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"Timah merupakan bahan baku utama material solder. Di Indonesia masih banyak sekali material solder yang mengandung bahan Pb yaitu Sn-Pb yang berbahaya bagi lingkungan dan kesehatan manusia. Untuk mendapatkan material solder ramah lingkungan, dilakukan penelitian Sn-xBi dan Sn-xBi-yAl dengan metode peleburan. Material paduan Sn-xBi telah dibuat dengan lima komposisi yang berbeda yaitu Sn-0Bi, Sn-10Bi, Sn-30Bi, Sn-52Bi dan Sn-70Bi, sedangkan paduan Sn-xBi-yAl dengan lima kandungan Al yang berbeda yaitu Sn-52Bi-0,05Al, Sn-52Bi-0,11Al, Sn-52Bi-0,14Al, Sn-52Bi-0,19Al dan Sn-52Bi-0,25Al. Karakterisasi sifat sifat material dilakukan dengan menggunakan, X-rd, DSC, LCR meter, Galvanostat, Ultrasonik. Hasil karakterisasi untuk Sn-xBi menghasilkan sifat yang optimal pada paduan Sn-52Bi yang mempunyai titik leleh 142,28oC dan tahanan jenis listrik 0,00022 ohm.m. Sedangkan untuk komposisi Sn-52Bi-yAl diperoleh yang optimum dengan titik leleh 144,6 oC dan hambatan jenisnya 0,0003 ohm m.

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Tin is primary material for solder. In Indonesia there are still many commercial solder containing Pb(Sn-37Pb) that are harmful for the environment and human health. In order to get the environmentally friendly solder material, this research was conducted to study the environmentally friendly solder material, this research was conducted to study the fabrication material alloy of Sn-xBi and Sn-xBi-yAl. Material alloy Sn-xBi has been made with five different compositions, namely Sn-0Bi, Sn-10Bi, Sn-30Bi, Sn-52Bi and Sn-0Bi, while the material alloy Sn-xBi-yAl was made with five Al different content, namely Sn-52Bi-0,05Al; Sn-52Bi-0,11Al; Sn-52Bi-0,14Al; Sn-52Bi-0,19Al and Sn-52Bi-0,25Al.

Material characterization were carried out using X-ray diffractometer, Differential Scanning Calorymeter, LCR meter, Galvanostat ad Ultrasonic. The results show, the optimum properties for Sn-xBi alloy is Sn-52Bi alloy with melting point at 142,28oC and specific electric resistance 0,00022m. Despite for Sn-52Bi-yAl has optimum with melting points at 144,6 oC and specific electric resistance 0,0003 ohm m."

"ABSTRAKPengerasan permukaan baja karbon rendah St41 telah dilakukan melalui proses boronisasi padat dengan tekanan mekanik. Sampel baja St41 dimasukkan kedalam wadah, ditimbun dengan serbuk boronisasi dalam bentuk campuran 5% boron karbida (B4C), 90% silicon karbida (SiC), 5% kalium borofluoride (KBF4), dan diberi tekanan 10 kN. Sampel yang telah dimasukkan dalam wadah, dipanaskan pada temperature 600, 700, 800, 900,dan 10000C selama 2, 4, 6, dan 8 jam pada masing-masing temperature. Pendinginan sampel dilakukan secara alamiah pada suhu kamar. Setelah dipanaskan, sampel dikarakterisasi dengan mikroskop optic, uji kekerasan mikro, X-RD, dan ketahanan aus. Morfologi dan ketebalan lapisan boride yang terjadi diamati dan diukur pada potongan melintang sampel. Untuk menentukan fase yang terjadi dilakukan pencocokan kurva dengan software Match berdasarkan data kristalografi. Untuk menganalisis fase secara kuantitatif digunakan software GSAS untuk menentukan ukuran kristalit rata-rata, dan parameter kisi, pada masing-masing fase yang terbentuk. Hasil penelitian menunjukkan bahwa dengan menambahkan tekanan mekanik untuk mencegah terjadinya oksidasi pada proses boronisasi padat dapat membentuk larutan padat intertisi lapisan besi boride pada permukaan baja St41. Dari hasil pengujian diperoleh kekerasan mikro pada permukaan lapisan besi boride sebesar 1703 HV dengan ketebalan 309 μm, dan ketahanan aus 36 kali ketahanan aus sampel semula. Harga kekerasan mikro dan ketebalan tersebut lebih besar jika dibandingkan dengan hasil-hasil penelitian terdahulu dan meningkat menjadi lebih dari 10 kali lipat harga kekerasan sampel semula. Dari hasil perhitungan diperoleh persamaan difusi D = D0 exp (-168,25 kJ/RT) dengan energi aktivasi sebesar 168,25 kJ.

