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"[Asam galat merupakan zat polifenol dengan kemampuan sitotoksik. Studisebelumnya menunjukkan turunan asam galat mampu menghambat pertumbuhansel kanker. Sampai saat ini, belum banyak studi yang mempelajari turunan alkilester galat dan turunan metoksi galat terhadap pertumbuhan kanker kolon. Tujuandari penelitian ini adalah untuk mengetahui aktivitas sitotoksik turunan alkil estergalat dan metoksi galat pada sel kanker kolon. Penelitian ini dilakukan dengandesain eksperimental secara in vitro. Kemampuan sitotoksik asam galat danturunannya diuji pada sel HCT116 (sel kanker kolon) dengan menggunakan MTS(3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2Htetrazolium)assay. Data yang diperoleh dianalisis untuk mendapatkan IC50 setiapsenyawa. Hasil penelitian menunjukkan modifikasi asam galat menjadi senyawametil galat, propil galat, butil galat, t-butil galat, amil galat, oktil galat dan ketigaturunan metoksi galat tidak menunjukkan peningkatan aktivitas sitotoksik denganpeningkatan konsentrasi yang diuji. Dari semua senyawa yang memilikikecenderungan menghambat, heptil galat memiliki aktivitas yang paling baik.Disimpulkan, metil galat, propil galat, butil galat, t-butil galat, amil galat, dan oktilgalat merupakan turunan alkil galat yang tidak aktif. Etil galat, isobutil galat,isoamil galat, dan heptil galat merupakan turunan alkil galat yang memiliki aktivitassitotoksik pada sel kanker kolon. Ketiga tur;Gallic acid is a polyphenol with anticancer activity. Previous studies had shown thatthe derivatives of gallic acid had cytotoxic activity in cancer cell. To date, fewstudies evaluated the activity of alkyl ester derivatives of gallic acid and methoxyderivatives of gallic acid in colon cancer cell. The objective of this study was toexamine the cytotoxic activity of alkyl ester derivatives and methoxy derivatives ofgallic acid in colon cancer cell. This study was conducted in in-vitro study inHCT116 colon cancer cell. Cytotoxic activity of gallic acid and its derivatives wereevaluated in HCT116 colon cancer cell using MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) assay. Data fromthis experiment was analyzed to obtain IC50 of each compound. The result showedthat modification of gallic acid to methyl gallate, propyl gallate, butyl gallat, t-butylgallate, pentyl gallate, octyl gallate and three methoxy derivatives of gallic acid didnot increase cytotoxic activity in all concentrations tested. Among all derivatives ofgallic acid, heptyl gallate has the best cytotoxic activity. In conclusion, methylgallate, propyl gallate, butyl gallate, t-butyl gallate, pentyl gallate, and octyl gallateare alkyl ester derivatives of gallic acid with no cytotoxic activity. Ethyl gallate,isobutyl gallate, isopentyl gallate, and heptyl gallate are active derivatives of gallicacid. All methoxy derivatives of gallic acid do not show any cytotoxic activity incolon cancer cell.;Gallic acid is a polyphenol with anticancer activity. Previous studies had shown thatthe derivatives of gallic acid had cytotoxic activity in cancer cell. To date, fewstudies evaluated the activity of alkyl ester derivatives of gallic acid and methoxyderivatives of gallic acid in colon cancer cell. The objective of this study was toexamine the cytotoxic activity of alkyl ester derivatives and methoxy derivatives ofgallic acid in colon cancer cell. This study was conducted in in-vitro study inHCT116 colon cancer cell. Cytotoxic activity of gallic acid and its derivatives wereevaluated in HCT116 colon cancer cell using MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) assay. Data fromthis experiment was analyzed to obtain IC50 of each compound. The result showedthat modification of gallic acid to methyl gallate, propyl gallate, butyl gallat, t-butylgallate, pentyl gallate, octyl gallate and three methoxy derivatives of gallic acid didnot increase cytotoxic activity in all concentrations tested. Among all derivatives ofgallic acid, heptyl gallate has the best cytotoxic activity. In conclusion, methylgallate, propyl gallate, butyl gallate, t-butyl gallate, pentyl gallate, and octyl gallateare alkyl ester derivatives of gallic acid with no cytotoxic activity. Ethyl gallate,isobutyl gallate, isopentyl gallate, and heptyl gallate are active derivatives of gallicacid. All methoxy derivatives of gallic acid do not show any cytotoxic activity incolon cancer cell., Gallic acid is a polyphenol with anticancer activity. Previous studies had shown thatthe derivatives of gallic acid had cytotoxic activity in cancer cell. To date, fewstudies evaluated the activity of alkyl ester derivatives of gallic acid and methoxyderivatives of gallic acid in colon cancer cell. The objective of this study was toexamine the cytotoxic activity of alkyl ester derivatives and methoxy derivatives ofgallic acid in colon cancer cell. This study was conducted in in-vitro study inHCT116 colon cancer cell. Cytotoxic activity of gallic acid and its derivatives wereevaluated in HCT116 colon cancer cell using MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) assay. Data fromthis experiment was analyzed to obtain IC50 of each compound. The result showedthat modification of gallic acid to methyl gallate, propyl gallate, butyl gallat, t-butylgallate, pentyl gallate, octyl gallate and three methoxy derivatives of gallic acid didnot increase cytotoxic activity in all concentrations tested. Among all derivatives ofgallic acid, heptyl gallate has the best cytotoxic activity. In conclusion, methylgallate, propyl gallate, butyl gallate, t-butyl gallate, pentyl gallate, and octyl gallateare alkyl ester derivatives of gallic acid with no cytotoxic activity. Ethyl gallate,isobutyl gallate, isopentyl gallate, and heptyl gallate are active derivatives of gallicacid. All methoxy derivatives of gallic acid do not show any cytotoxic activity incolon cancer cell.]"

