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1.
Clin Transl Med ; 12(1): e663, 2022 01.
Artigo em Inglês | MEDLINE | ID: mdl-35061932

RESUMO

BACKGROUND: The number of patients receiving anaesthesia is increasing, but the impact of general anaesthesia on the patient's immune system remains unclear. The aim of the present study is to investigate dynamics of systemic immune cell responses to anaesthesia during perioperative period at a single-cell solution. METHODS: The peripheral blood mononuclear cells (PBMCs) and clinical phenomes were harvested and recorded 1 day before anaesthesia and operation, just after anaesthesia (0 h), and 24 and 48 h after anaesthesia. Single-cell sequencing of PBMCs was performed with 10× genomics. Subsequently, data analysis was performed with R packages: Seurat, clusterProfiler and CellPhoneDB. RESULTS: We found that the cluster of CD56+ NK cells changed at 0 h and the cluster of monocytes increased at 24 and 48 h after anaesthesia. The characteristic genes of CD56+ NK cells were mainly enriched in the Jak-STAT signalling pathway and in cell adhesion molecules (24 h) and carbon metabolism (48 h). The communication between CD14+ monocytes and other cells decreased substantially 0 and 48 h after operation. The number of plasma cells enriched in protein export in men was substantially higher than that in women, although the total number in patients decreased 24 h after operation. CD14+ monocytes dominated that cell-cell communications appeared in females, while CD8+ NKT cells dominated that cell-cell communications appeared in male. The number of plasma cells increased substantially in patients with major surgical trauma, with enrichments of pentose phosphate pathway. The communications between plasma cells with other cells varied between surgical severities and anaesthetic forms. The intravenous anaesthesia caused major alterations of cell types, including CD14+ monocytes, plasmas cells and MAIT cells, as compared with inhalation anaesthesia. CONCLUSION: We initially reported the roles of perioperative anaesthesia/surgery in temporal phenomes of circulating immune cells at a single-cell solution. Thus, the protection against immune cell changes would benefit the recovery from anaesthesia/surgery.


Assuntos
Anestesia/normas , Leucócitos Mononucleares/citologia , Assistência Perioperatória/estatística & dados numéricos , Adulto , Anestesia/efeitos adversos , Anestesia/estatística & dados numéricos , Antígeno CD56/efeitos dos fármacos , Feminino , Humanos , Leucócitos Mononucleares/classificação , Masculino , Pessoa de Meia-Idade , Assistência Perioperatória/métodos
2.
Int J Sports Med ; 40(12): 803-809, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31476781

RESUMO

The use of injections to treat structural muscle injuries is controversially discussed. In our controlled in vitro study, we investigated the biological impact of Actovegin and Traumeel alone and in combination on primary human skeletal muscle cells. Cells were characterized by immunofluorescence staining for myogenic factor 5 (Myf5) and MyoD, and cultured with or without Actovegin and / or Traumeel. The effects of these agents were assayed by cell viability and gene expression of the specific markers MyoD, Myf5, neural adhesion molecule (NCAM), and CD31. Myotube formation was determined by myosin staining. Neither Actovegin nor Traumeel showed toxic effects or influenced cell viability significantly. High volumes of Actovegin down-regulated gene expression of NCAM after 3 days but had no effect on MyoD, Myf5, and CD31 gene expression. High volumes of Traumeel inhibited MyoD gene expression after 3 days, whereas after 7 days MyoD expression was significantly up-regulated. The combination of both agents did not significantly influence cell viability or gene expression. This is the first study demonstrating that Actovegin and Traumeel potentially modulate human skeletal muscle cells. The relevance of these in vitro findings has to be highlighted in further in vivo studies.