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ABSTRACT

Surface hardening of low carbon steel St41 has been done through the pack boronizing combining with mechanical pressure. The sample of St41 steel was inserted into the container, containing boronizing powder with a mixture of 5% in the form of boron carbide (B4C), 90% silicon carbide (SiC), 5% potassium borofluoride (KBF4), and given the mechanical pressure of 10 kN. Samples were heated at temperatures of 600, 700, 800, 900, and 10000C for 2, 4, 6, and 8 hours at each temperature. After heating, the samples were characterized by optical microscop, micro-hardness, X-RD, and wear resistance. Morphology and boride layer thicknes is observed and measured on a cross section of the sample. Quantitative phase analysis software GSAS used to determine phase, the average crystallite size, and lattice parameters of each phase formed. It is also obtained the surface layer hardness of iron boride was 1703 HV with a thickness of 309 μm, and wear resistance about 36 times than the wear resistance of the untreated sample. The hardness and the thickness is greater when compared with the results of previous studies 10 times to the hardness of untreated sample. Energy activation and diffusion equation have value 168,255 kJ and D = D0 exp (-168.25 kJ/RT)."

"Tujuan: Mengetahui pengaruh mutasi patogenik BRCA1/2 tumor terhadap kesintasan pasien advanced stage-high grade serous epithelial ovarian cancer di RSUPN Dr. Cipto Mangunkusumo, RSUP Persahabatan, dan RS MRCCC Siloam Jakarta.Metode: Sejumlah 68 sampel dari 144 pasien diagnosis high-grade serous epithelial ovarian cancer (HGSOC) stadium FIGO IIB-IV, periode 1 Januari 2015 sampai 31 Maret 2021, di RSUPN Dr. Cipto Mangunkusumo, RSUP Persahabatan, dan RS MRCCC Siloam Jakarta, menjalani pemeriksaan NGS mutasi patogenik BRCA1/2 tumor, dilibatkan dalam penelitian kohort historikal ini. Kami membandingkan karakteristik klinikopatologis pasien, dan hasil luaran kesintasan, setelah pasien menjalani tatalaksana primer, berdasarkan status mutasi patogenik BRCA1/2 tumor. Faktor terkait tatalaksana, yang diperkirakan berpengaruh terhadap hasil luaran kesintasan pasien, juga turut dianalisis dalam penelitian ini.Hasil: Angka kejadian mutasi patogenik BRCA1/2 tumor diketahui sebesar 27,94% (19/68). Antara kelompok mutasi patogenik BRCA1/2 tumor, dengan kelompok tanpa mutasi patogenik, tidak terdapat perbedaan statistik signifikan berdasarkan usia, paritas, indeks massa tubuh (kg/m2), riwayat kanker payudara, stadium FIGO 2014, kadar CA125 serum pre operatif (U/mL), volume cairan ascites intra operatif (mL), lesi residual pasca laparotomi debulking, pemberian neoadjuvant chemotherapy (NACT), pemberian kemoterapi adjuvant. Riwayat kanker keluarga terkait HBOC, merupakan variabel paling berpengaruh terhadap mutasi patogenik BRCA1/2 tumor. Kelompok dengan riwayat kanker keluarga terkait HBOC, berisiko 5,212 kali lebih besar mengalami mutasi patogenik BRCA1/2 tumor, dibandingkan dengan kelompok tanpa riwayat kanker tersebut (RR adjusted 5,212; 95%CI 1,495-18,167; nilai p=0,010).Pada kelompok mutasi patogenik BRCA1/2 tumor, kemungkinan meninggal 86% lebih rendah (RR adjusted 0,149; 95%CI 0,046-0,475; nilai p=0,001), dan median survival yang lebih baik (median 46 bulan; 95%CI 34,009-57,991; nilai p=0,001), apabila dibandingkan dengan kelompok tanpa mutasi patogenik (median 23 bulan; 95%CI 15,657-30,343; nilai p=0,001). Analisis multivariat menunjukkan mutasi patogenik BRCA1/2 tumor merupakan faktor prognostik independen yang baik terhadap hasil luaran kesintasan (RR adjusted 0,149; 95%CI 0,046-0,475; nilai p=0,001).Kesimpulan: Pasien advanced stage-high grade serous epithelial ovarian cancer, dengan mutasi patogenik BRCA1/2 tumor, memiliki kesintasan lebih baik, dibandingkan pasien tanpa mutasi patogenik BRCA1/2 tumor.

