Presentasi di International Conference CAL (IC-CAL) 2017

Presentasi di International Conference CAL (IC-CAL) 26 Oktober 2017 di UIN Sunan Gunung Djati, Bandung

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Penerima Pendanaan Penelitian Dan Pengabdian Masyarakat Di Perguruan Tinggi Tahun 2017. Kementerian Riset, Teknologi, Dan Pendidikan Tinggi Direktorat Jenderal Penguatan Riset Dan Pengembangan.

Alhamdulillah, Penelitian Produk Terapan (PPT) lolos pendanaan KemenRistek Dikti Direktorat Jenderal Penguatan Riset Dan Pengembangan. Semoga pelaksanaannya dimudahkan dan dilancarkan, hasilnya bermanfaat bagi peneliti/instansi dan masyarakat.

Perguruan Tinggi : Universitas Islam 45 Bekasi (Unisma Bekasi)
Skema : Penelitian Produk Terapan
Nama : Andi Hasad
Judul : Pengembangan Sistem Piconet Pervasive Pada Transmisi Data Rate Video Streaming Melalui Jaringan Bluetooth Sebagai Media Pembelajaran di Perguruan Tinggi

Dalam pendaanaan tahun 2017, tercatat 4 dosen (semua dari Fakultas Teknik Unisma Bekasi) yang lolos pendanaan skema Penelitian Produk Terapan (PPT), sedangkan dalam skema Penelitian Dosen Pemula (PDP), terdapat 10 dosen dari berbagai Fakultas yang dinyatakan lolos pendanaan. Selengkapnya sebagai berikut:

Penelitian Produk Terapan (PPT)

Penelitian Produk Terapan (PPT)

 Penerima Pendanaan Penelitian Dan Pengabdian Masyarakat Di Perguruan Tinggi Tahun 2017. Kementerian Riset, Teknologi, Dan Pendidikan Tinggi Direktorat Jenderal Penguatan Riset Dan Pengembangan.

Download surat resmi  Sumber Simlitabmas Ristek Dikti

Presentasi Seminar Usul Penelitian Produk Terapan dan Penelitian Unggulan Perguruan Tinggi Tahun 2016

Presentasi PPT 15-16082016

Seminar Usulan PPT 1

Seminar Usulan PPT 2

Ketua Peneliti dan Para Reviewer PPT 2016

Kegiatan Seminar Usulan Program Riset Terapan ( Penelitian Produk Terapan, Penelitian Unggulan Perguruan Tinggi) Tahun 2016 ini bertujuan antara lain:

  1. Mengundang para ketua peneliti (yang usulan penelitiannya lulus pada seleksi tahap pertama/Desk Evaluation) untuk mempresentasikan usul penelitiannya di hadapan para reviewer sebagai penilai.
  2. Menilai usulan penelitian ( Penelitian Produk Terapan, Penelitian Unggulan Perguruan TInggi) PTS Kelompok Binaan Tahun 2016 dari perguruan tinggi yang lulus seleksi tahap pertama.
  3. Untuk Ditetapkan sebagai calon penerima penelitian tahun 2017.
  4. Untuk memastikan tidak adanya duplikasi penelitian.

Dari Universitas Islam 45 Bekasi, ada 4 proposal yang dinyatakan lulus Desk Evaluation, dan masuk ke tahap berikutnya presentasi seminar usul penelitian, yaitu:

  1. Andi Hasad (Ketua Peneliti), Program Studi Teknik Elektronika,  Universitas Islam 45 Bekasi
  2. Sugeng (Ketua Peneliti), Program Studi Teknik Elektro, Universitas Islam 45 Bekasi
  3. Anita Setyowati Srie Gunarti (Ketua Peneliti), Program Studi Teknik Sipil,  Universitas Islam 45 Bekasi
  4. Rahmadya Trias Handayanto (Ketua Peneliti), Program Studi Teknik Komputer,  Universitas Islam 45 Bekasi

Ketua Peneliti PPT Unisma Bekasi

Salah satu reviewer Dikti pada kegiatan ini adalah Prof. Dr. Kuncoro, S.T., M.T., Guru Besar Universitas Sebelas Maret, Solo. Kegiatan ini berjalan lancar dan sukses , 15-16 Agustus 2016, berlokasi di Hotel Harris, Jl. Peta Bandung.

