BDNF and NGF is secreted by all adipocyte cultures with beigeBMP7(-) and beigeBMP7(+) secreting slightly higher amounts in comparison to white adipocytes. Conclusion: ADSCs and adipocytes alike are capable of expressing TLRs, but white adipocytes remain the highest expressing in both control and stimulated cultures. TLR2 is highly expressed in white and beige adipocytes whereas TLR4 showed no significant expression. LPS and METRNL trigger IL-6 and IL-8 secretion in adipocytes. Products of white adipocyte “browning” are capable of secreting higher amounts of BDNF and NGF in comparison to white adipocytes.

Understanding the obesity-related genes may provide future therapeutic strategies to modulate disease progression. UCP2 separates oxidative phosphorylation (OXPHOS) from ATP production in the inner mitochondria. Figure 1 shows the differences among UCP1, 2, 3. The main role of UCP2 is controlling the metabolism of energy in the cells [1-3]. Besides that, the expression of UCP2 is associated with chronic inflammation due to reactive oxygen species (ROS). In this regard, in injured cells and tissues, ROS could be decreased by reducing the proton motor force by the anti-inflammatory effect of UCP2 [4].

Introduction: the perennial pandemic: There are serious challenges posed by the SARS-CoV-2 virus and COVID-19 as the disease. With the persistence of the pandemic over one and half year, it is being feared that the COVID-19 may have become the new reality associated with human existence world over and the mankind may have to live with it for years or even decades. Further, the grievous nature of the disease is evolving further with genomic changes in the virus in form of mutations and evolution of variants, with enhanced infectivity and probably virulence. Acute and chronic phases of COVID-19: Epidemiologically, it is becoming clear that apart from the advanced age and pre-existing conditions, such as diabetes, cardiovascular, pulmonary, and renal diseases, certain constituent factors render some patients more vulnerable to more severe forms of the disease. These factors influence the COVID-19 manifestations, its course, and later the convalescence period as well as the newly defined ‘Long COVID phase. The substantial continuing morbidity after resolution of the infection indicates persisting multisystem effects of ‘Long Covid’. Lung damage associated with COVID-19: COVID-19 is primarily a respiratory disease presenting with a broad spectrum of respiratory tract involvement ranging from mild upper airway affliction to progressive life-threatening viral pneumonia and respiratory failure. It affects the respiratory system in various ways across the spectrum of disease severity, depending on age, immune status, and comorbidities. The symptoms may be mild, such as cough, shortness of breath and fevers, to severe and critical disease, including respiratory failure, shock, cytokine crisis, and multi-organ failure. Implications for the post-COVID care: Depending on the severity of respiratory inflammation and damage, as well as associated comorbidities, duration of injury and genetics, the progressive fibrosis leads to constriction and compression of lung tissues and damage to pulmonary microvasculature. Consequently, the COVID-19 patients with moderate/severe symptoms are likely to have a significant degree of long-term reduction in lung function. Depending on the severity of the disease, extensive and long-lasting damage to the lungs can occur, which may persist after resolution of the infection. Managing the long COVID’s challenges: Given global scale of the pandemic, the healthcare needs for patients with sequelae of COVID-19, especially in those with lung affliction are bound to increase in the near future. The challenge can be tackled by harnessing the existing healthcare infrastructure, development of scalable healthcare models and integration across various disciplines with a combination of pharmacological and non-pharmacological modalities. Following clinical and investigational assessment, the therapeutic strategy should depend on the disease manifestations, extent of damage in lungs and other organs, and associated complications.

The process of hypothermia in the clinical setting has been practiced for 50 years and is known for its neuroprotective properties. This paper describes histopathological changes either by an ice sludge mimicking accidental hypothermia (S-group n=7) or by endovascular core-cooling (C-group n=7). Focal infiltrates of neutrophilic granulocytes were found in five of seven brains in the S-group and in one of seven brains in the C-group. These granulocytes were found in the arachnoids, in vessels, in vessel walls, and in the cerebral cortex. Fungi, bacteria, lymphocytes or plasma were not found. This experimental study, mimicking accidental hypothermia, reported histopathologic features of aseptic inflammation. To our knowledge, such findings have not been described in hypothermic animals or humans before. We suggest that a local inflammatory response may be triggered in such cases of hypothermia.

