Background and Objectives In designing a resistance exercise program, intensity, rest, and exercise volume are important. Many studies have been conducted to find the most suitable resistance exercise program incorporating the above, and in particular, many prior studies have been conducted on intensity. This study attempted to determine the effective volume of exercise by analyzing the number of repetitions performed at intensities of 65% one-repetition maximum (1RM) and 75% 1RM during the bench press exercise, and the electromyography (EMG) response of the agonist muscle. Materials and Methods Eight males in their 20s were selected as study subjects and they performed five sets of bench presses at two levels of intensity (65% 1RM, 75% 1RM). The following results were obtained by measuring the number of repetitions and the EMG response according to the exercise intensity and sets during the workout. Results First, the number of repetitions showed a sharp drop from the first set to the third set at 65% 1RM intensity and showed no change in the fourth and fifth sets. At 75% 1RM intensity, the intensity of hypertrophy showed a gradual decrease from the first set to the fifth set. Second, at 75% 1RM exercise intensity, the pectoralis major, anterior deltoid and triceps brachii showed high muscle activity, and the activity of the anterior deltoid continued to increase from the first set to the fourth set at 65% 1RM intensity, and from the first set to the fifth set at 75% 1RM. Conclusion It was found that during the bench press exercise, three minutes of rest at 75% 1RM intensity, five sets of five sets, one minute rest at 65% 1RM intensity, and three sets of the exercise were effective.
Emeka, Promise M.;Rasool, Sahibzada T.;Morsy, Mohamed A.;Islam, Mohamed I. Hairul;Chohan, Muhammad S.
The Korean Journal of Physiology and Pharmacology
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v.25
no.4
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pp.321-331
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2021
Vancomycin, an antibiotic used occasionally as a last line of treatment for methicillin-resistant Staphylococcus aureus, is reportedly associated with nephrotoxicity. This study aimed at evaluating the protective effects of lutein against vancomycin-induced acute renal injury. Peroxisome proliferator-activated receptor gamma (PPARγ) and its associated role in renoprotection by lutein was also examined. Male BALB/c mice were divided into six treatment groups: control with normal saline, lutein (200 mg/kg), vancomycin (250 mg/kg), vancomycin (500 mg/kg), vancomycin (250 mg/kg) with lutein, and vancomycin (500 mg/kg) with lutein groups; they were euthanized after 7 days of treatment. Thereafter, samples of blood, urine, and kidney tissue of the mice were analyzed, followed by the determination of levels of N-acetyl-β-D-glucosaminidase (NAG) in the urine, renal creatine kinase; protein carbonyl, malondialdehyde, and caspase-3 in the kidney; and the expression of PPARγ, nuclear factor erythroid 2-related factor 2 (Nrf2), and nuclear factor-kappaB (NF-κB) in renal tissue. Results showed that the levels of protein carbonyl and malondialdehyde, and the activity of NAG, creatine kinase and caspase-3, were significantly increased in the vancomycin-treatment groups. Moreover, the levels of Nrf2 significantly decreased, while NF-κB expression increased. Lutein ameliorated these effects, and significantly increased PPARγ expression. Furthermore, it attenuated vancomycin-induced histological alterations such as, tissue necrosis and hypertrophy. Therefore, we conclude that lutein protects against vancomycin-induced renal injury by potentially upregulating PPARγ/Nrf2 expression in the renal tissues, and consequently downregulating the pathways: inflammation by NF-κB and apoptosis by caspase-3.