Hasil dari kegiatan ini merupakan pertimbangan bagi Direktorat Riset dan Pengabdian Masyarakat, Direktorat Jenderal Penguatan Riset dan Pengembangan, dalam menentukan usulan baru penelitian yang akan didanai pada tahun anggaran 2017.

Lampiran:

Undangan Peserta Seminar Usulan Penelitian Riset Terapan Tahun 2016 di Bandung

Lampiran Undangan Seminar Usul Riset Terapan

Sumber:

Panduan Kegiatan Seminar Susulan Program Riset Terapan ( Penelitian Produk Terapan, Penelitian Unggulan Perguruan Tinggi) PTS Kelompok Binaan. DRPM, Ditjen Penguatan Riset dan Pengembangan. Ristek DIKTI, 2016.

Particle and Fibre Toxicology

Mesothelioma: Do asbestos and carbon nanotubes pose the same health risk?. Carbon nanotubes (CNTs), the product of new technology, may be used in a wide range of applications. Because they present similarities to asbestos fibres in terms of their shape and size, it is legitimate to raise the question of their safety for human health. Recent animal and cellular studies suggest that CNTs elicit tissue and cell responses similar to those observed with asbestos fibres, which increases concern about the adverse biological effects of CNTs. While asbestos fibres’ mechanisms of action are not fully understood, sufficient results are available to develop hypotheses about the significant factors underlying their damaging effects. This review will summarize the current state of knowledge about the biological effects of CNTs and will discuss to what extent they present similarities to those of asbestos fibres. Finally, the characteristics of asbestos known to be associated with toxicity will be analyzed to address the possible impact of CNTs.

Introduction
Carbon nanotubes (CNTs) have unique chemical and physical characteristics as a result of their nanostructure. CNTs may be used in a wide range of applications, in fields as diverse as electronics and medicine. Due to their widespread use, it is important to determine the safety of CNTs for the protection of ecological systems and human health. Research to investigate the biological effects of CNTs is advancing today in order to foresee and prevent their potentially harmful effects. CNTs have fibrelike characteristics in terms of their elongated shape, dimensions and aspect ratio. As particles with at least one dimension of less than 100 nm, they correspond to High Aspect Ratio Nanoparticles (HARN) . In light of the health impact of mineral fibres, especially the fibrogenic and carcinogenic potency of asbestos fibres, and the health and socio-economical tragedies caused by unregulated asbestos utilization, the increasing development and uses of CNTs have triggered concern about their potential toxicity. In recent years, several publications have reported the effects of CNTs. Most studies have concerned animal and cell responses, focusing primarily on respiratory diseases, especially the inflammatory effects in the lung. However, while inhalation is one important probable route of contamination, it must be kept in mind that there are other relevant routes of exposure. A severe primary cancer, malignant mesothelioma (MM), has been closely linked to asbestos exposure . Epidemiological and animal studies have shown that asbestos fibres are not the only fibres to be associated with a risk of MM development. Epidemiological studies have demonstrated a higher incidence of MM in populations exposed to asbestiform and non-asbestos fibres. Some manmade vitreous fibres have caused MM in animal experiments. The question of whether CNTs might potentially be linked to MM development justifies further research in this area. Moreover, on the basis of the literature, CNTs have already shown effects in animals and in cell systems that are similar to those observed with asbestos fibres. Two recent studies showed the occurrence of MM in genetically-modified cancer-sensitized mice and in conventional Fischer 344 rats exposed to CNTs by intraperitoneal or intrascrotal administration respectively. These initial results underline the urgent need for information to further our knowledge about CNTs’ potential to cause MM.

