Nordic musculoskeletal questionnaire number of recorded “Yes’s”.
\r\n\tAlthough the microorganism was later described by several other researchers with multiple synonyms, Escherich was recognized as the first, establishing the definitive name of the microbe as Escherichia coli in 1954.
\r\n\tIn 1933, Alfred Adam showed that certain serotypes of "dyspepsia Koli" (as he called the diarrheagenic E. coli strains) were implicated in epidemics of pediatric diarrhoea. In 1944, Kauffman proposed a classification scheme that is still in use today for the purpose of differentiating commensal types from pathogens and subclassifying them.
\r\n\tEscherichia coli, in its natural habitat, lives in the intestines of most healthy mammals. It is the main facultative anaerobic organism of the digestive system. In healthy individuals, that is, if the bacterium does not acquire genetic elements that encode virulent factors, the bacterium acts as a commensal forming part of the intestinal microbiota and thus helping the absorption of nutrients.
\r\n\tIn humans, E. coli colonizes the gastrointestinal tract of a neonate by adhering to the mucus of the large intestine within a few hours of birth. Since then, it remains in a relationship of mutual benefit. However, these commensal strains can cause infections in immunosuppressed patients.
\r\n\r\n\tPathogenic strains of E. coli, on the other hand, as soon as they colonize a healthy host, can cause infections of varying severity in the intestine, urinary tract, meningitis, and sepsis, among other infections.
\r\n\tDiarrhea caused by pathogenic strains of E. coli is an important cause of death in children under 5 years of age, especially in sub-Saharan Africa and South Asia, where it is one of the four most important causes of moderate and severe diarrhea, potentially lethal An increase in mortality is associated with enteropathogenic strains.
\r\n\tUrinary tract infections are more common in women because of the short length of the urethra (25 to 50 mm) compared to men (about 15 cm). Among the elderly, urinary infections tend to be of the same proportion between men and women.
\r\n\tBecause the bacteria invariably enter the urinary tract through the urethra (an ascending infection), poor hygiene habits can predispose to infection; however, other factors become important, such as pregnancy, benign or malignant hypertrophy of the prostate, and in In many cases, the initiating event of the infection is unknown. Although ascending infections are the cause of lower urinary tract infections and cystitis, this is not necessarily the cause of upper infections such as pyelonephritis, which may have a hematogenous origin.
A considerable amount of interest has been placed on the discovery of novel naturally occurring plant-derived compounds for the treatment and prevention of various diseases. Bioactive compounds of plant origin have long been shown to possess strong ameliorative properties against various communicable and noncommunicable diseases [1, 2]. For example, since its traditional use during the 1950s, artemisinin, an antimalarial
Apigenin (PubChem CID: 5280443) is a natural flavone (4′,5,7-trihydroxyflavone) with the molecular formula C15H10O5 (MW 270.24 g/mol) that is abundantly present in fruits and vegetables, including parsley, chamomile, and celery (Figure 1) [9]. Apigenin was identified as the main yellow dye compound in the flowers of
The chemical structure of apigenin (4′,5,7-trihydroxyflavone).
In relation to its biological activities, increasing studies have demonstrated that apigenin displays a broad spectrum of anticarcinogenic properties as reviewed by Sung et al. [16]. Some of the well-studied mechanisms associated with the chemo-preventative capabilities of apigenin include its anti-inflammatory activity, its ability to suppress cell proliferation and oxidative stress, as well as its modulatory effect of autophagy and apoptosis [16, 17]. Interestingly, similar mechanisms have also been implicated in the development and aggravation of IR and its related complications. In a recent study, Jung et al. [18] showed that in addition to reducing circulating free fatty acids (FFAs), total cholesterol, and apolipoprotein B levels, apigenin modulated transcriptional factors linked with the development of obesity and related metabolic disturbances in high fat diet (HFD)-induced mice. This study showed that apigenin upregulated the expression of genes responsible for the regulation of beta-oxidation, oxidative phosphorylation, as well as electron transport chain and cholesterol homeostasis, which are all essential target sites for the control of substrate usage in cells. Although limited studies are reporting on its effect on skeletal muscle, two recent studies have shown that apigenin can regulate skeletal muscle function. For instance, Choi et al. [19] showed that this flavone improved mitochondrial function and exercise capacity by reducing the expression of atrophic genes such as RING-finger protein-1 and Atrogin 1 in mice fed HFD. Jang et al. [20] demonstrated that in C2C12 cells and skeletal muscle of C57BL/6 mice, this flavone promoted hypertrophy and myogenic differentiation by regulating protein arginine methyltransferase 7 (Prmt7)-peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)-G protein-coupled receptor 56 (GPR56) pathway, as well as the Prmt7-p38-myoD pathway. Although additional studies are required to further assess the impact of apigenin in the modulation of metabolic disease-related complications through the regulation of skeletal muscle function, the two aforementioned studies suggest that this flavone has a potential to protect against skeletal muscle weakness associated with metabolic complications.
\nAspalathin (PubChem CID: 11282394) is a natural
The chemical structure of aspalathin (3′-β-D-glucopyranosyl-2′,3,4,4′,6′- pentahydroxydihydrochalcone).
Relevant to its biological activity, the initial evidence demonstrated that aspalathin possess strong antioxidant properties by scavenging 2,2-diphenyl-β-picrylhydrazyl (DPPH) radical in vitro [28]. This effect was important since experimental and clinical studies support the notion that drug compounds that enhance intracellular antioxidant properties can further exhibit a wide range of beneficial effects against the development of metabolic syndrome [29]. In addition to its robust antioxidant activity [28, 30, 31, 32, 33, 34], aspalathin can ameliorate inflammation [35, 36, 37, 38, 39], protect cardiac cells exposed to high glucose concentrations [40, 41, 42, 43, 44], and also display glucose lowering properties [45, 46, 47, 48, 49, 50]. In addition to work by our group [46, 48], studies conducted by Kawano et al. [51] and Son et al. [50] have reported on the effect of pure aspalathin or an aspalathin rich green rooibos extract on the signaling mechanisms that regulate glucose and lipid metabolism in skeletal muscle. Activation of 5\' AMP-activated protein kinase (AMPK), an important kinase in the regulation of energy production, as well as increasing the expression and translocation of glucose transporter (GLUT) 4 have been the key molecular targets by aspalathin in the skeletal muscle. Thus, although additional evidence such as assessing the therapeutic effect of this dihydrochalcone on skeletal muscle biopsies of insulin-resistant human subjects is still necessary, its aforementioned potential to target AMPK, and improve glucose uptake is of major importance for future therapeutic development.
\nBerberine (PubChem CID: 2353) is a quaternary alkaloid (5,6-Dihydro-9,10-dimethoxybenzo[g]-1,3-benzodioxolo[5,6-a]quinolizinium) with the molecular formula C20H18 NO4+ (MW 336.37 g/mol) that is present in several plants including
The chemical structure of berberine (5,6-dihydro-9,10-dimethoxybenzo[g]-1,3-benzodioxolo[5,6-a]quinolizinium).
