Vous avez cherché: name four game which are played with a ball (Anglais - Malais)

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Anglais

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Anglais

a 3d arcade game with a ball

Malais

permainan arked 3d dengan bebola

Dernière mise à jour : 2014-08-15
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Anglais

allah will surely try you with a game which will be within the range of your hands and lances so that he might mark out those who fear him, even though he is beyond the reach of human perception.

Malais

demi sesungguhnya allah akan menguji kamu (semasa kamu berihram) dengan sesuatu dari binatang buruan yang mudah ditangkap oleh tangan kamu dan (mudah terkena) tikaman lembing-lembing kamu, supaya allah ketahui wujudnya sesiapa yang takut kepadanya semasa ia tidak melihatnya semasa ia tidak dilihat orang.

Dernière mise à jour : 2014-07-03
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Anglais

combined with a serum ferritin blood test to identify cytokine storms, it is meant to counter such developments, which are thought to be the cause of death in some affected people.

Malais

digabungkan dengan ujian darah feritin serum untuk mengenal pasti ribut sitokin, ini bermaksud untuk melawan perkembangan tersebut, yang dianggap sebagai punca kematian bagi beberapa orang yang dijangkiti.

Dernière mise à jour : 2020-08-25
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Anglais

or, they are like darkness upon a deep sea covered with a wave above which is another wave, above which are clouds, darkness piled one upon the other; when he stretches out his hand he can scarcely see it.

Malais

atau (orang-orang kafir itu keadaannya) adalah umpama keadaan (orang yang di dalam) gelap-gelita di lautan yang dalam, yang diliputi oleh ombak bertindih ombak; di sebelah atasnya pula awan tebal (demikianlah keadaannya) gelap-gelita berlapis-lapis - apabila orang itu mengeluarkan tangannya, ia tidak dapat melihatnya sama sekali.

Dernière mise à jour : 2014-07-03
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Anglais

since the invention of fire arms in the 1300s, there has been a steady and required need to tirelessly train with their use. firearms have always been tricky to get to grips with as a first time user, so repeated drills and exercises are used to develop muscle memory. developing a solid muscle memory and instinct for safe firearm use is the only way to operate efficiently in the field, without adrenaline and fear causing you to lock up or forget where the trigger is. as firearms (and other military equipment) have evolved, so has the way that war is fought. training no longer just requires weapons users to be proficient with their weapons and shoot on target like they did in the ‘old’ days. military training is now a much more cohesive and comprehensive form of training that covers everything from fitness to firearms drills, movement drills and vehicle training. these forms of training often involve training against other recruits to develop skills against ‘real’ opponents. how do you develop firearms skills and instinct without using real firearms, without potentially shooting fellow comrades? initially, (and still used by some) are blank ammunition. these munitions contain no bullet and are (relatively) safe for use with proper training. however, because there is no projectile used, there’s little adrenaline, little fear that a mistake could cause serious negative consequences and little learning under pressure. in comes simulated ammunition (simunition for short). with a small amount of modification (often just a new bolt carrier), a service weapon can be modified to shoot non-lethal projectiles called simunition. also, as a safety precaution, this modification prevents the weapon from firing standard cartridges. simunition is replacement ammunition that comes in a number of calibres and fires non-lethal, non-toxic rounds with muzzle energy of up to 5.6 joules (for reference, an airsoft 0.2g bb at 328fps is 1 joule). these rounds are typically accurate up to 30m and will provide a serious impact in those ranges and can even come with a marking option, similar to how paintballs work. operators are required to wear face protection due to the potential damage that these rounds could impart. these simulated ammunitions allow the gun to function exactly as it would with normal lethal cartridges and simulate the dangers that occur during combat. the weapons produce realistic sounds, cycle predictably and reload realistically, allowing the operator to practice drills whilst under genuine fire conditions. the rounds aren’t without their downsides, however. one downside is predominantly cost, as rounds cost roughly 3times the price of genuine ammunition, it can be difficult to justify the cost, not to mention the cost of weapon conversion kits. the use of these rounds also require special padding and face masks, which are not only an extra cost for forces to consider, but also impede and restrict the movement (particularly the ability to aim down sight) of the operator. finally, these systems are arguably no better than similar airsoft alternatives. systems such as systema ptws (professional training weapons) or celsius ctws are specifically designed for this use. they are designed to be 100% accurate compared to real firearms in operation, weight and look. yet, they are impossible to mistake a real fire arm for since they require batteries and bbs to operate. finally, ammunition is much cheaper and the muzzle velocity can be increased to match that of simunition rounds. the only negatives of these systems are the lack of realistic bolt movement and recoil, which is a requirement for most trainees to get familiar with.