Assuntos
Diferenciação Celular/efeitos dos fármacos , Heme/análogos & derivados , Minerais/farmacologia , Fibras Musculares Esqueléticas/fisiologia , Extratos Vegetais/farmacologia , Adulto , Idoso , Antígeno CD56/efeitos dos fármacos , Antígeno CD56/genética , Sobrevivência Celular , Células Cultivadas , Relação Dose-Resposta a Droga , Regulação para Baixo , Heme/farmacologia , Humanos , Masculino , Pessoa de Meia-Idade , Proteína MyoD/efeitos dos fármacos , Proteína MyoD/genética , Fator Regulador Miogênico 5/efeitos dos fármacos , Fator Regulador Miogênico 5/genética , Molécula-1 de Adesão Celular Endotelial a Plaquetas/efeitos dos fármacos , Molécula-1 de Adesão Celular Endotelial a Plaquetas/genética
3.
Br J Clin Pharmacol ; 82(5): 1333-1342, 2016 11.
Artigo em Inglês | MEDLINE | ID: mdl-27333593

RESUMO

AIM: Daclizumab high yield process (HYP) is a humanized IgG1 monoclonal antibody that binds to the α-subunit of the interleukin-2 receptor and is being developed for treatment of multiple sclerosis (MS). This manuscript characterized the pharmacokinetic-pharmacodynamic (PK-PD) relationships of daclizumab HYP in subjects with MS. METHODS: Approximately 1400 subjects and 7000 PD measurements for each of three biomarkers [CD25 occupancy, CD56bright natural killer (NK) cell count, regulatory T cell (Treg) count] from four clinical trials were analyzed using non-linear mixed effects modelling. Evaluated regimens included 150 or 300 mg subcutaneous (s.c.) every 4 weeks. RESULTS: CD25 occupancy was characterized using a sigmoidal maximum response (Emax ) model. Upon daclizumab HYP treatment, CD25 saturation was rapid with complete saturation occurring after approximately 7 h and maintained when daclizumab HYP serum concentration was ≥5 mg l-1 . After the last 150 mg s.c. dose, unoccupied CD25 returned to baseline levels in approximately 24 weeks, with daclizumab HYP serum concentration approximately ≤1 mgl-1 1L. CD56bright NK cell expansion was characterized using an indirect response model. Following daclizumab HYP 150 mg s.c. every 4 weeks, expansion plateaus approximately at week 36, at which the average maximum expansion ratio is 5.2. After the last dose, CD56bright NK cells gradually declined to baseline levels within 24 weeks. Treg reduction was characterized by a sigmoidal Emax model. Average maximum reduction of 60% occurred approximately 4 days post 150 mg s.c. dose. After the last dose, Tregs were projected to return to baseline levels in approximately 20 weeks. CONCLUSIONS: Robust PK-PD models of CD25 occupancy, CD56bright NK cell expansion and Treg reduction by daclizumab HYP were developed to characterize its key pharmacodynamic effects in the target patient population.


Assuntos
Anticorpos Monoclonais Humanizados/farmacologia , Anticorpos Monoclonais Humanizados/farmacocinética , Antígeno CD56/efeitos dos fármacos , Subunidade alfa de Receptor de Interleucina-2/efeitos dos fármacos , Células Matadoras Naturais/efeitos dos fármacos , Esclerose Múltipla/sangue , Linfócitos T Reguladores/efeitos dos fármacos , Anticorpos Monoclonais Humanizados/sangue , Ensaios Clínicos como Assunto , Daclizumabe , Humanos , Células Matadoras Naturais/citologia , Contagem de Linfócitos , Dinâmica não Linear , Linfócitos T Reguladores/citologia
4.
Braz J Infect Dis ; 14(4): 398-405, 2010.
Artigo em Inglês | MEDLINE | ID: mdl-20963327

RESUMO

Natural killer cells can be divided into five subpopulations based on the relative expression of CD16 and CD56 markers. The majority of natural killer cells are CD56(dim), which are considered to be the main cytotoxic effectors. A minority of the natural killer cells are CD56(bright), and function as an important source of immune-regulatory cytokines. Shifts of these subsets have been reported in patients with chronic hepatitis C virus infection. We sought to investigate the shift of natural killer subsets among Egyptian patients with chronic HCV and to analyze the influence of interferon therapy on this shift. We applied a flow cytometric analysis of peripheral blood natural killer subsets for 12 interferon-untreated and 12 interferon-treated patients with chronic HCV, in comparison to 10 control subjects. Among interferon-untreated patients, there was a significant reduction of CD56⁻16(+) (immature natural killer) cells. Among interferon-treated patients, the absolute count of natural killer cells was reduced, with expansion of the CD56(bright) subset and reduction of the CD56(dim)16(+) subset. Natural killer subset counts were not significantly correlated to HCV viral load and were not significantly different among interferon responders and non-responders. In conclusion, HCV infection in Egyptian patients has been observed to be statistically and significantly associated with reduction of the CD56⁻16(+)NK subset, while a statistically significant expansion of CD56(bright) and reduction of CD56(dim)16(+) subsets were observed after interferon therapy. Further studies are required to delineate the molecular basis of interferon-induced shift of natural killer subsets among patients with HCV.


