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"Cancer is a class of disease or disorders characterized by uncontrolled division of cells and the ability of these cells to invade other tissues. One new approach in dealing with cancer is through apoptotic regulators, which is the process of controlling cell growth by abnormally prolonging cell survival, facilitating the accumulation of transforming mutations and promoting resistance. This book uses oral cancers as the specific means to demonstrate this technique with this particular type of cancer, which is quite prevalent (and deadly) in India and other parts of Asia, in particular"--Provided by publisher."

"Our recent understanding of the cellular and molecular defects and the regulation of the apoptotic signalling pathways has resulted in rationally designed anticancer strategies and the development of novel agents that regulates apoptosis. A comprehensive review of all apoptotic-related anticancer therapies is not the purpose of this book. However, in the volume of this book with 11 chapters, we have described a number of novel apoptotic regulators that have shown promising value and also great feasibility for cancer treatment. These novel agents either occur naturally or are chemically synthes. "

"Penelitian ini dilakukan untuk melihat faktor proliferasi sel sebagai peyebab ketidaksiapan endometrium untuk implantasi setelah pemberian berbagai dosis rekombinan FSH (rFSH) dengan melihat tingkat ekspresi FSH-Reseptor (FSHR) dan ekspresi protein KI-67. Sampel penelitian ini adalah bahan biologi tersimpan (BBT) dari jaringan endometrium Macaca nemestrina. Total sampel 15, sampel terdiri dari tiga kelompok yang diberikan GnRH agonis dosis tetap dan rFSH dengan dosis stimulasi berbeda, yaitu 30IU, 50IU, dan 70IU dan satu kelompok kontrol. Tidak ditemukan perbedaan signifikan antara berbagai dosis rFSH yang diberikan dengan ekspresi FSHR dan ekspresi protein Ki67 pada sel endometrium Macaca nemestrina. Tingkat ekspresi FSHR dan ekspresi Ki67 ditemukan tidak berkorelasi siginifikan. Dosis rFSH yang lebih tinggi tidak menurunkan ekspresi FSHR dan Ki67 serta tidak terdapat korelasi antara ekspresi FSHR dengan ekspresi Ki67.

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This study was conducted to look at cell proliferation factors as causes of endometrial unpreparedness for implantation after administration of various recombinant FSH doses (rFSH) by looking at FSH-receptor (FSHR) expression and expression of KI-67 proteins. The study sample was stored biological material (SBM) from endometrial tissue of Macaca nemestrina. The total sample was 15, the sample consisted of three groups given fixed-dose GnRH agonists and different stimulation doses, namely 30IU, 50IU, and 70IU and one control group. we found not significantly different between various doses of rFSH with FSHR and Ki67 expression in endometrial tissue Macaca nemestrina. We found not correlation significantly between FSHR expression and Ki67 Expression endometrial tissue Macaca nemestrina. Higher rFSH doses did not reduce FSHR expression and Ki67 and there was no correlation between FSHR expression and Ki67 expression."

"Cell in the distress situation, denaturation of proteins may occur, and may also respond by expressing stress proteins. However, such homeostatis effort does not always succeed and even may lead to disease, including cancer. In distress situation also ensue much protein misfolding. Objective: This research were to explain the role of heat shock protein 40 (Hsp40) and HSP20 in pathogenesis of occured oral squamous cell carcinoma (OSSC) patient which realized human papiloma virus (HPV) infection. Material and method: Tissue biopsy frozen section were taken from BOSC and OSCC patients was cut into three part. Parrafin blocks were made from cutting I, which was subsequently stains with HE to ascertain the type of neoplasm. Cutting II was subjected to DNA isolation. The DNA isolation results were subjected to PCR to amplify L1-HPV gene for fixed the HPV stressor. Protein isolation was treated from cutting III, followed with Blottdot test by using anibody monoclonal anti Hsp40 and Hsp 70 and continued with measurement using densitometer to find the concentration of Hsp40 and Hsp70. The collected data were analyzed with F Test (Manova) and discriminant analysis. Result: This experiment showed the differences in concentration of Hsp40 (p<=0,070) and Hsp70 (p<=0,006) between benign oral squamous cell (BOSC) and OSCC patients which realized HPV infection. Conclusion: This experiment proved that OSCC patients which realized HPV infection indicated an up regulated of Hsp70 concentration, so that there was occurs misfolding of the proteins cell. The misfolding was ensue obstacle of apoptosis and to raise cell poliferation which to storm carcinogenesis. An up regulated of Hsp40 was role as co-chaperone."