Malais

sejak ciptaan senjata api pada tahun 1300-an, terdapat keperluan yang mantap dan diperlukan untuk melatih dengan lancar dengan penggunaannya. senjata api sentiasa sukar untuk mendapatkan cengkaman dengan sebagai pengguna kali pertama, jadi gerudi berulang dan senaman digunakan untuk membangunkan memori otot. membangunkan memori otot pepejal dan naluri untuk kegunaan senjata api yang selamat adalah satu-satunya cara untuk beroperasi dengan cekap di lapangan, tanpa adrenalin dan ketakutan menyebabkan anda terkunci atau lupa di mana pencetus. sebagai senjata api (dan mili lain

Dernière mise à jour : 2021-03-29
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Anglais

insulin receptors and insulin binding insulin mediates its actions through binding to insulin receptors. the insulin receptor was fi rst characterised in 1971. it consists of a heterotetramer consisting of 2 α and 2 β glycoprotein subunits linked by disulphide bonds and is located on the cell membrane.25 the gene coding for the insulin receptor is located on the short arm of chromosome 19.17 insulin binds to the extracellular α subunit, resulting in conformational change enabling atp to bind to the intracellular component of the β subunit.23 atp binding in turn triggers phosphorylation of the β subunit conferring tyrosine kinase activity. this enables tyrosine phosphorylation of intracellular substrate proteins known as insulin responsive substrates (irs). the irs can then bind other signalling molecules which mediate further cellular actions of insulin.25 there are four known specifi cally-named irs proteins. irs 1 and 2 have widely overlapping tissue distribution. irs 1 is phosphorylated by both the insulin receptor and insulinlike growth factor 1 (igf-1 see below) receptor, mediates the mitogenic effects of insulin and couples glucose sensing to insulin secretion with irs 1 proposed to be the major irs in skeletal muscle. irs 2, proposed to be the main irs in liver, mediates peripheral actions of insulin and growth of pancreatic β cells.25 irs 3 and 4 are less well characterised. irs 3 is found only in adipose tissue, β cells and liver and irs 4 in thymus, brain and kidney.26,27 phosphorylated irs proteins bind specifi c src-homology-2 domain proteins (sh2), which include important enzymes such as phosphatidylinositol 3-kinase (pi 3-kinase) and phosphotyrosine phosphatase shptp2 (or syp), and other proteins that lack enzymatic activity but which link irs-1 and other intracellular signalling systems, e.g. the adaptor protein grb2 which connects with the ras (rat sarcoma protein) pathway. pi 3-kinase promotes the translocation of glucose transporter proteins, glycogen, lipid and protein synthesis, anti-lipolysis and the control of hepatic gluconeogenesis.27 pi 3-kinase acts via serine and threonine kinases such as akt/protein kinase b (pkb), protein kinase c (pkc) and pi dependent protein kinases1& 2 (pipd 1&2). the ras pathway activates transcription factors and stimulates the growth promoting actions of insulin.25 thus broadly, pi 3-kinase mediates insulin’s metabolic effects, e.g. cellular glucose uptake, while ras signifi cantly mediates insulin’s mitogenic effects17,25 clin biochem rev vol 26 may 2005 i 23 insulin and insulin resistance together with other less well described actions. these pathways are presented schematically in figure 2. glucose transporter proteins glucose enters cells in an atp-independent manner by means of glucose transporter proteins (glut), of which at least 5 subtypes have been identifi ed28,29 (table 2). differing in characteristics such as km for maximal glucose transport and insulin dependency, they enable different cell types to utilise glucose according to their specifi c functions. for example, most brain cells, having glut 1 as the principal transporter protein, are able to move glucose intracellularly at very low blood glucose blood concentrations without the need for insulin. thus these neurons, which are principally dependent on glucose for intracellular energy, are able to extract it from the circulation and function despite the low glucose and insulin levels seen during the fasting state. on the other hand, adipose cells and muscle cells have glut 4 as the major glucose transporter protein, which requires insulin for its action and has a much higher km for glucose. this enables adipose tissue cells, whose function is to store excess energy, to respond to the higher glucose levels characteristic of the fed state, and allows glucose to enter the cells where fatty acid and glycerol synthesis is stimulated and lipolysis suppressed. however, where glucose and insulin levels fall to fasting values, glucose no longer enters the cells, promoting lipolysis. in muscle cells, intracellular glucose transport facilitates glycogen synthesis in the fed state.27 pi 3-kinase appears to be essential for the translocation of glut 4 to the cell membrane in muscle cells and adipocytes; this facilitates the downstream actions of this key intracellular enzyme.25 actions of insulin at the cellular level insulin’s actions at the cellular level encompass carbohydrate, lipid