Assuntos
Antivirais/uso terapêutico , Antígeno CD56/efeitos dos fármacos , Hepatite C Crônica/tratamento farmacológico , Interferons/uso terapêutico , Células Matadoras Naturais/efeitos dos fármacos , Adulto , Estudos de Casos e Controles , Estudos Transversais , Feminino , Citometria de Fluxo , Humanos , Masculino , Pessoa de Meia-Idade
5.
Neurol Sci ; 28(3): 121-6, 2007 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-17603762

RESUMO

We studied how interferon-beta (IFN-beta) treatment of relapsing-remitting multiple sclerosis (MS) affects subgroups of natural killer cells (NK cells). Following IFN-beta treatment, there was an expansion of CD56(Bright) NK-cells in the peripheral blood of MS patients, while at the same time the proportion of CD56(Dim) cells was diminished. In a control group, the proportion of CD56(Bright) NK-cells was significantly higher in secondary lymphoid tissues compared to the peripheral blood of the same individual. Our findings confirm that CD56(Bright) NK-cells preferably locate within the secondary lymphoid tissues, where they may interact with T cells and thereby contribute to the control of the disease activity in MS.


Assuntos
Antígeno CD56/efeitos dos fármacos , Fatores Imunológicos/uso terapêutico , Interferon beta/uso terapêutico , Células Matadoras Naturais/efeitos dos fármacos , Subpopulações de Linfócitos/efeitos dos fármacos , Esclerose Múltipla Recidivante-Remitente/imunologia , Adulto , Antígeno CD56/imunologia , Antígeno CD56/metabolismo , Feminino , Imunofluorescência , Humanos , Células Matadoras Naturais/imunologia , Células Matadoras Naturais/metabolismo , Subpopulações de Linfócitos/imunologia , Subpopulações de Linfócitos/metabolismo , Masculino , Pessoa de Meia-Idade , Esclerose Múltipla Recidivante-Remitente/sangue , Esclerose Múltipla Recidivante-Remitente/tratamento farmacológico
6.
FASEB J ; 21(10): 2323-34, 2007 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-17431094

RESUMO

Dendritic cells (DCs) and natural killer (NK) cells are essential components of the innate immunity and play a critical role in the first phase of host defense against infection. Interactions between DCs and NK cells have been demonstrated in a variety of settings, with evidence emerging of complex bidirectional crosstalk between the two cell types. The accessory HIV-1 Nef protein is a crucial determinant for viral replication and pathogenesis. We previously demonstrated that Nef, hijacking DC functional activity, subverts the DC arm of immune response to escape the adaptive immune attack. Here, we monitor the effect of Nef on the outcome of the innate immune response, focusing on the impact of Nef on DC/NK crosstalk. We demonstrate that Nef up-regulates the ability of DCs to stimulate the immunoregulatory NK cells (CD56(bright)) as assessed by the activated phenotype, up-regulation of their proliferative response and INF-gamma release. On the other hand, Nef-pulsed DCs inhibit cytotoxic NK cells (CD56(dim)), as assessed by the reduced HLA-DR surface expression, reduced proliferation and cytotoxic activity. Moreover, in the presence of Nef-pulsed DCs, we found a significant up-regulation of TNF-alpha secretion and a significant reduction of IL-10, GM-CSF, MIP-1alpha and RANTES secretion. Our findings suggest that the Nef-induced dysregulation in the DC/NK cell crosstalk may represent a potential mechanism through which HIV escapes innate immune surveillance.