There is evidence that complement components induce cell migration in mesenchymal stem cells and regulate cytokine production in osteoblastic cells thus playing a regulatory role in normal bone formation. The aim of the present study was to investigate the involvement of complement system in the differentiation of bone marrow cells in complement-depleted model of rheumatoid arthritis (RA). Arthritis was induced by intraarticular injection of zymosan in cobra venom factor (CVF)-treated mice depleted of functional complement. The expression of different markers by bone marrow [1], on fibroblasts (CD29), mesenchymal cells (CD105), dendritic cells (CD14, CD86), osteoclasts (CD265), cells expressing Dectin1 (CD369) and megakaryocytes (CD62P) was determined by flowcytometry. The lack of functional complement activity at the point of arthritis initiation (day 3) lead to an increase of fibroblast and megakaryocyte populations, to a decrease of mature and dectin1 positive populations, while the number of mesenchymal cells was not changed, all compared to arthritic mice. Immunohistochemical staining showed that low complement activity diminished arthritis-induced generation of megakaryocytes and platelets in BM. Chronic inflammation during erosive conditions such as rheumatoid arthritis, leads to dysregulated differentiation and prolifеration of bone cells, inflammation of synovial membrane and bone marrow, and degradation of cartilage and bone. Present results point that the lack of functional complement changed the ratio between different cell populations that can be used for determining the development and stage of rheumatoid arthritis and can help finding of new therapeutic approaches.

Growing evidence supports the hypothesis that endothelial cell-derived microparticles (MPs) might contribute to the pathogenesis of cardiovascular (CV) disease. Endothelial cell-derived MPs play a pivotal role in the regulation of the endogenous repair system, thrombosis, coagulation, inflammation, immunity and metabolic memory phenomenon. There is evidence that the MPs are secreted actively accompanied to other regulatory molecules. All these actively synthetizing and secreting factors include proteins, adhesion and intercellular signal molecules, peptides, lipids, free DNAs, microRNAs, and even microparticles (MPs) are defined as cellular secretome. The proteomic profile of secretome is under tightly control of genetic and epigenetic mechanisms, which may altered a secretion of the proteins involved into MPs’ organization. Finally, this may contribute the modification of MP’s after their secretion and throughout transfer to the target cells. As a result, communicative ability of endothelial cell-derived MPs may sufficiently worse. Subsequently, cross talk between some components of secretome might modulate delivering cargos of MPs and their regenerative and proliferative capabilities via intercellular signaling networks. The aim of the review is to discuss the effect of various components of secretome on MP-dependent effects on endothelium.

Transglutaminases are a family of Ca2+-dependent enzymes which catalyze post-translational modifications of proteins. The main activity of these enzymes is the cross-linking of glutaminyl residues of a protein/peptide substrate to lysyl residues of a protein/peptide co-substrate. In addition to lysyl residues, other second nucleophilic co-substrates may include monoamines or polyamines (to form mono-or bi-substituted/crosslinked adducts) or -OH groups (to form ester linkages). In absence of co-substrates, the nucleophile may be water, resulting in the net deamidation of the glutaminyl residue. Transglutaminase activity has been suggested to be involved in molecular mechanisms responsible for both physiological and pathological processes. In particular, transglutaminase activity has been shown to be responsible for human autoimmune diseases, and Celiac Disease is just one of them. Interestingly, neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, supranuclear palsy, Huntington’s disease and other polyglutamine diseases, are characterized in part by aberrant cerebral transglutaminase activity and by increased cross-linked proteins in affected brains. Here we describe the possible molecular mechanisms by which these enzymes could be responsible for such diseases and the possible use of transglutaminase inhibitors for patients with diseases characterized by aberrant transglutaminase activity.

Inflammation is a complex biological reaction induced by the alteration of tissue homeostasis, which occurs in response to the presence of a biological, chemical or physical agent in the body [1]. The acute inflammatory response is composed of an elaborate cascade of both proinflammatory and anti-inflammatory mediators, and balance between these mediators often determines the outcome after injury [2]. Generally during acute inflammation, cellular and molecular events and interactions reduce the risk of eventual injuries or infections. However, acute inflammation can become chronic, contributing to a variety of chronic inflammatory diseases [3]. Major micro circulatory events that occur during the inflammatory process include changes in vascular permeability, leukocyte recruitment and accumulation, and inflammatory mediator’s release [4]. 