and amino acid metabolism and mrna transcription and translation. carbohydrate metabolism insulin acts at multiple steps in carbohydrate metabolism. its effect on facilitated diffusion of glucose into fat and muscle cells via modulation of glut 4 translocation has been discussed. glycogen synthesis is increased, and glycogen breakdown decreased, by dephosphorylation of glycogen synthase and glycogen phosphorylase kinase respectively. glycolysis is stimulated and gluconeogenesis inhibited by dephosphorylation of pyruvate kinase (pk) and 2,6 biphosphate kinase. signalling intracellular energy abundance, insulin enhances the irreversible conversion of pyruvate to 24 i clin biochem rev vol 26 may 2005 wilcox g table 1. mediators of insulin secretion. stimulus nutrient hormone neural stimulatory glucose growth hormone β-adrenergic amino acids glucagon vagal (ketones) glp-1 (parasympathetic) gip secretin cholecystokinin gastrin vip gastrin releasing peptide inhibitory adrenocorticosteroids α-adrenergic somatostatin adrenalin noradrenalin galanin neuropeptide y calcitonin gene-related peptide (cgrp) prostaglandin e reference: adapted from reference 17. acetyl co-a by activation of the intra-mitochondrial enzyme complex pyruvate dehydrogenase. acetyl-coa may then be directly oxidised via the krebs’ cycle, or used for fatty acid synthesis.30 lipid metabolism insulin stimulates fatty acid synthesis in adipose tissue, liver and lactating mammary glands along with formation and storage of triglycerides in adipose tissue and liver. fatty acid synthesis is increased by activation and increased phosphorylation of acetyl-coa carboxylase, while fat oxidation is suppressed by inhibition of carnitine acyltransferase. triglyceride synthesis is stimulated by esterifi cation of glycerol phosphate, while triglyceride breakdown is suppressed by dephosphorylation of hormone sensitive lipase. cholesterol synthesis is increased by activation and dephosphorylation of hmg co-a reductase while cholesterol ester breakdown appears to be inhibited by dephosphorylation of cholesterol esterase. phospholipid metabolism is also infl uenced by insulin.28 protein synthesis insulin promotes protein synthesis in a range of tissues. there are effects on transcription of specifi c mrna, as well as translation of mrna into proteins in the ribosomes. examples of enhanced mrna transcription include the mrna for glucokinase, pk, fatty acid synthase and albumin in the liver, pyruvate carboxylase in the adipose tissue, casein in the mammary gland and amylase in the pancreas. insulin action decreases mrna for liver enzymes such as carbamoyl phosphate synthetase, a key enzyme in the urea cycle. effects on translation are widespread and infl uenced by both insulin itself and by various growth factors, e.g. igf-1.19,28 other ligands for the insulin receptor insulin-like growth factors (igf) are so-called because they have signifi cant structural homology with proinsulin but mainly mitogenic effects, signifi cantly regulated by growth hormone.31 igf-1 and 2 are coded for on the long arm of chromosome 12 and short arm of chromosome 11 respectively.32 they have specifi c receptors and bind with clin biochem rev vol 26 may 2005 i 25 insulin and insulin resistance figure 2. schematic presentation of insulin signalling pathways. adapted from references: 25, 28 & 35. see footnotes on page 22 for figure abbreviations. different affi nities to the various igf binding proteins. insulin can bind to the receptors for igf-1 and 2 but with much lower affi nity (10-2 and 5x10-3) respectively. igf-1 binds weakly to the insulin receptor, with only 1.25x10-3 the affi nity for the igf-1 receptor; it binds the igf-2 receptor with 1/4 the affi nity for the igf-2 receptor. igf-2 does not bind to the insulin receptor; it does bind the igf-1 receptor but with 1/3 the affi nity for the igf-2 receptor.29 therefore overlap in physiological functions is more limited in vivo. physiological role of insulin insulin is the pivotal hormone regulating cellular energy supply and macronutrient balance, directing anabolic processes of the fed state.27 insulin is essential for the intra-cellular transport of glucose into insulin-dependent tissues such as muscle and adipose tissue. signalling abundance of exogenous energy, adipose tissue fat breakdown is suppressed and its synthesis promoted. in muscle cells, glucose entry enables glycogen to be synthesised and stored, and for carbohydrates, rather than fatty acids (or amino acids) to be utilised as the immediately available energy source for muscle contraction. insulin therefore promotes glycogen and lipid synthesis in muscle cells, while suppressing lipolysis and gluconeogenesis from muscle amino acids. in the presence of an adequate supply of amino acids, insulin is anabolic in muscle.29 mechanisms of insulin resistance physiologically, at the whole body level, the actions of insulin are infl uenced by the interplay of other hormones. insulin, though the dominant hormone driving metabolic processes in the fed state, acts in concert with growth hormone and igf1; growth hormone is secreted in response to insulin, among other stimuli, preventing insulin-induced hypoglycaemia. other counter-regulatory hormones include glucagon, glucocorticoids and catecholamines. these hormones drive metabolic processes in the fasting state. glucagon promotes glycogenolysis, gluconeogenesis and ketogenesis. the ratio of insulin to glucagon determines the degree of phosphorylation or dephosphorylation of the relevant enzymes.29 catecholamines promote lipolysis and glycogenolysis; glucocorticoids promote muscle catabolism, gluconeogenesis and lipolysis. excess secretion of these hormones may contribute to insulin resistance in particular settings, but does not account for the vast majority of insulin resistant states. 