"The purposes of this study are to study the pathogenesis of oral cancer and to see the role play of oncogenes, onco-suppressor genes in cancer growth and their mutation type. There are many predisposing factors which may influence the development of cancer. The factors are divided intrinsic (hereditary) and extrinsic factors (bacteria, viruses, fungi, chemical, drugs, radiation, trauma, heat, cold and nutrition). These agents may act individually, in combination with other carcinogen (co-carcinogen) or in combination with other agents that do not in themselves causes cancer (promoters), but that help the carcinogens to mutate or depress cells, but in the mechanism still enigma. Oncogenes oncosuppressor genes are normal genes in human. Oncogenes functions are as growth factor (e.g. sis), growth factor receptor (e.g. erbB1), signal transducer (e.g. ras) or nuclear factor (e.g.myc, jun). Tumor (oral cancer) will be arises if oncogenes andonco-suppressor genes function are disturbed by some carcinogenand these genes have mutation, deletion, amplification or translocation. That was also related to the loss or inactivation of onco-suppressor genes such as p53, so that causes the loss of the normal growth regulation/strait control that associated with tumorigenesis."

"Latar belakang: Paparan hipoksia subletal (Hypoxia conditioning) diyakini memiliki efek neuroprotektif yang dapat meningkatkan resistensi sel dengan cara menginduksi perubahan ekspresi gen dan jalur sinyal intraseluler yang mengakibatkan adaptasi intraseluler melalui proses eritropoiesis, angiogenesis, transport glukosa dan glikolisis anaerobik melalui aktivitas gen HIF- 1 alpha. Penelitian mengenai hipoksia hipobarik intermiten (HHI) telah membuktikan bahwa induksi HHI menurunkan kerusakan jaringan otak pada korteks, dan meningkatkan densitas mikrovaskuler. HHI juga memicu respons neuroplastisitas pada sel otak sebagai upaya agar fungsi sel otak tidak terganggu. Tujuan: Menganalisis efek hipoksia hipobarik intermitten (HHI) terhadap neuroplastisitas jaringan otak dengan mengamati perubahan fungsi motorik dan kognitif serta peningkatan protein PSD95 sebagai respons adaptasi pasca induksi hipoksia hipobarik intermitten. Metode: 25 tikus Sprague-Dawley, dibagi menjadi 4 kelompok diinduksi HHI dan 1 kelompok sebagai kelompok kontrol.Induksi dilakukan dengan hypobaric chamber di Lakespra TNI AU dengan interval induksi 1 minggu selama 4 kali (hari-1, 8, 15 dan 22). Setelah induksi, kelompok itu diuji untuk parameter fisiologis menggunakan balok berjalan untuk mengukur fungsi motorik dan Y Maze untuk mengukur fungsi kognitif. Jaringan otak diambil untuk pemeriksaan reseptor neurotransmitter glutamat dan GABA serta protein PSD95. Hasil: kelompok perlakuan dengan 1,2,3,4 kali paparan hipoksia hypobarik tidak menunjukkan perbedaan yang signifikan dalam fungsi neuromotor kompleks, fungsi kognitif dan PSD 95 dibandingkan dengan kelompok kontrol (p> 0,05). Ekspresi reseptor GABA dan glutamat menurun secara signifikan di induksi pertama, namun meningkat secara signifikan pada kelompok induksi kedua dan ketiga dan untuk akhirnya menurun mendekati rerata kelompok kontrol. Kesimpulan: HHI menginduksi proses neuroplastisitas sebagai respon adaptasi terhadap paparan hipoksia hipobarik intermiten pada tikus Sprague-Dawley.