Berberine has a long history of medicinal use in traditional Chinese and Native American medicine [56] and has demonstrated a number of beneficial effects against metabolic complications, including amelioration of IR. Berberine demonstrated an enhanced effect to reduce body weight and raise plasma triglyceride levels while improving glucose tolerance and insulin action in both type 2 diabetic (
Curcumin, also known as diferuloylmethane (PubChem CID: 969516; (1E,6E)-1,7-Bis (4-hydroxy-3-methoxyphenyl) hepta-1,6-diene-3,5-dione), is a major polyphenolic derivative of turmeric (
The chemical structure of curcumin ((1E,6E)-1,7-bis(4-hydroxy-3-methoxyphenyl)hepta-1,6-diene-3,5-dione).
An increasing number of reviews has been published to keep track of the cumulative literature informing on the therapeutic potential of curcumin, including anticancer, antioxidant, anti-inflammatory, and antibacterial activities [70, 71, 72]. Relevant to its effect on skeletal muscle function. A study published in 2005 by Farid et al. [73] showed that curcumin failed to inhibit NF-κB activity, leading to its inability to ameliorate loss of muscle mass in the soleus. However, in a follow-up study published in 2008, curcumin presented enhanced effect in blocking sepsis-induced muscle proteolysis, at least in part by inhibiting NF-κB, and p38 activities in rats [74]. In L6 or C2C12 myotubes exposed to high palmitate concentrations as a model of IR, curcumin reversed IR by increasing glucose and FFA oxidation, at least in part by mediating LKB1-AMPK pathways, as well as suppressing insulin receptor substrate 1 (IRS-1) Ser307 and protein kinase B (AKT) phosphorylation [75, 76, 77]. Although similar evidence has been supported by in vivo experiments on skeletal muscle tissue of either diabetic or nondiabetic rodents [75, 77], curcumin displays an enhanced capacity to protect against oxidative stress associated complications by improving mitochondrial biogenesis, and other antioxidant mechanisms [78, 79, 80, 81]. This involves activation of the nuclear factor (erythroid-derived 2)-like 2 (NRF2) [82], an essential intracellular antioxidant response element that is a target of various natural products aiming to reduce metabolic disease-associated complications.
\nEpigallocatechin gallate (PubChem CID: 65064) is an ester of epigallocatechin and gallic acid ([(2R,3R)-5,7-dihydroxy-2-(3,4,5-trihydroxyphenyl)chroman-3-yl] 3,4,5-trihydroxybenzoate, with the molecular formula C22H18O11 (MW 458.375 g/mol), that is abundantly found in tea (Figure 5) [83]. Due to the popularity of green tea and as one of its major components, epigallocatechin gallate remains one of the highly consumed polyphenolic compounds [84]. Although it is detectable in its original form in human plasma after oral administration [85], epigallocatechin gallate is considered to have very low oral bioavailability profile as reviewed by Mereles and colleagues [86]. Although additional evidence is required to improve its bioavailability, there has been an extensive exploration of this polyphenolic compound for its chemopreventive properties. Among the 10 polyphenols present in green tea, epigallocatechin gallate was found to exhibit the most antiproliferative and antiapoptotic effects [87].
\nThe chemical structure of epigallocatechin gallate ([(2R,3R)-5,7-dihydroxy-2-(3,4,5-trihydroxyphenyl)chroman-3-yl] 3,4,5-trihydroxybenzoate).
It has already been established that epigallocatechin gallate can ameliorate complications linked with the development of the metabolic syndrome, by improving insulin sensitivity in both obese rodents and patients [88, 89, 90]. The enhanced therapeutic effect of this catechin has been associated with the modulation of various signaling pathways, including targeting of genes involved in cell survival, FFA regulation, mitochondrial energetics, intracellular antioxidant response, and others as reviewed by Singh and colleagues [91]. A number of studies have demonstrated several mechanisms associated with the ameliorative effect of epigallocatechin gallate on IR and associated complications in skeletal muscle. In addition to strengthening muscle integrity [92, 93, 94], accumulative data has been presented that this catechin can improve insulin sensitivity by enhancing glucose uptake, reduce lactate concentrations, enhancing mitochondrial capacity and stimulating beta-oxidation in cultured cells, or rodents as well as obese human subjects [95, 96, 97, 98, 99, 100]. Inhibition of oxidative stress, activation of AMPK, increased expression of PGC-1α, NAD-dependent protein deacetylase sirtuin-1 (SIRT1), nuclear respiratory factor 1, medium chain acyl coA decarboxylase, uncoupling protein 3 (UCP3), AKT, and peroxisome proliferator-activated receptor alpha (PPARα) are some of the mechanisms targeted by epigallocatechin to enhance skeletal muscle function in a diseased state [101, 102, 103, 104].
\nHesperidin (PubChem CID: 10621) is a flavanone glycoside ((2S)-5-hydroxy-2-(3-hydroxy-4-methoxyphenyl)-7-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-[[(2R,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxymethyl]oxan-2-yl]oxy-2,3-dihydrochromen-4-one) with the molecular formula C28H34O15 (MW 610.565 g/mol) that is present in high amounts in citrus fruits (Figure 6) [105]. Although it has a low bioavailability due to the rutinoside moiety attached to the flavonoid [106], hesperidin can be converted to glucuronides and sulfoglucuronides, which have been shown to be excreted in urine nearly 24 hours after the orange juice ingestion [107]. In a randomized controlled trial, Nielsen et al. [108] demonstrated that removal of the rhamnose group to yield hesperetin-7-glucoside improved the bioavailability of the aglycone hesperetin. Suggesting that additional interventions are required to improve the bioavailability of citrus flavonoids such as hesperidin.
\nThe chemical structure of hesperidin ((2S)-5-hydroxy-2-(3-hydroxy-4-methoxyphenyl)-7-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-[[(2R,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxymethyl]oxan-2-yl]oxy-2,3-dihydrochromen-4-one).
Increasing data has supported the notion that hesperidin possesses increased potential to lower raised blood glucose and lipid levels in various models of type 2 diabetes [109, 110, 111]. When administered in rats subjected to swimming exercise, this citrus flavonoid improved the biochemical and antioxidant profile of the animals [112]. This compound may induce its therapeutic effect through the regulation of genes implicated in insulin signaling such as insulin receptor substrate 1, GLUT2/4, and those linked with lipid metabolism, including sterol regulatory element–binding protein 1c (SREBP-1c), fatty acid synthase (FAS) and acetyl-CoA carboxylase [113]. Although data on its effect on skeletal muscle is currently limited, it can reverse IR by reducing muscle glycogen content and ischemia–reperfusion injury while promoting myogenic differentiation through the activation of MyoD-mediated myogenin expression in cultured cells and animals [109, 114, 115].