26 i clin biochem rev vol 26 may 2005 wilcox g table 2. glucose transporter proteins.26,27 isoform tissue distribution affi nity for glucose km characteristics gene location glut 1 brain microvessels, red blood cells placenta kidney all tissues high 1 mmol/l ubiquitous basal transporter chr 1 glut 2 liver kidney β cell small intestine low 15-20 mmol/l high km transporter insulin-independent chr 3 glut 3 brain neurons placenta foetal muscle all tissues high <1 mmol/l low km transporter found in glucosedependent tissues chr 12 glut 4 muscle cells fat cells heart medium 2.5-5 mmol/l sequestered intracellularly and translocates to cell surface in response to insulin chr 17 glut 5 small intestine testes medium 6 mmol/l high affi nity for fructose chr 1 insulin resistance in most cases is believed to be manifest at the cellular level via post-receptor defects in insulin signalling. despite promising fi ndings in experimental animals with respect to a range of insulin signalling defects, their relevance to human insulin resistance is presently unclear. possible mechanisms include down-regulation, defi ciencies or genetic polymorphisms of tyrosine phosphorylation of the insulin receptor, irs proteins or pip-3 kinase, or may involve abnormalities of glut 4 function.33 sites of insulin action and manifestations of insulin resistance the effects of insulin, insulin defi ciency and insulin resistance vary according to the physiological function of the tissues and organs concerned, and their dependence on insulin for metabolic processes. those tissues defi ned as insulin dependent, based on intracellular glucose transport, are principally adipose tissue and muscle. however, insulin’s actions are pleotropic and widespread, as are the manifestations of insulin resistance and the associated compensatory hyperinsulinaemia.3 muscle glucose uptake into muscle is essentially insulin dependent via glut 4, and muscle accounts for about 60-70% of whole-body insulin mediated uptake.34 in the fed state insulin promotes glycogen synthesis via activation of glycogen synthase. this enables energy to be released anaerobically via glycolysis, e.g. during intense muscular activity. muscle cells do not rely on glucose (or glycogen) for energy during the basal state, when insulin levels are low. insulin suppresses protein catabolism while insulin defi ciency promotes it, releasing amino acids for gluconeogenesis. in starvation, protein synthesis is reduced by 50%.35 whilst data regarding a direct anabolic effect of insulin are inconsistent, it is clearly permissive, modulating the phosphorylation status of intermediates in the protein synthetic pathway. in experimental studies, the insulin dose promoting protein synthesis is signifi cantly greater than the dose required to suppress proteolysis. insulin is anabolic in conjunction with growth hormone, igf-1 and suffi cient amino acids.35 in insulin resistance, muscle glycogen synthesis is impaired; this appears largely mediated by reduced intracellular glucose translocation.28 in regard to protein turnover, one study reported no difference between insulin resistant type 2 diabetics and controls, though this was at the expense of hyperinsulinaemia in this hyperinsulinemic euglycemic clamp study.36 adipose tissue intracellular glucose transport into adipocytes in the postprandial state is insulin-dependent via glut 4; it is estimated that adipose tissue accounts for about 10% of insulin stimulated whole body glucose uptake.34 insulin stimulates glucose uptake, promotes lipogenesis while suppressing lipolysis, and hence free fatty acid fl ux into the bloodstream. as adipocytes are not dependent on glucose in the basal state, intracellular energy may be supplied by fatty acid oxidation in insulin-defi cient states, whilst liberating free fatty acids into the circulation for direct utilization by other organs e.g. the heart, or in the liver where they are converted to ketone bodies. ketone bodies provide an alternative energy substrate for the brain during prolonged starvation.30 in insulin resistance the effects on adipose tissue are similar, but in the liver the increased free fatty acid fl ux tends to promote hepatic very low density lipoprotein (vldl) production37 whilst ketogenesis typically remains suppressed by the compensatory hyperinsulinaemia. furthermore, since lipoprotein lipase activity is insulin-dependent and impaired by insulin resistance, peripheral