• Journal of Hospice and Palliative Care
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• 제15권2호
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• pp.99-107
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• 2012

목적: 말기암환자의 여명 예측은 치료의 이득과 위해를 판단하는 잣대가 되고, 적절한 의료 중재 제공 및 환자의 자율성에 기초한 의사결정에 중요한 기준이 된다. 특히 많은 수의 말기암환자는 암성 식욕부진-악액질 증후군으로 사망에 이르기 때문에 본 연구에서는 이를 반영할 수 있는 혈장 렙틴 농도와 생존기간과의 연관성을 알아보고자 하였다. 방법: 2009년 7월부터 2010년 7월까지 13개월 동안, 만 20세 이상의 말기암환자 69명을 대상으로 혈장 렙틴 농도를 측정하고, 생존기간을 조사하였다. 나이, 성별, 원발암 부위, 암 치료 경력, 전이여부, 투약상황 및 활력증후, 백혈구 수, 혈색소, Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), C-반응성 단백질, 총 빌리루빈, 총 콜레스테롤, 알부민, 렙틴 등의 혈액검사를 시행하였다. 결과: 혈장 렙틴 농도와 성별, 나이, 백혈구 수, 혈색소, AST, ALT, 총 빌리루빈, C-반응성 단백질, 통증강도 등의 상관 관계 분석 결과 렙틴과 생존기간에는 통계적으로 유의한 양의 상관 관계를 보였으며, 단변량 분석한 결과 혈장 렙틴 농도는 생존기간과 통계적으로 경계수준의 유의한 관계를 보였으나, 단변량 분석에서 생존 기간에 유의한 영향을 미치는 성별, 백혈구 수, AST, ALT, 총 빌리루빈, 알부민, C-반응성 단백질을 포함하여 시행한 다변량 분석에서 혈장 렙틴 농도는 생존기간과 통계적으로 유의한 관계가 없는 것으로 나타났다. 결론: 암성 식욕부진-악액질 증후군과 관련이 있는 혈장 렙틴 농도와 말기암환자의 생존기간과는 통계적으로 유의한 연관성을 보이지는 않았다. 그러나, 소화기계암환자에 있어서는 혈장 렙틴 농도가 생존기간 예측인자로서 쓰일 수 있는 가능성을 보여주었다.

• Tuberculosis and Respiratory Diseases
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• 제44권5호
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• pp.1019-1029
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• 1997

연구배경 : 폐암 환자에서 체중감소와 영양결핍은 흔히 동반되며 체중감소가 있는 폐암 환자는 체중감소가 없는 환자보다 항암제 치료에 대한 반응이 좋지 않으며 예후도 나쁘다. 폐암환자에서의 체중감소는 안정시 에너지 소비(resting energy expenditure : REE)와 관계가 있다. 저자들은 폐암 환자에서 안정시 에너지 소비자 증가된 빈도를 알아보고 안정시 에너지 소비에 영향을 주는 인자를 알아보고자 하였다. 방 법 : 처음 진단된 31명의 폐암 환자를 대상을 안정시 에너지 소비를 측정하여 대조군과 비교하였다. 안정시 에너지 소비량은 ventilated hood system을 사용하여 간접 칼로리측정법(indirect calorimetry)으로 측정하였다. 안정시 에너지 소비량은 칼로리측정기로 측정한 산소 소모량과 이산화탄소 생성량을 이용하여 Weir공식으로 계산하였으며 안정시 에너지 소비량의 예측치는 Harris-Benedict공식으로 구하여 비교하였다. 결 과 : 안정시 에너지 소비량은 폐암 환자와 대조군에서 각각 $1415.5{\pm}237.0$(Kcal/day), $1253.6{\pm}174.6$(Kcal/day)로 폐암 환자에서 유의하게 더 높았으며 REE 백분율도 각각 $116.8{\pm}15.8$(%), $100.7{\pm}13.8$(%)로 폐암 환자에서 유의하게 더 높았다. REE백분율은 흡연, 주 증상의 기간, 폐기능 장애 정도, 무기폐유무, 폐암의 위치 등에 의한 차이는 없었으나 원격전이 유무에 따라서는 원격전이가 있었던 군과 없었던 군에서 각각 $127.0{\pm}17.3$(%), $113.8{\pm}11.6$(%)로 원격전이가 있었던 군에서 유의하게 더 높았다. 폐암 환자중에서 과대사 상태와 정상대사 상태사이에 흡연, 주 증상의 기간, 원발암의 용적, 원발암의 기관지 내시경상의 위치, 무기폐나 기관폐색의 유무, 폐암의 병기, 원격적인 유무에 따른 차이는 없었다. 결 론 : 폐암 환자에서 안정시 에너지 소비가 비교적 높은 빈도로 증가되어 있었으며 증가된 안정시 에너지 소비는 폐암의 원격천이 유무와 관계가 있었다.

