Atasi Limbah Dengan Bakteri Kurthia zopfii

Harian Surya 29 Januari 2007
Tingginya tingkat pencemaran di DAS Brantas yang kini mencapai 10-15 mg/liter atau diatas ambang baku mutu air sempat mengkhawatirkan masyarakat yang tinggal di aliran sungai. Pasalnya, sungai Brantas selama ini banyak digunakan untuk kebutuhan sehari-hari. Seperti mencuci, masak dan mandi.
Ironisnya, penyebab pencemaran sulit terdeteksi karena berasal dari limbah rumah tangga seperti sabun dan deterjen. Namun masalah itu kini tidak akan berlarut-larut andai masyarakat dan pemerintah daerah di Malang Raya mau mengaplikasikan hasil penelitian Ir Nur Hidayat MP, dosen Fakultas Teknologi Pertanian Unibraw.
Penelitian Ir Nur Hidayat MP bersama rekan-rekannya ini menemukan bakteri bernama Kurthia zopfii yang bisa menguraikan deterjen dan sabun menjadi senyawa yang tidak berbahaya.
"Kalau deterjen saja bisa diuraikan, tentu bahan kimia lain seperti kotoran manusia yang lebih ringan bisa dengan mudah diuraikan," terang Nur Hidayat saat ditemui Surya di ruang kerjanya, Senin (29/1).
Dijelaskan sekretaris jurusan Teknologi Industri Pertanian (TIP) FTP ini (kini ketua Lab Bioindustri), untuk bisa menguraikan deterjen, tinggal mencampurkan 1 cc bakteri kurthia zopfii ke dalam satu liter air atau kelipatannya. Bakteri ini akan memakan deterjen dan menguraikannya dalam hitungan jam. Sehingga air bisa langsung dialirkan ke sungai.
Istimewanya, usai memakan deterjen, bakteri ini akan berkembangbiak hingga mencapai populasi 100 juta. Pada tingkat populasi maksimal inilah ketika kondisi air sudah normal, bakteri ini akan mati dengan sendirinya dan mengendap menjadi senyawa organik.
"Senyawa organik bakteri ini bisa dimanfaatkan untuk kompos," terang Sie Ilmiah Perhimpunan Mikrobiologi Indonesia Cabang Malang (kini sekretaris). Bakteri ini juga bisa mengalahkan bakteri eschericia coli yang membahayakan kesehatan. Saat ini, lanjutnya, pihaknya tengah mengupayakan mendapatkan hak paten atas hasil penelitiannnya tersebut. Jika paten ini didapatkan, tidak menutup kemungkinan temuan ini akan dileparkan ke pasaran.
Penemuan mikrobakteri ini adalah yang kesekian kalinya dilakukan Nur Hidayat. Sebelumnya, Nur Hidayat juga menemukan bakteri bacillus thuringiensis varietas israelensis. Bakteri ini bisa digunakan untuk memakan jentik-jentik nyamuk pembawa virus demam berdarah.

High-density fermentation of microalga Chlorella protothecoides in bioreactor for microbio-diesel production

Applied Microbiology and Biotechnology
Volume 78, Number 1 / February, 2008 p:29-36

Wei Xiong, Xiufeng Li, Jinyi Xiang and Qingyu Wu1

Abstract
Agal-fermentation-based microbio-diesel production was realized through high-cell-density fermentation of Chlorella protothecoides and efficient transesterification process. Cell density achieved was 16.8 g l−1 in 184 h and 51.2 g l−1 in 167 h in a 5-l bioreactor by performing preliminary and improved fed-batch culture strategy, respectively. The lipid content was 57.8, 55.2, and 50.3% of cell dry weight from batch, primary, and improved fed-batch culture in 5-l bioreactor. Transesterification was catalyzed by immobilized lipase, and the conversion rate reached up to 98%. The properties of biodiesel from Chlorella were comparable to conventional diesel fuel and comply with US standard for Biodiesel. In a word, the approach including high-density fermentation of Chlorella and enzymatic transesterification process were set up and proved to be a promising alternative for biodiesel production.

