cyanic-selkie/wikianc huggingface dataset:
HIV
The clinical course of HIV-1 infection
Infection with HIV-1 is associated with a progressive loss of CD4+ T-cells (lymphocytes). This rate of loss can be measured and is used to determine the stage of infection. The loss of CD4+ T-cells is linked with an increase in viral load. The clinical course of HIV-infection generally includes three stages: primary infection, clinical latency and AIDS (Figure 1). HIV plasma levels during all stages of infection range from just 50 to 11 million virions per ml.
Primary infection
Primary, or acute infection is a period of rapid viral replication that immediately follows the individual's exposure to HIV. During primary HIV infection, most individuals (80 to 90%) develop an acute syndrome characterised by flu-like symptoms of fever, malaise, lymphadenopathy, pharyngitis, headache, myalgia, and sometimes a rash. Within an average of three weeks after transmission of HIV-1, a broad HIV-1 specific immune response occurs that includes seroconversion. Because of the nonspecific nature of these illnesses, it is often not recognized as a sign of HIV infection. Even if patients go to their doctors or a hospital, they will often be misdiagnosed as having one of the more common infectious diseases with the same symptoms. Since not all patients develop it, and since the same symptoms can be caused by many other common diseases, it cannot be used as an indicator of HIV infection. However, recognizing the syndrome is important because the patient is much more infectious during this period.
Clinical latency
A strong immune defense reduces the number of viral particles in the blood stream, marking the start of the infection's clinical latency stage (Figure 1). Clinical latency can vary between two weeks and 20 years. During this early phase of infection, HIV is active within lymphoid organs, where large amounts of virus become trapped in the follicular dendritic cells (FDC) network. The surrounding tissues that are rich in CD4+ T-cells also become infected, and viral particles accumulate both in infected cells and as free virus. Individuals who have entered into this phase are still infectious.
HIV structure and genome
HIV is different in structure from previously described retroviruses. It is around 120 nm in diameter (120 billionths of a meter; around 60 times smaller than a red blood cell) and roughly spherical.
HIV has several major genes coding for structural proteins that are found in all retroviruses, and several nonstructural ("accessory") genes that are unique to HIV. The gag gene provides the physical infrastructure of the virus; pol provides the basic enzymes by which retroviruses reproduce; the env gene supplies the proteins essential for viral attachment and entry into a target cell. The accessory proteins tat, rev, nef, vif, vpr, and vpu enhance virus production. Although called accessory proteins, tat and rev are essential for virus replication. In some strains of HIV, a mutation causes the production of an alternate accessory protein, Tev, from the fusion of tat, rev, and env.
The gp120 and gp41 proteins, both encoded by the env gene, enable the virus to attach to and fuse with target cells to initiate the infectious cycle. Both, especially gp120, have been considered as targets of future treatments or vaccines against HIV.
HIV tropism
The term viral tropism refers to the cell type that the virus infects and replicates in. HIV can infect a variety of cells such as CD4+ helper T-cells and macrophages that express the CD4 molecule on its surface. HIV-1 entry to macrophages and T helper cells is mediated not only through interaction of the virion envelope glycoproteins (gp120) with the CD4 molecule on the target cells but also with its chemokine coreceptors. Macrophage (M-tropic) strains of HIV-1, or non-syncitia-inducing strains (NSI) use the beta-chemokine receptor CCR5 for entry and are thus able to replicate in macrophages and CD4+ T-cells. The normal ligands for this receptor, RANTES, macrophage inflammatory protein (MIP)-1-beta and MIP-1-alpha, are able to suppress HIV-1 infection in vitro. This CCR5 coreceptor is used by almost all primary HIV-1 isolates regardless of viral genetic subtype. Indeed, macrophages play a key role in several critical aspects of HIV disease. They appear to be the first cells infected by HIV and perhaps the very source of HIV production when CD4+ cells are markedly depleted in the patient. Macrophages and microglial cells are the cells infected by HIV in the central nervous system. In tonsils and adenoids of HIV-infected patients, macrophages fuse into multinucleated giant cells that produce copious amounts of virus. T-tropic isolates, or syncitia-inducing (SI) strains replicate in primary CD4+ T-cells as well as in macrophages and use the alpha-chemokine receptor, CXCR4, for entry. The alpha-chemokine, SDF-1, a ligand for CXCR4, suppresses replication of T-tropic HIV-1 isolates. It does this by down regulating the expression of CXCR4 on the surface of these cells. Viruses that use only the CCR5 receptor are termed R5, those that only use CXCR4 are termed X4, and those that use both, X4R5. However, the use of coreceptor alone does not explain viral tropism, as not all R5 viruses are able to use CCR5 on macrophages for a productive infection. Some people are resistant to certain strains of HIV. An example of this is people with the CCR5-Δ32 mutation; these people are resistant to infection with R5 virus as the mutation does not allow HIV to bind to this coreceptor, impeding its ability to infect the target cell. HIV can also infect a subtype of dendritic cells, MDC-1, which probably constitute a major reservoir that maintains infection when T helper cell numbers have declined to extremely low levels.
Viral entry to the cell
The change in gp120's shape also exposes a portion of the gp41 glycoprotein, which was previously buried in the viral membrane and loosely bound to gp120. A fusion peptide within gp41 causes the fusion of the viral envelope and the host-cell envelope, allowing the capsid to enter the target cell. The exact mechanism by which gp41 causes the fusion is still largely unknown.
Once HIV has bound to the target cell, the HIV RNA and various enzymes, including but not limited to reverse transcriptase, integrase and protease, are injected into the cell.
Viral replication and transcription
Once the viral capsid has entered the cell, an enzyme called reverse transcriptase liberates the single-stranded (+)RNA from the attached viral proteins and copies it into a negatively sensed viral complementary DNA of 9 kb pairs (cDNA) (Figure 2). This process of reverse transcription is extremely error prone and it is during this step that mutations (such as drug resistance) are likely to arise. The reverse transcriptase then makes a complementary DNA strand to form a double-stranded viral DNA intermediate (vDNA). This new vDNA is then transported into the cell nucleus. The integration of the proviral DNA into the host genome is carried out by another viral enzyme called integrase. This is called the latent stage of HIV infection. To actively produce virus, certain transcription factors need to be present in the cell. The most important is called NF-kB (NF Kappa B) and is present once the T cell becomes activated. This means that those cells most likely to be killed by HIV are in fact those currently fighting infection.
Initially the integrated provirus is copied to mRNA which is then spliced into smaller chunks. These small chunks produce the regulatory proteins Tat (which encourages new virus production) and Rev. As Rev accumulates it gradually starts to inhibit mRNA splicing. At this stage the structural proteins Gag and Env are produced from the full-length mRNA. Additionally the full-length RNA is actually the virus genome, so it binds to the Gag protein and is packaged into new virus particles.
