Comparison of physical and anthropometrical parameters of teen-age male rowers, kayakers, canoers and sedentary school children

Objetivo: Comparar los parámetros antropométricos y físicos de los jóvenes remeros, kayakistas, canoeros y la población de control. Métodos: Nuestro estudio se llevó a cabo en 173 niños (n=53 remeros, edad=16,24±1,51 años; n=38 kayakistas, edad= 17,0±3,99 años; n= 37 canoeros, edad= 15,1±0,53 años; y grupo control, n=45, edad=15,0±0,46). Varios bioparámetros, altura corporal (cm), peso corporal (kg) e (índice de masa corporal) (kg/m2), grosor del pliegue cutáneo (mm) bíceps, tríceps, subescapular, suprailíaco y pantorrilla, diámetros de humorístico y fémur (cm), longitud del brazo (cm), longitud del brazo (cm), longitud de la parte delantera de la pierna (cm), longitud del muslo (cm), longitud del pie (cm), longitud de la parte superior del brazo, longitud del antebrazo (cm), hombro Se midieron la anchura (cm), la longitud del tronco (cm), la circunferencia del muslo y la pantorrilla (cm), el porcentaje de grasa corporal, la fuerza de agarre (derecha e izquierda) de las manos, la flexibilidad del tronco, la fuerza relativa de la espalda, los abdominales y las flexiones.Resultados:La altura corporal (cm) de los remeros masculinos fue mayor que la de los canoeros masculinos y el grupo control (p<0,05). El salto largo de pie (cm) de los remeros masculinos fue significativamente mayor que los kayakistas y el grupo de control (p<0,05). La flexibilidad de los remeros masculinos fue significativamente mayor que la de los piragüistas masculinos y el grupo de control (p<0.0.5). La fuerza relativa de la espalda (kg) de los remeros, kayakistas y canoeros masculinos fue significativamente mayor que la del grupo de control. Sentarse/minuto de los canoeros masculinos fue significativamente mayor que los remeros masculinos (p<0,01) y los kayakistas (p<0,05). El empuje hacia arriba/minuto de los canoistas masculinos se observó significativamente más alto que el grupo de control (p <0,01) y los kayakistas y remeros (p <0,05). La envergadura de los brazos de los remeros fue significativamente mayor que la del grupo control (p<0,01) y la de los kayakistas y canoeros (p<0,05). La longitud del antebrazo (cm) de los remeros masculinos fue significativamente mayor que la del grupo de control (p<0,01). También se encontró más alto en kayakistas y canoeros masculinos que en el grupo de control (p<0.05).Conclusión:Nuestros atletas tienen una diferencia significativa en algunos parámetros ya que están bien entrenados y el grupo de control no tiene entrenamiento previo en absoluto.Aim: It is to compare anthropometrical and physical parameters of teen-aged young male rowers, kayakers, canoers and control population. Methods: Our study was carried on 173 children (n=53 rowers, age=16.24±1.51 years; n=38 kayakers, age= 17.0±3.99 years; n= 37 canoers, age= 15.1±0.53 years; and control group, n=45, age=15.0±0.46). Several bio-parameters, body height (cm), body weight (kg) and (body mass index) (kg/m2), skin fold thickness (mm)  biceps, triceps, sub-scapula, supra-illiac and calf, diameters of humorous and femur (cm), arm length (cm), arm span (cm), fore leg length (cm), thigh length (cm), foot length (cm), upper arm length, fore arm length (cm), shoulder breadth (cm), trunk length (cm), thigh and calf girth (cm), body fat percentage, the grip strength (right and left ) hands, trunk flexibility, relative back strength, sit up, push up  were measured. Results: Body height (cm) of male rowers was higher than male canoers and control group (p<0.05). Standing broad jump (cm) of male rowers was significantly higher than kayakers and control group (p<0.05). Flexibility of male rowers was significantly higher than male canoers and control group (p<0.0.5). Relative back strength (kg) of male rowers, kayakers and canoers was significantly higher than control group. Sit up /minute of male canoers was significantly higher than both male rowers (p<0.01) and kayakers (p<0.05). Push up/minute of male canoers was noted higher significantly than control group (p<0.01) and kayakers and rower (p<0.05). The arm span of rowers was significantly higher than control group (p<0.01) and kayakers and canoers (p<0.05). Fore arm length (cm) of male rowers was significantly higher than control group (p<0.01). It was also found higher in male kayakers and canoers than control group (p<0.05). Conclusion: Our athletes have significant difference in some parameters as they are well trained and the control group has no such previous training at all