BACKGROUND/OBJECTIVES: Patients with chronic kidney disease (CKD) have a high concentration of uremic toxins in their blood and often experience muscle atrophy. Indoxyl sulfate (IS) is a uremic toxin produced by tryptophan metabolism. Although an elevated IS level may induce muscle dysfunction, the effect of IS on physiological concentration has not been elucidated. Additionally, the effects of ursolic acid (UA) on muscle hypertrophy have been reported in healthy models; however, it is unclear whether UA ameliorates muscle dysfunction associated with chronic diseases, such as CKD. Thus, this study aimed to investigate whether UA can improve the IS-induced impairment of mitochondrial biogenesis. MATERIALS/METHODS: C2C12 cells were incubated with or without IS (0.1 mM) and UA (1 or 2 μM) to elucidate the physiological effect of UA on CKD-related mitochondrial dysfunction and its related mechanisms using real-time reverse transcription-polymerase chain reaction, western blotting and enzyme-linked immunosorbent assay. RESULTS: IS suppressed the expression of differentiation marker genes without decreasing cell viability. IS decreased the mitochondrial DNA copy number and ATP levels by downregulating the genes pertaining to mitochondrial biogenesis (Ppargc1a, Nrf1, Tfam, Sirt1, and Mef2c), fusion (Mfn1 and Mfn2), oxidative phosphorylation (Cycs and Atp5b), and fatty acid oxidation (Pdk4, Acadm, Cpt1b, and Cd36). Furthermore, IS increased the intracellular mRNA and secretory protein levels of interleukin (IL)-6. Finally, UA ameliorated the IS-induced impairment in C2C12 cells. CONCLUSIONS: Our results indicated that UA improves the IS-induced impairment of mitochondrial biogenesis by affecting differentiation, ATP levels, and IL-6 secretion in C2C12 cells. Therefore, UA could be a novel therapeutic agent for CKD-induced muscle dysfunction.
Objectives : This study was conduct to compare of histological changes on four target organs which related with diabetes in streptozotocin-induced diabetic rats. Methods : Diabetes was induced in male Sprague-Dawley rats by consecutive injection of streptozotocin (STZ) at different doses of 30, 40 and 50 mg/kg for 5 days. After 4 weeks, all rats were sacrificed, five different organs such as pancreas, liver, kidney, and lung were isolated and observed their histological changes by hematoxylin and eosin (H&E), Periodic acid-Schiff (PAS) and Masson's trichrome staining. The changes of body weight, blood glucose, and food and water intake were also measured. Results : The multiple administration of STZ was induced diabetes in rats with hyperglycemia, decrease of body weight, increase water and food intake, and histopathological changes of target organs, compared with those of normal rats in both dose-dependent and time-dependent manner. In histological analysis, pancreas was showed decrease of the islet numbers with beta-cell loss. Kidney showed morphological damage with glomerulus hypertrophy, and also lung was showed bronchial epithelial damage with inflammatory cells infiltration. In liver, the portal vein and hepatic artery could not observed, and showed inflammatory cell infiltration with liver fibrosis. Conclusions : These results suggest that the increase of the capacity of STZ, each of the more chronic disease, it can be seen that the damage was deep. Thus, evaluate the resulting drug appropriate depending on the purpose of the model is expected to be selected.
[Purpose] Milk is a commonly ingested post-exercise recovery protein source. Casein protein, found in milk, is characterized by its slow digestion and absorption. Recently, several studies have been conducted with a focus on how pre-sleep casein protein intake could affect post-exercise recovery but our knowledge of the subject remains limited. This review aimed at presenting and discussing how pre-sleep casein protein ingestion affects post-exercise recovery and the details of its potential effector mechanisms. [Methods] We systematically reviewed the topics of 1) casein nutritional characteristics, 2) pre-sleep casein protein effects on post-exercise recovery, and 3) potential effector mechanisms of pre-sleep casein protein on post-exercise recovery, based on the currently available published studies on pre-sleep casein protein ingestion. [Results] Studies have shown that pre-sleep casein protein ingestion (timing: 30 minutes before sleep, amount of casein protein ingested: 40-48 g) could help post-exercise recovery and positively affect acute protein metabolism and exercise performance. In addition, studies have suggested that repeated pre-sleep casein protein ingestion for post-exercise recovery over a long period might also result in chronic effects that optimize intramuscular physiological adaptation (muscle strength and muscle hypertrophy). The potential mechanisms of pre-sleep casein protein ingestion that contribute to these effects include the following: 1) significantly increasing plasma amino acid availability during sleep, thereby increasing protein synthesis, inhibiting protein breakdown, and achieving a positive protein balance; and 2) weakening exercise-induced muscle damage or inflammatory responses, causing reduced muscle soreness. Future studies should focus on completely elucidating these potential mechanisms. [Conclusion] In conclusion, post-exercise ingestion of at least 40 g of casein protein, approximately 30 minutes before sleep and after a bout of resistance exercise in the evening, might be an effective nutritional intervention to facilitate muscle recovery.
