wow.

we literally just rolled into town about 45 minutes ago....i rushed in to put on tay's first day of school outfit- wet a brush to try and tame her crazy hair...i dumped the kennel, cooler, fishing rods, suitcases, and food in the middle of the floor so i could pack tay back in the car to get her to school on time. we went into the classroom and played baby dolls. i acted like i was looking for a bottle for the babies and snuck out of the door.... now i am back home staring at this mess i have created, hoping tay is having a wonderful first day of school and trying to inhale my coffee as fast as i can b/c i am so tired....seriously, is it only 9:30??

*image courtesy of rikshaw design

Obat Ginjal, dari Kumis Kucing hingga Sambiloto

Jumat, 4 September 2009 | 11:57 WIB

KOMPAS.com — Apa saja tanaman obat yang telah digunakan dan memiliki potensi untuk dijadikan pilihan alternatif ataupun pendamping pengobatan batu ginjal dan membantu meningkatkan kinerja ginjal?

Prof Dr Sumali Wiryowidagdo, Guru Besar Departemen Farmasi Fakultas MIPA UI, menyatakan bahwa beberapa tanaman obat sebenarnya layak disebut herba rasional karena telah dibuktikan selama bertahun-tahun meski secara empiris. Tanaman obat ini paling tidak telah teruji khasiat, efektivitas, dan keamanannya. Jenis-jenis herba yang dapat digunakan untuk mengatasi gangguan ginjal dan kandung kemih di antaranya:

KUMIS KUCING
Bersifat diuretik, bermanfaat untuk mengatasi infeksi kandung kemih, infeksi saluran kemih, kencing batu, batu kantung empedu, dan sebagai antipiretik.
Komponen berkhasiat: Eupatrin, sinensetin, 3-hidroksi-tetrametil flavon dan siphonol A-E.
Cara meramu: Kumis kucing dan meniran, masing-masing 30 gram, direbus. Setelah dingin airnya diminum.

LOBAK
Sebagai peluruh batu ginjal. Cara meramu: 200 gram lobak dibuat jus, lalu disaring dan diminum untuk satu hari.

TAPAK LIMAN
Seluruh bagian tanaman dapat dimanfaatkan sebagai peluruh batu ginjal, untuk meningkatkan kinerja ginjal, antiseptik, antiradang, dan penurun panas.
Komponen berkhasiat deoxy, isodeoxyelephantopin, dan seskuiterpena.
Cara meramu: Rebus 1.530 gram tanaman yang telah dikeringkan, airnya diminum.

PEGAGAN
Bersifat antibakteri, menyembuhkan luka, antiradang, antioksidan, dan meningkatkan kinerja ginjal. Telah melalui beberapa uji praklinis untuk antibakteri, ginjal, dan antitumor. Digunakan sebagai obat untuk membantu penyembuhan luka dan radang pada saluran kemih.
Cara meramu: Daun segar sebanyak 50-80 gram direbus, airnya diminum.

DAUN SENDOK
Bermanfaat sebagai antiinflamasi, melarutkan batu ginjal, meningkatkan kerja ginjal, dan sebagai antibakteri.
Komponen kimia: Plantaginin, - homoplantaginin, katalpol.
Cara meramu: Rebus 15-30 gram daun dengan 2 gelas air sampai tinggal 1 gelas, lalu minum.

TEMPUYUNG
Sebagai peluruh kemih, melarutkan batu empedu, dan meningkatkan kinerja ginjal. Komponen kimia: Flavonoid dan aeskulin.
Cara meramu: 5 lembar daun tempuyung, 5 lembar daun alpukat, 5 lembar daun sawi tanah direbus dengan 3 gelas air hingga tersisa 2 gelas. Minum setelah dingin.
Cara lain: 5 lembar daun tempuyung, 6 buah jagung muda, dan gula aren secukupnya direbus, airnya diminum.