Chronic rhinosinusitis (CRS) is an inflammatory condition involving nasal passages and the paranasal sinuses for 12 weeks or longer [1]. It can be subdivided into three types: CRS with nasal polyposis (CRS with NP), CRS without nasal polyposis (CRS without NP), and Allergic fungal rhinosinusitis (AFRS). To diagnose CRS we require at least two of four of its cardinal signs/symptoms (nasal obstruction, mucopurulent discharge, facial pain/pressure, and decreased sense of smell). In addition, direct visualization or imaging for objective documentation of mucosal inflammation is required. CRS therapy is aimed to reduce its symptoms and improve quality of life as it cannot be cured in most patients. Thus, the goals of its therapy include the following:

Xanthogranulomatous cholecystitis is a rare benign inflammatory disease of gallbladder that may be misdiagnosed as carcinoma of the gallbladder intraoperative or in pre-operative imaging. Intramural accumulation of lipid-laden macrophages and acute and chronic inflammatory cells is the hallmark of the disease. The xanthogranulomatous inflammation can be very severe and can spill over to the neighboring structures like liver, bowel and stomach resulting in dense adhesions, abscess formation, perforation, and fistulous communication with adjacent bowel [1-3]. Cholecysto-colic fistula is a rare and late complication of gallstones roughly found 1 in every 1,000 cholecystectomies. Clinical featuresThe clinical features are variable and non-specific. Patients with cholecysto-colonic fistula often present with symptoms of acute cholecystitis and preoperative diagnostic tools often fail to show the fistula. Hence most cases it is an on table diagnosis. ManagementTreatment involves closing the fistula and performing an open or laparoscopic cholecystectomy.

COVID-19 virus structural components: The 2019-nCoV, also called SARS-CoV-2, was first reported in Wuhan, China in December 2019. The disease was named Coronavirus Disease 2019 (COVID-19) and the virus responsible for it as the COVID-19 virus, respectively, by WHO. The 2019-nCoV has a round, elliptic or pleomorphic form with a diameter of 60–140 nm. It has single-stranded RNA genome containing 29891 nucleotides, a lipid shell, and spike, envelope, membrane and hemagglutinin-esterase (HE) proteins. Steps in progression of COVID-19 illness: Once inside the airways, the S protein on the viral surface recognizes and mediates the attachment to host ACE-2 receptors and gains access to endoplasmic reticulum. The HE protein facilitates the S protein-mediated cell entry and virus spread through the mucosa, helping the virus to attack the ACE2-bearing cells lining the airways and infecting upper as well as lower respiratory tracts. With the dying cells sloughing down and filling the airways, the virus is carried deeper into the lungs. In addition, the virus is able to infect ACE2-bearing cells in other organs, including the blood vessels, gut and kidneys. With the viral infestation, the activated immune system leads to inflammation, pyrexia and pulmonary edema. The hyperactivated immune response, called cytokine storm in extreme cases, can damage various organs apart from lungs and increases susceptibility to infectious bacteria especially in those suffering from chronic diseases. The current therapeutics for COVID-19: At present, there is no specific antiviral treatment available for the disease. The milder cases may need no treatment. In moderate to severe cases, the clinical management includes infection prevention and control measures, and symptomatic and supportive care, including supplementary oxygen therapy. In the critically ill patients, mechanical ventilation is required for respiratory failure and hemodynamic support is imperative for managing circulatory failure and septic shock. Conclusion: Confusion, despair and hopes: There is no vaccine for preexposure prophylaxis or postexposure management. There are no specific approved drugs for the treatment for the disease. A number of drugs approved for other conditions as well as several investigational drugs are being canned and studied in several clinical trials for their likely role in COVID-19 prophylaxis or treatment. The future seems afflicted with dormant therapeutic options as well as faux Espoir or false hopes. As obvious, not all clinical trials will be successful, but having so many efforts in progress, some may succeed and provide a positive solution. Right now, though, confusion and despair prevail.