Interestingly, HIV-1 and HIV-2 appear to package their RNA differently; HIV-1 will bind to any appropriate RNA whereas HIV-2 will preferentially bind to the mRNA which was used to create the Gag protein itself. This may mean that HIV-1 is better able to mutate (HIV-1 causes AIDS faster than HIV-2 and is the majority species of the virus).
Viral assembly and release
The final step of the viral cycle, assembly of new HIV-1 virions, begins at the plasma membrane of the host cell. The Env polyprotein (gp160) goes through the endoplasmic reticulum and is transported to the Golgi complex where it is cleaved by protease and processed into the two HIV envelope glycoproteins gp41 and gp120. These are transported to the plasma membrane of the host cell where gp41 anchors the gp120 to the membrane of the infected cell. The Gag (p55) and Gag-Pol (p160) polyproteins also associate with the inner surface of the plasma membrane along with the HIV genomic RNA as the forming virion begins to bud from the host cell. Maturation either occurs in the forming bud or in the immature virion after it buds from the host cell. During maturation, HIV proteases (proteinases) cleave the polyproteins into individual functional HIV proteins and enzymes. The various structural components then assemble to produce a mature HIV virion. This step can be inhibited by drugs. The virus is then able to infect another cell.
Genetic variability of HIV
One of the major characteristics of HIV is its high genetic variability as a result of its fast replication cycle and the high error rate and recombinogenic properties of reverse transcriptase. This means that different genomic combinations may be generated within an individual who is infected by genetically different HIV strains. Recombination results when a cell is simultaneously infected by two different strains of HIV and one RNA transcript from two different viral strains are encapsidated into the same virion particle. This virion then infects a new cell where it undergoes replication. During this phase, the reverse transcriptase, by jumping back and forth between the two different RNA templates, will generate a newly synthesized retroviral DNA sequence that is a recombinant between the two parental genomes. This recombination is most obvious when it occurs between subtypes.
Three groups of HIV-1 have been identified on the basis of differences in env: M, N and O (Figure 4). Group M is the most prevalent and is subdivided into eight subtypes, based on the whole genome, that are each geographically distinct. The most prevalent are subtypes B (found predominantly in North America and Europe), A and D (found predominantly in Africa), and C (found predominantly in Africa and Asia) (Figure 5); these subtypes form branches in the phylogenetic tree representing the lineage of the M group of HIV-1 (Figure 4). Coinfection with distinct subtypes gives rise to circulating recombinant forms (CRFs).
In 2000, the last year in which an analysis of global subtype prevalence was made, 47.2% of infections worldwide were of subtype C, 26.7% were of subtype A/CRF02_AG, 12.3% were of subtype B, 5.3% were of subtype D, 3.2% were of CRF_AE, and the remaining 5.3% were composed of other subtypes and CRFs (Figure 5). Almost 95% of all HIV research currently taking place is focused on subtype B, while a few laboratories focus on other subtypes.
Treatment
HIV infection is a chronic infectious disease that can be treated, but not yet cured. There are effective means of preventing complications and delaying progression to AIDS. At the present time, not all persons infected with HIV have progressed to AIDS, but it is generally believed that the majority will. People with HIV infection need to receive education about the disease and treatment so that they can be active partners in decision making with their health care provider.
A combination of several antiretroviral agents, termed Highly Active Anti-Retroviral Therapy HAART, has been highly effective in reducing the number of HIV particles in the blood stream (as measured by a blood test called the viral load). This can improve T-cell counts. This is not a cure for HIV, and people on HAART with suppressed levels of HIV can still transmit the virus to others through sex or sharing of needles. There is good evidence that if the levels of HIV remain suppressed and the CD4 count remains greater than 200, then the quality and length of life can be significantly improved and prolonged. Improved antiretroviral inhibitors against proteins such as Reverse transcriptase, Integrase and Tat are being researched and developed. One of the most promising new therapies is a new class of drugs called fusion or entry inhibitors.
Current recommendations for treatment include at least a three drug effective regime to induce complete cease of viral replication and reduce the incidence of new mutations. Current drug classes include NNRTI, NRTI, NtRTI, PI, FI. Each of the drugs in these classes represent individual pharmacodynamics and toxicities, requiring expert knowledge to appropriately select and dose an effective combination.
Post-exposure prophylaxis (PEP) with a course of antiviral drugs is also thought to reduce the risk of seroconversion after high risk exposure (unprotected anal or vaginal sex) to HIV. To be effective, it must be started as soon as possible after exposure and no later than 72 hours post-exposure. The treatment for HIV lasts four weeks. While there is compelling data to suggest that PEP after HIV exposure is extremely effective, there have been cases where it has failed.
As yet, no vaccine has been developed to prevent HIV infection or disease in people who are not yet infected with HIV, but the potential worldwide public health benefits of such a preventive vaccine are vast. Researchers in many countries are seeking to produce such a vaccine, including through the International AIDS Vaccine Initiative.
Epidemiology
UNAIDS and the WHO estimate that AIDS has killed more than 25 million people since it was first recognized in 1981, making it one of the most destructive epidemics in recorded history. Despite recent, improved access to antiretroviral treatment and care in many regions of the world, the AIDS epidemic claimed an estimated 2.8 million (between 2.4 and 3.3 million) lives in 2005 of which more than half a million (570,000) were children.
Globally, between 33.4 and 46 million people currently live with HIV. In 2005, between 3.4 and 6.2 million people were newly infected and between 2.4 and 3.3 million people with AIDS died, an increase from 2004 and the highest number since 1981.
Sub-Saharan Africa remains by far the worst-affected region, with an estimated 21.6 to 27.4 million people currently living with HIV. Two million [1.5–3.0 million] of them are children younger than 15 years of age. More than 64% of all people living with HIV are in sub-Saharan Africa, as are more than three quarters (76%) of all women living with HIV. In 2005, there were 12.0 million [10.6–13.6 million] AIDS orphans living in sub-Saharan Africa 2005. South & South East Asia are second worst affected with 15%. AIDS accounts for the deaths of 500,000 children in this region. Two-thirds of HIV/AIDS infections in Asia occur in India, with an estimated 5.7 million infections (estimated 3.4 - 9.4 million) (0.9% of population), surpassing South Africa's estimated 5.5 million (4.9-6.1 million) (11.9% of population) infections, making it the country with the highest number of HIV infections in the world.
The latest evaluation report of the World Bank's Operations Evaluation Department assesses the development effectiveness of the World Bank's country-level HIV/AIDS assistance defined as policy dialogue, analytic work, and lending with the explicit objective of reducing the scope or impact of the AIDS epidemic. This is the first comprehensive evaluation of the World Bank's HIV/AIDS support to countries, from the beginning of the epidemic through mid-2004. Because the Bank's assistance is for implementation of government programmes by government, it provides important insights on how national AIDS programmes can be made more effective.
