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PubMed2003

Effects of reducing dietary protein, methionine, choline, folic acid, and vitamin B12 during the late stages of the egg production cycle on performance and eggshell quality.

A series of four experiments was conducted to determine whether-shell quality during the late stages of egg production can be improved by using diets that are effective in reducing egg size. The experiments involved dietary manipulation of protein, methionine, choline, folic acid, and vitamin B12. In experiment 1, reducing dietary protein in combination of reducing the dietary methionine and choline or this diet without supplemental folic acid and vitamin B12 resulted in reduced egg weight and improved shell quality. However, egg production also was drastically reduced. In experiment 2, reducing the dietary level of methionine, without adding supplemental choline, folic acid, and vitamin B12 reduced egg size and improved shell quality, but egg production was reduced as well. In this experiment reducing the dietary methionine without supplemental folic acid and vitamin B12 reduced egg size and improved shell quality with no adverse effect on egg production. In experiment 3, reducing the dietary level of methionine and choline or reducing the dietary level of choline, folic acid, and vitamin B12 reduced egg size and improved shell quality without adverse effects on egg production. On the other hand, reducing dietary methionine, folic acid, vitamin B12, and supplemental choline reduced egg weight and improved shell quality but lowered egg production. In experiment 4, reducing dietary methionine together with reducing choline and vitamin B12 reduced egg size and improved shell quality with no adverse effect on egg production. The results of this series of experiments generally indicate that certain manipulations of the combination of methionine, choline, folic acid, and vitamin B12 have the potential to reduce egg weight and improve shell quality without affecting egg production during the latter stages of the egg production cycle.

Animal Feed↗

PubMed2002

Perturbations in choline metabolism cause neural tube defects in mouse embryos in vitro.

A role for choline during early stages of mammalian embryogenesis has not been established, although recent studies show that inhibitors of choline uptake and metabolism, 2-dimethylaminoethanol (DMAE), and 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine (ET-18-OCH3), produce neural tube defects in mouse embryos grown in vitro. To determine potential mechanisms responsible for these abnormalities, choline metabolism in the presence or absence of these inhibitors was evaluated in cultured, neurulating mouse embryos by using chromatographic techniques. Results showed that 90%-95% of 14C-choline was incorporated into phosphocholine and phosphatidylcholine (PtdCho), which was metabolized to sphingomyelin. Choline was oxidized to betaine, and betaine homocysteine methyltransferase was expressed. Acetylcholine was synthesized in yolk sacs, but 70 kDa choline acetyltransferase was undetectable by immunoblot. DMAE reduced embryonic choline uptake and inhibited phosphocholine, PtdCho, phosphatidylethanolamine (PtdEtn), and sphingomyelin synthesis. ET-18-OCH3 also inhibited PtdCho synthesis. In embryos and yolk sacs incubated with 3H-ethanolamine, 95% of recovered label was PtdEtn, but PtdEtn was not converted to PtdCho, which suggested that phosphatidylethanolamine methyltransferase (PeMT) activity was absent. In ET-18-OCH3 treated yolk sacs, PtdEtn was increased, but PtdCho was still not generated through PeMT. Results suggest that endogenous PtdCho synthesis is important during neurulation and that perturbed choline metabolism contributes to neural tube defects produced by DMAE and ET-18-OCH3.

Acetylcholine↗

PubMed2003

11C-choline PET for the detection of bone and soft tissue tumours in comparison with FDG PET.

We assessed and compared the usefulness of C-choline positron emission tomography (PET) with that of 2-[ F]fluoro-2-deoxy-D-glucose (FDG) PET for the differentiation between benign and malignant bone and soft tissue tumours. A total of 43 patients with 45 lesions were included. C-choline PET and FDG PET were performed from 5 and 40 min, respectively, after injection of 275-370 MBq tracer. PET data were evaluated by using the standardized uptake value (SUV) and were analysed according to the pathological data. C-choline uptake in malignancies was 4.9+/-2.1 (n=14), which was significantly higher than that in benign lesions (2.5+/-1.7, n=31) (P <0.0001). The sensitivity, specificity and accuracy of C-choline PET were 100%, 64.5% and 75.6%, respectively, when 2.59 of the SUV was used as the cut-off value. The FDG uptake in malignancies was 5.1+/-4.2 (n=14) and was also significantly larger than that in benign lesions 2.9+/-2.9 (n=31) (P<0.003). The sensitivity, specificity and accuracy of FDG PET were 85.7%, 41.9% and 55.6%, respectively (cut-off=1.83). The C-choline uptake in the lesions correlated with FDG uptake ( r=0.61, P<0.003). In receiver operating characteristic (ROC) analysis, the area under the ROC curve for C-choline PET (area=0.847) was higher than that for FDG PET (area=0.717). This study showed that C-choline PET was superior to FDG PET in differentiation between malignant and benign lesion in bone and soft tissue tumours. C-choline PET might be useful as a screening method for malignant bone and soft tissue tumours.