Keywords
Agal-fermentation-based microbio-diesel (AFMD) - Chlorella protothecoides - Fed-batch - High-density fermentation - Immobilized lipase

Tawaran Iptek Vucer UJI dsb

Ada tawaran pengajuanpengabdian kepada masyarakat tahun anggaran 2009 mencakup:
1. kegiatan:
a. Penerapan IPTEKS
b. Program VUCER
c. Penerapan IPTEKS - UKM (IPTEKS MULTI YEARS)
d. Program pengembangan usaha:
1. MKU
2. KBPK
3. KWU
4. KKU
5. UJI

2. Usul harus memenuhi format

3. Besaran Dana:
a. IPTEK 7,5 juta
b. VUCER mak 15 jt
c. IPTEK UKM ( 3 tahuan maksimal 100 jt)
d. Kewirausahaan 15 0 30 jt
e. UJI seperti IPTEK_UKM

4. Waktu 8 bulan

selamat bekerja untuk membuat proposal.

The nutritive quality of maize-soybean (70:30) tempe flour

Plant Foods for Human Nutrition (Formerly Qualitas Plantarum)

Volume 47 no 5 June 1995

J. Tchango Tchango

Abstract

The nutritive quality of maize-soybean (70:30) tempe flour manufactured by fermentation withRhizopus oligosporus: Rhizopus orysae (1:1) was determined using weanling rats. Mould fermentation of maize-soybean mixture did not significantly affect its proximate composition. It increased the content of reducing sugars, total acids and aminonitrogen by about 43, 195 and 482 percent, respectively, and decreased phytate content by 46 percent. In vitro iron absorption for maize flour and maize-soybean tempe flour was 2.46 and 5.51 percent, respectively. Protein Efficiency Ratio (PER) and Net Protein Ratio (NPR) for maize-soybean tempe flour and skim-milk diets were 2.71 and 2.96, respectively, for PER, and 3.31 and 3.51, respectively, for NPR. In vivo protein digestibility of the two products was 95.0 and 98.0 percent, respectively.

Key words Maize-soybean tempe flour - Minerals bioavailability - Mould fermentation - Phytate - Protein quality - Proximate composition

Virology: The battle within

Melinda Wenner, Nature 451, 388-389 (2008)

Viral and microbial interactions within living tissues are more complex than previously thought. Melinda Wenner explores whether a periodic table of the infectious could help sort out the mess.

In 2001, Paulo Lusso asked his colleague Leonid Margolis for a favour. Lusso, a virologist at the San Raffaele Scientific Institute in Milan, Italy, had recently discovered that HIV patients are often co-infected with human herpesvirus 6 (HHV-6). Although typically benign, HHV-6 seemed to hasten HIV progression, and no one knew why. Lusso was studying HHV-6's effects on lymphoid cells but wanted to see what the virus did to whole pieces of lymphoid tissue. So he asked Margolis, a virologist at the US National Institute of Child Health and Human Development in Bethesda, Maryland, and an expert on three-dimensional-tissue, to perform some experiments for him.
Margolis agreed. Human lymph-node tissue was hard to come by, but tonsils, which doctors remove from patients all the time, are also lymphoid tissue — and Margolis had developed an experimental tonsil-tissue system to study HIV pathogenesis. Because HHV-6 infection was often found alongside HIV, Margolis and his colleague Jean-Charles Grivel co-infected tonsil tissue with both viruses. He predicted that the herpesvirus, normally suppressed by the immune system, would be free to replicate in immune-compromised HIV-infected tissue.
But, weeks later, when Grivel analysed the infected tissue, something was wrong. HIV wasn't replicating. Although excited, the scientists didn't want to jump to conclusions, so Grivel performed the experiments again. “There was another three weeks of waiting, which was really very emotional,” Margolis says. Nevertheless, they got the same result. “We couldn't believe our eyes,” Margolis says. HHV-6, at least in this situation, seemed to protect against HIV1.
So infectious agents interact with each other and with hosts in unpredictable ways. An average human body is rife with viruses, and benign and not-so-benign bacteria as well as 'endogenous retroviruses', which buried themselves in the human genome eons ago. This crowded house is a different beast from the sterile cell lines used as models. Scientists such as Margolis therefore argue for a broader approach to virology — one that involves studying infections in a more true-to-life context, predicting their interactions and sometimes taking the unexpected good with the usual bad that infections bring.