• Radiation Oncology Journal
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• 제13권3호
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• pp.259-266
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• 1995

Purpose : The aim of this study is to analyze the survival rate, treatment failure and complication of radiation therapy alone in stage III uterine cervical cancer. Materials and Methods : From January 1980 through December 1985, 227 patients with stage III uterine cervical cancer treated with radiation therapy at Kosin Medical Center were retrospectively studied. Among 227 patients, 72 patients($317{\%}$) were stage IIIa, and 155 patients($68.3{\%}$) were stage IIIb according to FIGO classification. Age distribution was 32-71 years (median: 62 years). Sixty nine patients($95.8{\%}$) in stage IIIa and 150 patient ($96.8{\%}$) in stage IIIb were squamous cell carcinoma. pelvic lymph node metastasis at initial diagnosis was 8 patients($11.1{\%}$) in stage IIIa and 29 patients($18.7{\%}$) in stage IIIb, Among 72 patients with stage IIIa, 36 patients ($50{\%}$) were treated with external radiation therapy alone by conventional technique (180-200 cGy/fr.) and 36 patients($50{\%}$) were treated with external radiation therapy with intracavitary radiotherapy(ICR) with $Cs^{137}$ sources, and among 155 patients with stage IIIb, 80 patients ($51.6{\%}$) were treated with external radiation therapy alone and 75 patients ($48.4{\%}$) were treated with external radiation therapy with ICR. Total radiation doses of stage IIIa and IIIb were 65-105 Gy(median: 78.5 Gy) and 65-125.5 Gy (median 83.5 Gy). Survival rate was calculated by life-table method. Results : Complete response rates were $58.3{\%}$(42 patients) in stage IIIa and $56.1{\%}$(87 patients) in stage IIIb. Overall 5 year survival rates were $57{\%}$ in stage IIIa and $40{\%}$ in stage IIIb. Five year survival rates by radiation technique in stage IIIa and IIIb were $64{\%},\;40{\%}$ in the group treated in combination of external radiation and ICR, and $50\%,\;40\%$ in the group of external radiation therapy alone(P=NS). Five year survival rates by response of radiation therapy in stage IIIa and IIIb were $90\%,\;66\%$ in responder group and $10\%,\;7\%$ in non-responder group (P<0.001) There were statistically no significant differences of 5 year survival rate by total radiation doses and external radiation doses(40 Gy vs 50 Gy) of whole or true pelvis in stage IIIa and IIIb(P=NS). Treatment failures rates were $40.3\%$(29 patients) in stage IIla and $57.4\%$(89 patients) in stage IIIb. 17 patients ($23.6\%$) in stage IIIa and 46 patients ($29.7\%$) in stage IIIb experienced complications. Total radiation doses more than 85 Gy produced serious complication in both stage IIIa($50\%$) and IIIb($50\%$). Serious complication rates were higher in group received external radiation doses of 50 Gy than 40 Gy to whole or true pelvis in stage IIIa and IIIb. Serious rectal complication developed in rectal doses more than 65 Gy, and serious bladder complication developed in bladder doses more than 75 Gy. Major cause of death was cachexia due to locoregional failure in both stage IIIa($34.7\%$) and IIIb($43.9\%$). Conclusion : From this study, we found that external radiation therapy with ICR was found to have a tendency to be superior to external radiation therapy alone in survival rate, local control rate and complication rate but not different in statistics, and external radiation doses of 50 Gy than 40 Gy to whole or true pelvis produced serious rectal and bladder complications in stage III uterine cervical cancer.