MM is a primary tumour of the serosas caused by the neoplastic transformation of mesothelial cells. In populations exposed to asbestos fibres, MM mainly occurs in the pleura, and to a lesser extent in the peritoneum and pericardium. MM is considered to be highly specific to asbestos exposure, and is found in from 60% to over 80% of cases. In France, the calculated risk of MM attributable to occupational asbestos exposure was estimated at 83.2% (95% CI 76.8 to 89.6) in men, and 38.4% (95% CI 26.8 to 50.0) in women. Many studies carried out to investigate pleural and mesothelial cell response to asbestos fibres have made it possible to reach sound hypotheses about the mechanism of action of asbestos fibres in neoplastic mesothelial cell transformation.
The aim of the present review is to explore whether our knowledge of the mechanism of action of asbestos fibres could offer a useful paradigm to provide a warning or predict the risk of CNTs, to interpret data on animal and cellular responses, and to evaluate their potential health effects. For the purposes of our discussion, we consider three points: (i) the fate of asbestos fibres following exposure; (ii) their effects on mesothelial cells and the biological mechanism associated with the cell response; (iii) the nature of the fibre parameters involved in the harmful effects, and their similarities with CNT characteristics. We begin with a summary of current knowledge on the toxicology of CNTs, then look at asbestos fibres’ mechanisms of action, focusing on carcinogenic effects at the pleural level. Finally, we address the similarities between asbestos and CNTs.

Toxicology of CNTs

Context of toxicological studies on CNT

Various kinds of CNTS have been the focus of toxicological studies. CNTs are heterogeneous in terms of their structure, impurities and physico-chemical properties. Both single-walled (SWCNTs) and multi-walled (MWC- NTs) CNTs have been examined in toxicological studies, including commercial and laboratory-made CNTs, whether purified or used as produced. The effects of CNTs have been investigated following in vivo exposure of rodents, and on several types of cells in culture. Most studies concerned pulmonary toxicity . Animal experiments mainly focused on inflammatory responses after exposure by intratracheal instillation or aspiration, or intraperitoneal injection. In vitro cell systems with several types of mammalian cells have been used to study inflammatory responses and genotoxicity. A few in vivo and in vitro studies were related to dermal toxicity, and some in vitro studies focused on neurons. Toxicity test systems on procaryotes were also used to assess genotoxicity. Here our focus will be on respiratory effects.


Biological effects of CNTs
Translocation
Biodistribution of CNTs after deposition in the lung or via other routes has been poorly investigated. A translocation of SWCNTs in various organs has been reported by several authors. In a recent study, MWCNTs deposited by intratracheal instillation in rats revealed clearance due to macrophage uptake and the lymphatic system without evidence of crossing the pulmonary barrier, six months after instillation. It can be noted that macrophage and lymphatic clearance was also demonstrated following administration or exposure to asbestos fibres. Erdely et al.  suggest that the release of soluble inflammatory factors could circulate to the vascular blood compartment after lung deposition of CNTs. The release of circulating factors must be taken into consideration to account for fibre effects. While asbestos fibres have been detected in the pleura, soluble molecules could also account for the pleural response , and genotoxicity may be due to clastogenic factors. Additional studies are needed to determine the pharmacokinetics of CNTs. Regarding the numerous varieties of CNTs associated with a broad scale of physical and physico-chemical properties, fundamental studies will be necessary to establish the parameters leading the translocation process. Biological effects on mesothelial cells In vivo effects on mesothelial cells Six recently-published studies concerned CNTs’ effects on mesothelial cells. Three reported findings from animal experiments and three from cell system studies. One animal experiment concerned the mesothelial cell inflammatory response and pathological changes after intraperitoneal injection. The authors exposed C57Bl/6 mice to four samples of MWCNTs of different sizes and aggregation states. There was one sample of “short” MWC-NTs (from NanoLab, Inc; mean diameter: 14.8 ± 0.5 nm; mean length: 1–5 μm); two samples of “long” MWCNTs (Long1, from Mitsui & Co.; mean diameter: 84.9 ± 1.9 nm; mean length: 40–50 μm [24% > 15 μm of length]; Long2 from Univ. Manchester; mean diameter: 165 ± 4.7 nm; mean length: 20–100 μm [84% > 15 μm of length]); and one sample of more tangled MWCNTs (from NanoLab, Inc.; mean diameter: 10.4 ± 0.3 nm; mean length: 5–20 μm), as well as carbon black. At the same time, two samples of amosite fibres were tested; these were short fibres (4.5% > 15 μm of length) and long fibres (50.4% > 15 μm of length) known to be differently pathogenic in rodents. In prior experiments, inhalation and intraperitoneal exposure in rats to long amosite fibres revealed greater pathogenicity than short fibres in terms of fibrosis and cancer. In the study reported by Poland et al., inflammation was assessed after injection of 50 μg of MWCNTs/mouse, after 24 h and seven days. The end points were quantification of inflammation in peritoneal lavage and histology of diaphragm. Only long samples of MWCNTs and of amosite produced inflammation and granulomas. Histological analyses revealed the occurrence of “frustrated phagocytosis” by macrophages. These results thus demonstrated some similarities between the responses to the long forms of amosite and MWCNTs. Several of the effects of asbestos were also found with CNTs. There were higher inflammatory responses with samples of long fibres. Only the samples that contained long fibres caused granulomas and “frustrated phagocytosis”.