CEPLUKAN
Sebagai peluruh batu dan meningkatkan kerja ginjal, bersifat analgesik, antitumor, dan antiseptik.
Komponen kimia: Fisalin B, D, F dan withangulatin A. Saat ini pengembangan penelitian diarahkan untuk membuktikan potensinya sebagai antikanker.
Cara meramu: Konsumsi langsung buahnya atau air rebusan daun secukupnya.

ALANG ALANG
Sebagai infus rimpang, sebagai peluruh batu dan meningkatkan kerja ginjal, menurunkan tekanan darah, sekaligus pereda panas dalam. Hasil penelitian membuktikan tanaman ini tidak beracun, dan praktis penggunaannya karena cukup direbus.
Kandungan kimia: Arundoin, fernenol, isoarborinol, silindrin, dan skopoletin.

DAUN ALPUKAT
Perasan daun alpukat berkhasiat sebagai peluruh batu ginjal dan meningkatkan kerja ginjal. Seduhan daun sebagai pelarut batu ginjal kalsium. Komponen kimia: Polifenol, flavonoid, alkolodi, dan saponin.

KEJI BELING
Daun berkhasiat sebagai peluruh dan pelarut batu ginjal dan batu kandung empedu.
Untuk batu kandung kemih: Rebus bersama tongkol jagung muda.
Untuk batu ginjal: Campur dengan daun menirandan daun ungu. Dapat juga dicampur dengan tempuyung dan tongkol jagung muda.

MENIRAN
Digunakan sebagai peluruh batu ginjal dan mengurangi infeksi sekaligus mempertahankan kinerja ginjal, meningkatkan daya tahan tubuh.
Untuk ramuan diuretik: 20 gram herba direbus selama 15 menit, lalu diminum.
Komponen kimia: Flavonoid kuersitrin, kuersitrin, isokuersitrin, filantin, dan nirantin.

DAUN SAMBILOTO
Digunakan bila terjadi komplikasi penghancuran batu ginjal, nanah dalam saluran kencing, dan atau darah dalam saluran kencing. Berfungsi sebagai diuretik dan peningkat daya tahan tubuh. Komponen kimia: Andirgafolida, neoandrografolida, homoandrografolida, andrografin.
Cara meramu: Rebus daun segar atau yang telah dikeringkan secukupnya. (GHS/ken)

http://kesehatan.kompas.com/read/xml/2009/09/04/11575663/obat.ginjal.dari.kumis.kucing.hingga.sambiloto

Note:

Kombinasi herbal yg selama ini efektif utk atasi batu ginjal adalah Meniran dan Tempuyung. Jika ingin mendapatkan kapsul herbal tsb bisa contact sy di 081310343598 atau email budiprakoso98@gmail.com.

Animal Models of Atherosclerosis: LDL

Researchers have developed a number of animal models of atherosclerosis (fatty/fibrous lesions in the arteries that influence heart attack risk) to study the factors that affect its development. In the next two posts, I will argue that these models rely on a massive increase in LDL, up to 10-fold, due to overloading the cholesterol metabolism of herbivorous species with excessive dietary cholesterol. This also greatly increases oxidized LDL, leading to atherosclerosis. I will discuss the role of saturated fat, which often receives the blame, in this process.

A reader recently sent me a reference to an interesting paper titled "Dietary Fat Saturation Effects on Low-density-lipoprotein Concentrations and Metabolism in Various Animal Models". It's a review of animal studies that have looked at the effect of different fats on LDL concentration as of 1997. 

When an investigator wants to study diet-induced atherosclerosis, first he selects a species that's susceptible to it. These are generally herbivorous or nearly herbivorous species such as rabbits, guinea pigs, hamsters, and several species of monkey. Then, he feeds it an "atherogenic diet". This is typically a combination of 0.1 to 1% cholesterol by weight, plus 20-40% of calories as fat. The fat can come from a variety of sources, but animal fats or saturated vegetable fats are typical. The remainder of the diet is processed grains, vitamin and mineral supplements, and often casein for protein.