Assuntos
Antígeno CD56/fisiologia , Células Dendríticas/imunologia , Produtos do Gene nef/farmacologia , Células Matadoras Naturais/imunologia , Síndrome da Imunodeficiência Adquirida/imunologia , Antígeno CD56/classificação , Antígeno CD56/efeitos dos fármacos , Divisão Celular , Células Dendríticas/efeitos dos fármacos , Células Dendríticas/virologia , Citometria de Fluxo , Produtos do Gene nef/fisiologia , Fator Estimulador de Colônias de Granulócitos e Macrófagos/metabolismo , Humanos , Interleucina-10/metabolismo , Células Matadoras Naturais/efeitos dos fármacos , Células Matadoras Naturais/virologia , Proteínas Recombinantes/farmacologia , Replicação Viral/fisiologia , Produtos do Gene nef do Vírus da Imunodeficiência Humana
7.
Auris Nasus Larynx ; 31(3): 239-45, 2004 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-15364358

RESUMO

Interleukin-12 (IL-12) plays a critical role in producing an immune response, as indicated in many ways, e.g., induction of interferon-gamma (IFN-gamma), and augmentation of the cytotoxic activity of resting activated T cells and natural killer (NK) cells. In this study, we examined whether intratumoral injection of a recombinant retrovirus vector expressing IL-12s induce antitumor and antiangiogenic effects in a murine model using a murine head and neck squamous cell carcinoma (NR-S1). In vitro the levels of vascular endothelial growth factor (VEGF) mRNA and protein expression were decreased in IL-12 gene transfected NR-S1 cell. in vivo direct IL-12 gene therapy resulted in significantly remarkable inhibition of tumor growth compared to the control group. The tumor regression by direct IL-12 gene therapy was also associated with decreased vessel density, and apoptosis and increased infiltration of CD8(+) T cells and CD56(+) NK cells in the tumor increased. Also, the number of IFN-gamma expressed cells of spleen cells was increased in the treatment group compared with the control group. These results suggested that direct IL-12 gene therapy appears to be effective in reducing tumor growth by triggering both antiangiogenic effects and an immunological enhancing mechanism through induction of IFN-gamma.


Assuntos
Inibidores da Angiogênese/uso terapêutico , Carcinoma de Células Escamosas/terapia , Terapia Genética/métodos , Neoplasias de Cabeça e Pescoço/terapia , Interleucina-12/uso terapêutico , Inibidores da Angiogênese/administração & dosagem , Inibidores da Angiogênese/farmacologia , Animais , Antígeno CD56/efeitos dos fármacos , Antígeno CD56/imunologia , Antígenos CD8/efeitos dos fármacos , Antígenos CD8/imunologia , Carcinoma de Células Escamosas/química , Carcinoma de Células Escamosas/imunologia , Contagem de Células , Linhagem Celular Tumoral , Neoplasias de Cabeça e Pescoço/química , Neoplasias de Cabeça e Pescoço/imunologia , Imuno-Histoquímica , Técnicas In Vitro , Injeções , Interferon gama/imunologia , Interferon gama/metabolismo , Interleucina-12/administração & dosagem , Interleucina-12/farmacologia , Células Matadoras Naturais/metabolismo , Linfócitos do Interstício Tumoral/química , Camundongos , RNA Mensageiro/efeitos dos fármacos , Transfecção/métodos , Fator A de Crescimento do Endotélio Vascular/metabolismo
8.
Psychiatry Res ; 113(1-2): 1-15, 2002 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-12467941

RESUMO

Alterations in immune function are associated with major depression and have been related to changes in endocrine function. We investigated whether alterations in immune function were associated with altered basal hypothalamic-pituitary-adrenal (HPA) function (salivary cortisol) and lymphocyte sensitivity to dexamethasone (DEX) intake (1 mg PO). The latter was explored by comparing the impact of DEX-induced changes on peripheral lymphocyte redistribution and expression of adhesion molecules (beta2 integrins and L-selectin). The study included 36 inpatients with treatment-resistant major depression (unipolar subtype) and 31 matched healthy controls. The dexamethasone suppression test (DST) was carried out and used to classify 10 patients as HPA axis non-suppressors. The latter presented significantly higher post-DEX salivary cortisol levels than DST suppressors, 82.0 vs. 8.9 nM l(-1) h(-1). No differences in basal salivary cortisol levels were found between patients and controls. Changes in cell redistribution (CD4(+), CD8(+), CD19(+), CD56(+) and HLADR(+) cells) after DEX administration were more prominent in controls than in patients, but the effects of DEX varied dependent on whether patients exhibited DEX-induced suppression of cortisol secretion. Glucocorticoid-induced suppression of adhesion molecule expression was also generally less marked in patients than controls. Our data indicate that alterations in immune function and steroid regulation associated with depression are not related to elevated basal levels of cortisol and further suggest that lymphocyte steroid resistance is associated with drug-resistant depression.