"Kejadian kanker kolon mayoritas terjadi secara sporadik. Berbagai faktor non-inherited yang dipikirkan sebagai penyebab kanker kolon merupakan kombinasi antara faktor diet dan lingkungan. Kedua faktor ini menyebabkan mutasi somatik pada berbagai gen spesifik dalam pembentukan kanker kolon. Di antara berbagai faktor, butirat (dibentuk dalam proses fermentasi fiber) mungkin mempunyai peranan yang penting sebagai zat kemoprotektif terhadap kanker kolon. Sumber butirat dalam makanan sehari-hari berasal dari makanan yang mengandung kulit gandum. Pada tingkat molekuler, butirat menyebabkan asetilasi histon, meningkatkan diferensiasi berbagai sel, menginduksi terjadinya apoptosis dan meregulasi ekspresi dari berbagai onkogen. Faktor-faktor ini yang menjadi alasan butirat mempunyai efek protektif terhadap kanker kolon. (Med J Indones 2003; 12: 127-31)

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The majority of colon cancers occur sporadically. They are thougth to be caused by non-inherited factors such as a combination of diet and environmental factors, which result in somatic mutations of specific genes. Among dietary factors butyrate which is derived from fermentable fibers may have important role as chemoprotector against colorectal cancer. The source of butyrate in daily diet mostly come from wheat products especially wheat bran. At molecular level, butyrate causes hystone acetylation, favours differentiation, induces apoptosis and regulates the expressions of various oncogens. These effects suggest that butyrate may be protective against colorectal cancers. (Med J Indones 2003; 12: 127-31)"

"Fiber is not digested or absorbed in the small intestine. The main site of action of fiber is in the colon. Inthe colon, fiber will increase stool output and frequency. Increase stool water, dilute the colonic content,reduce the toxins, bile acid, increase colonic fermentation and also stimulate probiotic growth.Some meta-analysis of observational epidemologic and case contro studies have faund a protectiveeffect of dietary fiber against colon cancer that increase with intake. Therefore, the high fiber diet is healthy recommendation to prevent various gastrointestinal disorders."