In the 35 African nations with the highest prevalence, average life expectancy is 48.3 years—6.5 years less than it would be without the disease. For the eleven countries in Africa with prevalence rates above 13%, life expectancy is 47.7 years—11.0 years less than would be expected without HIV/AIDS.
Alternative theories
A minority of scientists and activists question the connection between HIV and AIDS, or the existence of HIV, or the validity of current testing methods. These claims are met with resistance by, and often evoke frustration and hostility from, most of the scientific community, who accuse the dissidents of ignoring evidence in favor of HIV's role in AIDS, and irresponsibly posing a dangerous threat to public health by their continued activities. Dissidents assert that the current mainstream approach to AIDS, based on HIV causation, has resulted in inaccurate diagnoses, psychological terror, toxic treatments, and a squandering of public funds. The debate and controversy regarding this issue from the early 1980s to the present has provoked heated emotions and passions from both sides.
Mesir
Républik Arab Mesir, leuwih dikenal salaku Mesir, (مصر, Miṣr) mangrupa hiji nagara nu kalobaannana wewengkonna aya di Afrika bagian kalér-wétan.
Lega wewengkonna kira-kira 997.739 km² Mesir nyapluk Samananjung Sinai (dianggap sabagé bagian ti Asia Kidul-Kulon), teras kalobaannnana wewengkonna aya di Afrika Kalér. Mesir tepung wates jeung Libya di kulon, Sudan di kidul, jalur Gaza jeung Israél di kidul-wétan. Watesna jeung cai nyaéta liwat Laut Tengah di kalér jeung Laut Beureum di wétan.
Mayoritas populasi Mesir nyicingan di sisi Sungai Nil (kira-kira 40.000 km²). Kalobaannana daratan mangrupa bagian ti sagara keusik Sahara nu jarang dicicingan.
Politik
Mesir bentukna républik ti 18 Juni 1953. Mohamed Hosni Mubarak geus ngajabat salaku Présidén Mesir dina lima période, ti 14 Oktober 1981 saenggeus rajapati Présidén Mohammed Anwar el-Sadat. Salian éta, manéhna mingpin ogé Partai Démokrat Nasional. Perdana Menteri Mesir, Dr. Ahmed Nazif diistrénan dina 9 Juli 2004 pikeun ngagentosan Dr. Atef Ebeid.
Kakawasaan di Mesir diatur ngagunakeun sistem semiprésidénsial multipartai. Téoritisna, kakawasaan éksekutif dibagi antara présidén jeung perdana menteri tapi dina praktikna kakawasaan musat dina présidén, nu dina kiwari dipilih dina pamilu nu kandidatna tunggal. Mesir ngayaan ogé pamilu parlemén multipartéy.
Dina ahir Februari 2005, Présidén Mubarak ngabéwarakeun parobahan aturan pamilihan présidén nuju ka pamilu multikandidat. Pikeun kahiji kalina, ti 1952, rahayat Mesir mibanda kasempetan pikeun milih pamingpin ti daptar sababaraha kandidat. Tapi, aturan nu anyar ogé nerapkeun sababaraha batesan sangkan rupa-rupa inohong, kawas Ayman Nour, heunteu bisa sihungan dina pamilihan jeung Mubarak meunang deui dina pamilu.
Dina ahir Januari 2011, rahayat Mesir ménta Présidén nu waktos éta maréntah, Hosni Mubarak, pikeun mundur ti jabatanna. Nepi ka 18 poé aksi démonstrasi gedé méntaan Présidén Hosni Mubarak mundur, ahirnya dina kaping 11 Fébruari 2011, Hosni Mubarak resmi mundurkeun awak.
Démografi
Mesir mangrupa nagara Arab nu populasina panglobana, kira-kira 74 juta jalmi. Méh sakabéh populasi musat di sapanjang Walungan Nil, utamana Iskandariyah jeung Kairo, jeung sapanjang Délta Nil jeung deukeut Terusan Suéz. Méh 90% ti populasina mangrupa pangagem Islam jeung sisana Kristen (utamana didominasi Koptik.
Pangaruh Méditérania (kawas Arab jeung Italia) jeung Arab muncul di kalér, jeung aya sababaraha populasi asli hideung di kidul. Loba téori geus diusulkeun ngeunaan asal urang Mesir, tapi euweuh nu konklusif, jeung nu panglobana ditarima nyaéta yén masarakat Mesir téh mangrupa campuran ti urang Afrika Wétan jeung Asiatik nu pindah ka lebak Nil saenggeus jaman és. Urang Mesir ngagunakeun basa ti kulawarga Afro-Asiatik (saméméhna dikenal salaku Hamito-semitic).
Babagian Administratif
Mesir dibagi kana 26 kagubernuran (muhafazat; tunggal – muhafazah):
Atikan
Sajarahna, modérnisasi atikan di Mesir mimitina ti pangenalan kamajuan ilmu pangaweruh jeung téhnologi Napoléon Bonaparté wanci panalukan Mesir. Kamajuan ilmu pangaweruh jeung téhnologi nu dipiboga ku Napoléon Bonaparté ti Perancis ieu, méré inspirasi nu kuat kana para panganyar Mesir pikeun ngalaksanakeun modérnisasi atikan di Mesir nu dianggapna stagnan. Di antara inohong-inohong éta, Jamaluddin al-Afghani, Muhammad Abduh, jeung Muhammad Ali Pasha.
Sistem Atikan di nagara Mesir kaasup:
Lawe Polak, Lawe Sumur, Aceh Tenggara
Lawe Polak nyaéta salah sahiji Gampong di kacamatan Lawe Sumur, Kabupatén Aceh Tenggara, Propinsi Acéh, Indonésia.
Hégarmanah, Cikarang Timur, Bekasi
Hégarmanah nyaéta salah sahiji désa di kacamatan Cikarang Timur, Kabupatén Bekasi, Propinsi Jawa Barat, Indonésia.
Autokorélasi
Autokorélasi mangrupa salah sahiji alat matematika anu remen digunakeun dina signal processing keur analisa fungsi atawa deret nilai, saperti domain waktu signals. Autokorélasi nyaéta cross-correlation hiji signal jeung signalna sorangan. Autokorélasi ilahar dipaké keur manggihkeun pola "pengulangan" dina signal, saperti nangtukeun aya périodeu signal nu kaganggu atawa keur identifikasi frékuénsi dasar signal nu teu mibanda komponen frékuénsi, tapi mangaruhan kana frékuénsi nu harmonis.
Harti
bédana definisi autokorélasi nu dipaké gumantung kana widang elmu nu ditalungtik nu satemenna teu sarua. Dina sababaraha widang elmu istilahna diganti ku autocovariance.