Adolescent↗

PubMed2003

A comparative study of 11C-choline PET and [18F]fluorodeoxyglucose PET in the evaluation of lung cancer.

The purpose of this study was to compare the diagnostic value of 11C-choline positron emission tomography (PET) and [18F]fluorodeoxyglucose (FDG) PET imaging in the detection of primary lung cancer and mediastinal lymph node metastases. Seventeen patients with histologically proven primary lung cancer were examined with both 11C-choline and FDG PET within a week of each study. Lung cancers were analysed visually and semiquantitatively using the ratio of tumour-to-normal radioactivity (T/N ratio) and standardized uptake value (SUV). Mediastinal lymph node metastases were analysed visually. Although both techniques delineated focal lesions with an increase in tracer accumulation in 13 patients, FDG PET identified three additional patients in whom 11C-choline PET did not visualize any lesion. In the detection of lung cancer <2 cm in size, FDG PET provided higher sensitivity (six of seven, 85.7%) than 11C-choline PET (four of seven, 57.1%). The T/N ratio and SUV were significantly higher with FDG PET (T/N ratio, 7.43+/-6.22; SUV, 4.05+/-3.05) than these were with 11C-choline PET (T/N ratio, 2.93+/-1.19; SUV, 2.93+/-0.79) (P<0.001). There was a significant positive correlation between the T/N ratios and SUVs of FDG and 11C-choline. In the assessment of mediastinal lymph node involvement, FDG PET detected lymph node metastases in two patients who were negative on 11C-choline PET, whereas both techniques could not detect tumour involvement in one patient. Both techniques have clinical value for the non-invasive detection of primary lung cancer that is 2 cm or greater in size. However, FDG PET is superior to 11C-choline PET in the detection of lung cancer that is less than 2 cm in diameter and in mediastinal lymph node metastases.

Adenocarcinoma↗

PubMed2003

Value of [11C]choline-positron emission tomography for re-staging prostate cancer: a comparison with [18F]fluorodeoxyglucose-positron emission tomography.

PURPOSE: We compared [11C]choline-positron emission tomography (PET) with [18F]fluorodeoxyglucose-PET for re-staging prostate cancer in a group of 100 patients. MATERIALS AND METHODS: A total of 100 consecutive patients referred for whole body [18F]fluorodeoxyglucose-PET for clinical prostate re-staging after radical treatment for prostate cancer were retrospectively included in the study. Mean prostate specific antigen (PSA) was 6.57 ng./ml. In all cases [11C]choline-PET was also performed. PET studies were done with a multiring device 5 minutes after intravenous injection of approximately 370 MBq. [11C]choline and 60 minutes after injection of approximately 370 MBq. [18F]fluorodeoxyglucose. PET findings were compared with those obtained with different conventional imaging and with PSA assessed at the time of PET and 1 year later. RESULTS: Areas of abnormal focal increases were noted in 47% of patients on [11C]choline-PET and in 27% on [18F]fluorodeoxyglucose-PET. Of the 100 patients 49 had positive conventional imaging findings. All except 14 [11C]choline-PET findings were concordant with conventional imaging, including 6 negative and 8 positive conventional imaging results. All except 1 [11C]choline-PET negative cases also had negative conventional imaging after 1 year. PSA at 1 year remained stable or decreased in 80% and 62% of [11C]choline-PET negative and positive cases, respectively. CONCLUSIONS: [11C]choline-PET seems to be useful for re-staging prostatectomy cases with increasing serum PSA levels. It is superior to [18F]fluorodeoxyglucose-PET and complementary to conventional imaging but with the advantage of staging disease at a single step.