Let's put that amount of cholesterol into human context. Assuming the average person eats about 2 pounds dry weight of food per day, 0.5% cholesterol would be 4.5 grams. That's the equivalent of:

• 17.5 pounds of beef steak, or
• 3.8 pounds of beef liver, or
• 22.5 eggs

Per day. Now feed that to an herbivore that's not adapted to clearing cholesterol. You can imagine it doesn't do their blood lipids any favors. For example, in one study, compared to a low-fat, low-cholesterol "control diet", a diet of 20% hydrogenated coconut oil plus 0.12% cholesterol caused hamsters' LDL to increase by more than 7-fold. A polyunsaturated fat (PUFA) rich diet caused LDL to increase less. This study is typical, and the interpretation is typical as well: SFA raises LDL. But there's another possible explanation: in the absence of unnatural amounts of dietary cholesterol, PUFA reduces LDL in some species, and SFA has very little effect on it in most.

It's important to remember that the relevance of this hamster experiment to humans is unclear. No one is claiming that reducing saturated fat and cholesterol will reduce a human's LDL by 7-fold.  

But let's get back to the animal models. The hypothesis the paper addresses is that saturated fat raises LDL in animal models. If that is true, it should be able to raise LDL even in the absence of added cholesterol. So let's consider only the studies that didn't add extra cholesterol to the diets. And if saturated fat raises LDL, it should also do it relative to monounsaturated fat (MUFA- like olive oil), rather than only in comparison to PUFA, which has a known cholesterol-lowering effect. So let's narrow the studies further to those that compared SFA-rich fats, MUFA-rich fats and PUFA-rich fats. In Fernandez et al. (1989), investigators fed guinea pigs 35% of calories from corn oil (PUFA), olive oil (MUFA) or lard (MUFA-SFA). Here's what their LDL looked like:
The same investigators published two more studies showing similar results over the next five years. The next study was published by Khosla et al. in 1992. They fed cebus and rhesus monkeys cholesterol-free diets containing 40% of calories from safflower oil (PUFA), high-oleic safflower oil (MUFA) or palm oil (SFA-MUFA). How was their LDL?
None of the differences were statistically significant. Khosla and colleagues published another study with the same result in 1993. This is hardly supportive of the idea that saturated fat raises LDL in animal models. The most you can say is that PUFA lowers LDL in some, but not all, species. There is no indication from these studies that SFA raises LDL in the absence of excessive dietary cholesterol. I didn't cherry pick studies here; this is every study in the review paper that met my two criteria of no added cholesterol and a MUFA comparison group.

The bottom line is that experimental models of atherosclerosis appear to rely on overloading herbivorous species with dietary cholesterol that they are not equipped to clear. SFA does exacerbate the increase in LDL caused by cholesterol overload. But in the absence of excess cholesterol, it does not necessarily raise LDL even in species ill-equipped to digest these types of fats. Dietary cholesterol has a modest effect on LDL cholesterol in humans, and it has even less effect on LDL particle number, a more important measure. So there may not be a cholesterol overload for saturated fat to exacerbate in humans. 

PUFA vegetable oils do lower LDL in humans, and the effect appears to persist for at least a few years (probably indefinitely). But the evidence is not conclusive that lowering cholesterol in this way actually prevents heart attacks.

Dr. Stephan

After a very challenging summer, I've finally turned in my written thesis, so it's official: I have my Ph.D. I'm publishing the abstract below. These findings should all be published in peer-reviewed journals in the next 6 months.


Ataxin-7 Conserved Motifs Determine the Severity of the Neurodegenerative Disorder Spinocerebellar Ataxia Type 7 in Transgenic Mice and Influence Lifespan in Yeast

Spinocerebellar ataxia type 7 (SCA7) is an autosomal dominant, progressive neurodegenerative disorder whose characteristic features are cerebellar ataxia, dysarthria, and retinal cone-rod dystrophy culminating in blindness. SCA7 is caused by an abnormally long glutamine-coding CAG repeat in the SCA7 gene, which encodes the protein Ataxin-7.