\nLuteolin (PubChem CID: 5280445) is a flavone glycoside (2-(3,4-Dihydroxyphenyl)- 5,7-dihydroxy-4-chromenone) with the molecular formula C15H10O6 (MW 286.239 g/mol) that is rich in various dietary sources such as fruits, vegetables, and teas (Figure 7) [116]. As with most flavonoids, during its metabolism luteolin is broken down to its glucuronides, which can eventually pass through intestinal mucosa as shown by Yasuda and colleagues [117]. Although studies reporting on the pharmacokinetic profile of luteolin in human subjects are limited, this flavone is quickly absorbed in rats and can be detected in urine and feces while showing a slow elimination rate [118]. Furthermore, luteolin from peanut hull extract can be easily absorbed compared to the pure compound, with its absorption more efficient in the jejunum and duodenum than in the colon and ileum [119]. Alternatively, luteolin-loaded solid lipid nanoparticles prepared by hot microemulsion ultrasonic technique can also improve the solubility and increase the compound concentration in plasma of rats [120].
\nThe chemical structure of luteolin (2-(3,4-dihydroxyphenyl)- 5,7-dihydroxy-4-chromenone).
In addition to its strong antioxidant effects [121], in vitro experiments have provided evidence that luteolin possesses chemopreventive and anti-inflammatory properties [122, 123]. Hydroxyl groups and 2–3 double bond remain key structural features of luteolin that are linked to its enhanced therapeutic effect [124]. Recent studies show that this flavone attenuates hepatic steatosis and IR by upregulating PPARγ protein expression and activating AMPKα1 signaling, which may be linked to the improvement in circulating FFA levels in diet-induced obese mice [125, 126]. However, only a few studies have reported on the effect of luteolin on the skeletal muscle. Available literature has reported on its effect in preventing lipopolysaccharide-induced muscle atrophy, oxidative stress-induced tissue injury and inflammation, partly through regulation of atrogin-1/MAFbx expression, and c-Jun N-terminal kinases (JNK) phosphorylation reported on [127, 128, 129].
\nNaringenin (PubChem CID: 932) is a flavanone (5,7-dihydroxy-2-(4-hydroxyphenyl)chroman-4-one) with the molecular formula C15H12O5 (MW 272.256 g/mol) that is also predominantly found in citrus fruits (Figure 8) [130]. The chemical structure of naringenin comprises three hydroxy groups at the 4′, 5, and 7 carbons while its glycoside, naringin contains an additional disaccharide neohesperidose that is linked via its carbon end. Although naringenin can be detected as monoglucuronides in plasma and urine after ingestion of orange fruit juice in human subjects [131], the bioavailability of naringenin can be influenced by its glycosidic moiety. Felgines et al. [132] demonstrated that kinetics of absorption of naringenin and naringenin-7-glucoside was similar. In addition, naringenin-7-rhamnoglucoside exhibited a delay in its intestinal absorption, resulting in decreased bioavailability after ingestion in rats. On the other hand, complexation of naringenin with hydroxypropoyl-β-cyclodextrin has been another viable alternative to improve the bioavailability of naringenin, which is important to enhance its therapeutic potential [133].
\nThe chemical structure of naringenin (5,7-dihydroxy-2-(4-hydroxyphenyl)chroman-4-one).
Naringenin is among the well-studied citrus flavonoids shown to prevent complications associated with IR and the metabolic syndrome. Its role in preventing the deterioration in skeletal muscle mass and protecting against metabolic associated complication is summarized. In low-density lipoprotein (LDL) receptor–null (Ldlr−/−) mice fed HFD, this flavanone reduced fasting hyperinsulinemia, improved glucose utilization and increased insulin sensitivity through regulation of SREBP-1c–mediated lipogenesis [134]. It stimulated glucose uptake but failed to have a significant effect on basal or insulin-stimulated AKT phosphorylation while significantly increasing AMPK phosphorylation/activation in cultured L6 myotubes [135]. Bhattacharya and colleagues showed that naringenin stimulates glucose uptake, indicating a dependence on GLUT4 activity as well as phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) and/or p38MAPK activity [136]. Maintenance of muscle mass by reducing muscle diacylglycerol content, improving hyperinsulinemia, promoting phosphorylation of p38/MAPK via estrogen receptor beta (ERβ), lowering reactive oxygen species (ROS) production, and enhancing tyrosine phosphorylation are other mechanisms associated with protective effect of naringenin in either cultured cells or in vivo animal models [137, 138, 139, 140].
\nQuercetin (PubChem CID: 5280343) is classified as a flavonol (2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-4H-chromen-4-one) with the molecular formula C15H10O7 (MW 302.238 g/mol) that is abundantly found in various fruits and vegetables (Figure 9) [141]. Quercetin is one of the most abundant dietary flavonoids that is rapidly metabolized to glucuronides and sulfates that can be detected in plasma and urine [142]. Although oral bioavailability of quercetin remains low, the type of sugar moiety attached to its structure may affect its absorption. This has been as demonstrated with quercetin glycosides from onion which have a higher absorption rate compared to apple-derived quercetin [143, 144]. Quercetin-4’-
The chemical structure of quercetin (2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-4H-chromen-4-one).
Quercetin exhibits a wide range of biological functions. Although Stewart et al. [146] failed to show any beneficial effect of quercetin against IR in diet induced-obese mice, other researchers have shown that this flavonol plays a major role in modulating several signaling pathways to reverse metabolic syndrome and improve skeletal muscle function, either in vitro on cultured cells or in vivo in animals and samples from human subjects [148, 149, 150, 151, 152, 153, 154, 155, 156, 157, 158, 159, 160, 161, 162, 163, 164, 165, 166, 167, 168]. In L6 myotubes and skeletal muscle of genetical modified (
Resveratrol (PubChem CID: 445154) is a phytoalexin stilbenoid (3,5,4′-trihydroxy-trans-stilbene) with the molecular formula C14H12O3 (MW 228.247 g/mol) that is present in abundant amounts in various food sources such as grapes, blueberries, and red wine (Figure 10) [169]. Upon ingestion, resveratrol can be metabolized to form conjugated sulfates and glucuronides, namely resveratrol monosulfate, monosulfate dihydroresveratrol, and monoglucuronide dihydroresveratrol, as reviewed by Gambini and colleagues [170]. Although the bioavailability of resveratrol is considered low, it can vary depending on the method of administration and type of dietary source ingested [171]. The dimethyl ether analog of resveratrol, pterostilbene, has been shown to exhibit a higher bioavailability, in terms of total plasma levels of both the parent compound and metabolites than does resveratrol [172]. However, Li et al. [173] showed that intravenous and oral pharmacokinetic characteristics of trans-resveratrol can be improved through encapsulating with PP123 self-assembling lecithin-based mixed polymeric micelles. Suggesting that alternative methods to improve the bioavailability of resveratrol are required, which may translate to enhanced therapeutic potential in vivo.