Statistik
Dina statistik, fungsi autokorelasi (ACF) keur deret waktu diskrit atawa hiji prosés Xt hartina korelasi antara prosés dina titik nu béda tur béda waktu oge. Lamun Xt mibanda mean μ jeung varian σ2 mangka definisi ACF nyaéta nu mana E nyaéta nilai ekspektasi. Nilai ekspektasi ieu teu bisa dipaké sacara umum keur sakabéh deret waktu atawa prosés lamun nilai varian sarua jeung nol (keur prosés nu konstan) atawa tak hingga. Fungsi ieu mibanda harti nu umum lamun dihartikeun mibanda sifat nu aktraktif dina rentang [−1, 1], nu mana 1 nunjukkeun korelasi nu sampurna sarta −1 nunjukkeun anti-korelasi nu sampurna.
Lamun Xt mangrupa orde-dua statis mangka ACF ngan gumantung kana béda antara t jeung s sarta bisa digambarkeun salaku fungsi variabel tunggal. Hal ieu geus ilahar maké rumus nu umum nyaéta, lamun k mangrupa lag (|t - s|). Dina sababarha widang elmu digambarkeun ku normalisasi σ2 sarta maké watesan autocorrelation nu kadangkala disebut ogé autocovariance. Keur conto panjang deret waktu n, X1, X2 ... Xn nu mana méan jeung varian dipikanyaho mangka nilai estimasi-na ditangtukeun tina keur.
Lamun nilai méan atawa varian keur prosés ieu teu dipikanyaho mangka μ sarta σ2 bisa diganti ku rumus standar keur sampel méan jeung sampel varian sanajan hasilna nujul kana bias dina nilai estimasi-na.
Signal processing
Dina signal processing, definisi teu di handap salawasna dipaké bari teu maké normalisasi, nyaéta, teu ngurangan méan sarta ngabagi ku varianna.
Singapura
Singapura (Singapura; ; சிங்கப்பூர், Ciŋkappūr), ngaran resmina Républik Singapura (Republik Singapura; ; சிங்கப்பூர் குடியரசு, Ciŋkappūr Kudiyarasu), nyaéta hiji nagara pulo nu perenahna di tungtung kidul Jajirah Malayu. Singapura ayana 137 kilométer (85 mi) kalereun hatulistiwa, kiduleun nagara bagéan Johor, Malaysia sarta kalereun Kapuloan Riau Indonésia. Kalayan legana nu ukur 704.0 km² (272 sq mi), Singapura mangrupa salah sahiji nagara kota nu ngan saeutik nyesa kénéh sadunya, tur mangrupa nagara pangleutikna di Asia Tenggara.
Autokorélasi
Signal processing
Upamana signal f(t), autokorelasi kontinyu Rff(τ) salawasna dihartikeun salaku integral korelasi-silang kontinyu tina f(t)-na sorangan, dina lag τ.
nu mana f* nunjukkeun kompleks konjuget sarta lingkaran nunjukkeun konvolusi. Keur fungsi ril, f* = f.
Autokorelasi diskrit R at lag j keur signal diskrit xn nyaéta
Definisi di handap dipaké keur signals nu mangrupa integral kuadrat atawa jumlah kuadrat, nyaéta nu énérgina kawates. Signals nu "pamungkas salawasna" dianggap gaganti prosés acak, nu mana diperlukeun definisi nu béda, dumasar kana nilai ekspektasi. Keur proses acak statis nu leuwih lega, autokorelasi dihartikeun salaku
Singapura
Tumbu luar
Jalan-jalan
Autokorélasi
Signal processing
Keur prosés anu henteu stationary, mangrupa fungsi tina t, atawa n oge.
Alternatipna, signals nu salawasna pamungkas bisa dirobah kana analisa fungsi autokorelasi keur waktu nu pondok, maké integral waktu nu kawengku (Tempo short-time Fourier transform keur prosés nu pakait.)
Singapura
Tumbu luar
Peta
Autokorélasi
Signal processing
Autokorelasi multi-dimension bisa dihartikeun ku cara nu sarua. Contona, dina autokorelasi tilu dimenasi dina kuadrat-jumlah signal diskrit bisa jadi
Lamu nilai méan dikurangkeun tina signal saméméh diitung dina fungsi autokorelasi, fungsi nu dihasilkeun disebut ogé fungsi auto-covarian.
Sipat
Saterusna arek dijelaskeun sipat autokorélasi dina hiji-dimensi, sabab satemenna loba sipat hiji-dimensi nu gampang keur dipaké dina kasus multi-dimensi.
Autokorélasi dina analisa regresi
Dina regression analysis ngagunakeun time series, autokorélasi nyaéta sesa tina ieu masalah, sarta nuju ka arah bias nu luhur dina estimasi statistical significance tina koefisien estimasi, saperti dina T statistic. Tes standar keur ayana autokorélasi nyaéta Durbin-Watson statistic atawa, lamun ngajelaskeun variabel kaasup lagged dependent variable, Durbin's h statistic.
Respon keur autokorélasi kaasup differencing data sarta ayana struktur "lag" dina estimasi.
Aksara Gedé
Aksara Gedé atawa dina basa Indonésia disebut huruf kapital mangrupa aksara anu miboga wangun jeung ukuran husus. Salah sahiji fungsi ieu aksara nyaéta bisa digunakeun dina awal kecap unggal kalimah, nuliskeun ngaran jelema atawa tokoh (inohong)
Aksara Gedé dina Alpabét
Bagan di handap mangrupa larapna aksara gedé dina alpabét
Fungsi Aksara Gedé
Ngalarapkeun fungsi aksara gedé dina kalimah bisa pasing-pasing dumasar udaganana. Fungsi aksara gedé di antarana larap dina :
1. Aksara gedé digunakeun pikeun nuliskeun aksara kahiji di awal kalimah.
Conto:
(aksara anu dimiringkeun mangrupa larapna aksara gedé di awal kalimah).
2. Aksara gedé digunakeun nalika nuliskeun aksara kahiji dina awal kalimah cutatan langsung.
(aksara anu dimiringkeun mangrupa larapna aksara gedé dina kalimah anu aya cutatan langsungna).
3. Aksara gedé dipaké pikeun nuliskeun aksara kahiji dina kecap anu aya patalina jeung hal-hal kaagamaan, kitab, jeung jenengan Allah (kaasup kecap sulur-Na).
(aksara anu dimiringkeun mangrupa larapna aksara gedé dina hal-hal kaagamaan).