Ataxin-7 contains several conserved motifs that may influence the toxicity of the glutamine tract. Among these are three conserved regions (conserved block I – III), two caspase-7 cleavage sites, a nuclear export signal and two monopartite nuclear localization signals (NLS). Previous investigations have shown that the caspase-7 cleavage site D266 is required for the full toxicity of the Ataxin-7 protein in cell culture. We generated SCA7 transgenic mice expressing a 92 CAG version of the human SCA7 cDNA, with and without a D266N mutation. Mice carrying the D266N mutation were protected from SCA7-like neurodegeneration, behavioral signs and shortened lifespan.

To further characterize the role of conserved motifs in SCA7 pathology, we generated SCA7 transgenic mice carrying point mutations in both C-terminal NLSs (KKRK -> KAAK). Previous work has shown that nuclear localization is an important step in the pathology of CAG repeat disorders. We observed that mice lacking C-terminal NLS activity were substantially protected from degeneration of the retina and cerebellum, SCA7-like behavioral signs and shortened lifespan.

Age is the primary risk factor for neurodegenerative disease. Even in the absence of overt disease, the aging brain shows histopathological and molecular changes reminiscent of neurodegeneration. To explore the link between neurodegenerative disease and aging, we have examined the replicative lifespan of Saccharomyces cerevisiae missing the SCA7 ortholog, SGF73. This strain exhibits an unusually long lifespan, which is dependent on the function of the NAD+-dependent deacetylase SIR2. We present evidence that the extended lifespan of the SGF73 null strain is due to the influence of Sgf73 on the activity of Sir2 and the histone deubiquitinase Ubp8. Furthermore, we show that the level of ubiquitinated H2B is elevated in an SCA7 transgenic mouse line, indicating that an alteration in Ubp8 activity may play a role in SCA7 pathology and that aging and neurodegeneration may share a common mechanism.

Sejarah Kereta Api ( lokomotif )

Sejarah perkeretaapian sama seperti sejarah alat transportasi umumnya yang diawali dengan penemuan roda. Mulanya dikenal kereta kuda yang hanya terdiri dari satu kereta (rangkaian), kemudian dibuatlah kereta kuda yang menarik lebih dari satu rangkaian serta berjalan di jalur tertentu yang terbuat dari besi (rel) dan dinamakan sepur. Ini digunakan khususnya di daerah pertambangan tempat terdapat lori yang dirangkaikan dan ditarik dengan tenaga kuda.

Setelah James Watt menemukan mesin uap, Nicolas Cugnot membuat kendaraan beroda tiga berbahan bakar uap. Orang-orang menyebut kendaraan itu sebagai kuda besi. Kemudian Richard Trevithick membuat mesin lokomotif yang dirangkaikan dengan kereta dan memanfaatkannya pada pertunjukan di depan masyarakat umum. George Stephenson menyempurnakan lokomotif yang memenangi perlombaan balap lokomotif dan digunakan di jalur Liverpool-Manchester. Waktu itu lokomotif uap yang digunakan berkonstruksi belalang. Penyempurnaan demi penyempurnaan dilakukan untuk mendapatkan lokomotif uap yang lebih efektif, berdaya besar, dan mampu menarik kereta lebih banyak.

Penemuan listrik oleh Michael Faraday membuat beberapa penemuan peralatan listrik yang diikuti penemuan motor listrik. Motor listrik kemudian digunakan untuk membuat trem listrik yang merupakan cikal bakal kereta api listrik. Kemudian Rudolf Diesel memunculkan kereta api bermesin diesel yang lebih bertenaga dan lebih efisien dibandingkan dengan lokomotif uap. Seiring dengan berkembangnya teknologi kelistrikan dan magnet yang lebih maju, dibuatlah kereta api magnet yang memiliki kecepatan di atas kecepatan kereta api biasa. Jepang dalam waktu dekade 1960-an mengoperasikan KA Super Ekspress Shinkanzen dengan rute Tokyo-Osaka yang akhirnya dikembangkan lagi sehingga menjangkau hampir seluruh Jepang. Kemudian Perancis mengoperasikan kereta api serupa dengan nama TGV.