\nThe chemical structure of resveratrol (3,5,4′-trihydroxy-trans-stilbene).
Resveratrol has displayed a variety of antidiabetic effects in rodent models. In addition, resveratrol attenuates thermal hyperalgesia, cold allodynia, as well as raised serum lipid levels [174, 175, 176]. In diabetic individuals, resveratrol administration is associated with significantly improved glucose and insulin control [177]. The systematic search of evidence linking resveratrol and IR in skeletal muscle revealed up to 18 studies published between 2007 and 2017, with 9 papers produced between 2016 and 2017, suggesting that this phytoalexin stilbenoid is increasingly explored for therapeutic effect against metabolic associated complications. Although Williams and colleagues showed no effect on insulin signaling pathways [178], stimulation of glucose uptake by resveratrol in cultured C2C12 cells or skeletal muscle has been linked with activation of extracellular signal-related kinase/p38/PI3K [179]. Its effect in promoting glucose uptake and improving insulin sensitivity was also associated with increased NAD-dependent protein deacetylase sirtuin-1 (SIRT1) expression, activation of AMPK while abolishing phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), JNK, and IκB kinase α/β (IKKα/IKKβ) [180, 181, 182, 183, 184, 185, 186, 187, 188, 189, 190]. Other documented beneficial effect of resveratrol includes inhibiting ischemia–reperfusion injury through its potent antioxidant properties [191], reducing cell proliferation through upregulating PGC-1α [192], promoting muscle regeneration and attenuating the impact of ROS [193], and elevated forearm skeletal muscle mitochondrial capacity [194].
\nRutin (PubChem CID: 5280805) is a glycoside combining the flavonol quercetin and the disaccharide rutinose (2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-3-[α-L-rhamnopyranosyl-(1→6)-β- D-glucopyranosyloxy]-4H-chromen-4-one) with the molecular formula C27H30O16 (MW 610.521 g/mol) that is found in many plants and fruits, as well as tea infusions (Figure 11) [195]. Upon oral administration, rutin can be metabolized into sulfates and glucuronides of quercetin that are detected in blood, whereas unchanged forms of rutin and quercetin were not detected [142, 196]. Although quercetin glycosides from onions demonstrate an enhanced absorptive capacity than pure aglycones [143, 144], some studies have showed that rutin has a lower oral absorption rate than quercetin [142, 197]. However, as with the use of natural deep eutectic solvents [198], alternative methods to improve the absorptive capacity of rutin is tested to improve therapeutic effect in vivo.
\nThe chemical structure of rutin (2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-3-[α-L-rhamnopyranosyl-(1→6)-β-D-glucopyranosyloxy]-4H-chromen-4-one).
Like quercetin, rutin exhibits a wide variety of biological properties, mostly attributed to its strong antioxidant properties [199, 200]. It is accomplished that rutin displays enhanced potential to improve insulin sensitivity by regulating genes involved in glucose and lipid metabolism such as GLUT4, PPARγ, and tyrosine phosphatase 1B in cultured cells or skeletal muscle of rodents [201, 202, 203, 204]. However, from the study by Zyma et al. [205], that demonstrated that rutin induces conformational changes in the myosin structure of skeletal muscle of rabbits accompanied by an increase in ATPase activity, accumulative evidence has supported muscle strengthening capacity of this polyphenol. For example, Su et al. [206] presented data showing that rutin promoted skeletal muscle endurance capacity by modulating markers of mitochondrial biogenesis such as PGC-1α and SIRT1 expression in ICR mice subjected to a weight-loaded forced swim test. These findings were further supported by data showing that rutin increased the mitochondrial size and mitochondrial DNA content as well as gene expression related to mitochondrial biogenesis, such as PGC1-α, NRF-1, transcription factor A, and SIRT1 [207, 208].
\nSulforaphane (PubChem CID: 5350) is an isothiocyanate (1-isothiocyanato-4-methylsulfinylbutane) with the molecular formula C6H11NOS2 (MW 177.28 g/mol) that is found in cruciferous vegetables such as cabbages, broccoli, and brussels sprouts (Figure 12) [209]. Although sulforaphane displays a dose-dependent pharmacokinetic behavior, as higher doses show reduced absorptive potential, lower doses of the compound can be rapidly absorbed in rats following intravenous administration, with the absolute bioavailability being able to reach 82% [210]. In human subjects consuming fresh broccoli sprouts or the broccoli sprout extract, with each estimated to provide 200 μmol sulforaphane daily, the compound metabolites were found to be three times higher in plasma and urine of sprout consumers, suggesting enhanced sulforaphane absorption from sprouts [211]. Therefore, dietary form and dosing schedule of sulforaphane may influence impact absorption and therapeutic potential in human subjects.
\nThe chemical structure of sulforaphane (1-isothiocyanato-4-methylsulfinylbutane).
Sulforaphane has received a considerable interest due to its ability to simultaneously control multiple cellular targets involved in various metabolic complications. For instance, in rats fed HFD, this isothiocyanate has displayed an enhanced hypoglycemic potential as well as the elevation of GLUT3 expression in the cerebral cortex and hypothalamus, leading to improved glucose tolerance [212]. Other studies [213, 214] have supported the beneficial effect of sulforaphane or its stable precursor glucoraphanin, to reverse IR, mostly through its robust antioxidant properties. In skeletal muscle, sulforaphane has exhaustive exercise-induced muscle damage, reducing muscle glycogen content, and enhanced exercise endurance capacity through inhibition of pro-inflammatory response and enhancing antioxidant response by upregulating NRF2 expression [215, 216, 217, 218, 219, 220].
\nNatural compounds have gained popularity for their potential beneficial effect to fight metabolic diseases due to their less adverse effect compared to synthetic drugs. Furthermore, natural compounds serve as a valuable source for the discovery of new drugs. Currently, knowledge shows that natural compounds can ameliorate IR, however, the gap in scientific evidence of plant-derived therapeutic benefits still exist due to the slow rate of translation of animal studies findings into human clinical trials. In this chapter, evidently reported the great potential and the future promise of natural compounds for the management and treatment of metabolic disorders, specifically IR, obesity, and T2D. Therefore, further research is required to assess the use of natural compounds alone or in combination with well know antidiabetic drugs might result in synergistic and enhanced effects in combating metabolic diseases.
\nThis work was supported by the Biomedical Research and Innovation Platform of the South African Medical Research Council (SAMRC) baseline funding and the South African National Research Foundation (NRF; grant number 87836 to SE Mazibuko-Mbeje). The grant holders acknowledge that opinions, findings, and conclusions or recommendations expressed in any publication generated by the SAMRC or NRF supported research are those of the authors, and that the SAMRC and NRF accept no liability whatsoever in this regard. PVD was partially supported as a Post-Doctoral Fellow by funding from the SAMRC.