Aged↗

PubMed1999

Increased choline kinase activity in 1,2-dimethylhydrazine-induced rat colon cancer.

Cancer cells acquire particular characteristics that benefit their proliferation. We previously reported that human colon cancers examined had increased choline kinase activity and phosphocholine levels. The elevated phosphocholine levels were in part due to both activation of choline kinase and increased choline kinase alpha protein levels. In this report, we analyzed choline kinase, which catalyzes the phosphorylation of choline to produce phosphocholine, in rat 1,2-dimethylhydrazine (DMH)-induced colon cancer. This study is the first to demonstrate increased choline kinase alpha enzymatic activity, protein levels, and mRNA levels in DMH-induced colon cancer as well as human colon cancer, although phosphocholine was not increased in DMH-induced rat cancer. The increase in the mRNA level was partly due to an increase in the transcription of the choline kinase alpha gene. The increased choline kinase activity may be a specific characteristic acquired by cancer cells that benefits their proliferation.

1,2-Dimethylhydrazine↗

PubMed1986

Grouping of human ejaculates according to the degree of coagulation and the relationship to the levels of choline and cholinesterase.

Human ejaculates were divided into 3 groups (I, II and III) according to the extent of their coagulation and the levels of free choline and cholinesterase were determined together with seminal vesicular N-acetylamino sugar and prostatic (zinc) marker components. Coagulation was determined as the percent coagulum (CG) at 5 min after ejaculation. The mean (+/- SEM) values for CG at 5 min in groups I, II and III were 6 +/- 2, 43 +/- 4 and 79 +/- 2, respectively. The time for 100% liquefaction in the 3 groups were 4.7 +/- 0.8, 12.9 +/- 1.4 and 19.1 +/- 2.1 min, respectively. Group III had significantly higher levels of choline and cholinesterase activity than groups I and II. The choline level was correlated significantly (r = 0.58) with the concentration of N-acetylamino sugar, but there was no correlation with the level of zinc. Evaluation of the level of choline in prostatic fluid, in semen from azoospermic men and in ejaculates with different CG values suggested that the level of choline may provide valuable information about activity of the seminal vesicles. Release of choline in group I was only 33 and 50% of that groups III and II, respectively. 60% of the total release of choline occurred during the liquefaction phase. The mean activity of cholinesterase in the prostate was only 27% lower than that found in seminal plasma. The liquefaction time and the concentration of choline, N-acetylamino sugar and zinc decreased significantly in ejaculates after 2 days of abstinence.

Acetylglucosamine↗

PubMed2006

Drastic reduction in the virulence of Streptococcus pneumoniae expressing type 2 capsular polysaccharide but lacking choline residues in the cell wall.

The role of capsular polysaccharides and several virulence-related proteins in the pathogenic potential of Streptococcus pneumoniae has been studied extensively. Much less information is available about the role of the pneumococcal cell wall in virulence. In this communication we describe an experimental system that has allowed us to test - in a global way - the role of choline, a structural component of the pneumococcal cell wall, in virulence. We constructed double mutants of S. pneumoniae which have lost the auxotrophic requirement for choline and which were also blocked from utilizing choline from the growth medium. Such a double mutant expressing type 2 capsule but completely lacking choline residues from its cell wall grew well both in vitro and also in the blood of infected mice, but showed striking reduction of virulence approaching that of a capsule-free strain in several models of pneumococcal disease including the capacity to attach and invade a human nasopharyngeal cell line; nasal colonization and intraperitoneal and intravenous inoculation in the mouse. The findings allow one to separate the choline requirement of S. pneumoniae into two sharply defined classes: the need for choline in growth and replication which can be effectively bypassed and the need for choline in pneumococcal virulence that appears to be irreplaceable. The double mutant should be a useful experimental tool to dissect the mechanism of choline requirement in various stages of pneumococcal virulence.

Animals↗

PubMed1980

The utilization of choline and acetyl coenzyme A for the synthesis of acetylcholine.