4. Aksara gedé dipaké pikeun nuliskeun hiji gelar kahormatan anu dituturkeun ku ngaran macakal
(aksara anu dimiringkeun mangrupa larapna aksara gedé dina ngaran gelar kahormatan)
5. Aksara gedé dipaké pikeun nuliskeun ngaran jalma, tokoh, atawa inohong
6. Aksara gedé digunakeun pikeun nuliskeun aksara kahiji dina ngaran bangsa, sélér bangsa, jeung basa
(aksara anu dimiringkeun mangrupa larapna aksara gedé dina nuliskeun ngaran bangsa, basa, jeung sélér bangsa)
7. Aksara gedé dipaké pikeun nuliskeun ngaran taun, bulan, poé, hari raya, jeung kajadian sajarah
(aksara anu dimiringkeun mangrupa larapna aksara gedé dina nuliskeun ngaran poé, hari raya, jeung kajadian sajarah)
969
Taun ka-969 Maséhi dina Kalénder Grégorian.
Aksara Gedé
Fungsi Aksara Gedé
8. Aksara gedé dipaké pikeun nuliskeun aksara kahiji ngaran-ngaran dina istilah géografi.
Contona:
(aksara anu dimiringkeun mangrupa larapna aksara gedé dina nuliskeun ngaran-ngaran dina istilah géografi)
9. Aksara gedé dipaké pikeun nuliskeun ngaran resmi badan, lembaga pamaréntahan, katatanagaraan, jeung ngaran dokumén resmi.
Conto
'''10. Aksara gedé dipaké pikeun nuliskeun ngaran buku, majalah, surat kabar, jeung judul karangan. (Kecuali kata hubung)'''
(aksara anu dimiringkeun mangrupa larapna aksara gedé dina nuliskeun ngaran buku, majalah, surat kabar, jeung judul karangan)
11. Aksara gedé dipaké pikeun nuliskeun singgetan gelar jeung sesebutan.
12. Aksara gedé dipaké pikeun nuliskeun aksara kahiji anu nuduhkeun pancakaki (saperti bapak, ema, kakang, emang, uwa, jst) anu dipaké pikeun gaganti kecap sulur atawa sesebutan.
13. Aksara gedé dipaké pikeun nuliskeun aksara kahiji kecap anu nuduhkeun jujuluk.
2016 RF40
Ari 2016 RF40 mangrupa hiji astéroid. Ieu asteroid téh bagéan tina astéroid Amor, anu nganjrek deukeut jeung marcapada. Ékséntrisitas orbit ieu astéroid kacatet gedéna 0.156, sedengkeun magnitudo mutlakna 21.6. Ari nu jadi référénsina mah nyaéta MPO 409569.
Bebentukan
Kawas sakumna astéroid, ieu astéroid kabentuk tina nébula panonpoé primordial minangka beubeulahan planétisimal, objék di nébula marcapada ngora nu teu cukup badag pikeun robah jadi planét.
(88254) 2001 FM129
Ari (88254) 2001 FM129 mangrupa hiji astéroid. Ieu asteroid téh bagéan tina astéroid Apollo, anu nganjrek deukeut jeung marcapada. Ékséntrisitas orbit ieu astéroid kacatet gedéna 0.630, sedengkeun magnitudo mutlakna 17.6. Ari nu jadi référénsina mah nyaéta MPO�341230.
Bebentukan
Kawas sakumna astéroid, ieu astéroid kabentuk tina nébula panonpoé primordial minangka beubeulahan planétisimal, objék di nébula marcapada ngora nu teu cukup badag pikeun robah jadi planét.
Toto Katon, Punggur, Lampung Tengah
Toto Katon nyaéta salah sahiji Désa di kacamatan Punggur, Kabupatén Lampung Tengah, Propinsi Sumatra Kalér, Indonésia.
Toto Katon, Punggur, Lampung Tengah
Ad Dukhon
Surah Ad-Dukhon (Bahasa Arab:الدخان, Halimun) nyaéta surah ka-44 dina Al-Quran anu kaasup ogé kana golongan surah Makkiyah. Surah ieu disebut Ad-Dukhon sabab ti ayat 10 nepi ka 15 nyaritakeun azab halimun anu ditimpakeun ka jalma kafir. Surah Ad-Dukhon kaasup surah ka-25 tina 29 surah anu dimimitian ku huruf muqattha’ah jeung surah ka-5 ti 7 surah anu dimimitian ku huruf muqattha’ah Ha Mim (Hamimat).
Pokok Eusina
Téma-téma anu diangkat di surah ieu nyaéta ngeunaan jalma-jalma anu ingkar kana hari kiamat sarta nyebutkeun yén Allah SWT. teu nyiptakeun nanaon di antara langit jeung bumi. Surah ieu ogé ngagambarkeun tanda-tanda kiamat sarta kaayaan jelema-jelema anu loba dosa dina mangsa kiamat. Salian ti éta, dicaritakeun ogé sapotong cari tentang Nabi Musa AS. sarta nasib Fir'aun jeung kaumna anu ingkar ka gusti Allah SWT.
Azab Mangrupa Halimun
Dumasar riwayat Al-Bukhari, carita ngeunaan azab halimun éta bisa diringkes jadi kieu: Masarakat kafir Mekkah ngahalangan medarna agama Islam sarta kalakuan doraka aranjeuna ka Nabi Muhammad SAW. geus ngaleuwihan wates. ku sabab éta, Rasulullah ngadoa ka Allah SWT méh jalma-jalma kafir éta ditimpa ku azab sakumaha azab usum halodo anu ditimpakeun ka jalma anu ingkar ka Nabi Yusuf AS. Doa ieu dikobul ku Allah dugi ka jalma-jalma kafir éta ngadahar tulang jeung bangké bakat ku kalaparan. Aranjeuna ngadua ka Allah méh dipaparin pitulung, tapi Allah teu ngabulkeun waé. Nu katingali ngan ukur halimun anu nutupan tetempoanana.
Akhirna aranjeuna nyungkeun ka Rasulullah sangkan anjeuna kersa ngadua nyungkeun dipaparin hujan ka Allah. Teu lila, Allah ngabulkeun doa Rasulullah. Tapi saatos hujan diturunkeun, masarakat kafir Mekkah jadi kafir deui jiga asalna. Ku kituna, Allah SWT ngajangjikeun yén aranjeuna bakal ditimpakeun azab anu kacida peurihna.