Background: The development of COVID-19 having been set apart as the third presentation of an exceptionally pathogenic coronavirus into the human populace after the extreme intense SARS-COV and MERS-COV in the twenty-first century. The infection itself doesn’t make a crucial commitment to mortality, anyway “cytokine storm” created by the unreasonable invulnerable reaction activated by the virus can result in a hyperinflammatory response of lung tissues and deadly lung injury, and in this way increment death rate. In this manner, immunomodulatory medications ought to likewise be remembered for treatment of COVID-19. Presentation of the hypothesis: the virus particles invade the respiratory mucosa firstly and infect other cells, triggering a series of immune responses and the production of cytokine storm in the body, which may be associated with the critical condition of COVID-19 patients. Once a cytokine storm is formed, the immune system may not be able to kill the virus, but it will certainly kill many normal cells in the lung, which will seriously damage the of lung function. Patients will have respiratory failure until they die of hypoxia. It is not yet clear what the death rate of Covid-19 will be, though the best estimate right now is that it is around 1 percent, 10 times more lethal than seasonal flu due to cytokines storm which trigger a violent attack by the immune system to the body, cause acute respiratory distress syndrome (ARDS) and multiple organ failure, and finally lead to death in severe cases of COVID-19 infection. Therefore, inhibiting cytokine storm can significantly reduce inflammatory injury in lung tissues. Pyridostigmine (PDG), cholinergic anti-inflammatory pathway (CAP) is a neural mechanism that modulates inflammation through the release of acetylcholine (ACh), resulting in decreased synthesis of inflammatory cytokines such as TNF-α and IL-1. This finding emphasis, the nervous and immune systems work collaboratively during infection and inflammation. Implications of the hypothesis: Administrations of Pyridostigmine (PDG) as cholinergic agonist inhibits the inflammatory response and lower the mortality of COVID-19 patients. Likewise, activation of the CAP during systemic inflammation down-regulates the production and release of inflammatory cytokines. 

Corona Virus Disease-2019 (COVID-19) has become one of the most serious diseases in the history of mankind. It has captured the entire world and solutions are yet to be discovered to fight this global crisis. The outcomes of COVID-19 are influenced by a variety of pre-existing factors. The secondary microbial infections are one of the prominent ones that are major contributors for Antimicrobial Resistance (AMR) as they warrant the use of antimicrobial medications. The present review aimed at exploring the potential relationship between AMR under such circumstances and COVID-19 related outcomes. The published literature across the globe has delineated that the impact of COVID-19 may have worsened by a great degree due to the presence of secondary infections majorly bacterial ones. The consequences of COVID-19 have been fatal and a significant proportion can be a major attributor to AMR, either directly or indirectly. Although, there is a dearth of studies that can establish a very strong and direct relationship between AMR and negative COVID-19 outcomes so in-depth research on this topic is required to further explain this relationship in detail. 

Background: Combination of extracts from multiple plants are typically used in ethnomedicine to putatively offer more potent chemotherapeutic and chemopreventive effects than that of individual extracts from single plants. Aqueous extracts from two multipurpose plants Strophanthus hispidus (roots) and Aframomum meleguta (seeds) are topically co-administered in the nasal cavities for the ethnomedicinal management of chronic sinusitis. Aim: This study assessed the potential phytochemical synergy between constituent extracts of Strophanthus hispidus (roots) and Aframomum meleguta (seeds) in its anti-inflammation, anti-microbial and anti-oxidant effects. Methods and Materials: Broth dilution assay assessed anti-microbial activities. DPPH radical scavenging assay examined the scope of anti-oxidant activities and inhibition of carrageenan-induced 7-day old chick feet oedema revealed anti-inflammatory activities. Results: Anti-microbial activities of individual plant extracts in broth dilution assay showed comparable potency to that of the co-extract mixture. Similarly, individual extracts showed levels of DPPH radical scavenging activities in anti-oxidant assay that was comparable to those found for the co-extract mixture. In contrast to these two effects, inhibition of carrageenan-induced 7-day old chick feet oedema revealed an anti-inflammatory activity evoked by co-extract mixtures that was greater than the sum of the individual potencies of the two extracts. Conclusion: The potential phytochemical synergy of the two plants extracts in its anti-inflammatory response largely validates ethnomedicinal practice and generally confirms growing literature reports that ascribe the net pharmacological activities of herbal extracts to the combined multi-activities of unique phytochemical entities at multiple target sites.