• Journal of Ginseng Research
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• 제47권6호
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• pp.726-734
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• 2023

Background: Skeletal muscles play a key role in physical activity and energy metabolism. The loss of skeletal muscle mass can cause problems related to metabolism and physical activity. Studies are being conducted to prevent such diseases by increasing the mass and regeneration capacity of muscles. Ginsenoside Rg5 has been reported to exhibit a broad range of pharmacological activities. However, studies on the effects of Rg5 on muscle differentiation and growth are scarce. Methods: To investigate the effects of Rg5 on myogenesis, C2C12 myoblasts were induced to differentiate with Rg5, followed by immunoblotting, immunostaining, and qRT-PCR for myogenic markers and promyogenic signaling (p38MAPK). Immunoprecipitation confirmed that Rg5 increased the interaction between MyoD and E2A via p38MAPK. To investigate the effects of Rg5 on prevention of muscle mass loss, C2C12 myotubes were treated with dexamethasone to induce muscle atrophy. Immunoblotting, immunostaining, and qRT-PCR were performed for myogenic markers, Akt/mTOR signaling for protein synthesis, and atrophy-related genes (Atrogin-1 and MuRF1). Results: Rg5 promoted C2C12 myoblast differentiation through phosphorylation of p38MAPK and MyoD/E2A heterodimerization. Furthermore, Rg5 stimulated C2C12 myotube hypertrophy via phosphorylation of Akt/mTOR. Phosphorylation of Akt induces FoxO3a phosphorylation, which reduces the expression of Atrogin-1 and MuRF1. Conclusion: This study provides an understanding of how Rg5 promotes myogenesis and hypertrophy and prevents dexamethasone-induced muscle atrophy. The study is the first, to the best of our knowledge, to show that Rg5 promotes muscle regeneration and to suggest that Rg5 can be used for therapeutic intervention of muscle weakness and atrophy, including cancer cachexia.

• Radiation Oncology Journal
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• 제8권2호
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• pp.241-253
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• 1990

1980.6.부터 1985.12.까지 고신의료원 치료방사선과에서 방사선 단독 치료한 병기 IIb 자궁경부암 환자 331명에 대하여 후향적으로 생존율 치료 실패 및 합병증 등에 영향을 미칠 수 있는 방사선 치료요소들을 분석조사 하였다. 5년 생존율과 무병생존율은 각각 $82.8{\%}$와 $82.4{\%}$였다. 방사선 치료 6주 경과에 분석한 골반내 관해율은 전골반 외부 조사후 강내조사한 예에서는 $98.6{\%}$였고 축소조사한 추가 치료한 예에서는 $71.6{\%}$였다. 전골반 방사선 조사후 완전관해를 보였던 예에서의 5년 생존율은 $98.9{\%}$였지만 국소치료실패 및 원격전이한 예에서는 $12.9{\%}$였다. Point A에 $7500{\~}8500$ cGy를 조사한 예에서는 $88.5{\%}$의 5년 생존율을 보였고 합병증은 $4.9{\%}$였지만 그 이상의 조사량에서는 생존율은 증가한지 않았고 합병증만 증가하였다. $18.7{\%}$(62예)에서 치료실패를 보였는데, 이중국소치료실패가 $72.6{\%}$(45예), 국소 및 골반임파 치료실패가 $3.2{\%}$(2예)였으며 원격전이 실패는 $24{\%}$(15)였다. 합병증은 $15.1{\%}$(50예)였는데 이중 $42{\%}$가 직장 출혈 및 협착이였다. Point A의 조사량은 8500 cGy가 합병증 유발의한계 조사량 이였으며 합병증의 $70{\%}$가 그 이상의 조사양에서 발생하였다. 직장 합병증은 6500 cGy이상에서 발생하였고 방광합병증은 7500 cGy이상에서 발생하였다. 사망의 원인으로는 국소치료실패로 인한 전신쇠약이 대다수였으며 전체 사망원인으로는 국소치료 실패로 인한 전신쇠약이 대다수였으며 전체 사망원인의 $73.7{\%}$였고 그외 폐, 간, 뼈 전이순이였으며 방사선합병증으로 인한 사망은 3예에 지나지 않았다. 상기와 같은 결과에 대한 결론으로 크기가 아주 큰 종양이나 Barrel형태의 종양의 방사선 치료에는 지금 많이 사용되고 있는 4000 cGy이상의 외부 조사량이 강내조사전에 골반관해를 성취하기 위해 필요한 것을 알 수 있었다.