Carita ngeunaan azab ieu dijelaskeun ti ayat 10 nepi ka ayat 15 surah Ad-Dukhon anu eusina:
'''« فَارْتَقِبْ يَوْمَ تَأْتِي السَّماءُ بِدُخانٍ مُبينٍ. يَغْشَى النَّاسَ هٰذا عَذابٌ أَليمٌ. رَبَّنَا اكْشِفْ عَنَّا الْعَذابَ إِنَّا مُؤْمِنُونَ »'''
'''« أَنَّى لَهُمُ الذِّكْرى‏ وَ قَدْ جاءَهُمْ رَسُولٌ مُبينٌ. ثُمَّ تَوَلَّوْا عَنْهُ وَ قالُوا مُعَلَّمٌ مَجْنُونٌ. إِنَّا كاشِفُوا الْعَذابِ قَليلاً إِنَّكُمْ عائِدُونَ »'''
"Mangka tungguan hiji wanci di mana langit mawa halimun anu nyata, anu ngawengku manusa. Ieu azab anu peurih. (Aranjeuna ngadoa), "Ya Tuhan kami, leungitkeun azab ieu ti kami. Saleresna kami bakal iman." Kumaha aranjeuna bisa narima pépéling, padahal geus datang ka aranjeuna hiji rosul anu ngémbarkeun penjelasan. Terus maranéhna ingkar ka rosul éta bari nyebutkeun, "Anjeun téh jelema anu narima ajaran ti jelema anu teu waras?" Saleresna (lamun) Kami ngaleungitkeun siksaan éta saeutik waé ogé, anjeun bakal balik deui (jadi ingkar)." (QS Ad-Dukhon [44]:10-15)
Pemerihan, Krui Kidul, Pesisir Kulon
Pemerihan nyaéta salah sahiji Désa di kacamatan Krui Kidul, Kabupatén Pesisir Kulon, Propinsi Sumatra Kalér, Indonésia.
Basa Asmat Unir Sirau
Basa Asmat Unir Sirau nyaéta basa wewengkon anu aya di Indonésia. Panyaturna aya di 1 propinsi nyaéta propinsi Papua, nu dumuk di 1 kabupaten/kota.
968
Taun ka-968 Maséhi dina Kalénder Grégorian.
Gala Gala Pangkailan, Porsea, Toba Samosir
Gala Gala Pangkailan nyaéta salah sahiji Désa di kacamatan Porsea, Kabupatén Toba Samosir, Propinsi Sumatra Kalér, Indonésia.
Gala Gala Pangkailan, Porsea, Toba Samosir
Pante Cermen Paloh, Padang Tiji, Pidie
Pante Cermen Paloh nyaéta salah sahiji Gampong di kacamatan Padang Tiji, Kabupatén Pidie, Propinsi Acéh, Indonésia.
Pante Cermen Paloh, Padang Tiji, Pidie
Perkebunan Pulo Rambung, Bahorok, Langkat
Perkebunan Pulo Rambung nyaéta salah sahiji Désa di kacamatan Bahorok, Kabupatén Langkat, Propinsi Sumatra Kalér, Indonésia.
Paya, Manggeng, Aceh Barat Daya
Paya nyaéta salah sahiji Gampong di kacamatan Manggeng, Kabupatén Aceh Barat Daya, Propinsi Acéh, Indonésia.
Jatibaru, Cikarang Timur, Bekasi
Jatibaru nyaéta salah sahiji désa di kacamatan Cikarang Timur, Kabupatén Bekasi, Propinsi Jawa Barat, Indonésia.
Mandala, Dukupuntang, Cirebon
Mandala nyaéta salah sahiji désa di kacamatan Dukupuntang, Kabupatén Cirebon, Propinsi Jawa Barat, Indonésia.
2013 HG19
Ari 2013 HG19 mangrupa hiji astéroid. Ieu asteroid téh bagéan tina astéroid Amor, anu nganjrek deukeut jeung marcapada. Ékséntrisitas orbit ieu astéroid kacatet gedéna 0.291, sedengkeun magnitudo mutlakna 25.4. Ari nu jadi référénsina mah nyaéta MPO 263186.
Bebentukan
Kawas sakumna astéroid, ieu astéroid kabentuk tina nébula panonpoé primordial minangka beubeulahan planétisimal, objék di nébula marcapada ngora nu teu cukup badag pikeun robah jadi planét.
Lawes Sumur Sepakat, Lawe Sumur, Aceh Tenggara
Lawes Sumur Sepakat nyaéta salah sahiji Gampong di kacamatan Lawe Sumur, Kabupatén Aceh Tenggara, Propinsi Acéh, Indonésia.
Lawes Sumur Sepakat, Lawe Sumur, Aceh Tenggara
(513550) 2010 NG3
Bebentukan
Kawas sakumna astéroid, ieu astéroid kabentuk tina nébula panonpoé primordial minangka beubeulahan planétisimal, objék di nébula marcapada ngora nu teu cukup badag pikeun robah jadi planét.
Koto Tengah, Tanah Kampung, Sungai Penuh
Koto Tengah nyaéta salah sahiji désa di kacamatan Tanah Kampung, Kota Sungai Penuh, Propinsi Jambi, Indonésia.
Tanggul Angin, Punggur, Lampung Tengah
Tanggul Angin nyaéta salah sahiji Désa di kacamatan Punggur, Kabupatén Lampung Tengah, Propinsi Sumatra Kalér, Indonésia.
Tanggul Angin, Punggur, Lampung Tengah
2010 JH87
Ari 2010 JH87 mangrupa hiji astéroid. Ieu asteroid téh bagéan tina astéroid Apollo, anu nganjrek deukeut jeung marcapada. Ékséntrisitas orbit ieu astéroid kacatet gedéna 0.540, sedengkeun magnitudo mutlakna 19.6. Ari nu jadi référénsina mah nyaéta MPO�288491.
Bebentukan
Kawas sakumna astéroid, ieu astéroid kabentuk tina nébula panonpoé primordial minangka beubeulahan planétisimal, objék di nébula marcapada ngora nu teu cukup badag pikeun robah jadi planét.
Seuneulop, Manggeng, Aceh Barat Daya
Seuneulop nyaéta salah sahiji Gampong di kacamatan Manggeng, Kabupatén Aceh Barat Daya, Propinsi Acéh, Indonésia.
Mandiri Sejati, Krui Kidul, Pesisir Kulon
Mandiri Sejati nyaéta salah sahiji Désa di kacamatan Krui Kidul, Kabupatén Pesisir Kulon, Propinsi Sumatra Kalér, Indonésia.
Mandiri Sejati, Krui Selatan, Pesisir Barat
Basa Atam
Basa Atam nyaéta basa wewengkon anu aya di Indonésia. Panyaturna aya di 1 propinsi nyaéta propinsi Papua, nu dumuk di 1 kabupaten/kota.
967
Taun ka-967 Maséhi dina Kalénder Grégorian.
Jatireja, Cikarang Timur, Bekasi
Jatireja nyaéta salah sahiji désa di kacamatan Cikarang Timur, Kabupatén Bekasi, Propinsi Jawa Barat, Indonésia.
Pasar Paloh, Padang Tiji, Pidie
Pasar Paloh nyaéta salah sahiji Gampong di kacamatan Padang Tiji, Kabupatén Pidie, Propinsi Acéh, Indonésia.
Pasar Paloh, Padang Tiji, Pidie
Lhok Puntoy, Manggeng, Aceh Barat Daya
Lhok Puntoy nyaéta salah sahiji Gampong di kacamatan Manggeng, Kabupatén Aceh Barat Daya, Propinsi Acéh, Indonésia.