"ABSTRAKBackground One of the highest mortality rates among all cancer types is colon cancer. In 2011 statistic data, colon cancer is placed on the 3rd mortality rate. Inflammation has been considered an etiology for the development of colon cancer thus knowing the pathogenesis and development of inflammatory related colon cancer, further diagnosis method and treatment can be developed.Method Administration of Dextran Sodium Sulfate 1 during the first week and continued with peritoneal injection of Azoxymethane on mice strain C3H and BALB C. The mice are sacrificed on 2 months, 4 months, and 6 months after AOM injection. Mice colons are then taken in the middle part of the colon for 1 cm. The specimens are analyzed using HE staining with high magnification. Inflammatory foci counting are done in all microscopic fields of the specimen. The result of which are tabulated and further analyzed using Kolmogorov Smirnov Test and ANOVA Test to check the significancy.Results Macroscopically, the colonic mucosa of the mice shows a lot of proliferating nodules in the 4 months and 6 months specimen. Microscopically, we found that the inflammatory foci have a tendency of decrease in number throughout the months. Based on the analytical data, the progression of inflammatory foci is constant among all three different months. Conclusion Inflammatory foci development in colon carcinogenesis AOM DSS mice model is strongly correlates with the administration of DSS. 1 week of DSS administration has a constant inflammatory foci number in 6 months of colon carcinogenesis development.

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ABSTRACTKanker kolon merupakan salah satu jenis kanker yang menyebabkan angka kematian tinggi. Menurut data statistik tahun 2011, angka kematian kanker kolon mencapai urutan ke-3 dibanding dengan kanker lainnya. Inflamasi pada kolon adalah salah satu penyebab terjadinya kanker kolon, sehingga dengan mengetahui proses patogenesis kanker kolon yang beretiologi inflamasi dapat menjadi dasar untuk pengembangan metoda diagnosis dan penyembuhan.Metode: Pemberian mencit dengan Dextran Sodium Sulfate 1 selama satu minggu pertama yang dilanjutkan dengan injeksi Azoxymethane pada jenis mencit C3H dan BALB/C. Mencit kemudian dikorbankan pada bulan ke 2, 4, dan 6 setelah injeksi AOM. Bagian tengah kolon mencit diambil sepanjang 1 cm. Setelah itu, specimen dianalisa menggunakan pewarnaan HE dengan lapang pandang besar pada mikroskop. Fokus inflamasi dihitung pada seluruh area lapang pandang pada setiap specimen. Data hasil focus inflamasi kemudian dianalisa menggunakan tes Kolmogorov-Smirnov dan ANOVA untuk mengetahui signifikansi data.Hasil: Pada hasil makroskopik, terlihat mukosa kolon mencit bernodul banyak pada specimen bulan ke 4 dan ke 6. Pada hasil mikroskopik, fokus inflamasi cenderung menurun seiring dengan waktu. Sedangkan, analisa data menunjukkan bahwa perkembangan fokus inflamasi terlihat konstan pada seluruh spesimen.Kesimpulan: Perkembangan fokus inflamasi pada proses karsinogenesis kolon sangat berhubungan dengan pemberian DSS. Pada eksperimen ini, pemberian 1 minggu DSS pada awal bulan memperlihatkan perkembangan fokus inflamasi yang konstan selama 6 bulan."

