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PubMed1987

Real-time hexose monophosphate shunt activity in light- and dark-adapted rabbit retinas.

Correlation proton nuclear magnetic resonance spectroscopy was performed on light- and dark-adapted rabbit retinas to elucidate real-time hexose monophosphate shunt (HMPS) activity. Light significantly stimulated retinal HMPS initially, which consumed 17% more glucose than that in dark-adapted retinas. The glucose consumption eventually declined to 16% of total, the baseline level, after 60 min of light exposure. In contrast, dark-adapted retinas showed an initial HMPS activity of 29% total glucose consumption, which declined to the basal level after 40 min. Lactate production appeared stable in both sets of retinas. Tert-butyl hydroperoxide (1 mM) also stimulated the shunt; however, a combination of light-adaptation and tert-butyl hydroperoxide did not stimulate the shunt additively. These data indicate that the retina has limited HMPS capacity.

Adaptation, Physiological↗

PubMed1978

Creatine kinase and hexose phosphate isomerase activity in skeletal muscles of healthy male adults.

Creatine kinase (CPK) and hexose phosphate isomerase (PHI) activities were measured in surgically obtained skeletal muscle samples of healthy adult men (n = 45). Median values of 4,200 for CPK and 275 for PHI (U/g wet weight, 37 degrees C) were found. Duplicate determinations on 7 samples divided and treated separately gave a very good reproducibility. There is a significant relationship between the activity of the two enzymes (r = +0.798, p less than 0.001). The mean activity levels were for both enzymes higher in m. vastus medialis quadricipitis and m. triceps brachii, c. long., than in vastus lateralis quadric. and in deltoideus. PHI frequency distribution was not of the normal type but probably bimodal, suggesting muscle types with lower and higher glycolytic rate in man.

Adolescent↗

PubMed1977

Microsomal hexose-6-phosphate dehydrogenase in injured liver.

Hexose-6-phosphate dehydrogenase (H6PD) in rat liver microsomes was clearly differentiated kinetically, immunologically and electrophoretically from glucose-6-phosphate dehydrogenase (G6PD) localized in liver supernatants. Although the soluble G6PD activity increased upon liver injuries induced by CCl4 and thioacetamide, the H6PD activity decreased markedly 1-2 days following administrations of these hepatotoxins. The specific activity of H6PD remained fairly constant under other experimental conditions where the levels of the soluble G6PD activity increased.

Alcohol Oxidoreductases↗

PubMed1976

Mechanisms of methylene blue stimulation of the hexose monophosphate shunt in erythrocytes.

The response of the hexose monophosphate shunt in erythrocytes was studied with the ionization chamber-electrometer apparatus to measure continuously 14CO2 derived from 14C-labeled substrates. The effect of methylene blue at high (0.1 mM) and low (1 muM) concentrations was evaluated under different gas mixtures; air, carbon monoxide, and 6% carbon monoxide in air. The latter gas mixture results in nearly 100% carboxyhemoglobin but provides a physiologic partial pressure of oxygen. The extent to which pentose is recycled through the shunt in response to methylene blue stimulation was examined with radioactive glucose substrates labeled on the first, second, and third carbon positions. Generation of hydrogen peroxide after stimulation of erythrocytes with methylene blue was evaluated by the catalase-aminotriazole trapping technique, [14C]formate oxidation, and oxidation of reduced glutatione. Stimulation of the shunt with 1 muM methylene blue was markedly impaired in the absence of oxyhemoglobin, but stimulation with 0.1 mM methylene blue was only slightly impaired under the carbon monoxide-air mixture. The higher concentration of methylene blue produced evidence of hydrogen peroxide generation of all three techniques. Despite the evidence for the involvement of oxygen, oxyhemoglobin, and hydrogen peroxide in the response to methylene blue, cells containing methemoglobin induced by sodium nitrite or from a patient with congenital methemoglobinemia responded normally to methylene blue in the absence of oxygen. These experiments indicate that the reactions induced by methylene blue in erythrocytes are more complex than generally thought and that high concentrations are associated with production of peroxide.

Carbon Dioxide↗

PubMed1984

Proton secretion by stimulated neutrophils. Significance of hexose monophosphate shunt activity as source of electrons and protons for the respiratory burst.

Phagocytosis by neutrophils is accompanied by a burst in O2 consumption and activation of the hexose monophosphate shunt (HMPS). Proton secretion equal to the amount of O2 consumed is an additional feature of the respiratory burst, but its source has not been identified, nor has the source of all electrons donated to O2 in the respiratory burst. We chemically quantitated total CO2 generation in human neutrophils and found that proton secretion elicited by phagocytosis was accompanied by a stoichiometric increase in CO2 generation. Addition of carbonic anhydrase and its inhibitors had no effect on either the quantities of CO2 measured or the quantities of protons secreted. Therefore, the CO2 generated in the respiratory burst of stimulated neutrophils is hydrated to form H2CO3, which then dissociates, accounting for the observed proton secretion. Furthermore, the CO2 generated corresponds to the O2 consumed with a respiratory quotient of nearly 1. We conclude on the basis of this and previous studies that the HMPS activity is the source of both the electrons for the NADPH oxidase and of protons secreted in association with the respiratory burst.

Carbonic Anhydrases↗

PubMed1980

Immunohistochemical localization of hexose 6-phosphate dehydrogenase in various organs of the rat.

Distribution of hexose 6-phosphate dehydrogenase in various organs of the rat has been studied by a peroxidase-labeled antibody method in order to find some clue to elucidating the, as yet unclear, function of this enzyme. As a result, the following cells were found to contain this enzyme in relative abundance: hepatic parenchymal cells, ovarian lutein and theca interna cells, testicular interstitial cells, striated ducts and serous tubular portions of the submandibular gland, plasma cells and the P3 segment of proximal convolutions, and collecting tubules of the cortex and inner medulla of the kidney. Although the role of this enzyme in salivary glands and in plasma cells is unclear at present, the results obtained with steroidogenic cells, liver cells, and renal tubules appear to suggest the possibility that this enzyme might be involved in drug and steroid metabolism.