Acetylcholine synthesis in rat brain synaptosomes was investigated with regard to the intracellular sources of its two precursors, acetyl coenzyme A and choline. Investigations with alpha-cyano-4-hydroxycinnamate, an inhibitor of mitochondrial pyruvate transport, indicated that pyruvate must be utilized by pyruvate dehydrogenase located in the mitochondria, rather than in the cytoplasm, as recently proposed. Evidence for a small, intracellular pool of choline available for acetylcholine synthesis was obtained under three experimental conditions. (1) Bromopyruvate competitively inhibited high-affinity choline transport, perhaps because of accumulation of intracellular choline which was not acetylated when acetyl coenzyme A production was blocked. (2) Choline that was accumulated under high-affinity transport conditions while acetyl coenzyme A production was impaired was subsequently acetylated when acetyl coenzyme A production was resumed. (3) Newly synthesized acetylcholine had a lower specific activity than that of choline in the medium. These results indicate that the acetyl coenzyme A that is used for the synthesis of acetylcholine is derived from mitochondrial pyruvate dehydrogenase and that there is a small pool of choline within cholinergic nerve endings available for acetylcholine synthesis, supporting the proposal that the high-affinity transport and acetylation of choline are kinetically coupled.

Acetyl Coenzyme A↗

PubMed1981

Effect of increasing choline, in vivo and in vitro, on the synthesis of acetylcholine in a sympathetic ganglion.

The experiments described in this paper were designed to test whether increasing choline availability over normal physiological levels increases acetylcholine synthesis in the cat's superior cervical ganglion. When ganglia were perfused with Krebs solution, an increase in the medium's choline concentration over physiological (10(-5)M) levels increased tissue choline but did not increase tissue acetylcholine or the release of acetylcholine from stimulated ganglia. However, increasing plasma choline in the whole animal increased ganglionic acetylcholine levels. The basis for this difference in the effects of in vivo and in vitro exposure to elevated choline levels on the tissue acetylcholine content was found to involve plasma factor(s), rather than indirect actions of choline, and the acetylcholine content of isolated ganglia was increased when the tissue was perfused with plasma, instead of Krebs solution, containing 10(-3)M-choline. The extra acetylcholine generated by this procedure was associated with a subsequent transient increase in transmitter release during short intervals of stimulation, but most of the extra acetylcholine was not readily available for release from stimulated ganglia. It is concluded that increasing choline available to sympathetic ganglia over physiological concentration does not have a sustained effect on the turnover of releasable transmitter under the conditions of these experiments.

Acetylcholine↗

PubMed1981

Alterations of acetylcholine and choline metabolism in mammalian preparations treated with beta-bungarotoxin.

We have studied the effects of beta-bungarotoxin on acetylcholine and choline metabolism in central and peripheral cholinergic preparations using a gas chromatographic-mass spectrometric assay for acetylcholine and choline. In contrast with previous reports, beta-Bungarotoxin did not inhibit the high-affinity uptake of labeled choline or the synthesis of acetylcholine in rat brain synaptosomal fractions. However, the toxin did cause a significant increase of medium choline when it was incubated with synaptosomal fractions. This increase of endogenous choline in the medium may account for the previously reported inhibition of choline uptake because of a dilution of the specific activity of the labeled choline in the medium. Several experiments are reported in which a further characterization was made of the effect of beta-bungarotoxin on medium choline. beta-Bungarotoxin was also shown to cause a large increase of acetylcholine release from rat brain minces and a depletion of the acetylcholine content of minces. A similar phenomenon was found in diaphragm preparations that were exposed continuously to beta-bungarotoxin. However, diaphragms that were treated for only 30 min with toxin showed the previously reported increase of acetylcholine content. beta-bungarotoxin did not have any measurable effect on acetylcholine turnover in smooth muscle preparations from guinea pig ileum. These results help to explain certain inconsistencies in the literature regarding the action of beta-bungarotoxin.

Acetylcholine↗

PubMed1982

Increase in exogenous choline fails to elevate the content or turnover rate of cortical, striatal, or hippocampal acetylcholine.

The present experiments were designed to test whether increasing the availability of choline to rat brain increases the rate of acetylcholine synthesis in that organ. The content of choline and acetylcholine and the turnover rate of acetylcholine in striatum, hippocampus, and cerebral cortex were measured following changes in dietary choline, intraperitoneal choline, or intravenous infusion of choline. Increasing plasma choline caused some increase in tissue choline but did not increase acetylcholine levels nor acetylcholine turnover rate in any of the areas of brain studied. Indeed, in hippocampus, choline decreased the turnover rate of acetylcholine.