High blood pressure (HBP) is a strong, independent and etiologically relevant risk factor for cardiovascular and therefore, the leading cause of preventable deaths worldwide. Hypertension has high medical and social costs. Due to its many associated complications, the use of medical services create high costs with medications which represent almost half of the estimated direct expenses. Free distribution of more than 15 medications for HyPERtension and DIAbetes (HIPERDIA program) clearly shows the important role of drugs in the Brazilian Government’s effort to tackle these two diseases. Notwithstanding, the prevalence of HBP is rising in parallel with other NCDs. It is known that HBP results from environmental and genetic factors, and interactions among them. Our ancestors were often faced with survival stresses, including famine, water and sodium deprivation. As results of natural selection, the survival pressures drove our evolution to shape a thrifty genotype, which favored/promoted energy-saving and sodium/water preservation. However, with the switch to a sodium- and energy-rich diets and sedentary lifestyle, the thrifty genotype and ancient frugal alleles, are no longer advantageous, and may be maladaptive to disease phenotype, resulting in hypertension, obesity and insulin resistance syndrome. Low-grade chronic inflammation and oxidative stress would be the underlying mechanisms for these diseases. HBP is often associated with unhealthy lifestyles such as consumption of high fat and/or high-salt diets and physical inactivity. Therefore, alternatively to medicine drugs, lifestyle and behavioral modifications are stressed for the prevention, treatment, and control of hypertension. A lifestyle modification program (LSM) involving dietary counseling and regularly supervised physical activity (“Move for Health”) has been used for decades, in our group, for NCDs primary care. Retrospective (2006-2016) data from 1317 subjects have shown the top quartile of blood pressure(142.2/88.5mmHg) differing from the lower quartile (120.6/69.2mmHg) by being older, with lower schooling, lower income and, lower physical activity and aerobic capacity. Additionally, the P75 showed higher intake of CHO, saturated fat and sodium along with lower-diet quality score with a more processed foods. They showed higher body fatness and prevalence of metabolic syndrome along with higher pro-inflammatory and peroxidative activities and insulin resistance. In this free-demand sample, the HBP rate was 51.2% for SBP and 42.7% for DBP. The rate of undiagnosed HBP was 9.8% and only 1/3 of medicated patients were controlled for HBP. After 10 weeks of LSM the HBP normalization achieved 17.8% for SBP and 9.3% for DBP with a net effectiveness of 8.5% and 2.4%, respectively. The reduction of HBP by LSM was followed by increased aerobic conditioning and reduced intake of processed foods along with decreased values of BMI, abdominal fatness, insulin resistance, pro-inflammatory and peroxydative activities. Importantly, once applied nationwide this LSM would save HBP medication for 3.1 million of hypertensives at an economic saving costs of US$ 1.47 billion a year!

Platelet vesiculation is common factor contributing in coagulation and thromboembolism in patients with atrial fibrillation (AF). Platelet-derived vesicles are involved in the coagulation, thromboembolism, microvascular inflammation, arterial stiffness, vascular calcification, atherosclerotic plaque shaping and rupture, endothelial dysfunction, cardiac remodelling, and kidney dysfunction. Recent clinical studies have revealed elevated concentrations of platelet-derived vesicles in peripheral blood of patients with current AF and history of AF. The aim of the mini review is to discuss the role of platelet-derived micro vesicles as predictive biomarker in AF. Serial measures of circulating levels of platelet-derived vesicules are discussed to be useful in stratification of AF patients at risk of thromboembolic complications, but there is limiting evidence regarding their predictive value that requires further investigations in large clinical trials.

The Federal and State governments have declared the presence of an opioid addiction pandemic in the United States claiming the lives of more than 55,000 in 2015 (Rudd RA, Seth P, David F and Scholl L. 2016). The pharmaceutical manufacturers of the numerous FDA-approved opioid drugs are raking in more than $5 billion per year with about 2 million chronic pain sufferers addicted. The irony of this narcotic use and abuse conundrum is the existence of evidence-based technology for drug-free pain management which is not covered for reimbursement among public and private third-party payers. Therefore, this paper is presented to propose a pilot study to demonstrate the efficacy of resolving the chronic inflammation, edema and ischemia that causes non-malignant chronic pain with PEMF therapy, a non-invasive, non-thermal radio transmission of electrical impulses, thereby invalidating the legitimacy of prescribing opioid analgesics in such cases.