\nThe authors report no conflicts of interest. All authors are responsible for the content and writing of the chapter.
AKT | protein kinase B |
AMPK | 5\' AMP-activated protein kinase |
ATP | adenosine triphosphate |
CD36 | cluster of differentiation 36 |
DPPH | 2,2-diphenyl-β-picrylhydrazyl |
ERβ | estrogen receptor beta |
FAS | fatty acid synthase |
FFA | free fatty acid |
GLUT | glucose transporter |
HFD | high fat diet |
IR | insulin resistance |
IRS-1 | suppressing insulin receptor substrate 1 |
JNK | c-Jun N-terminal kinases |
LDL | low density lipoprotein |
LKB1 | serine/threonine kinase 11 |
MAPK | mitogen-activated protein kinase |
MW | molecular weight |
NF-κB | nuclear factor kappa-light-chain-enhancer of activated B cells |
NRF2 | nuclear factor (erythroid-derived 2)-like 2 |
PGC-1α | peroxisome proliferator-activated receptor gamma coactivator 1-alpha |
PI3K | phosphatidylinositol-4,5-bisphosphate 3-kinase |
PPAR | peroxisome proliferator-activated receptor |
Prmt7 | protein arginine methyltransferase 7 |
SIRT1 | NAD-dependent protein deacetylase sirtuin-1 |
SREBP-1c | sterol regulatory element–binding protein 1c |
T2D | type 2 diabetes mellitus |
UCP | uncoupling protein |
Hospital workers are highly susceptible to musculoskeletal disorders due to the regular lifting, positioning, and transporting of patients, combined with a fast pace work environment and a general collective temperament of putting their patients’ health before their own [1]. Upon closer review, the EP/Cath lab subset of the rural hospital workforce appears to be especially susceptible to the specific musculoskeletal disorder of low back pain. This has been attributed to the sustained forward-flexed postures they commonly maintain while working in the operating room [2], combined with a shortage of rural physicians and less community-based resources available to rural hospital staff as compared to their urban counterparts [3]. As a strategy to address this dilemma, exercise and physical activity routines, health education, and continued management support have been broadly promoted as cost-effective programs which are powerful enough to improve the health of the workforce, yet also produce a positive return on investment [4]. In theory the implementation of these low cost/low risk programs is a sound strategy based on evidence-based guidelines. The American College of Physicians strongly recommends nonpharmacologic treatments for chronic low back pain, including exercise and mindfulness-based stress reduction, because the benefits clearly outweigh the risk [5]. In practice, though, limited time and the inability to incorporate the program into everyday work routines have been found to be the two main reasons why these worksite-based fitness programs have failed to produce significant findings [6]. To overcome these barriers, hospital management must concurrently have the social, financial, and strategic investments in place which complement and support these specific wellness interventions to realize significant and lasting reductions in musculoskeletal disorders [7]. Unfortunately, the extent to which these investments have been made by hospital management, and thus perceived effective by the EP/Cath lab workforce, is unknown. Thus, the objective of this study was to determine the prevalence of low back pain in rural EP/Cath laboratories and the significance of exercise and physical activity routines, health education, and continued management support as low back pain prevention strategies in the rural EP/Cath lab community.
Those individuals who worked in the EP/Cath laboratories of two rural hospitals in the state Arkansas were eligible to participate in the study. A convenience sample design was used, and all research data were collected through the electronic transmission of a Qualtrics survey. The survey included three general sections: Nordic Musculoskeletal Questionnaire (NMQ), demographics/applicable work practice details, and low back pain prevention strategies. The first section featuring the NMQ was used to calculate the prevalence of musculoskeletal symptoms within the study population. The NMQ was developed for the analysis of musculoskeletal symptoms, [8] and has been validated and applied to a wide range of occupational groups, including nursing [9]. Additionally, the validity and reliability of the NMQ was assessed to be moderate to high and its use appropriate for epidemiological research related to musculoskeletal disorders [10]. The second section on demographics/applicable work practice assessed height, weight, gender, age, number of years worked in an EP/Cath lab setting, number of hours per week in a lead apron, and percentage of average shift spent standing in the lab. The third section on low back pain prevention strategies assessed exercise and physical activity routines, health education, and continued management support. These questions were developed through the examination of peer-reviewed journal articles, scientific posters, and government websites which promote specific behaviors or actions that had the potential to prevent or reduce low back pain [11].
A total of 45 participants were invited to participate in the study. Upon receiving IRB approval, the survey was sent to the work email address of all study participants. Data were deidentified and summarized using Microsoft Excel. Analysis showed fifteen individuals either selected they did not want to participant in the study or did not complete the survey in its entirety and thus, were omitted from the final data set. Ultimately, a total of 30 completed surveys were included in the final data set for analysis.
The first section of the survey featuring the NMQ assessed the prevalence of musculoskeletal symptoms in nine different regions of the body. The largest group, 18 (60%), stated they experienced pain in the lower back (L4 to S1) spinal level, while 12 (40%) reported no low back pain. Among the 60% of respondents who have experienced low back pain, eight (26.67%) had trouble in the last week and six (20%) were prevented from doing their normal work (at home or away from home) (Table 1).
Region of Body | Recorded “Yes” (n = 30) |
---|---|
Neck | 46.67% |
Trouble in the last 12 months | 14 |
Prevented from normal work | 1 |
Trouble in the last 7 days | 4 |
Shoulders | 40.00% |
Trouble in the last 12 months | 12 |
Prevented from normal work | 2 |
Trouble in the last 7 days | 4 |
Elbows | 13.33% |
Trouble in the last 12 months | 4 |
Prevented from normal work | 1 |
Trouble in the last 7 days | 1 |
Wrists/Hands | 13.33% |
Trouble in the last 12 months | 4 |
Prevented from normal work | 1 |
Trouble in the last 7 days | 1 |
Upper Back | 36.67% |
Trouble in the last 12 months | 11 |
Prevented from normal work | 1 |
Trouble in the last 7 days | 3 |
Lower Back | 60.00% |
Trouble in the last 12 months | 18 |
Prevented from normal work | 6 |
Trouble in the last 7 days | 8 |
Hips/Thighs | 26.67% |
Trouble in the last 12 months | 8 |
Prevented from normal work | 3 |
Trouble in the last 7 days | 2 |
Knees | 23.33% |
Trouble in the last 12 months | 7 |
Prevented from normal work | 2 |
Trouble in the last 7 days | 4 |
Feet/Ankles | 30.00% |
Trouble in the last 12 months | 9 |
Prevented from normal work | 1 |
Trouble in the last 7 days | 5 |
Per Person Mean and SD | 4.57 ± 4.03 |
Nordic musculoskeletal questionnaire number of recorded “Yes’s”.