Influence Of Systematic Training On Morpho-Physiological And Motor Ability Profiles Of Indian Young Female Rowers, Kayakers And Canoers

International Journal of Exercise Science 16(6): 744-755, 2023. Our study was carried on junior female athletes (22 rowers, 11 kayakers and 7 canoers) adopting systemic training to explore the possible training manipulation that can be implicated in these three kinds of water sports, might be in a different way. Several morpho-physiological parameters and motor ability profiles were measured by standard methods. Accordingly, body weight (kg), performing time of 2.4 km run (sec), 6×10 meters shuttle run/agility (sec) of female rowers were reduced progressively and significantly from Preparatory Period (PP1) to General Practice Period (GPP) i.e., from (59.41±4.84) to (52.23±5.34), (773.04±92.64) to (566.19±80.84) and (17.91±0.96) to (14.79±0.6) respectively. In case of kayakers, the time to cover 6×10 meters shuttle run was decreased from (18.42±0.63) to (16.61±0.79) and standing vertical jump (cm) was increased from (24.64±4.65) to (38.18±5.65) significantly from initial PPI to final GPP with considerable changes in between the phases. Body weight (kg), performing time of 60 meters standing start (sec), 2.4 km run (sec) and 6×10 meters shuttle run of female canoers were found to be decreased maximally from PP1 to GPP, following eight successive training phases from (58.56±3.98) to (49.88±4.39), (10.96±0.42) to (9.35±0.29), (802.57±32.40) to (632.57±57.38) and (10.96±0.42) to (9.35±0.29) respectively and also decreased considerably between other training phases. Standing broad jump (cm), standing vertical jump (cm), sit up/min, and push up/min performance were also found to be increased maximally from PP1 to GPP i.e., from (180.71±9.01) to (252.12±7.76), (27±4.16) to (41.14±1.86), (43±7.72) to (96±15.13) and from (34.43±7.50) to (88.28±4.85) respectively and also considerably between other training phases. Training as designed and incorporated in the present study significantly improves motor ability in all three groups. More discrete training can be prescribed for better fitness

Anti-tumor effect of fruit rind of Myristica malabarica in an Ehrlich ascites carcinoma model

Background: Among the various modalities of anti-cancer treatment, cancer chemotherapy plays a very vital role. The alarming side effects being its main drawback leads to relentless research for newer agents. A new natural agent with promising anti-cancer properties from in-vitro studies leads to this study. Here we have evaluated the anti-tumor activity of a crude extract of fruit rind of Myristica malabarica in an Ehrlich ascites carcinoma model in mice.Methods: A murine model of cancer was established with i.p. inoculation of Ehrlich Ascites carcinoma (EAC) cells; animals were divided into five groups (including normal control) to observe the inhibitory effect of a crude extract of the fruit rind of Myristica malabarica/rampatri (0-100mg/kg b.w. i.p.) as compared with methotrexate (0.4mg/kg bw., i.p.). Blood and ascitic fluid were collected on the 10th day for analysis.Results: In the EAC model, there was an increase in tumor volume, tumor weight, and tumor packed cell volume, which was decreased by rampatri (50 and 100mg/kg bw) along with an increase in the mean survival time (MST). Rampatri caused minimal alterations in hematological parameters, renal functions remained unchanged but an increase in hepatic SGOT was demonstrated.Conclusions: The crude extract of rampatri (containing Malabaricones) exhibited significant anti-tumor activity with minimal effect on hematological and renal functions

Effectiveness of malabaricone-A in P-glycoprotein over-expressing cancer cell lines