(Marie-Claude F Jaurand*1,2 , Annie Renier1,2 and Julien Daubriac1,2 Address: 1 INSERM, U674, Fondation Jean Dausset – CEPH, Paris, F-75010, France and 2 Université Paris 7, Paris, F-75013, France)

Maternal exposure to nanoparticulate titanium dioxide

Nanotechnology is developing rapidly throughout the world and the production of novel man-made nanoparticles is increasing, it is therefore of concern that nanomaterials have the potential to affect human health. The purpose of this study was to investigate the effects of maternal exposure to nano-sized anatase titanium dioxide (TiO2 ) on gene expression in the brain during the developmental period using cDNA microarray analysis combined with Gene Ontology (GO) and Medical Subject Headings (MeSH) terms information.

Results: Analysis of gene expression using GO terms indicated that expression levels of genes associated with apoptosis were altered in the brain of newborn pups, and those associated with brain development were altered in early age. The genes associated with response to oxidative stress were changed in the brains of 2 and 3 weeks old mice. Changes of the expression of genes associated with neurotransmitters and psychiatric diseases were found using MeSH terms.

Conclusion: Maternal exposure of mice to TiO2 nanoparticles may affect the expression of genes related to the development and function of the central nervous system.

The small size of nanoparticles can bestow unique trans­locational properties . It has been reported that nano-sized elemental carbon particles (36 nm) inhaled by adult rats were translocated into extrapulmonary organs, such as liver. A subsequent study showed that intranasally instilled carbon black nanoparticles can be translocated to the central nervous system, including cerebrum, cerebel­lum, and olfactory bulb via the olfactory nerve . In a recent study, Takeda et al.  found that TiO2 nanoparti­cles administrated subcutaneously to pregnant mice were transferred from the mother to the fetal brain, and induced apoptosis in the mitral cells of the olfactory bulb of mice exposed maternally to the nanoparticles. Fetal brains are easily affected by blood-borne substances, including nano-sized materials, to a much greater extent than adult brains because the development of the blood-brain barrier in the fetal brains is incomplete . Taking these observations into consideration, functional altera­tions of the central nervous system induced by maternal exposure to nanoparticles need to be investigated. To ana­lyze the effect of maternal exposure to TiO2 nanoparticles on the early stages of development of the brain, we used microarray technology and gene expression profiles by functional annotation of genes using Gene Ontology (GO) terms and Medical Subject Headings (MeSH) terms.

Methods

Titanium dioxide nanoparticles

TiO2 nanopowder (particle size 2570 nm; surface area 2025 m2/g; crystal form anatase) was purchased from Sigma-Aldrich Japan Inc. (Tokyo, Japan) and used as TiO2 nanoparticles. The nanopowder was suspended in saline (Otsuka Pharmaceutical Factory Inc., Tokushima, Japan) with 0.05% (v/v) Tween 80 and sonicated for more than 30 minutes immediately before administration.