Assuntos
Antidepressivos/uso terapêutico , Moléculas de Adesão Celular/efeitos dos fármacos , Moléculas de Adesão Celular/metabolismo , Transtorno Depressivo Maior/tratamento farmacológico , Transtorno Depressivo Maior/metabolismo , Dexametasona/farmacologia , Dexametasona/uso terapêutico , Glucocorticoides/farmacologia , Glucocorticoides/uso terapêutico , Linfócitos T/efeitos dos fármacos , Linfócitos T/metabolismo , Adulto , Idoso , Anticorpos Monoclonais , Antígenos CD19/efeitos dos fármacos , Antígenos CD19/imunologia , Antígenos CD19/metabolismo , Antígenos CD4/efeitos dos fármacos , Antígenos CD4/imunologia , Antígenos CD4/metabolismo , Antígeno CD56/efeitos dos fármacos , Antígeno CD56/imunologia , Antígeno CD56/metabolismo , Antígenos CD8/efeitos dos fármacos , Antígenos CD8/imunologia , Antígenos CD8/metabolismo , Transtorno Depressivo Maior/imunologia , Resistência a Medicamentos , Feminino , Antígenos HLA-DR/efeitos dos fármacos , Antígenos HLA-DR/imunologia , Antígenos HLA-DR/metabolismo , Humanos , Hidrocortisona/análise , Hidrocortisona/metabolismo , Sistema Hipotálamo-Hipofisário/efeitos dos fármacos , Sistema Hipotálamo-Hipofisário/imunologia , Sistema Hipotálamo-Hipofisário/metabolismo , Imunofenotipagem , Masculino , Pessoa de Meia-Idade , Sistema Hipófise-Suprarrenal/efeitos dos fármacos , Sistema Hipófise-Suprarrenal/imunologia , Sistema Hipófise-Suprarrenal/metabolismo , Saliva/química , Linfócitos T/imunologia
9.
Biol Trace Elem Res ; 86(2): 123-36, 2002 May.
Artigo em Inglês | MEDLINE | ID: mdl-12008975

RESUMO

The role of alpha-tocopherol (alpha-toco) and selenium (Se) on human lymphocyte oxidative stress and T-cells proliferation were studied by flow cytometry. We measured the hydrogen peroxide and glutathione levels in cultured human T-lymphocytes and the proliferation of their subsets: T-helper/inducer, T-suppressor/cytotoxic, and natural killer and interleukin-2 receptors upon stimulation by the mitogens phytohemaglutinin (PHA) and lipopolysaccharide (LPS). The results indicate that early stimulation by mitogens is affected by the glutathione and hydrogen peroxide status of the T-lymphocytes. The addition of 100 microM or 500 microM alpha-toco or 0.5 microM Se alone shows weak antioxidant and immunostimulant properties. When combined, an enhanced antioxidant and immunoregulatory effect was observed. The present findings indicate that alpha-toco and Se have interactive effects as oxygen radical scavengers, thus promoting human lymphocyte response to antigens. This suggests that micronutrient status is an important factor in considering when interpreting the results of in vitro assays of lymphocyte function.


Assuntos
Antioxidantes/farmacologia , Linfócitos/efeitos dos fármacos , Linfócitos/imunologia , Selênio/farmacologia , alfa-Tocoferol/farmacologia , Antioxidantes/metabolismo , Antígenos CD4/efeitos dos fármacos , Antígeno CD56/efeitos dos fármacos , Antígenos CD8/efeitos dos fármacos , Diferenciação Celular/efeitos dos fármacos , Divisão Celular/efeitos dos fármacos , Células Cultivadas , Sinergismo Farmacológico , Glutationa/metabolismo , Humanos , Peróxido de Hidrogênio/metabolismo , Lipopolissacarídeos/toxicidade , Subpopulações de Linfócitos/efeitos dos fármacos , Mitógenos/toxicidade , Fito-Hemaglutininas/toxicidade , Receptores de Interleucina-2/efeitos dos fármacos
10.
Int J Hematol ; 72(4): 463-5, 2000 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-11197212