Background: A major impediment in treatment for cancers is resistance to chemotherapy and is primarily attributed to over-expression of efflux pumps. This study aimed to establish the cytotoxicity of malabaricone-A (MAL-A) in P-glycoprotein/multidrug resistance (P-gp/MDR) over-expressing hematopoietic cancer cell lines.Methods: Leukemia and multiple myeloma cell lines were indirectly evaluated for their P-gp/MDR status by examining Calcein-AM fluorescence and cell viability was assessed by the MTS-PMS assay.Results: The fluorescence of calcein was significantly decreased in three cell lines LP-1, RPMI-8226 and CEM-ADR 5000 and reversal with verapamil endorsed their P-gp/MDR activity. The mean IC50 of MAL-A in these MDR+ cell lines (5.40±1.41 to 12.33±0.78 µg/ml) was comparable with the MDR- leukemic (9.72±1.08 to 19.26±0.75 µg/ml) and multiple myeloma cell lines (9.65±0.39 to 18.05±0.17 μg/ml).Conclusions: Irrespective of their P-gp activity, the cytotoxicity of MAL-A was comparable, making it worthy of future pharmacological consideration in multidrug resistance

Malabaricone-A Induces A Redox Imbalance That Mediates Apoptosis in U937 Cell Line

BACKGROUND: The 'two-faced' character of reactive oxygen species (ROS) plays an important role in cancer biology by acting both as secondary messengers in intracellular signaling cascades and sustaining the oncogenic phenotype of cancer cells, while on the other hand, it triggers an oxidative assault that causes a redox imbalance translating into an apoptotic cell death. PRINCIPAL FINDINGS: Using a tetrazolium [{3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl}-2H-tetrazolium] based cell viability assay, we evaluated the cytotoxicity of a plant derived diarylnonanoid, malabaricone-A on leukemic cell lines U937 and MOLT-3. This cytotoxicity hinged on its ability to cause a redox imbalance via its ability to increase ROS, measured by flow cytometry using 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate and by decreasing glutathione peroxidase activity. This redox imbalance mediated apoptosis was evident by an increase in cytosolic [Ca(2+)], externalization of phosphatidyl serine as also depolarization of the mitochondrial membrane potential as measured by flow cytometry. There was concomitant peroxidation of cardiolipin, release of free cytochrome c to cytosol along with activation of caspases 9, 8 and 3. This led to cleavage of the DNA repair enzyme, poly (ADP-ribose) polymerase that caused DNA damage as proved by labeling with 4',6-diamidino-2-phenylindole (DAPI); furthermore, terminal deoxy ribonucleotide transferase catalysed incorporation of deoxy uridine triphosphate confirmed DNA nicking and was accompanied by arrest of cell cycle progression. CONCLUSIONS: Taken together, compounds like MAL-A having pro-oxidant activity mediate their cytotoxicity in leukemic cells via induction of oxidative stress triggering a caspase dependent apoptosis

Influence of polymorphisms in TNF-α and IL1β on susceptibility to alcohol induced liver diseases and therapeutic potential of miR-124-3p impeding TNF-α/IL1β mediated multi-cellular signaling in liver microenvironment