Age-related macular degeneration (AMD) is one of the leading causes of blindness in elderly individuals. However, the currently used intravitreal injections of anti-vascular endothelial growth factor are invasive, and repetitive injections are also accompanied by a risk of intraocular infection. The pathogenic mechanism of AMD is still not completely understood, but a multifactorial mechanism that combines genetic predisposition and environmental factors, including cellular senescence, has been suggested. Cellular senescence refers to the accumulation of cells that stop dividing due to the presence of free radicals and DNA damage. Characteristics of senescent cells include nuclear hypertrophy, increased levels of cell cycle inhibitors such as p16 and p21, and resistance to apoptosis. Senolytic drugs remove senescent cells by targeting the main characteristics of these cells. One of the senolytic drugs, ABT-263, which inhibits the antiapoptotic functions of Bcl-2 and Bcl-xL, may be a new treatment for AMD patients because it targets senescent retinal pigment epithelium (RPE) cells. We proved that it selectively kills doxorubicin (Dox)-induced senescent ARPE-19 cells by activating apoptosis. By removing senescent cells, the expression of inflammatory cytokines was reduced, and the proliferation of the remaining cells was increased. When ABT-263 was orally administered to the mouse model of senescent RPE cells induced by Dox, we confirmed that senescent RPE cells were selectively removed and retinal degeneration was alleviated. Therefore, we suggest that ABT-263, which removes senescent RPE cells through its senolytic effect, has the potential to be the first orally administered senolytic drug for the treatment of AMD.
Ischemia-reperfusion results in excess reactive oxygen species (ROS) that affect myocardial cell damage. ROS production inhibition is effectively proposed in treating cardiovascular diseases including myocardial hypertrophy. Studies have shown that oxidizing cultured cells in in vitro experiments gradually decreases the permeability of mitochondrial membranes time- and concentration-dependent, resulting in increased mitochondrial membrane damage due to secondary ROS production and cardiolipin loss. However, recent studies have shown that 5-iodo-6-amino-1,2-benzopyrone (INH2BP), an anticancer and antiviral drug, inhibited peroxynitrite-induced cell damage in in vitro and alleviated partial or overall inflammation in animal experiments. Therefore, in this paper, we studied the preventive effect of INH2BP on H9c2 cells derived from mouse heart damaged by oxidative stress using 700 μM of hydrogen peroxide. As a result of oxidative stress to H9c2 cells by hydrogen peroxide whether the treatment of INH2BP or not, hydrogen peroxide caused serious damage in H9c2 cells. These results were confirmed with cell viability and Hoechst 33342 assays. And this damage was through cell death. However, it was confirmed that H9c2 cells pretreated with INH2BP significantly reduced cell death by hydrogen peroxide. In addition, measurements with DCF-DA assay to determine whether ROS is produced in H9c2 cells treated with only hydrogen peroxide produced ROS significantly, but H9c2 cells pretreated with INH2BP significantly reduced ROS production by hydrogen peroxide. Taken together, it is believed that INH2BP can be useful for the prevention and treatment of cardiovascular diseases induced through oxidative stress such as heart damage caused by ischemia/reperfusion.