RESUMO

Chronic natural killer (NK) lymphocytosis involves a persistent increase in CD56+ large granular lymphocytes (LGLs) that is sometimes associated with immune-mediated complications, such as anemia and neutropenia. However, aplastic anemia (AA) is a rare complication. Here we describe 2 patients with severe AA who presented with persistent increases in NK cells. Their LGLs were positive for CD56, CD16, and intracellular interferon (IFN)-gamma but negative for CD3, Fas-ligand, and T-cell receptor rearrangement, findings that are compatible with NK cells. Not only the number of NK cells, but NK activity as well, was increased in both patients. The number of NK cells changed according to hematologic recovery and relapse in 1 case. Thus, there seemed to be a close relationship between NK cells and the progression of AA, at least in this instance. Further investigation of the clinical course of similar cases and the characteristics of NK cells is necessary.


Assuntos
Anemia Aplástica/complicações , Células Matadoras Naturais , Linfocitose/etiologia , Idoso , Anemia Aplástica/sangue , Antígeno CD56/sangue , Antígeno CD56/efeitos dos fármacos , Doença Crônica , Humanos , Imunossupressores/farmacologia , Imunossupressores/uso terapêutico , Células Matadoras Naturais/patologia , Linfocitose/sangue , Masculino , Pessoa de Meia-Idade , Contagem de Plaquetas
11.
Med Sci Sports Exerc ; 31(11): 1528-34, 1999 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-10589853

RESUMO

PURPOSE: Athletes who use anabolic steroids get larger and stronger muscles. How this is reflected at the level of the muscle fibers has not yet been established and was the topic of this investigation. METHODS: Muscle biopsies were obtained from the trapezius muscles of high-level power lifters who have reported the use of anabolic steroids in high doses for several years and from high-level power lifters who have never used these drugs. Enzyme-immunohistochemical investigation was performed to assess muscle fiber types, fiber area, myonuclear number, frequency of satellite cells, and fibers expressing developmental protein isoforms. RESULTS: The overall muscle fiber composition was the same in both groups. The mean area for each fiber type in the reported steroid users was larger than that in the nonsteroid users (P < 0.05). The number of myonuclei and the proportion of central nuclei were also significantly higher in the reported steroid users (P < 0.05). Likewise, the frequency of fibers expressing developmental protein isoforms was significantly higher in the reported steroid users group (P < 0.05). CONCLUSION: Intake of anabolic steroids and strength-training induce an increase in muscle size by both hypertrophy and the formation of new muscle fibers. We propose that activation of satellite cells is a key process and is enhanced by the steroid use. The incorporation of the satellite cells into preexisting fibers to maintain a constant nuclear to cytoplasmic ratio seems to be a fundamental mechanism for muscle fiber growth. Although all the subjects in this study have the same level of performance, the possibility of genetic differences between the two groups cannot be completely excluded.


Assuntos
Anabolizantes/farmacologia , Fibras Musculares Esqueléticas/efeitos dos fármacos , Músculo Esquelético/efeitos dos fármacos , Adenosina Trifosfatases/análise , Adenosina Trifosfatases/efeitos dos fármacos , Adulto , Biópsia , Antígeno CD56/análise , Antígeno CD56/efeitos dos fármacos , Núcleo Celular/efeitos dos fármacos , Humanos , Hipertrofia , Imuno-Histoquímica , Fibras Musculares de Contração Rápida/efeitos dos fármacos , Fibras Musculares Esqueléticas/citologia , Fibras Musculares de Contração Lenta/efeitos dos fármacos , Proteínas Musculares/análise , Proteínas Musculares/efeitos dos fármacos , Músculo Esquelético/citologia , Miofibrilas/efeitos dos fármacos , Miofibrilas/ultraestrutura , Cadeias Pesadas de Miosina/análise , Cadeias Pesadas de Miosina/efeitos dos fármacos , Isoformas de Proteínas/análise , Isoformas de Proteínas/efeitos dos fármacos , Levantamento de Peso
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