Animals and treatments

Pregnant ICR mice, purchased from Japan SLC Inc. (Shi­zuoka, Japan), were housed in a room under controlled temperature (23 ± 1 °C), humidity (55 ± 5%) and light (12 h light/12 h dark cycle with light on at 8:00 a.m.) with ad libitum access to food and water. Pregnant mice were transported carefully to minimize stress factors by Sankyo Labo Service Co., Inc (Tokyo, Japan). All animals were handled in accordance with institutional and national guidelines for the care and use of laboratory animals.

A 100 μL volume of TiO2 suspended at 1 μg/μL was injected subcutaneously into pregnant mice (n = 15) on gestational days 6, 9, 12, and 15 for the exposure group, while 100 μL of vehicle alone was injected into pregnant mice (n = 14) as a control group. Brain tissue was obtained from male fetuses on embryonic day (ED) 16 (n = 8/group) and from male pups on postnatal days 2 (n = 10/group), 7 (n = 10/group), 14 (n = 9/group), and 21 (n = 9/group).

Total RNA extraction

Whole brains were immediately frozen in liquid nitrogen and kept at -80 °C. Frozen tissue was homogenized and extracted with Isogen (Nippon Gene Co., Ltd., Tokyo, Japan) while well stirred by a Vortex-Genie 2 (Scientific Industries, Tokyo, Japan). Total RNA was isolated accord­ing to the manufacture’s protocol and suspended in TE buffer (10 mM Tris-HCl, pH 8.0, 1 mM EDTA).

Complementary DNA microarray analysis

Figure 1. Summary of the extracted terms with genes differentially expressed in the maternal TiO2 exposure group.RNAs for microarray analysis were pooled for each group, purified using the RNeasy Micro Kit (Qiagen, Hilden, Ger­many) and reverse-transcribed to yield complementary DNA (cDNA) labeled with the fluorescent dye Cy3 or Cy5 using the SuperScript Indirect cDNA Labeling Core Kit (Invitrogen, CA, USA) and the SuperScript Indirect cDNA Labeling System Purification Kit (Invitrogen). Cy3- and Cy5-labeled samples were purified using the CyScribe GFX Purification Kit (GE Healthcare Bio-Sciences, Little Chalfont, UK). The generated targets were mixed and sub­jected to hybridization to an NIA mouse 15 K Microarray v2.0 (AGC Techno Glass Co. Ltd., Chiba, Japan) consist­ing of 16, 192 gene probes. Microarrays were scanned with two different photomultiplier sensitivities by a ScanArray (Packard BioChip Technologies, MA, USA). The scanner output images were normalized and signal quantification was performed using ScanArray Express (Perkin Elmer, MA, USA) and TIBCO Spotfire (TIBCO Software Inc., CA, USA). Normalization was used so that the overall inten­sity ratio of Cy3 and Cy5 was equal to 1. Statistical analy­sis was done with analysis of variance (ANOVA) and the level of statistical significance was set at P < 0.05.

Functional analysis of microarray data with gene annotation

A total of 37 GO terms and 66 MeSH terms associated with anatomy, brain development and associated pep­tides, neurotransmitters, hormones, behavior and psycho­logical phenomena, brain related disorders, oxidative stress, inflammation, and cell death were selected ; and 2838 and 3625 genes were annotated by GO and MeSH terms, respectively, using the gene reference database PubGene (https://server.pubgene.com/online/  PubGene/, Pub Gene AS, Oslo, NOR). These annotations were updated in April, 2008. The genes for which upregu­lation and downregulation were detected were catego­rized with GO and MeSH terms. The enrichment factor for each category was defined as (nf/n)/(Nf/N), where nf is the number of differentially expressed genes within the category, n is the total number of genes within that same category, Nf is the number of differentially expressed genes on the entire microarray, and N is the total number of genes on the microarray. Statistical analysis was per­formed using Fisher’s exact test with hypergeometric dis­tribution and the level of statistical significance was set at P < 0.05.

(Midori Shimizu , Hitoshi Tainaka , Taro Oba , Keisuke Mizuo , Masakazu Umezawa and Ken Takeda, Department of Hygienic Chemistry, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Chiba 278-8510, Japan and Research Center for Health Sciences of Nanoparticles, Research Institute for Science and Technology, Tokyo University of Science, Yamazaki 2641, Noda-shi, Chiba 278-8510, Japan)