"ABSTRAK Pembedahan terbuka kolorektal mempunyai morbiditas yang tinggi. Laparoskopi kolorektal pertama kali diperkenalkan pada tahun 1991 dengan hasil morbiditas pascabedah yang rendah. Penelitian ini mengambil total sampel subjek kanker kolorektal yang menjalani pembedahan laparoskopi pada tahun 2010 hingga 2015. Data ditabulasi dan dianalsis untuk mendapatkan hasil jangka pendek dan kesintasan lima tahun. Didapatkan 65 data dengan 21 kasus kolon 32,3 dan 44 kasus rektum 67,7 ; 34 pria 52,3 31 wanita 47,7 dengan rata ndash;rata usia 57,17 tahun SD 13.380 . Pada kelompok kolon didapatkan rata ndash;rata durasi bedah 216,75 menit SD 65,94 dan kehilangan darah 159,75 mL SD 125,47 . Median VAS adalah empat; diet, mobilisasi dan lama rawat pascabedah didapatkan pada dua, empat dan tujuh hari. Kesintasan lima tahun pasien didapatkan 83 . Tidak ada komplikasi, pembedahan ulang dan infeksi luka operasi ILO pada kelompok ini. Pada kelompok rektum rata ndash;rata durasi bedah adalah 305,97 min SD 94,23 dan perdarahan intra operasi 150 mL SD 50 . Median VAS pascabedah tiga, diet dan mobilisasi pascabedah dua hari dan empat hari. Lama rawat pascabedah delapan hari. Kesintasan lima tahun adalah 58,5 . Morbiditas pascabedah lebih rendah dengan pembedahan laparoskopi dengan hasil kesintasan keseluruhan yang tidak berbeda dengan kesintasan pasien kanker kolorektal yang ditangani sebelumnya. ABSTRACT Conventional colorectal cancer surgery is often associated with high post operative moribidities. Laparoscopic colorectal surgery has reduced post operative morbidities with same survival outcomes of open surgery. Retrospective data of laparoscopic colorectal cancer surgery from 2010 to 2015 were collected, tabulated and analyzed to get early results and five years survival rate. There were 65 data, 21 colon cancer 32.3 and 44 rectal cancer 67.7 . Higher incidence of male patients n 34, 52.3 than female n 31, 47.7 with mean age of 57,17 13.38 years. Length of operation for colon group was 216.75 SD 65.94 mins with intra operative blood loss 159.75 SD 125.47 mL and post operative pain, on visual analog score VAS , was 4 2 5 . Post operative diet, mobilization and length of stay were 2 1 3 days, 4 2 7 days and 7 4 12 days respectively. The five years survival rate was 83 . In rectal group, length of operation was 305,97 SD 94,23 mins with intra operative blood loss 150 SD 50 mL. Post operative VAS, diet, mobilization and length of stay were 3 2 5 , 2 1 4 days, 4 2 22 days and 8 5 36 days respectively. Five years survival rate was 58.5 . Post operative morbidities in colorectal cancer decreases with laparoscopic resection with satisfactory overall survival rate."

"Colon polyp is a term used for abnormality from bulging tissue above surrounding colonic mucosal layer. Adenoma polyp was the commonly found polyp that progress to colorectal cancer. Most of those patients was asymptomatic. Undetected and unmanaged polyp was a risk factors of colorectal cancer even."

"ABSTRACTPurpose: Postoperative pneumonia affects the length of stay and mortality after surgery in elderly patients with colorectal cancer (CRC). We aimed to determine the risk factors of postoperative pneumonia in elderly patients with CRC, and to evaluate the impact of laparoscopic surgery on elderly patients with CRC.Methods: We retrospectively investigated 1473 patients ≥ 80 years of age who underwent surgery for stage 0-III CRC between 2003 and 2007. Using a multivariate analysis, we determined the risk factors for pneumonia occurrence from each baseline characteristic.Results: Among all included patients, 26 (1.8%) experienced postoperative pneumonia, and restrictive respiratory impairment, obstructive respiratory impairment, history of cerebrovascular events, and open surgery were determined as risk factors (odds ratio [95% confidence interval], 2.78 [1.22-6.20], 2.71 [1.22-6.30], 3.60 [1.37-8.55], and 3.57 [1.22-15.2], respectively). Furthermore, postoperative pneumonia was more frequently accompanied by increasing cumulative numbers of these risk factors (area under the receiver operating characteristic curve = 0.763).Conclusions: Laparoscopic surgery may be safely performed in elderly CRC patients, even those with respiratory impairment and a history of cerebrovascular events."