• Toxicological Research
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• 제8권2호
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• pp.343-357
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• 1992

Tumor necrosis factor-${\alpha}$(TNF), a polypeptide hormone secreted primarily by activated macrophages, was originally identified on the basis of its ability to cause hemorrhagic necrosis and tumor regression in vivo. Subsequently, TNF has been shown to be an important component of the host responses to infection and cancer and may mediate the wasting syndrome known as cachexia. These systemic actions of TNF are reflected in its diverse effects on target cells in vitro. TNF initiates its diverse cellular actions by binding to specific cell surface receptors. Although TNF receptors have been identified on most of animal cells, regulation of these receptors and the mechanisms which transduce TNF receptor binding into cellular responses are not well understood. Therefore, in the present study, the mechanisms how TNF receptors are being regulated and how TNF receptor binding is being transduced into cellular responses were investigated in rat liver plasma membranes (PM) and ME-180 human cervical carcinoma cell lines. $^{125}I$-TNF bound to high ($K_d=1.51{\pm}0.35nM$)affinity receptors in rat liver PM. Solubilization of PM with 1% Triton X-100 increased both high affinity (from $0.33{\pm}0.04\;to\;1.67{\pm}0.05$ pmoles/mg protein) and low affinity (from $1.92{\pm}0.16\;to\;7.57{\pm}0.50$ pmoles/mg protein) TNF binding without affecting the affinities for TNF, suggesting the presence of a large latent pool of TNF receptors. Affinity labeling of receptors whether from PM or solubilized PM resulted in cross-linking of $^{125}I$-TNF into $M_r$ 130 kDa, 90 kDa and 66kDa complexes. Thus, the properties of the latent TNF receptors were similar to those initially accessible to TNF. To determine if exposure of latent receptors is regulated by TNF, $^{125}I$-TNF binding to control and TNF-pretreated membranes were assayed. Specific binding was increased by pretreatment with TNF (P<0.05), demonstrating that hepatic PM contains latent TNF receptors whose exposure is promoted by TNF. Homologous up-regulation of TNF receptors may, in part, be responsible for sustained hepatic responsiveness during chronic exposure to TNF. As a next step, the post-receptor events induced by TNF were examined. Although the signal transduction pathways for TNF have not been delineated clearly, the actions of many other hormones are mediated by the reversible phosphorylation of specific enzymes or target proteins. The present study demonstrated that TNF induces phosphorylation of 28 kDa protein (p28). Two dimensional soidum dodecyl sulfate-polyacrylamide gel electrophoresis(SDS-PAGE) resolved the 28kDa phosphoprotein into two isoforms having pIs of 6.2 and 6.1. The pIs and relative molecular weight of p28 were consistent with those of a previously characterized mRNA cap binding protein. mRNA cap binding proteins are a class of translation initiation factors that recognize the 7-methylguanosine cap structure found on the 5' end of eukaryotic mRNAs. In vitro, these proteins are defined by their specific elution from affinity columns composed of 7-methylguanosine 5'-triphosphate($m^7$GTP)-Sepharose. Affinity purification of mRNA cap binding proteins from control and TNF treated ME-180 cells proved that TNF rapidly stimulates phosphorylation of an mRNA cap binding protein. Phosphorylation occurred in several cell types that are important in vitro models of TNF action. The mRNA cap binding protein phosphorylated in response to TNF treatment was purifice, sequenced, and identified as the proto-oncogene product eukaryotic initiation factor-4E(eIF-4E). These data show that phosphorylation of a key component of the cellular translational machinery is a common early event in the diverse cellular actions of TNF.