Acetylcholine↗

PubMed1988

Binding of [3H]hemicholinium-3 to the high-affinity choline transporter in electric organ synaptosomal membranes.

Sodium-dependent binding of [3H]hemicholinium-3 was observed to be 10-fold higher with presynaptic membranes from the electric organ than with electroplaque membranes and this binding site copurified with synaptosomal membranes. The KD for specific [3H]hemicholinium-3 binding was found to be 31 +/- 4 nM and the Bmax, 5.0 +/- 0.2 pmol/mg protein; a Ki of 16 nM was estimated for hemicholinium-3 as a competitive inhibitor of high-affinity choline transport in electric organ synaptosomes. Choline and choline analogues were equally potent as inhibitors of [3H]choline uptake and [3H]hemicholinium-3 binding. Tubocurarine and oxotremorine also inhibited uptake and binding, but carbachol was without effect in both tests. These findings suggest that [3H]hemicholinium binds to the high-affinity choline transporter present at the cholinergic nerve terminal membrane. A comparison of maximal velocities for choline transport and the maximal number of hemicholinium-3 binding sites indicated that the high-affinity choline transporter has an apparent turnover number of about 3s-1 at 20 degrees C under resting conditions. The high transport rates observed in electric organ synaptosomes are likely due to the high density of high-affinity choline transporters in this tissue, estimated on the basis of [3H]hemicholinium-3 binding to be of the order of 100/micron2 of synaptosomal membrane.

Amino Alcohols↗

PubMed1988

Kinetics of choline uptake into isolated rat forebrain microvessels: evidence of endocrine modulation.

The active uptake of [methyl-3H]choline into isolated rat brain microvessel suspension was studied as a likely guide to the transport of choline across the blood-brain barrier. The method consisted primarily of incubation of the suspension with a fixed concentration of labeled choline in the presence of increasing concentrations of unlabeled choline or any other inhibitor (I) of active uptake, defined as the difference in uptake at 37 degrees and 0 degrees C. From the linear regression of (1/V) against [I], the following values of Vmax (nmol g-1 min-1) and Km (microM) were obtained for choline: 2-month-old males, 10.6 +/- 3.8 and 6.1 +/- 0.9; 3-month old random females, 28.4 +/- 5.9 and 12.6 +/- 4.0; females at metaestrus, 17.8 +/- 10.3 and 8.3 +/- 5.0; at diestrus, 31.1 +/- 9.3 and 13.0 +/- 2.6; at proestrus, 54.9 +/- 2.2 and 14.0 +/- 1.5; at estrus, 19.2 +/- 2.2 and 2.6 +/- 1.7. The differences between males and random females (p less than 0.018) and between females at proestrus and estrus (p less than 0.005) are significant. It is suggested that these inter- and intrasex variations in choline uptake reflect a dynamic adjustment of supply in accordance with brain demand for choline at the time of assay. Hemicholinium-3 was an effective inhibitor of choline uptake, Ki = 14.0 +/- 8.5 microM; dimethylaminoethanol was much less effective; and imipramine had no measurable effect.

Animals↗

PubMed1991

Stereospecificity of high- and low-affinity transport of choline analogues into rat cortical synaptosomes.

The present experiments used methylcholines to examine the stereoselectivity of choline transport into rat synaptosomes. R(+)-alpha-methylcholine and S(+)-beta-methylcholine were significantly better inhibitors of the high-affinity choline transport system than were their enantiomers. Although both enantiomers of alpha- and of beta-methylcholine inhibited [3H]choline transport, only R(+)-alpha-methylcholine and S(+)-beta-methylcholine could be transported by the high-affinity choline uptake mechanism. Therefore, we conclude that the chiral requirements for recognition of and for transport by the high-affinity transporter are clearly different. In addition to high-affinity choline transport, Na(+)-independent low-affinity transport was measured. This process transported R(+)-alpha-methylcholine, but not S(-)-alpha-methylcholine; however, it showed no stereoselectivity for the enantiomers of beta-methylcholine. Thus, high- and low-affinity choline transport mechanisms exhibit distinct differences in their substrate selectivities. We suggest that the stereoselective properties of choline transport might present a unique opportunity to study choline uptake and metabolism.

Animals↗

PubMed1993

Phosphorylation of rat brain choline acetyltransferase and its relationship to enzyme activity.