When we compare our study to a sample of Radiologic Technologists study who similarly wear lead aprons1, the current study showed a higher overall pervasiveness of low back pain (60% to 47.62%) but less low back pain symptoms on the short-term basis (33.33% to 26.67%). Despite these discrepancies, low back pain was found to be the most prevalent musculoskeletal symptom recorded in both studies. Another significant finding in this study is the data showed an increase in the prevalence of low back pain once five years of service in an EP/Cath lab setting has been completed (58–61%) (Table 2). To provide a sense of comparison, Goldstein, et al. in (2004) likewise reported an upward trajectory in the prevalence of low back pain among Interventional Cardiologists as the number of years of service increased [12].
Total | LBP | No LBP | |
---|---|---|---|
Number | 30 | 18 | 12 |
Height (inches) | 67.30 ± 5.47 | 67.28 ± 5.54 | 67.33 ± 5.61 |
Weight (pounds) | 196.17 ± 31.79 | 194.44 ± 36.58 | 198.75 ± 24.16 |
Gender (% male) | 46.67 | 44.44 | 50.00 |
Age | 40.93 ± 11.92 | 38.67 ± 9.93 | 44.33 ± 14.20 |
Years working in EP/Cath lab setting | 9.53 ± 9.79 | 8.22 ± 6.60 | 11.50 ± 13.36 |
under 5 | 12 | 7 | 5 |
5–10 | 8 | 6 | 2 |
11–16 | 4 | 2 | 2 |
17–20 | 4 | 3 | 1 |
21 or more | 2 | 0 | 2 |
Hours per week in lead apron | 18.13 ± 10.45 | 16.17 ± 10.53 | 21.08 ± 10.02 |
% of shift spent standing in lab | 60.50 ± 24.96 | 59.44 ± 26.51 | 62.08 ± 23.50 |
Demographics/applicable work practice details stratified by the presence or absence of low Back pain (LBP).
Finally, the top two prevention strategies reported by those with low back pain were “regularly complete at least 150 minutes per week of moderate-intensity aerobic physical activity” and “if a worksite-based fitness program will be offered to you at your department, will you be interested on joining it for at least a year” (Table 3). As motivation to exercise appears to be high, interestingly no responses were recorded when asked if their worksite-based fitness program occurred on company time or if low back pain and other musculoskeletal symptoms were periodically evaluated. In addition, only one response was recorded when asked if ergonomic-related topics were discussed during team meetings. These findings suggest it is the cultural norm of the EP/Cath lab community to believe it is the personal responsibility of the employee rather than shared responsibility of the employee and hospital (EP/Cath lab) management to address the widespread low back pain present in the workforce, personified by only 36.67% of respondents reporting “hospital management believes improvements in physical conditioning will help to prolong career.”
Prevention Strategy | LBP (n = 18) | No LBP (n = 12) |
---|---|---|
Currently participate in early morning fitness program | 6 | 5 |
Yes: Includes strength training exercises | 6 | 4 |
Yes: Includes stretching exercises | 5 | 5 |
Yes: Overall do you do your fitness program regularly | 5 | 4 |
Worksite-based fitness program currently offered to dept | 4 | 5 |
Yes: Occurred on company-time | 0 | 0 |
Yes: Each class included exercises targeting the various muscle groups of the body | 4 | 5 |
Yes: Customized around dept’s specific needs, preferred communication methods, and resources available to the employees to help create a sense of ownership | 2 | 1 |
If a worksite-based fitness program will be offered to you at your department, will you be interested on joining it for at least a year | 10 | 1 |
Yes: How often to hold class (days/week) | 3 Responses: Daily 6 Responses: 3x 1 Response: 1x | 1 Response: Daily |
Yes: How long to hold class (minutes) | 2 Responses: 10–15 6 Responses: 15–20 2 Responses: Other | 1 Response: 10–15 |
Yes: Led by a faciliator or instructor | 7 | 1 |
Ergonomic-related topics discussed during team meetings | 0 | 1 |
Yes: Includes discussion on poor posture(s) | 0 | 1 |
Yes: Includes discussion on stress management | 0 | 1 |
Yes: Includes discussion on active coping strategies | 0 | 1 |
Yes: Strategies developed to overcome limited time to stretch | 0 | 1 |
Yes: Strategies developed to overcome lack of regular breaks | 0 | 1 |
Yes: Strategies developed to overcome requirement to keep the body in a sustained forward-flexed posture during surgery | 0 | 1 |
Regularly complete at least 150 minutes per week of moderate-intensity aerobic physical activity | 10 | 3 |
Regularly complete stretching exercises | 6 | 6 |
Regularly complete strength training exercises two or more days/week | 8 | 4 |
Yes: Systematically change number of sets, reps, or weight used in strength training program | 7 | 4 |
Yes: Know how to engage the deep core muscles | 7 | 4 |
Hospital management believes improvements in physical conditioning will help to prolong career | 6 | 5 |
Low back pain and other musculoskeletal symptoms periodically evaluated | 0 | 0 |
Functional Movement Screen or another validated screening tool periodically used to identify faulty movement patterns or muscular imbalances | 1 | 2 |
Prevention strategies completed by EP/Cath lab physicians, managers, and technicians stratified by the presence or absence of low Back pain (LBP).
The primary goal of this study was to illustrate the prevalence and generalized characteristics of back pain among EP and Cath laboratories in rural hospital settings. Conclusions that may be drawn from this study are the prevalence of low back pain demonstrated within this study were consistent when compared to available studies, low back pain is a common condition among EP and Cath lab employees, and several low cost/low risk preventative strategies for reducing musculoskeletal symptoms in the workforce are not currently being completed by those who participated in the study.