uptake of triglycerides from vldl is also diminished. these mechanisms contribute to the observed hypertriglyceridaemia of insulin resistance.38 in addition to free fatty acids, adipose tissue secretes a number of cytokines which have systemic effects on insulin resistance. these include il-6, tnfα, plasminogen activator inhibitor 1 (pai-1), angiotensinogen and leptin which are associated with increased insulin resistance, and adiponectin with reduced insulin resistance.39 tnfα and il-6 impair insulin signalling, lipolysis and endothelial function. il-6 production is enhanced by sympathetic nervous system activation, e.g. stress.39 adipose tissue depots differ in their response to insulin.35 adipocytes from diabetic and insulin resistant individuals have reduced glut 4 translocation, impaired intracellular signalling via reduced irs-1 gene and protein expression, impaired insulin-stimulated pip-3 kinase and akt (protein kinase b).34 liver while glucose uptake into the liver is not insulin-dependent, it accounts for about 30% of whole body insulin-mediated glucose disposal,34 with insulin being needed to facilitate key metabolic processes. through intracellular signalling described above, glycogen synthesis is stimulated while protein synthesis and lipoprotein metabolism are modulated.30 gluconeogenesis and ketone body production are inhibited. mitogenic effects of insulin (and growth hormone) are mediated via hepatic production of insulin-like growth factors and potentially via suppression of sex-hormone binding globulin (shbg) production.28 whilst in insulin defi ciency, e.g. starvation, these processes are more uniformly affected, this is not necessarily the case with insulin resistance. compensatory hyperinsulinaemia, differential insulin resistance and differential tissue requirements may dissociate these processes.3 resistance to clin biochem rev vol 26 may 2005 i 27 insulin and insulin resistance insulin’s metabolic effects results in increased glucose output via increased gluconeogenesis (as in starvation), however, unlike starvation, compensatory hyperinsulinaemia depresses shbg production and promotes insulin’s mitogenic effects. alterations in lipoprotein metabolism represent a major hepatic manifestation of insulin resistance. increased free fatty acid delivery, and reduced vldl catabolism by insulin resistant adipocytes, results in increased hepatic triglyceride content and vldl secretion.38 hepatic synthesis of creactive protein, fi brinogen and pai-1 is induced in response to adipocyte-derived pro-infl ammatory cytokines such as tnfα and il-6. insulin may also increase factor vii gene expression.39 endothelium and vasculature insulin and its actions play an important role in various aspects of endothelial function, e.g. nitric oxide production, while insulin resistance is strongly associated with endothelial dysfunction. whether these associations are causal, or mediated by common mechanisms, awaits clarifi cation. the functions of vascular endothelial cells are critical to many aspects of cardiovascular biology, with endothelial dysfunction being seen at a very early stage of atherosclerosis and its associated clinical risk factors. endothelial cells not only provide the physical lining of the blood vessels but secrete various factors infl uencing vessel tone, platelet function, coagulation and fi brinolysis. clinical problems develop when these processes are in imbalance. nitric oxide (no) is the major factor in large arteries mediating endothelial dependent relaxation. it also inhibits platelet aggregation, cell adhesion and smooth muscle cell proliferation. no is synthesised from l-arginine, molecular oxygen and nadph, via the activity of endothelial enzyme nitric oxide synthase (enos), and its cofactors tetrahydrobiopterin, fl avin adenine dinucleotide and fl avin mononucleotide. interestingly, arginine is a potent secretatogue for insulin and there is a fi nal common pathway for the intracellular signalling of both enos and insulin. insulin enhances tetrahydrobiopterin production by stimulating its biosynthetic enzyme gtp cyclohydrolase, and stimulates enos by calcium-independent phosphorylation of enos at serine and threonine residues via pip-3 kinase and akt (protein kinase b). thus nitric oxide production is enhanced. insulin also promotes release of the vasoconstrictor endothelin while tnfα decreases enos expression and induces von willebrand factor release. in insulin resistance tetrahydrobiopterin levels are reduced, the pathways for enos stimulation are downregulated, and vasodilator responses to insulin and cholinergic agonists are impaired. insulin’s ability to counteract the tnfαmediated akt dephosphorylation in endothelial cells is also lost. free fatty acids, elevated in insulin resistant states, also inhibit enos activity, decreasing no production. the compensatory hyperinsulinaemia that accompanies insulin resistance is associated with increased levels of procoagulant factors such as pai-1. these factors are thought to contribute to the enhanced platelet aggregation seen in insulin resistant states. endothelin 1 secret