Background and aimsAlcoholic liver disease (ALD) is the leading cause of the liver cirrhosis related death worldwide. Excessive alcohol consumption resulting enhanced gut permeability which trigger sensitization of inflammatory cells to bacterial endotoxins and induces secretion of cytokines, chemokines leading to activation of stellate cells, neutrophil infiltration and hepatocyte injury followed by steatohepatitis, fibrosis and cirrhosis. But all chronic alcoholics are not susceptible to ALD. This study investigated the causes of differential immune responses among ALD patients and alcoholic controls (ALC) to identify genetic risk factors and assessed the therapeutic potential of a microRNA, miR-124-3p.Materials and methodsBio-Plex Pro™ Human Chemokine analysis/qRT-PCR array was used for identification of deregulated immune genes. Sequencing/luciferase assay/ELISA detected and confirmed the polymorphisms. THP1 co-cultured with HepG2/LX2/HUVEC and apoptosis assay/qRT-PCR/neutrophil migration assay were employed as required.ResultsThe combined data analysis of the GSE143318/Bio-Plex Pro™ Human Chemokine array and qRT-PCR array revealed that six genes (TNFα/IL1β/IL8/MCP1/IL6/TGFβ) were commonly overexpressed in both serum/liver tissue of ALD-patients compared to ALC. The promoter sequence analysis of these 6 genes among ALD (n=322)/ALC (n=168) samples revealed that only two SNPs, rs361525(G/A) at -238 in TNF-α/rs1143627(C/T) at -31 in IL1β were independently associated with ALD respectively. To evaluate the functional implication of these SNPs on ALD development, the serum level of TNF-α/IL1β was verified and observed significantly higher in ALD patients with risk genotypes TNF-α-238GA/IL1β-31CT+TT than TNF-α-238GG/IL1β-31CC. The TNF-α/IL1β promoter Luciferase-reporter assays showed significantly elevated level of luciferase activities with risk genotypes -238AA/-31TT than -238GG/-31CC respectively. Furthermore, treatment of conditioned medium of TNF-α/IL1β over-expressed THP1 cells to HepG2/LX2/HUVEC cells independently showed enhanced level of ER stress and apoptosis in HepG2/increased TGFβ and collagen-I production by LX2/huge neutrophil infiltration through endothelial layer. However, restoration of miR-124-3p in THP1 attenuated such inter-cellular communications and hepatocyte damage/collagen production/neutrophil infiltration were prohibited. Target analysis/luciferase-reporter assays revealed that both TNF-α/IL1β were inhibited by miR-124-3p along with multiple genes from TLR4 signaling/apoptosis/fibrogenesis pathways including MYD88, TRAF3/TRADD, Caspase8/PDGFRA, TGFβR2/MCP1, and ICAM1 respectively.ConclusionThus, rs361525(G/A) in TNF-α and rs1143627(C/T) in IL1β gene may be used as early predictors of ALD susceptibility among East Indian population. Impeding overexpressed TNF-α/IL1β and various genes from associated immune response pathways, miR-124-3p exhibits robust therapeutic potential for ALD patients

Berberine Chloride Mediates Its Anti-Leishmanial Activity via Differential Regulation of the Mitogen Activated Protein Kinase Pathway in Macrophages

BACKGROUND: A complex interplay between Leishmania and macrophages influences parasite survival and necessitates disruption of signaling molecules, eventually resulting in impairment of macrophage function. In this study, we demonstrate the immunomodulatory activity of Berberine chloride in Leishmania infected macrophages. PRINCIPAL FINDINGS: The IC(50) of Berberine chloride, a quaternary isoquinoline alkaloid was tested in an amastigote macrophage model and its safety index measured by a cell viability assay. It eliminated intracellular amastigotes, the IC(50) being 2.8 fold lower than its IC(50) in promastigotes (7.10 µM vs. 2.54 µM) and showed a safety index >16. Levels of intracellular and extracellular nitric oxide (NO) as measured by flow cytometry and Griess assay respectively showed that Berberine chloride in Leishmania infected macrophages increased production of NO. Measurement of the mRNA expression of iNOS, IL-12 and IL-10 by RT-PCR along with levels of IL-12p40 and IL-10 by ELISA showed that in infected macrophages, Berberine chloride enhanced expression of iNOS and IL-12p40, concomitant with a downregulation of IL-10. The phosphorylation status of extracellular signal related kinase (ERK1/2) and p38 mitogen activated protein kinase (p38 MAPK) was studied by western blotting. In infected macrophages, Berberine chloride caused a time dependent activation of p38 MAPK along with deactivation of ERK1/2; addition of a p38 MAPK inhibitor SB203580 inhibited the increased generation of NO and IL-12p40 by Berberine chloride as also prevented its decrease of IL-10. CONCLUSIONS: Berberine chloride modulated macrophage effector responses via the mitogen activated protein kinase (MAPK) pathway, highlighting the importance of MAPKs as an antiparasite target