2000 CP101
Ari 2000 CP101 mangrupa hiji astéroid. Ieu asteroid téh bagéan tina astéroid Apollo, anu nganjrek deukeut jeung marcapada. Ékséntrisitas orbit ieu astéroid kacatet gedéna 0.619, sedengkeun magnitudo mutlakna 19.9. Ari nu jadi référénsina mah nyaéta MPO�227395.
Bebentukan
Kawas sakumna astéroid, ieu astéroid kabentuk tina nébula panonpoé primordial minangka beubeulahan planétisimal, objék di nébula marcapada ngora nu teu cukup badag pikeun robah jadi planét.
Sindangmekar, Dukupuntang, Cirebon
Sindangmekar nyaéta salah sahiji désa di kacamatan Dukupuntang, Kabupatén Cirebon, Propinsi Jawa Barat, Indonésia.
Ngesti Rahayu, Punggur, Lampung Tengah
Ngesti Rahayu nyaéta salah sahiji Désa di kacamatan Punggur, Kabupatén Lampung Tengah, Propinsi Sumatra Kalér, Indonésia.
Ngesti Rahayu, Punggur, Lampung Tengah
Basa Auye
Basa Auye nyaéta basa wewengkon anu aya di Indonésia. Panyaturna aya di 1 propinsi nyaéta propinsi Papua, nu dumuk di 1 kabupaten/kota.
Setia Baru, Lawe Sumur, Aceh Tenggara
Setia Baru nyaéta salah sahiji Gampong di kacamatan Lawe Sumur, Kabupatén Aceh Tenggara, Propinsi Acéh, Indonésia.
Mesjid Paloh, Padang Tiji, Pidie
Mesjid Paloh nyaéta salah sahiji Gampong di kacamatan Padang Tiji, Kabupatén Pidie, Propinsi Acéh, Indonésia.
2014 YZ41
Ari 2014 YZ41 mangrupa hiji astéroid. Ieu asteroid téh bagéan tina astéroid Apollo, anu nganjrek deukeut jeung marcapada. Ékséntrisitas orbit ieu astéroid kacatet gedéna 0.374, sedengkeun magnitudo mutlakna 23.6. Ari nu jadi référénsina mah nyaéta MPO�342304.
Bebentukan
Kawas sakumna astéroid, ieu astéroid kabentuk tina nébula panonpoé primordial minangka beubeulahan planétisimal, objék di nébula marcapada ngora nu teu cukup badag pikeun robah jadi planét.
Tanjung Bunga, Tanah Kampung, Sungai Penuh
Tanjung Bunga nyaéta salah sahiji désa di kacamatan Tanah Kampung, Kota Sungai Penuh, Propinsi Jambi, Indonésia.
Tanjung Bunga, Tanah Kampung, Sungai Penuh
2013 AD32
Ari 2013 AD32 mangrupa hiji astéroid. Ieu asteroid téh bagéan tina astéroid Apollo, anu nganjrek deukeut jeung marcapada. Ékséntrisitas orbit ieu astéroid kacatet gedéna 0.601, sedengkeun magnitudo mutlakna 25.1. Ari nu jadi référénsina mah nyaéta MPO�250171.
Bebentukan
Kawas sakumna astéroid, ieu astéroid kabentuk tina nébula panonpoé primordial minangka beubeulahan planétisimal, objék di nébula marcapada ngora nu teu cukup badag pikeun robah jadi planét.
966
Taun ka-966 Maséhi dina Kalénder Grégorian.
Musam Pembangunan, Bahorok, Langkat
Musam Pembangunan nyaéta salah sahiji Désa di kacamatan Bahorok, Kabupatén Langkat, Propinsi Sumatra Kalér, Indonésia.
Mojopahit, Punggur, Lampung Tengah
Mojopahit nyaéta salah sahiji Désa di kacamatan Punggur, Kabupatén Lampung Tengah, Propinsi Sumatra Kalér, Indonésia.
Mojopahit, Punggur, Lampung Tengah
2016 GU2
Ari 2016 GU2 mangrupa hiji astéroid. Ieu asteroid téh bagéan tina astéroid Apollo, anu nganjrek deukeut jeung marcapada. Ékséntrisitas orbit ieu astéroid kacatet gedéna 0.958, sedengkeun magnitudo mutlakna 24.0. Ari nu jadi référénsina mah nyaéta MPO�386974.
Bebentukan
Kawas sakumna astéroid, ieu astéroid kabentuk tina nébula panonpoé primordial minangka beubeulahan planétisimal, objék di nébula marcapada ngora nu teu cukup badag pikeun robah jadi planét.
Ladang Panah, Manggeng, Aceh Barat Daya
Ladang Panah nyaéta salah sahiji Gampong di kacamatan Manggeng, Kabupatén Aceh Barat Daya, Propinsi Acéh, Indonésia.
Padang Raya, Krui Kidul, Pesisir Kulon
Padang Raya nyaéta salah sahiji Désa di kacamatan Krui Kidul, Kabupatén Pesisir Kulon, Propinsi Sumatra Kalér, Indonésia.
Padang Raya, Krui Selatan, Pesisir Barat
2007 DY
Ari 2007 DY mangrupa hiji astéroid. Ieu asteroid téh bagéan tina astéroid Apollo, anu nganjrek deukeut jeung marcapada. Ékséntrisitas orbit ieu astéroid kacatet gedéna 0.595, sedengkeun magnitudo mutlakna 19.6. Ari nu jadi référénsina mah nyaéta MPO�119700.
Ujung Bandar, Bahorok, Langkat
Ujung Bandar nyaéta salah sahiji Désa di kacamatan Bahorok, Kabupatén Langkat, Propinsi Sumatra Kalér, Indonésia.
Balap motor Grand Prix
Kajuaraan dunya balap motor Grand Prix mimiti diayakeun ku Fédération Internationale de Motocyclisme (FIM) taun 1949. Harita sacara tradisional geus dilaksanakeun sababaraha balapan di masing-masing acara pikeun sagala rupa kelas motor, dumasar kapasitas mesin, sarta kelas pikeun sidecars (motor gandéngan nu ditapelkeun digigir). Kelas-kelas nu aya harita nyaéta 50 cc, 125 cc, 250 cc, 350 cc, sarta 500 cc pikeun motor nu ditumpakan ku sorangan, sarta 350 cc jeung 500 cc pikeun motor sidecars. Taun 1950-an sarta sapanjang taun 1960-an, motor mesin 4 Tak pinunjul di sakuliah kelas. Dina panungtungan taun 1960-an, motor mesin 2 mimiti pinunjul di kelas-kelas leutik. Dina taun 1970-an motor mesin 2 Tak bener-bener nyingkahkeun mesin-mesin 4 Tak. Dina taun 1979, Honda ngusahakeun mesin 4 Tak di kelas utama kalayan nurunkeun motor NR500, tapi proyék ieu gagal, sarta dina taun 1983 Honda ngahontal kameunangan kalayan motor 500 cc 2 Tak. Dina taun 1983, kelas 350 cc pamustunganna dieureunkeun. Kelas 50 cc diganti ku kelas 80 cc dina taun 1984, antukna kelas nu mindeng didominasi ku purah balap ti Spanyol jeung Italia dieureunkeun taun 1990. Kelas sidecars ogé dieureunkeun tina kajuaraan dunya taun 1990-an, nu aya tinggal kelas 125 cc, 250 cc, sarta kelas 500 cc.