Malais

Dernière mise à jour : 2021-04-26
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Anglais

set or unset values of shell options and positional parameters. change the value of shell attributes and positional parameters, or display the names and values of shell variables. options: -a mark variables which are modified or created for export. -b notify of job termination immediately. -e exit immediately if a command exits with a non-zero status. -f disable file name generation (globbing). -h remember the location of commands as they are looked up. -k all assignment arguments are placed in the environment for a command, not just those that precede the command name. -m job control is enabled. -n read commands but do not execute them. -o option-name set the variable corresponding to option-name: allexport same as -a braceexpand same as -b emacs use an emacs-style line editing interface errexit same as -e errtrace same as -e functrace same as -t hashall same as -h histexpand same as -h history enable command history ignoreeof the shell will not exit upon reading eof interactive-comments allow comments to appear in interactive commands keyword same as -k monitor same as -m noclobber same as -c noexec same as -n noglob same as -f nolog currently accepted but ignored notify same as -b nounset same as -u onecmd same as -t physical same as -p pipefail the return value of a pipeline is the status of the last command to exit with a non-zero status, or zero if no command exited with a non-zero status posix change the behavior of bash where the default operation differs from the posix standard to match the standard privileged same as -p verbose same as -v vi use a vi-style line editing interface xtrace same as -x -p turned on whenever the real and effective user ids do not match. disables processing of the $env file and importing of shell functions. turning this option off causes the effective uid and gid to be set to the real uid and gid. -t exit after reading and executing one command. -u treat unset variables as an error when substituting. -v print shell input lines as they are read. -x print commands and their arguments as they are executed. -b the shell will perform brace expansion -c if set, disallow existing regular files to be overwritten by redirection of output. -e if set, the err trap is inherited by shell functions. -h enable ! style history substitution. this flag is on by default when the shell is interactive. -p if set, do not follow symbolic links when executing commands such as cd which change the current directory. -t if set, the debug trap is inherited by shell functions. -- assign any remaining arguments to the positional parameters. if there are no remaining arguments, the positional parameters are unset. - assign any remaining arguments to the positional parameters. the -x and -v options are turned off. using + rather than - causes these flags to be turned off. the flags can also be used upon invocation of the shell. the current set of flags may be found in $-. the remaining n args are positional parameters and are assigned, in order, to $1, $2, .. $n. if no args are given, all shell variables are printed. exit status: returns success unless an invalid option is given.