Generation of redox imbalance mediates the cytotoxic effectof Malabaricone-A in a multidrug resistant cell line

Multidrug resistance (MDR) refers to cross-resistance to a range of structurally and functionally unrelated compounds, and is accompanied by an elevated expression of ATP driven cell-membrane transporters. The cytotoxicity of Malabaricone-A (MAL-A), a diarylnonanoid derived from Myristica malabarica was demonstrated in leukemic cell lines, but its effectiveness in drug-resistant cancer cell lines has not been evaluated. Accordingly, this study tested its cytotoxic potential in a T-lymphoblastic leukemic cell line, CCRF CEM and its MDR counterpart, CEM/ADR5000. The effectiveness of MAL-A was 1.8 fold higher in CEM/ADR5000 than CCRF CEM cell line, the IC50 being value 5.40 ± 1.41 vs. 9.72 ± 1.08 µg/ml, respectively, suggesting that MAL-A demonstrated ‘collateral sensitivity’. This cytotoxicity of MAL-A was attributed to an enhanced generation of oxidative stress, as the IC50 value increased following the addition of an anti-oxidant, N-acetyl cysteine (NAC). Furthermore, MAL-A depleted glutathione and inhibited glutathione peroxidase activity, which too contributed towards generation of a redox imbalance. This culminated in an apoptosis mediated cell death as evident by mitochondrial membrane depolarization, enhanced caspase-3 activity, increased externalization of phosphatidylserine and an increase in the sub G0/G1 population. Collectively, compounds with pro-oxidant activity have promising therapeutic potential in drug resistant phenotypes, worthy of future pharmacological consideration

The variable chemotherapeutic response of Malabaricone-A in leukemic and solid tumor cell lines depends on the degree of redox imbalance