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Background: Sublethal exposure to hypoxia known as hypoxia preconditioning is believed to have neuroprotective effect. Hypoxia preconditioning induces changes in gene expression and intracellular signaling pathways that lead to the emergence of intracellular adaptation through the process of erythropoiesis, angiogenesis, glucose transport and anaerobic glycolysis through HIF- 1 alpha gene activity. Intermittent hypobaric hypoxic conditions (IHH) which occurs at high altitude such as during flight, is a common condition that causes exposure to hypoxia preconditioning. HHI induction decreased brain cortical tissue damage, and increased microvascular density. The aim of the present study is to investigate the effect of hypoxic preconditioning on the function of neuronal cells.

Aims: to investigate the neuroplasticity responses after intermittent hypobaric hypoxia induction on cerebral function (complex neuromotor function,cognitive function, PSD95 and neurotransmitter transduction).

Method: A total of 25 Sprague-Dawley rats were divided into 4 groups of IHH and 1 group as control. The 4 IHH groups were exposed to intermittent hypobaric hypoxia in Indonesian Air Force Institute of Aviation Medicine hypobaric chamber, by 1 week interval for 4 times (day-1, 8, 15 and 22). After the induction, the groups were evaluated for physiological parameters using walking beam to measure the complex neuromotor function and Y maze to measure the cognitive function. The brain was taken for immunochemistry and ELISA analysis.

Results: the group treated with 1,2,3,4 times exposure to hypobaric hypoxia shows no significant differences in complex neuromotor function,cognitive function and PSD95 compare to control group ( p>0.05). The level of GABA and glutamate receptor decreased significantly in induction 1, but raised significantly in group induction 2 and 3 compare to control group.

Conclution: IHH induced neuroplasticity as adaptation respons to hypobaric intermittent hypoxia in Sprague-Dawley rats."

"This book in order to stimulate the discussion of how the knowledge gained in the emerging field of oxidative stress in cancer biology can be utilized to more effectively design interventions to enhance therapeutic responses while causing fewer treatment limiting complications. The chapters contained in this volume provide highly informative emerging perspectives on how that selective enhancement of oxidative stress in cancerous tissues can be used as a target for enhancing therapeutic outcomes as well as how selective inhibition of oxidative stress could spare normal tissue damage and inhibit carcinogenesis. "

"This book explores the development and use of innovative computational and mathematical approaches for modeling the vascular development of tumors. Covers modeling of the angiogenesis cascade, and integrates vasculature development with tumor growth dynamics."

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Karsinoma sel skuamosa rongga mulut (KSS-RM) merupakan keganasan yang