Malais

tetap atau nyahtetap nilai bagi pilihan shell dan parameter berkedudukan. ubah nilai atribut shell dan parameter berkedudukan, atau papar nama dan nilai pembolehubah shell. pilihan: -a tanda pembolehubah yang diubahsuai atau dicipta untuk eksport. -b maklum penamatan kerja secara serta-merta. -e keluar serta-merta jika perintah wujud dengan status bukan-sifar. -f lumpuhkan penjanaan nama fail (globbing). -h ingat lokasi perintah bila ia dicari. -k semua argumen tugasan diletak dalam persekitaran untuk perintah, bukan bagi yang mendahului nama perintah. -m kawalan kerja dibenarkan. -n baca perintah tetapi jangan lakukannya -o option-name tetapkan pembolehubah yang berkaitan dengan option-name: allexport sama seperti -a braceexpand sama seperti -b emacs guna antaramuka penyuntingan baris gaya-emacs errexit sama seperti -e errtrace sama seperti -e functrace sama seperti -t hashall sama seperti -h histexpand sama seperti -h history benarkan sejarah perintah abai shell tdak akan keluar bila membaca eof interactive-comments benarkan ulasan muncul dalam perintah interaktif keyword sama seperti -k monitor sama seperti -m noclobber sama seperti -c noexec sama seperti -n noglob sama seperti -f nolog buat masa ini diterima tetapi diabaikan notify sama seperti -b nounset sama seperti -u onecmd sama seperti -t physical sama seperti -p pipefail nilai kembali talian paip ialah status perintah terakhir wujud dengan status bukan-sifar, atau sifar jika tiada perintah keluar dengan bukan-sifar posix ubah kelakuan bash yang mana operasi lalai berbeza dengan piawai posix untuk sepadan dengan piawai privileged sama seperti -p verbose sama seperti -v vi guna antaramuka penyuntingan baris gaya-vi xtrace sama seperti -x -p dihidupkan bila id pengguna efektif tidak sepadan. lumpuhkan pemprosesan fail $env dan mengimport fungsi shell. matikan pilihan ini menyebabkan uid dan gid efektif ditetapkan kepada uid dan gid sebenar. -t keluar selepas membaca dan melakukan satu perintah. -u anfggap nyahtetap pembolehubah sebagai ralat bila mengganti. -v cetak baris input shell sebagaimana ia dibaca. -x perintah cetak dan argumennya sebagaimana ia dilakukan. -b shell akan buat pengembangan teguh -c jika ditetapkan, tidak benarkan fail nalar sedia ada ditulis ganti secara arah semula output. -e jika ditetapkan, jerat err diwarisi oleh fungsi shell. -h benarkan penggantian sejaraj gaya !. bendera ini dihidupkan secara lalai bila shell adalah interaktif. -p jika ditetapkan, jangan ikut pautan simbolik bila melakukan perintah seperti cd yang menukar direktori semasa. -t jika ditetapkan, jerat debug diwarisi oleh fungsi shell. -- umpuk mana-mana argumen berbaki ke parameter berkedudukan. jika tiada argumen berbaki, parameter berkedudukan tidak dinyahtetap. - umpuk mana-mana argumen berbaki ke parameter berkedudukan. pilihan -x dan -v dimatikan. penggunaan + berbanding - menyebabkan bendera ini dimatikan. bendera juga boleh digunakan semasa invokasi shell. set bendera semasa boleh ditemui dalam $-. arg berbaki adalah parameter berkedudukan dan diumpuk, dalam tertib, sehingga $1, $2, .. $n. jika tiada args diberi, semua pembolehubah shell dicetak. status keluar: kembali berjaya melainkan pilihan tidak sah diberi.

Dernière mise à jour : 2014-08-15
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Anglais

this key contains a list of hosts which are connected to directly, rather than via the proxy (if it is active). the values can be hostnames, domains (using an initial wildcard like *.foo.com), ip host addresses (both ipv4 and ipv6) and network addresses with a netmask (something like 192.168.0.0/24).

Malais

kekunci ini mengandungi senarai hos yang disambung secara terus, bukannya melalui proksi (jika ia aktif). nilai boleh jadi nama hos, domain (menggunakan kad liar awalan seperti *.sebol.com), alamat hos ip (kedua-dua ipv4 dan ipv6) dan alamat rangkaian dengan netmask (seperti 192.168.0.0/24).