Pedaran
Motor Grand Prix nyaéta mesin balap nu dijieun husus sarta teu dijual pikeun dibeuli ku masyarakat umum sarta teu meunang dipaké di jalan umum. Ieu béda kalayan sababaraha kategori balap dumasar produksi, saperti Superbike sarta Isle of Man TT Races nu ngaluarkeun motor vérsi modifikasi nu dijual atawa sadia pikeun umum.
Kiwari kajuaraan dibagi kana tilu kelas : MotoGP, Moto2 sarta Moto3. Sakabéh kelas ngagunakeun mesin 4 Tak. Taun 2010 kelas 250cc diganti ku kelas Moto2 600 cc mesin 4 tak. taun 2012 kelas 125cc diganti ku kelas Moto3 250cc mesin 4 tak kalayan wates beurat 65 kg kalayan béngsin, sarta kapasitas mesin pikeun MotoGP dironjatkeun tina 800 cc ka 1.000 cc.
Kajuaraan dunya balap motor Grand Prix FIM mimiti diorganisir ku Fédération Internationale de Motocyclisme taun 1949. Hak komérsial kiwari dipibanda ku Dorna Sports, kalayan FIM minangka badan sanksi olahraga. Tim-tim diwakilan ku International Road Racing Teams Association (IRTA) sarta produsén ku Motorcycle Sport Manufacturers Association (MSMA). Aturan sarta parobahan tetekon diputuskeun antara opat éntitas, kalayan Dorna ngalakukeun ngumpulkeun sora sacara tie-breaking. Dina kasus modifikasi téknis, MSMA wenang sacara sapihak ngalakukeun atawa ngavéto parobahan kalayan sora buleud di antara para anggotanna. Kaopat éntitas ieu ngawangun Komisi Grand Prix.
Balap motor Grand Prix kelas utama geus robah sacara dramatis dina sababraha taun panungtung. Ti tengah-tengan taun 1970 nepi ka taun 2001, kelas utama balap motor Grand Prix ngarobah mesin 500 cc kalayan maksimal opat séher, teu paduli naha mesin éta 2-Tak atawa 4- Tak.
Dina taun 2002, parobahan tetekon diwanohkeun. Aturan kasebut ngidinan produsén milih antara mesin 2-Tak 500 cc atawa mesin 4-Tak ti 990 cc. Pabrikan ogé diidinan pikeun ngagunakeun pilihan konfigurasi mesin maranéhna. Sanajan waragad ngaronjat badag dina ngawangun mesin 4-Tak, lantaran kaleuwihan kapasitas 490cc. Mesin 4-Tak bisa gancang pinunjul ti saingan 2-Tak. Akibatna, taun 2003 euweuh mesin 2-Tak dina balapan MotoGP. Kelas 125 cc jeung 250 cc masih maké mesin 2-Tak.
Dina taun 2007, kelas MotoGP kapasitas mesin maksimum dikurangan jadi 800 cc salila minimal lima taun. Pikeun usum 2012 kapasitasna geus ngaronjat deu jadi 1.000 cc.
2015 FE36
Bebentukan
Kawas sakumna astéroid, ieu astéroid kabentuk tina nébula panonpoé primordial minangka beubeulahan planétisimal, objék di nébula marcapada ngora nu teu cukup badag pikeun robah jadi planét.
Teger Miko, Lawe Sumur, Aceh Tenggara
Teger Miko nyaéta salah sahiji Gampong di kacamatan Lawe Sumur, Kabupatén Aceh Tenggara, Propinsi Acéh, Indonésia.
Balap motor Grand Prix
Pedaran
Kalender balap taun 2008 ngawengku 18 rintakan di 15 nagara nu béda (Qatar, Spanyol nu ngayakeun tilu rintakan, Portugal, China, Prancis, Itali, Britania Raya, Walanda, Jérman, Amérika dua rintakan, Républik Céko, San Marino, Jepang, Australia sarta Malaysia). Eksklusif pikeun kelas MotoGP, aya ogé rintakan Amérika di Mazda Raceway Laguna Seca di Monterey, California, pikeun kelas 800 cc wungkul; ku sabab paddock teu cukup gedé pikeun dua kelas lianna. Dina taun 2008, MotoGP diayakeun di Indianapolis Motor Speedway nu munggaran dina jalur nu anyar disiapkeun. Katilu kelas kasebut dijadwalkeun balap tapi angin tarik sarta hujan antukna kelas 250 cc teu jadi balap. Balapan MotoGP di Indianapolis ngalawan arah jarum jam, kalayan "snake pit" kompléks ngaliwatan garis start-finish saancan ka péngkolan hiji jalur pondok sarta asup bagéan tengah sirkuit.
965
Taun ka-965 Maséhi dina Kalénder Grégorian.
Balap motor Grand Prix
Pedaran
Grid ngawengku tilu kolom (Opat pikeun kelas 125 cc sarta kelas 250 cc) sarta bisa asup sakitar 20 urang purah balap. Posisi grid diputuskeun dina urutan kualifikasi kacepatan, kalayan nu panggancangna di posisi pole atwa posisi kahiji. Balapan lumangsung kira-kira 45 menit, setiap balapan mangrupa pagancang-gancang ti awal nepi ka ahir tanpa ngadu bahan beuleum atawa gilinding.
Taun 2005, tetekon bandéra pikeun MotoGP diwanohkeun. Saméméhna, lamun mimiti balapan garing terus turun hujan, patugas ngébérkeun bandéra beurem (balapan eureun) sarta diteruskeun atawa dibalikan deui maké gilinding husus baseuh. Ayeuna, nalika hujan turun, bandera bodas dikébérkeun, nandakeun yén purah balap bisa asup pit pikeun ngaganti motor nu béda gilindingna Sagédkngeun béda gilinding, motor cuaca baseuh mibanda rém rotor waja sarta brake pads nu béda tibatan rém karbon sarta pedal nu digunakeun dina motor 'garing'. ku sabab rém karbon kudu kaayan panas supaya pungsina hadé, sedengkeun cai ngalantarankeun tiis. Suspénsi ogé 'ngahipuan' rada naék ku sabab cuaca baseuh.