menempati urutan ke-6 dari seluruh kasus kanker di dunia. Pembedahanmerupakan terapi utama KSS-RM namun pada KSS-RM lanjut lokal,pembedahan merupakan tantangan bagi dokter bedah karena struktur anatomiyang rumit dan dampaknya terhadap kualitas hidup penderita Oleh karena itudipikirkan pemberian kemoterapi neoadjuvan (KN) pada KSS-RM stadium lanjutlokal untuk mengecilkan tumor. Kemoresistensi merupakan masalah pemberianKN pada KSS-RM stadium lanjut lokal akibat microenvironment yang hipoksikditandai dengan peningkatan ekspresi HIF-1α. Kemoresistensi juga diregulasi olehmiR-210 serta peningkatan ekspresi penanda sel punca CD44 dan CD133.Melatonin memiliki efek antioksidan kuat dan efek onkostatik sehinggadiharapkan dapat memperbaiki kondisi hipoksia tumor.Penelitian ini merupakan uji klinis dengan desain paralel acak tersamarpembanding plasebo, yang dilaksanakan pada bulan Juni 2017 hingga Juli 2018,bertujuan untuk mengetahui efektivitas melatonin dalam meningkatkan responsklinis penderita KSS-RM stadium lanjut lokal yang diberikan kemoterapineoadjuvan dan apakah melatonin dapat memperbaiki hipoksia yang ditandaidengan penurunan ekspresi HIF-1α, miR-210, CD44, dan CD133. Sebanyak 50pasien KSS-RM stadium lanjut lokal dari RSCM dan RSKD dirandomisasi.Sebanyak 25 pasien mendapat kombinasi melatonin dan KN (taksan, sisplatin,dan 5-fluorourasil) dan 25 pasien lainnya mendapat KN saja. Sebanyak 25 pasienyang menyelesaikan protokol penelitian (13 pasien kelompok melatonin dan 12pasien kelompok plasebo). Perubahan ekspresi HIF-1α, miR-210, CD44, danCD133 yang diukur dari jaringan biopsi sebelum terapi dan jaringan biopsi/eksisiluas pasca terapi, menggunakan metode qRT-PCR absolute quantification. Selainitu untuk menilai respons klinis digunakan RECIST 1.1 sebelum dan sesudah KN.Melatonin 20 mg perhari menurunkan ekspresi HIF-1α (p = 0,301), miR-210 (p =0,767), dan CD44 (p = 0,103) namun tidak bermakna jika dibandingkan plasebo.Ekspresi CD133 meningkat pada kedua kelompok melatonin dan plasebo (p =0,301) walaupun tidak bermakna. Melatonin 20 mg perhari selama 1 minggusebelum KN pertama dimulai sampai KN selesai tidak memberikan perbedaanrespons positif yang bermakna pada dua kelompok. Penurunan konsentrasi HIF-1a dan CD133 tidak diikuti penurunan persentase sisa tumor. Pada kelompokmelatonin, ekspresi CD44 dan miR-210 menurun diikuti penurunan persentasesisa tumor yang tidak bermakna dibandingkan plasebo. Pada kelompok yangmendapat melatonin, persentase sisa tumor 21,35% lebih rendah dibandingkankelompok plasebo meskipun tidak berbeda bermakna (p = 0,531).

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Squamous cell carcinoma of the oral cancer (OSCC) is the sixth most common

malignancy of all malignant tumors. Surgery is the mainstay of treatment for oralcavity cancers. Surgery in locally advanced OSCC presents many challengesprimarily because the head and neck region have many critical structures that canbe damaged by tumor or treatment. Damage to these structures can result insignificant structural, cosmetic and functional deficits that negatively impactquality of life. Therefore, it is thought that neoadjuvant chemotherapy (KN) inlocal advanced stage OSCC is to shrink the tumor. The chemoresistancy is aproblem of KN administration in locally advanced OSCC due to a hypoxicmicroenvironment characterized by increased expression of HIF-1α. Thechemoresistancy is also regulated by miR-210 as well as increased expression ofCD44 and CD133 stem cell markers. Melatonin has powerful antioxidant effectsand oncostatic effects that are expected to improve tumor hypoxia.This study is a double-blind, randomized clinical trial, which was carried out inJune 2017 to July 2018 to determine the effectiveness of melatonin in improvingthe clinical response of locally advanced OSCC patients given neoadjuvantchemotherapy and whether melatonin can improve hypoxia marked by decreasedexpression of HIF-1α, miR-210, CD44, and CD133. Only 25 patients hadcompleted the study protocol, 13 in melatonin group and 12 in placebo group. Thedifference in HIF-1α, miR-210, CD44, and CD133 expression were measured as adelta concentration using absolute quantification qRT-PCR. The concentration ofthe biomolecular markers within the tumor tissue taken from the first biopsy (pretreatment)were determined using qRT-PCR then subtracted from theconcentration of biomarkers taken from the second biopsy. The clinical responsewas assessed using RECIST 1.1.The administration of melatonin 20 mg/day decreased the expression of HIF-1α(p = 0,301), miR-210 (p = 0,767), and CD44 (p = 0,103) but not statisticallysignificant. CD133 expression increased in both group melatonin and placebo (p= 0,301). Melatonin 20 mg per day for 1 week before NC was started until NCwas completed did not give a significant difference in positive responses in thetwo groups. The decrease concentrations of HIF-1 and CD133 were not followedby a decrease in the percentage of remaining tumors. The melatonin groupshowed a decrement in CD44 and miR-210 followed by a decrement in thepercentage of remaining tumors that were not significant compared to placebo. Inthis study, melatonin did not increase the clinical response although there is21.35% decrement in tumor mass in melatonin group compare (p = 0,531).

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