Choline acetyltransferase catalyzes the formation of acetylcholine from choline and acetyl-CoA in cholinergic neurons. The present study examined conditions for modulation of kinase-mediated phosphorylation of this enzyme. By using a monospecific polyclonal rabbit anti-human choline acetyltransferase antibody to immunoprecipitate cytosolic and membrane-associated subcellular pools of enzyme from rat hippocampal synaptosomes, we determined that only the cytosolic fraction of the enzyme (67,000 +/- 730 daltons) was phosphorylated under basal, unstimulated conditions. The quantity of this endogenous phosphoprotein was dependent, in part, upon the level of intracellular calcium, with 32Pi incorporation into the enzyme in nerve terminals incubated in nominally calcium-free medium only 43 +/- 7% of control. The corresponding enzymatic activity of cytosolic choline acetyltransferase did not appear to be altered by lowered cytosolic calcium, whereas membrane-associated choline acetyltransferase activity was decreased to 58 +/- 11% of control. Depolarization of synaptosomes with 50 microM veratridine neither altered the extent of phosphorylation or specific activity of cytosolic choline acetyltransferase, nor induced detectable phosphorylation of membrane-associated choline acetyltransferase, although the specific activity of the membrane-associated enzyme was increased to 132 +/- 5% of control. In summary, phosphorylation of choline acetyltransferase does not appear to regulate cholinergic neurotransmission by a direct action on catalytic activity of the enzyme.

Animals↗

PubMed2004

Choline availability modulates human neuroblastoma cell proliferation and alters the methylation of the promoter region of the cyclin-dependent kinase inhibitor 3 gene.

Choline is an important methyl donor and a component of membrane phospholipids. In this study, we tested the hypothesis that choline availability can modulate cell proliferation and the methylation of genes that regulate cell cycling. In several other model systems, hypomethylation of cytosine bases that are followed by a guanosine (CpG) sites in the promoter region of a gene is associated with increased gene expression. We found that in choline-deficient IMR-32 neuroblastoma cells, the promoter of the cyclin-dependent kinase inhibitor 3 gene (CDKN3) was hypomethylated. This change was associated with increased expression of CDKN3 and increased levels of its gene product, kinase-associated phosphatase (KAP), which inhibits the G(1)/S transition of the cell cycle by dephosphorylating cyclin-dependent kinases. Choline deficiency also reduced global DNA methylation. The percentage of cells that accumulated bromodeoxyuridine (proportional to cell proliferation) was 1.8 times lower in the choline-deficient cells than in the control cells. Phosphorylated retinoblastoma (p110) levels were 3 times lower in the choline-deficient cells than in control cells. These findings suggest that the mechanism whereby choline deficiency inhibits cell proliferation involves hypomethylation of key genes regulating cell cycling. This may be a mechanism for our previously reported observation that stem cell proliferation in hippocampus neuroepithelium is decreased in choline-deficient rat and mouse fetuses.

Base Sequence↗

PubMed1982

Potassium activation of [3H]-choline accumulation by isolated sympathetic ganglia of the rat.

1 The effect of K-depolarization on the uptake of low and high concentrations of [3H]-choline by isolated superior sympathetic ganglia of the rat has been studied. 2 In unstimulated ganglia, the uptake of [3H]-choline (0.1 microM) ('high affinity uptake') was unaffected by denervation or by hemicholinium-3 (HC-3), suggesting uptake by structures other than cholinergic nerve terminals. 3 K-depolarization of the ganglia increased [3H]-choline accumulation by the high affinity uptake process but in contrast the 'low affinity' accumulation of [3H]-choline (100 microM) was decreased. 4 The K-activated, 'high affinity' component of choline uptake was highly sodium-dependent, inhibited by HC-3, and was abolished by denervation. 5 In incubation conditions designed to prevent transmitter release (Ca-free medium and high-Mg medium), the K-activated uptake of [3H]-choline was abolished. 6 It is concluded that in unstimulated ganglia, there is little choline uptake by nerve terminals. However, when the terminals are depolarized, choline uptake is increased by the activation of a sodium-dependent, HC-3-sensitive transport process. The activation of this uptake process is apparently associated with the release of acetylcholine from the terminals, or by changes in ionic fluxes, and not by the depolarization per se.

Animals↗