That microbes can benefit their hosts is by no means new. For example, bacteria living in the human gut are known to influence immune function, and help our body absorb nutrients. But only recently have scientists suggested that infectious viruses could provide their hosts with benefits as well. Viruses influence the host immune system in significant — and occasionally beneficial — ways, a concept that isn't surprising when one considers that they have been interacting with immune systems for millions of years.
Recently, Herbert 'Skip' Virgin, an immunologist at Washington University School of Medicine in St Louis, Missouri, infected mice with dormant viruses genetically similar to human Epstein–Barr virus and human cytomegalovirus. These viruses, he found, protected the mice from the bacterial pathogens Listeria monocytogenes and Yersinia pestis . Virgin and his colleagues suggest that the viruses upregulate the production of immune factors that prevent further infection rather than interacting directly with the microbes2.
Helping or hindering?
The endogenous retroviruses that cemented their place in human history by infecting the eggs and sperm of our ancestors account for more than 8% of our genome, and some report that as much as half of our genome is composed of fragmented viruses. These viruses seem to influence immune function; for example, the susceptibility of mice to Friend virus, a strain of murine leukaemia virus, is controlled by two genes derived from endogenous retroviruses3. Some have proposed that endogenous retroviruses, long fixed in mammalian genomes, provide the immunosuppression that allows a fetus to develop in its mother's body, despite the differences between the immune systems.
Viruses also interact with each other directly, as Margolis discovered for himself in 2001. Similar viruses sometimes compete with each other, causing one to eventually 'win over' a cell and literally block infection by others. Viruses that are different enough from each other can co-infect cells cooperatively; in a process known as complementation, one virus provides another with a useful protein that it co-opts for its own use. Occasionally, viruses become dependent on other viruses. One such example is hepatitis D, which requires the presence of hepatitis B in order to replicate.
Margolis uncovered why HHV-6 prevents HIV replication under certain conditions. A subtype of HIV, most often found in early infection, generally gains entry into the cell by binding the receptor CCR5. When HHV-6 infects first, however, it instigates production of an immune chemical that binds to CCR5 receptors, blocking HIV's access. HIV can develop resistance to this chemical over time and HHV-6 co-infection may exert selective pressure on HIV to become immune-resistant, or switch to a different co-receptor — a change accompanied by increased HIV virulence. This explains the often poor prognosis of patients infected by both viruses.

Other human viruses influence HIV replication. Margolis found that human herpesvirus 7 (HHV-7) inhibits HIV replication, albeit via a different mechanism from HHV-6 (ref. 4). In 1998, two groups independently reported that HIV patients infected with a seemingly innocuous hepatitis-like virus called GBV-C live longer, although neither group knew why. The studies piqued the interest of Jack Stapleton, director of the University of Iowa's Helen C. Levitt Center for Viral Pathogenesis and Disease in Iowa City, who was, at the time, running an AIDS clinic while studying hepatitis C–HIV interaction.

“We thought it was a statistical fluke and that it wouldn't hold up in a larger study,” Stapleton recalls. With access to hundreds of samples, Stapleton decided to replicate the GBV-C study on a group of 362 HIV patients from his clinic. What he found surprised him and confirmed the findings: “If patients had [GBV-C], they were three times more likely to be alive at follow-up,” he says5. Stapleton's subsequent research, along with work completed by a group in Germany, has shown that a GBV-C peptide interferes with early replication of HIV, and that GBV-C, like HHV-6, increases production of an immune chemical that blocks HIV's entry into the cell.
Always dangerous
No one would suggest purposefully infecting individuals with a persistent infection to ward off HIV. After all, one of the hallmarks of viruses is that they evolve quickly. “Any virus that is not causing disease has the potential to cause disease,” says Robert Gallo, director of the Institute of Human Virology at the University of Maryland School of Medicine in Baltimore, and the co-discoverer of HIV. That said, Gallo, who worked with Lusso on the HHV-6 discovery, and his team recently tested the immune chemical produced during HHV-6 infection as a vaginal microbicide in macaque monkeys and found that it significantly lowered risk of contracting a monkey-infecting version of HIV6.
To make further progress, scientists need to expand which viruses they study, and how they study them, Margolis says. They need to use tissue systems that preserve immune function and cellular communication, because cells within tissues communicate with one another differently and have a different architecture than do cells that are cultured in vitro.