Purpose: The ‘two-faced’ character of reactive oxygen species (ROS) plays an important role in cancer biology by acting as secondary messengers in intracellular signaling cascades, enhancing cell proliferation and survival, thereby sustaining the oncogenic phenotype. Conversely, enhanced generation of ROS can trigger an oxidative assault leading to a redox imbalance translating into an apoptotic cell death. Intrinsically, cancer cells have higher basal levels of ROS which if supplemented by additional oxidative insult by pro-oxidants can be cytotoxic, an example being Malabaricone-A (MAL-A). MAL-A is a plant derived diarylnonanoid, purified from fruit rind of the plant Myristica malabarica whose anti-cancer activity has been demonstrated in leukemic cell lines, the modality of cell death being apoptosis. This study aimed to compare the degree of effectiveness of MAL-A in leukemic vs. solid tumor cell lines.Methods: The cytotoxicity of MAL-A was evaluated by the MTS-PMS cell viability assay in leukemic cell lines (MOLT3, K562 and HL-60) and compared with solid tumor cell lines (MCF7, A549 and HepG2); further studies then proceeded with MOLT3 vs. MCF7 and A549. The contribution of redox imbalance in MAL-A induced cytotoxicity was confirmed by pre-incubating cells with an antioxidant, N-acetyl-l-cysteine (NAC) or a thiol depletor, buthionine sulfoximine (BSO). MAL-A induced redox imbalance was quantitated by flow cytometry, by measuring the generation of ROS and levels of non protein thiols using dichlorofluorescein diacetate (CM-H2DCFDA) and 5-chloromethylfluorescein diacetate (CMFDA) respectively. The activities of glutathione peroxidase (GPx), superoxide dismutase, catalase (CAT), NAD(P)H dehydrogenase (quinone 1) NQO1 and glutathione-S-transferase GST were measured spectrophotometrically. The mitochondrial involvement of MAL-A induced cell death was measured by evaluation of cardiolipin peroxidation using 10-N-nonyl acridine orange (NAO), transition pore activity with calcein-AM, while the mitochondrial transmembrane electrochemical gradient (∆ψm) was measured by JC-1, fluorescence being acquired in a flow cytometer. The apoptotic mode of cell death was evaluated by double staining with annexin V-FITC and propidium iodide (PI), cell cycle analysis by flow cytometry and caspase-3 activity spectrophotometrically. The expression of Nrf2 and HO-1 was examined by western blotting. Results: MAL-A demonstrated a higher degree of cytotoxicity in three leukemic cell lines whose IC50 ranged from 12.70 ± 0.10 to 18.10 ± 0.95 µg/ml, whereas in three solid tumor cell lines, the IC50 ranged from 28.10 ± 0.58 to 55.26 ± 5.90 µg/ml. This higher degree of cytotoxicity in MOLT3, a leukemic cell line was due to a higher induction of redox imbalance, evident by both an increased generation of ROS and concomitant depletion of thiols. This was confirmed by pre-incubation with NAC and BSO, wherein NAC decreased MAL-A induced cytotoxicity by 2.04 fold while BSO enhanced MAL-A cytotoxicity and decreased the IC50 by 5.60 fold. However, in solid tumor cell lines (MCF7 and A549), NAC minimally decreased MAL-A induced cytotoxicity, and BSO increased the IC50 by 1.96 and 2.39 fold respectively. Furthermore, the generation of ROS by MAL-A increased maximally in MOLT3 as the fluorescence increased from 44.28 ± 7.85 to 273.99 ± 32.78, and to a lesser degree in solid tumor cell lines, MCF7 (44.28 ± 14.89 to 207.97 ± 70.64) and A549 (37.87 ± 3.24 to 147.12 ± 38.53). In all three cell lines there was a concomitant depletion of thiols as in MOLT3, the GMFC decreased from 340.65 ± 60.39 to 62.67 ± 11.32, in MCF7 (277.82 ± 50.32 to 100.39 ± 31.93) and in A549 (274.05 ± 59.13 to 83.15 ± 21.43). In MOLT3 as compared to MCF7 and A549, decrease in the activities of GPx, CAT, NQO1 and GST was substantially greater. In all cell lines, the MAL-A induced redox imbalance translated into triggering of initial mitochondrial apoptotic events. Here again, MAL-A induced a higher degree of cardiolipin peroxidation in MOLT3 (67.01%) than MCF7 and A549 (29.15% and 44.30%), as also down regulated the mitochondrial transition pore activity from baseline to a higher extent, GMFC being 48.05 ± 2.37 to 10.70 ± 3.97 (MOLT3), 43.55 ± 3.36 to 15.36 ± 0.60 (MCF7) and 39.58 ± 0.4 to 12.65 ± 1.56 (A549). Perturbation of mitochondrial membrane potential evident by a decrease in the ratio of red/green (J-aggregates/monomers) was 134 fold (14.73/0.11) in MOLT3, 45 fold in MCF7 (20.72/0.46) and 34 fold in A549 (22.01/0.64). The extent of apoptosis using a similar concentration of MAL-A was maximal in MOLT3, wherein a 105 fold increase in annexin V binding was evident (0.83 ± 0.51 to 87.08 ± 9.85%) whereas it increased by 43.11 fold in MCF7 (0.69 ± 0.30 to 29.75 ± 11.79%) and 47.52 fold in A549 (0.61 ± 0.31 to 28.99 ± 17.21%). MAL-A induced apoptosis was also associated with a higher degree of caspase-3 activity in MOLT3 vs. MCF7 or A549 which translated into halting of cell cycle progression, evident by an increment in the sub-G0/G1 population [19.26 fold in MOLT3 (0.95 ± 0.45 vs. 18.30 ± 1.90%), 11.01 fold in MCF7 (0.97 ± 0.37 vs. 10.68 ± 0.69%) and 8.58 fold in A549 (1.06 ± 0.45 vs. 9.10 ± 1.05%)]. MAL-A effectively inhibited Nrf2 and HO-1, more prominently in MOLT3. Furthermore, the decreased expression of Nrf2 in MOLT3 correlated with the decreased activities of NQO1 and GST, suggesting that targeting of the Nrf2 anti-oxidant pathway could be considered. Conclusion: Taken together, MAL-A a pro-oxidant compound is likely to be more effective in leukemias, meriting further pharmacological consideration