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Objective: To evaluate the impact of pathogenic BRCA1/2 tumor mutational status on advanced stage- high grade serous epithelial ovarian cancer survival outcome at RSUPN Dr. Cipto Mangunkusumo, RSUP Persahabatan, and RS MRCCC Siloam Jakarta.

Methods: A total 68 of 144 patients diagnosed with FIGO 2014 stage IIB-IV high grade serous epithelial ovarian cancer (HGSOC) between January 1st, 2015 until March 31st, 2021, at RSUPN Dr. Cipto Mangunkusumo, RSUP Persahabatan, and RS MRCCC Siloam Jakarta, underwent NGS tumor BRCA1/2 gene testing, and were included in this cohort hystorical study. We compared patients clinicopathological characteristics, and survival outcomes after primary treatment, according to pathogenic BRCA1/2 tumor mutational status. Treatment-related factors that might affect patients’ survival outcome were also investigated.

Results: The BRCA1/2 pathogenic tumor mutations prevalence was observed in this study 27.94% (19/68). There were no significant statistical differences in age, parity, body mass index (kg/m2), previous breast cancer history, FIGO 2014 staging, pre-operative serum CA 125 level (U/mL), intra operative ascites volume (mL), post cytoreductive surgery residual lesion, neoadjuvant chemotherapy (NACT), and adjuvant chemotherapy administration, between the pathogenic tumor BRCA1/2 mutation, and no pathogenic tumor BRCA1/2 mutation groups. The hereditary breast ovarian cancer family history (HBOC) variable has the strongest correlation with pathogenic tumor BRCA1/2 mutation. The group with a family history of HBOC-related cancer had a 5.212 times greater risk of developing pathogenic BRCA1/2 tumor mutations, compared with the group without a history of those cancer (RR adjusted 5.212; 95%CI 1.495-18.167; p value=0.010).

The pathogenic BRCA1/2 tumor mutation group displayed better survival outcome. In the pathogenic BRCA1/2 tumor mutation group, the likelihood of dying was 86% lower (RR adjusted 0.149; 95%CI 0.046-0.475; p-value=0.001), and the median survival was better (median 46 months; 95%CI 34.009- 57.991; p value=0.001), than without pathogenic BRCA1/2 tumor mutations group (median 23 months; 95%CI 15.657-30.343; p value=0.001). The multivariate analyses identified pathogenic BRCA1/2 tumor mutation as an independent favorable prognostic factor for survival outcome (RR adjusted 0.149; 95%CI 0.046-0.475; p-value=0.001).

Conclusions: In advanced stage-HGSOC, patients with pathogenic BRCA1/2 tumor mutations have a better prognosis with longer survival outcome than those without pathogenic BRCA1/2 tumor mutations."