Moreover, Margolis suggests, scientists should study infections in tissues harbouring the same persistent viruses present in humans. “If you study a pathogen such as HIV in a cell-culture model where there is no immune system, there is no effect from other microbes that are in the normal state in an infected human,” says Stapleton. “You're really missing important factors that will influence the pathogenesis.”

What would be ideal, says Margolis, is a table, not unlike Mendeleev's table of the elements, for infectious agents. “I fantasize about creating a periodic table of microbes,” he says. Each cell in the table might feature the name of the microbe, the immune factors it affects, the receptors it uses and the signalling systems it incorporates, he says. Just as the elemental version predicts how two substances react with one another, the periodic table of microbes would predict how two microbes interact in the human body.

“It's off the wall, but it could generate enormous insights,” says Michael Lederman, the director of the Center for AIDS Research at Case Western Reserve University in Cleveland, Ohio. Other scientists say that although such a table may have some practical value, the concept is potentially more interesting as a catalyst for scientific ideas and approaches. Philip Murphy, chief of the Laboratory of Molecular Immunology at the US National Institute of Allergy and Infectious Diseases in Bethesda, Maryland, says that scientists can only get so far with existing tissue and animal models. “Pathogens are very host-limited, so there is a whole range of human pathogens that you could never do an experiment with in mice models,” he says. For example, although Margolis's lymphoid-tissue model is incredibly useful, he says, there are a number of pathogens that will never infect lymphoid tissue. Scientists will, in other words, need to get creative.
Expanding the study of virology in these ways is challenging for other reasons, too. It is difficult, for example, for a scientist with expertise in DNA viruses such as herpesviruses to study their interactions with RNA viruses such as HIV. But collaboration can help, and although broadening the context of virology might make experiments more complicated, it will also make them more realistic, Margolis says. “In a more complicated system, you probably can understand less,” he admits. “But what you understand is really relevant.”

Gunakan Kedelai Hitam dan Kacang Hijau

Surabaya, Kompas - Perajin tempe bisa mengganti bahan baku kedelai putih yang harganya semakin mahal dengan kedelai hitam dan kacang hijau. Beragam jenis kacang-kacangan lain juga bisa dipakai sebagai bahan baku tempe.
Pakar teknologi pangan dari Universitas Brawijaya, Malang, Nur Hidayat, mengatakan, sebenarnya semua jenis kacang-kacangan bisa dipakai untuk membuat tempe. Tetapi, saat ini hanya kedelai hitam dan kacang hijau yang paling mudah digunakan. "Jumlah produksi kedua jenis tumbuhan itu bisa memenuhi kebutuhan pembuat tempe," ujarnya dari Malang, Selasa (15/1).
Kedua jenis kacang tersebut juga biasa dipasok petani dalam negeri sehingga tidak perlu khawatir terpengaruh kenaikan harga di pasar global. "Harganya relatif lebih murah dibandingkan dengan kedelai kuning saat ini," tuturnya.
Memang, rasa tempe dari kedua kacang itu berbeda dibandingkan dengan tempe kedelai kuning. Kalaupun ingin lebih terasa seperti tempe sekarang, bisa dicampur dengan sedikit kedelai kuning.
Pengurus Yayasan Tempe Indonesia, Arsiniati M Brata, mengatakan, sebagai alternatif bisa juga dipilih kacang koro dan kecipir. Tetapi, kedua jenis kacang itu harus diperkecil ukurannya. "Tempe koro dianggap kurang menarik karena koronya besar-besar. Kalau diperkecil mungkin lebih menarik," tuturnya.
Di beberapa daerah, tempe berbahan baku demikian sudah dikenal. Namun, tempe-tempe itu memang kurang populer dibandingkan dengan tempe kedelai putih. "Ada banyak alternatif bahan baku bisa dipakai," ujar guru besar emeritus ilmu gizi Universitas Airlangga itu.
Penggunaan bahan baku alternatif itu lebih baik dibandingkan dengan apa yang dilakukan perajin sekarang ini. Saat ini sebagian perajin mencampur kedelai dengan singkong atau jagung. "Penggunaan campuran itu membuat tempe mengandung karbohidrat. Kandungan karbohidrat membuat tempe berasa asam dan kaya bakteri," ujarnya. (RAZ)