Kim, Beom-Jun;Lee, Yun-Whan;You, Hi-Jin;Hwang, Na-Hyun;Kim, Deok-Woo
Medical Lasers
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v.8
no.1
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pp.7-12
/
2019
Background and Objectives Skin and soft tissue defects can be treated according to a range of strategies, such as local flap, skin graft, biological dressing, or free flap. On the other hand, free tissue transfer usually leaves a distinct scar with an inconsistency of color or hypertrophy. This problem is highlighted if the defect is located on the face, which could have devastating effects on a patient's psychosocial health. Materials and Methods The authors used an erbium : yttrium-aluminum-garnet (Er:YAG) laser to resurface the free flap skin and match the color with the surrounding facial skin. This study evaluated the effectiveness of laser skin resurfacing on the harmonious color matching of transferred flap. Patients who had undergone laser resurfacing on facial flap skin between January 2014 and December 2018 were reviewed retrospectively. An ablative 2,940-nm fractional Er:YAG laser treatment was delivered to the entire flap skin at 21 J/cm2 with the treatment end-point of pinpoint bleeding. Several months later, the clinical photographs were analyzed. The L*a*b* color co-ordinates of both the flap and surrounding normal skin were measured using Adobe Photoshop. The L*a*b* color difference (ΔE) for the scar and normal surrounding skin were calculated using the following equation: ${\Delta}E=\sqrt{({\Delta}L)^2+({\Delta}a)^2+({\Delta}b)^2}$ Results All five patients were satisfied with the more natural appearance of the flaps. The ΔE values decreased significantly from the pre-treatment mean value of 19.64 to the post-treatment mean value of 11.39 (Wilcoxon signed-rank test, p = 0.043). Conclusion Ablative laser resurfacing can improve the aesthetic outcome of free tissue transfer on the face.
Purpose: Crohn's disease (CD) is a chronic, idiopathic bowel disorder that can progress to partial or complete bowel obstruction. At present, there are no reliable diagnostic tests that can readily distinguish between acute inflammatory, purely fibrotic and mixed inflammatory and fibrotic. Our aim is to study the utility of contrast enhanced ultrasound (CEUS) in combination with shear wave elastography (SWE) to differentiate fibrotic from inflammatory strictures in children with obstructive CD of the terminal ileum. Methods: Twenty-five (19 male) children between 2016-2021 with CD of the terminal ileum were recruited into the study. Among these patients, 22 had CEUS kinetic measurements of tissue perfusion, including wash-in slope (dB/sec), peak intensity (dB), time to peak intensity (sec), area under the curve (AUC) (dB sec), and SWE. In total, 11 patients required surgery due to bowel obstruction. Histopathologic analysis was performed by a pathologist who was blinded to the CEUS and SWE test results. Results: Patients that underwent surgical resection had significantly higher mean area under the curve on CEUS compared to patients responsive to medical therapy (p=0.03). The AUC also correlated with the degree of hypertrophy and the percent fibrosis of the muscularis propria, as determined by histopathologic grading (p<0.01). There was no difference in the mean elastography measurements between these two patient groups. Conclusion: CEUS is a useful radiological technique that can help identify pediatric patients with medically refractory obstructive fibrotic strictures of the terminal ileum that should be considered for early surgical resection.
Ahmed H. Moustafa;Heba F. Pasha;Manar A. Abas;Adel M. Aboregela
Anatomy and Cell Biology
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v.56
no.1
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pp.109-121
/
2023
Thioacetamide (TAA) exposure and hepatitis C virus infection are usually associated with renal dysfunction. Sofosbuvir (SFV) and daclatasvir (DAC) drugs combination has great value in the treatment of hepatitis C. The study aimed to identify the nephrotoxic effects of TAA and to evaluate the ameliorative role of SFV and DAC in this condition. Forty-eight adult male albino rats were divided into eight groups and received saline (control), SFV, DAC, SFV+DAC, TAA, TAA+SFV, TAA+DAC and TAA+SFV+DAC for eight weeks. Kidney and blood samples were retrieved and processed for histological (Hematoxylin and Eosin and Masson's trichrome), immunohistochemical (α-smooth muscle actin), and biochemical analysis (urea, creatinine, total protein, albumin, malondialdehyde, reduced glutathione, superoxide dismutase, and tumor necrosis factor-α). Examination revealed marked destruction of renal tubules on exposure to TAA with either hypertrophy or atrophy of glomeruli, increase in collagen deposition, and wide expression of α-smooth muscle actin. Also, significant disturbance in kidney functions, oxidative stress markers, and tumor necrosis factor-α. Supplementation with either SFV or DAC produced mild improvement in the tissue and laboratory markers. Moreover, the combination of both drugs greatly refined the pathology induced by TAA at the cellular and laboratory levels. However, there are still significant differences when compared to the control. In conclusion, SFV and DAC combination partially but greatly ameliorated the renal damage induced by TAA which might be enhanced with further supplementations to give new hope for those with nephropathy associated with hepatitis.
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