Dernière mise à jour : 2014-08-15
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Anglais

welcome to dselect's main package listing. you will be presented with a list of packages which are installed or available for installation. since you do not have the privilege necessary to update package states, you are in a read-only mode. you can navigate around the list using the cursor keys (please see the `keystrokes' help screen), observe the status of the packages and read information about them. you should read the list of keys and the explanations of the display. much on-line help is available, please make use of it - press `?' at any time for help. when you have finished browsing, press `q' or to quit. press to leave help and enter the list now.

Malais

selamat datang ke penyenaraian pakej utama dselect. anda akan dihadirkan dengan satu senarai pakej yang dipasang atau tersedia untuk pemasangan. oleh kerana anda tidak mempunyai keistimewaan yang diperlukan untuk kemaskini keadaan pakej, anda kini berada didalam mod baca-sahaja. anda boleh pandu arah disekitar senarai menggunakan kekunci kursor (sila rujuk skrin bantuan `ketukan kekunci'), perhati status pakej dan baca maklumat mengenainya. anda patut baca senarai kekunci dan paparan penerangnnya. bantuan atas-talian juga tersedia, sila gunakkanya - tekan `?' pada bila-bila masa untuk bantuan. bila anda telah selesai melayar, tekan `q' atau untuk keluar. tekan untuk tinggalkan bantuan dan masuk ke senarai sekarang.

Dernière mise à jour : 2014-08-15
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Anglais

welcome to dselect's main package listing. you will be presented with a list of packages which are installed or available for installation. you can navigate around the list using the cursor keys, mark packages for installation (using `+') or deinstallation (using `-'). packages can be marked either singly or in groups; initially you will see that the line `all packages' is selected. `+', `-' and so on will affect all the packages described by the highlighted line. some of your choices will cause conflicts or dependency problems; you will be given a sub-list of the relevant packages, so that you can solve the problems. you should read the list of keys and the explanations of the display. much on-line help is available, please make use of it - press `?' at any time for help. when you have finished selecting packages, press to confirm changes, or `x' to quit without saving changes. a final check on conflicts and dependencies will be done - here too you may see a sublist. press to leave help and enter the list now.

Malais

selamat datang ke penyenaraian pakej utama dselect. anda akan dihadirkan dengan senarai pakej yang dipasang atau tersedia untuk pemasangan. anda boleh pandua arah disekitar senarai menggunakan kekunci kursor, tanpa pakej untuk pemasangan (guna `+') atau nyahpasang (guna `-'). pakej boleh ditanda sama ada secara tunggal atau kumpulan; awalnya anda akan lihat baris `semua pakej' dipilih. `+', `-' dan seterusnya akan mempengaruhi semua pakej yang diterangkan oleh baris tersorot. beberapa pilihan anda akan menyebabkan konflik atau masalah dependensi; anda akan diberikan sub-senarai pakej yang berkaitan, supaya anda dapat selesaikan masalahnya. anda patut baca senarai kekunci dan penerangan yang dipaparkan. bantuan atas-talian juga tersedia, sila gunakannya - tekan `?' pada bila-bila masa untuk dapatkan bantuan. bila anda selesai memilih pakej, tekan untuk sahkan perubahan, atau `x' untuk keluar tanpa menyimpan perubahan. satu semakan akhir pada konflik dan dependensi akan dibuat - disini jugaanda dapat lihat subsenarainya. tekan untuk tinggalkan bantuan dan masukkan ke senarai sekarang.

Dernière mise à jour : 2014-08-15
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Avertissement : un formatage HTML invisible est présent

Anglais

this key contains a list of hosts which are connected to directly, rather than via the proxy (if it is active). the values can be hostnames, domains (using an initial wildcard like *.foo.com), ip host addresses (both ipv4 and ipv6) and network addresses with a netmask (something like 192.168.0.0/24).

Malais

kekunci ini mengandungi senarai hos yang disambung secara terus, bukannya melalui proksi (jika ia aktif). nilai boleh jadi namahos, domain (menggunakan wildcard awalan seperti *.sebol.com), alamat hos ip (kedua-dua ipv4 dan ipv6) dan alamat rangkaian dengan netmask (seperti 192.168.0.0/24).

Dernière mise à jour : 2014-08-20
Fréquence d'utilisation : 2
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