kompas, 16 Januari 2008 (Humaniora)
http://kompas.com/kompas-cetak/0801/16/humaniora/4168787.htm

seminar nasional PATPI 2008

Pada 14 - 16 Oktober 2008 akan diadakan semanar nasional dan kongres PATPI di Palembang. dengan tema "Peranan Ilmu dan Teknologi dalam Meningkatkan Kualitas dan Ketahanan Pangan untuk Mmperluas Akses Pasar" dengan 3 subtema yaitu:
1. Teknologi Proses Pangan
a. Diversivikasi dan pengembangan produk pangan
b. keteknikan Pangan
c. Pengawetan Pangan
d. Bioteknologi Pangan
e. Pengemasan Pangan

2. Manajemen Pangan
a. Sosial ekonomi Produk Pangan
b. Pemasaran Produk Pangan
c. Kebijakan Pangan

3. Keamanan dan Kesehatan Pangan
a. Keamanan Pangan
b. Gizi dan Biokimia Pangan
c. Toksikologi
d. Penangan dan Pemanfaatan Limbah

bagi yang menginginkan informasi lebih lanjut silahkan hubungi email patpi2008@yahoo.com atau di blog ptp2007.wordpress.com

Abstrak Jurnal tentang Aspergillus niger

The Weak-Acid Preservative Sorbic Acid Is Decarboxylated and Detoxified by a Phenylacrylic Acid Decarboxylase, PadA1, in the Spoilage Mold Aspergillus niger

Andrew Plumridge, Malcolm Stratford, Kenneth C. Lowe, and David B. Archer
Applied and Environmental Microbiology, January 2008, p. 550-552, Vol. 74, No. 2

Resistance to sorbic and cinnamic acids is mediated by a phenylacrylic acid decarboxylase (PadA1) in Aspergillus niger. A. niger padA1 mutants are unable to decarboxylate sorbic and cinnamic acids, and the MIC of sorbic acid required to inhibit spore germination was reduced by 50% in padA1 mutants.

(Hasil poling terbanyak tentang abstrak jurnal, maka hari ini kami tampilkan abstrak dari Jurnal, mengenai topik tertentu, jika diinginkan silahkan tulis pada komentar, dan akan kami usahakan. terima kasih)

Hasil Rapat Lab Bulan Januari

Pada hari Rabu, 9 Januari 2008 telah diadkan rapat dengan hasil.
Koordinator untuk:
1. Penulisan Manual Analisis Manajemen dan Teknologi Limbah: Bu Atifah
2. Penulisan dalam Jurnal Teakreditasi: Pak Wignyanto
3. Koordinator Pelatihan: Bu Nia dan Bu Neneng
4. Koordinator seminar: Pak Nur

Diharapkan semua koordinator melaporkan program kegiatannya pada rapat bulan Februari.

Dalam rapat juga diputuskan adanya sumbangan dana bagi yang menerima dana penelitian atau pengabdian.
Sehubungan dengan program S3 bu Hindun dan selesainya S2 Bu neneng maka diadakan perubahan pembimbingan skripsi.

selamat bekerja.
Ka. lab

Bu Sri Suhartini sudah Selesai Sekolah

Bulan Januari 2008 ini Bu Sri Suhartini telah menyelesaikan s2 di Queensland Univerity dan mulai aktif kembali. dengan demikian saat ini sudah tidak ada lagi dosen di Lab Bioindustri yang berpendidikan S1.

Untuk berikutnya bu Neneng (panggilan beliau) akan lebih banyak mengajar yang ebrkait dengan limbah dan lingkungan sesuai yang dipelajari.

selamat datang dan bergabung dan berjarya kembali dengan laboratorium tercinta