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He also obtained an MSc in Molecular and Genetic Medicine, and a Ph.D. in Clinical Immunology and Human Genetics from the University of Sheffield, UK. He also completed a short-term fellowship in Pediatric Clinical Immunology and Bone Marrow Transplantation at Newcastle General Hospital, England. Dr. Rezaei is a Full Professor of Immunology and Vice Dean of International Affairs and Research, at the School of Medicine, Tehran University of Medical Sciences, and the co-founder and head of the Research Center for Immunodeficiencies. He is also the founding president of the Universal Scientific Education and Research Network (USERN). Dr. Rezaei has directed more than 100 research projects and has designed and participated in several international collaborative projects. He is an editor, editorial assistant, or editorial board member of more than forty international journals. He has edited more than 50 international books, presented more than 500 lectures/posters in congresses/meetings, and published more than 1,100 scientific papers in international journals.",institutionString:"Tehran University of Medical Sciences",institution:{name:"Tehran University of Medical Sciences",country:{name:"Iran"}}},{id:"180733",title:"Dr.",name:"Jean",middleName:null,surname:"Engohang-Ndong",slug:"jean-engohang-ndong",fullName:"Jean Engohang-Ndong",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/180733/images/system/180733.png",biography:"Dr. Jean Engohang-Ndong was born and raised in Gabon. After obtaining his Associate Degree of Science at the University of Science and Technology of Masuku, Gabon, he continued his education in France where he obtained his BS, MS, and Ph.D. in Medical Microbiology. He worked as a post-doctoral fellow at the Public Health Research Institute (PHRI), Newark, NJ for four years before accepting a three-year faculty position at Brigham Young University-Hawaii. Dr. Engohang-Ndong is a tenured faculty member with the academic rank of Full Professor at Kent State University, Ohio, where he teaches a wide range of biological science courses and pursues his research in medical and environmental microbiology. Recently, he expanded his research interest to epidemiology and biostatistics of chronic diseases in Gabon.",institutionString:"Kent State University",institution:{name:"Kent State University",country:{name:"United States of America"}}},{id:"188773",title:"Prof.",name:"Emmanuel",middleName:null,surname:"Drouet",slug:"emmanuel-drouet",fullName:"Emmanuel Drouet",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/188773/images/system/188773.png",biography:"Emmanuel Drouet, PharmD, is a Professor of Virology at the Faculty of Pharmacy, the University Grenoble-Alpes, France. As a head scientist at the Institute of Structural Biology in Grenoble, Dr. Drouet’s research investigates persisting viruses in humans (RNA and DNA viruses) and the balance with our host immune system. He focuses on these viruses’ effects on humans (both their impact on pathology and their symbiotic relationships in humans). He has an excellent track record in the herpesvirus field, and his group is engaged in clinical research in the field of Epstein-Barr virus diseases. He is the editor of the online Encyclopedia of Environment and he coordinates the Universal Health Coverage education program for the BioHealth Computing Schools of the European Institute of Science.",institutionString:null,institution:{name:"Grenoble Alpes University",country:{name:"France"}}},{id:"131400",title:"Prof.",name:"Alfonso J.",middleName:null,surname:"Rodriguez-Morales",slug:"alfonso-j.-rodriguez-morales",fullName:"Alfonso J. Rodriguez-Morales",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/131400/images/system/131400.png",biography:"Dr. Rodriguez-Morales is an expert in tropical and emerging diseases, particularly zoonotic and vector-borne diseases (especially arboviral diseases). He is the president of the Travel Medicine Committee of the Pan-American Infectious Diseases Association (API), as well as the president of the Colombian Association of Infectious Diseases (ACIN). He is a member of the Committee on Tropical Medicine, Zoonoses, and Travel Medicine of ACIN. He is a vice-president of the Latin American Society for Travel Medicine (SLAMVI) and a Member of the Council of the International Society for Infectious Diseases (ISID). Since 2014, he has been recognized as a Senior Researcher, at the Ministry of Science of Colombia. He is a professor at the Faculty of Medicine of the Fundacion Universitaria Autonoma de las Americas, in Pereira, Risaralda, Colombia. He is an External Professor, Master in Research on Tropical Medicine and International Health, Universitat de Barcelona, Spain. He is also a professor at the Master in Clinical Epidemiology and Biostatistics, Universidad Científica del Sur, Lima, Peru. In 2021 he has been awarded the “Raul Isturiz Award” Medal of the API. Also, in 2021, he was awarded with the “Jose Felix Patiño” Asclepius Staff Medal of the Colombian Medical College, due to his scientific contributions to COVID-19 during the pandemic. He is currently the Editor in Chief of the journal Travel Medicine and Infectious Diseases. His Scopus H index is 47 (Google Scholar H index, 68).",institutionString:"Institución Universitaria Visión de las Américas, Colombia",institution:null},{id:"332819",title:"Dr.",name:"Chukwudi Michael",middleName:"Michael",surname:"Egbuche",slug:"chukwudi-michael-egbuche",fullName:"Chukwudi Michael Egbuche",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/332819/images/14624_n.jpg",biography:"I an Dr. Chukwudi Michael Egbuche. I am a Senior Lecturer in the Department of Parasitology and Entomology, Nnamdi Azikiwe University, Awka.",institutionString:null,institution:{name:"Nnamdi Azikiwe University",country:{name:"Nigeria"}}},{id:"284232",title:"Mr.",name:"Nikunj",middleName:"U",surname:"Tandel",slug:"nikunj-tandel",fullName:"Nikunj Tandel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/284232/images/8275_n.jpg",biography:'Mr. Nikunj Tandel has completed his Master\'s degree in Biotechnology from VIT University, India in the year of 2012. He is having 8 years of research experience especially in the field of malaria epidemiology, immunology, and nanoparticle-based drug delivery system against the infectious diseases, autoimmune disorders and cancer. He has worked for the NIH funded-International Center of Excellence in Malaria Research project "Center for the study of complex malaria in India (CSCMi)" in collaboration with New York University. The preliminary objectives of the study are to understand and develop the evidence-based tools and interventions for the control and prevention of malaria in different sites of the INDIA. Alongside, with the help of next-generation genomics study, the team has studied the antimalarial drug resistance in India. Further, he has extended his research in the development of Humanized mice for the study of liver-stage malaria and identification of molecular marker(s) for the Artemisinin resistance. At present, his research focuses on understanding the role of B cells in the activation of CD8+ T cells in malaria. Received the CSIR-SRF (Senior Research Fellow) award-2018, FIMSA (Federation of Immunological Societies of Asia-Oceania) Travel Bursary award to attend the IUIS-IIS-FIMSA Immunology course-2019',institutionString:"Nirma University",institution:{name:"Nirma University",country:{name:"India"}}},{id:"334383",title:"Ph.D.",name:"Simone",middleName:"Ulrich",surname:"Ulrich Picoli",slug:"simone-ulrich-picoli",fullName:"Simone Ulrich Picoli",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/334383/images/15919_n.jpg",biography:"Graduated in Pharmacy from Universidade Luterana do Brasil (1999), Master in Agricultural and Environmental Microbiology from Federal University of Rio Grande do Sul (2002), Specialization in Clinical Microbiology from Universidade de São Paulo, USP (2007) and PhD in Sciences in Gastroenterology and Hepatology (2012). She is currently an Adjunct Professor at Feevale University in Medicine and Biomedicine courses and a permanent professor of the Academic Master\\'s Degree in Virology. She has experience in the field of Microbiology, with an emphasis on Bacteriology, working mainly on the following topics: bacteriophages, bacterial resistance, clinical microbiology and food microbiology.",institutionString:null,institution:{name:"Universidade Feevale",country:{name:"Brazil"}}},{id:"229220",title:"Dr.",name:"Amjad",middleName:"Islam",surname:"Aqib",slug:"amjad-aqib",fullName:"Amjad Aqib",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/229220/images/system/229220.png",biography:"Dr. Amjad Islam Aqib obtained a DVM and MSc (Hons) from University of Agriculture Faisalabad (UAF), Pakistan, and a PhD from the University of Veterinary and Animal Sciences Lahore, Pakistan. Dr. Aqib joined the Department of Clinical Medicine and Surgery at UAF for one year as an assistant professor where he developed a research laboratory designated for pathogenic bacteria. Since 2018, he has been Assistant Professor/Officer in-charge, Department of Medicine, Manager Research Operations and Development-ORIC, and President One Health Club at Cholistan University of Veterinary and Animal Sciences, Bahawalpur, Pakistan. He has nearly 100 publications to his credit. His research interests include epidemiological patterns and molecular analysis of antimicrobial resistance and modulation and vaccine development against animal pathogens of public health concern.",institutionString:"Cholistan University of Veterinary and Animal Sciences",institution:null},{id:"62900",title:"Prof.",name:"Fethi",middleName:null,surname:"Derbel",slug:"fethi-derbel",fullName:"Fethi Derbel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/62900/images/system/62900.jpeg",biography:"Professor Fethi Derbel was born in 1960 in Tunisia. He received his medical degree from the Sousse Faculty of Medicine at Sousse, University of Sousse, Tunisia. He completed his surgical residency in General Surgery at the University Hospital Farhat Hached of Sousse and was a member of the Unit of Liver Transplantation in the University of Rennes, France. He then worked in the Department of Surgery at the Sahloul University Hospital in Sousse. Professor Derbel is presently working at the Clinique les Oliviers, Sousse, Tunisia. His hospital activities are mostly concerned with laparoscopic, colorectal, pancreatic, hepatobiliary, and gastric surgery. He is also very interested in hernia surgery and performs ventral hernia repairs and inguinal hernia repairs. He has been a member of the GREPA and Tunisian Hernia Society (THS). During his residency, he managed patients suffering from diabetic foot, and he was very interested in this pathology. For this reason, he decided to coordinate a book project dealing with the diabetic foot. Professor Derbel has published many articles in journals and collaborates intensively with IntechOpen Access Publisher as an editor.",institutionString:"Clinique les Oliviers",institution:null},{id:"300144",title:"Dr.",name:"Meriem",middleName:null,surname:"Braiki",slug:"meriem-braiki",fullName:"Meriem Braiki",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/300144/images/system/300144.jpg",biography:"Dr. Meriem Braiki is a specialist in pediatric surgeon from Tunisia. She was born in 1985. She received her medical degree from the University of Medicine at Sousse, Tunisia. She achieved her surgical residency training periods in Pediatric Surgery departments at University Hospitals in Monastir, Tunis and France.\r\nShe is currently working at the Pediatric surgery department, Sidi Bouzid Hospital, Tunisia. Her hospital activities are mostly concerned with laparoscopic, parietal, urological and digestive surgery. She has published several articles in diffrent journals.",institutionString:"Sidi Bouzid Regional Hospital",institution:null},{id:"229481",title:"Dr.",name:"Erika M.",middleName:"Martins",surname:"de Carvalho",slug:"erika-m.-de-carvalho",fullName:"Erika M. de Carvalho",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/229481/images/6397_n.jpg",biography:null,institutionString:null,institution:{name:"Oswaldo Cruz Foundation",country:{name:"Brazil"}}},{id:"186537",title:"Prof.",name:"Tonay",middleName:null,surname:"Inceboz",slug:"tonay-inceboz",fullName:"Tonay Inceboz",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/186537/images/system/186537.jfif",biography:"I was graduated from Ege University of Medical Faculty (Turkey) in 1988 and completed his Med. PhD degree in Medical Parasitology at the same university. I became an Associate Professor in 2008 and Professor in 2014. I am currently working as a Professor at the Department of Medical Parasitology at Dokuz Eylul University, Izmir, Turkey.\n\nI have given many lectures, presentations in different academic meetings. I have more than 60 articles in peer-reviewed journals, 18 book chapters, 1 book editorship.\n\nMy research interests are Echinococcus granulosus, Echinococcus multilocularis (diagnosis, life cycle, in vitro and in vivo cultivation), and Trichomonas vaginalis (diagnosis, PCR, and in vitro cultivation).",institutionString:"Dokuz Eylül University",institution:{name:"Dokuz Eylül University",country:{name:"Turkey"}}},{id:"71812",title:"Prof.",name:"Hanem Fathy",middleName:"Fathy",surname:"Khater",slug:"hanem-fathy-khater",fullName:"Hanem Fathy Khater",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/71812/images/1167_n.jpg",biography:"Prof. Khater is a Professor of Parasitology at Benha University, Egypt. She studied for her doctoral degree, at the Department of Entomology, College of Agriculture, Food and Natural Resources, University of Missouri, Columbia, USA. She has completed her Ph.D. degrees in Parasitology in Egypt, from where she got the award for “the best scientific Ph.D. dissertation”. She worked at the School of Biological Sciences, Bristol, England, the UK in controlling insects of medical and veterinary importance as a grant from Newton Mosharafa, the British Council. Her research is focused on searching of pesticides against mosquitoes, house flies, lice, green bottle fly, camel nasal botfly, soft and hard ticks, mites, and the diamondback moth as well as control of several parasites using safe and natural materials to avoid drug resistances and environmental contamination.",institutionString:null,institution:{name:"Banha University",country:{name:"Egypt"}}},{id:"99780",title:"Prof.",name:"Omolade",middleName:"Olayinka",surname:"Okwa",slug:"omolade-okwa",fullName:"Omolade Okwa",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/99780/images/system/99780.jpg",biography:"Omolade Olayinka Okwa is presently a Professor of Parasitology at Lagos State University, Nigeria. She has a PhD in Parasitology (1997), an MSc in Cellular Parasitology (1992), and a BSc (Hons) Zoology (1990) all from the University of Ibadan, Nigeria. She teaches parasitology at the undergraduate and postgraduate levels. She was a recipient of a Commonwealth fellowship supported by British Council tenable at the Centre for Entomology and Parasitology (CAEP), Keele University, United Kingdom between 2004 and 2005. She was awarded an Honorary Visiting Research Fellow at the same university from 2005 to 2007. \nShe has been an external examiner to the Department of Veterinary Microbiology and Parasitology, University of Ibadan, MSc programme between 2010 and 2012. She is a member of the Nigerian Society of Experimental Biology (NISEB), Parasitology and Public Health Society of Nigeria (PPSN), Science Association of Nigeria (SAN), Zoological Society of Nigeria (ZSN), and is Vice Chairperson of the Organisation of Women in Science (OWSG), LASU chapter. She served as Head of Department of Zoology and Environmental Biology, Lagos State University from 2007 to 2010 and 2014 to 2016. 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