Animals↗

PubMed1984

Short communication. Glycogenosis Ib: neutrophil microbicidal defects due to impaired hexose monophosphate shunt.

We studied neutrophil microbicidal function and oxidative metabolic activity in a patient with glycogenosis Ib. The intracellular killing defect and the respiratory burst abnormality in gycogenosis Ib neutrophils were confirmed. The impaired oxygen-dependent microbicidal activity was shown to result from impaired hexose monophosphate shunt activity (impaired endogenous NADPH synthesis) and could be corrected by homogenization of the cells, followed by the addition of exogenous NADPH. Our data are thus consistent with a possible role for glucose-6-phosphate transport in neutrophil microbicidal function. We recommend a continuous prophylaxis with co-trimoxazole in patients with glycogen storage disease Ib.

Adolescent↗

PubMed1994

Uridine diphosphate hexoses in leukocytes and fibroblasts of classic galactosemics and patients with other metabolic diseases.

To examine uridine diphosphate hexose (UDPhexose) content of cells that have more complete metabolic patterns than erythrocytes, which have been commonly used in the study of galactosemia, the concentrations of uridine diphosphate galactose (UDPgalactose) and uridine diphosphate glucose (UDPglucose) were determined in white blood cells (WBC) and fibroblasts cultured from skin biopsies. Leukocyte UDPgalactose and UDPglucose values were determined in 60 normal individuals, 14 classic galactosemics, and 18 patients with other metabolic diseases on protein-restricted and low-lactose diets. There was no difference in the average concentration of these compounds between any of these groups. There was no relationship between age and WBC UDPhexose content or correlation of WBC and erythrocyte UDPhexose levels in the same blood specimens. WBC from galactosemic individuals differ from their red blood cells because the former do not show the low average UDPgalactose levels and abnormal UDPglucose to UDPgalactose ratio previously reported for erythrocytes from galactose-1-phosphate uridyltransferase-deficient individuals. Fibroblast cell lines from 10 normal and 10 galactosemic individuals, cultured and grown to confluence in glucose medium, also showed no difference in nucleotide sugar concentrations. Thus far, of the cell types easily available, red blood cells appear to be unique in showing an abnormality in nucleotide sugar metabolism. The fact that galactosemic fibroblasts demonstrate no abnormality in the concentration of these compounds suggests that the defective galactosylation that has been observed in galactosemic fibroblasts is not due to unavailability of UDPgalactose.

Adolescent↗

PubMed1986

Isoproterenol reduces insulin stimulation of hexose uptake by rat adipocytes via a postinsulin binding alteration.

The present studies have investigated the acute changes previously reported in insulin binding and insulin action that occur in fat cells after a 30-min treatment with isoproterenol. We find that the marked reduction in high affinity insulin binding can be explained by a drop in the pH of the incubation medium from 7.4 to 6.9, a change associated with the accelerated production of FFA. The alteration in insulin binding may explain the rightward shift in the insulin dose response for the stimulation of glucose transport. When the incubation medium is modified to prevent the pH change, isoproterenol stimulation fails to reduce insulin binding. In addition, the tyrosine kinase activity of the insulin receptor isolated from isoproterenol-treated cells is not altered, at least as measured by the phosphorylation of tyrosine residues on the artificial substrate, Glu80Tyr20. There are, however, changes produced in the insulin stimulation of 2-deoxy-D-glucose uptake. The response of the cells to a maximum effective concentration of insulin is reduced 35% by a 30-min treatment with 0.1 microM isoproterenol. This change occurs in parallel with a moderate rightward shift in the insulin dose-response curve. Thus, isoproterenol treatment rapidly alters the ability of the adipocyte hexose transport system to respond to insulin, but the responsible alteration(s) is located beyond the insulin-binding site and possibly beyond the insulin receptor itself.

Adipose Tissue↗

PubMed2005

A study of the hexose-6-phosphate dehydrogenase gene R453Q and 11beta-hydroxysteroid dehydrogenase type 1 gene 83557insA polymorphisms in the polycystic ovary syndrome.

CONTEXT: The R453Q variant in the hexose-6-phosphate dehydrogenase gene (H6PD) and 83557insA mutations in 11beta-hydroxysteroid dehydrogenase (11betaHSD) type 1 gene (HSD11B1) interact, resulting in cortisone reductase deficiency (CRD), a rare disorder characterized by a polycystic ovary syndrome (PCOS)-like phenotype. OBJECTIVE: The objective was to study these mutations in PCOS. DESIGN: The design was a case-control study. SETTING: The study was conducted in an academic hospital. PARTICIPANTS: A total of 116 PCOS patients and 76 nonhyperandrogenic controls participated. MAIN OUTCOME MEASURES: Genotype distributions and influence of genotypes on clinical and biochemical variables and, in 28 patients and 12 controls, estimates of 11betaHSD oxoreductase activity were the main outcome measures. RESULTS: Four controls and five patients presented three of four mutant alleles in H6PD R453Q and HSD11B1 83557insA, which is the genotype observed in some subjects with CRD. Estimates of 11betaHSD oxoreductase activity were measured in six of these nine women, ruling out CRD. Moreover, H6PD R453Q and HSD11B1 83557insA genotypes, either separately or in combination, did not influence 11betaHSD oxoreductase activity. The distribution of H6PD R453Q genotypes (R/R, R/Q, and Q/Q) was different in patients and controls (42% of controls and 63% of PCOS patients were R/R; 53% of controls and 31% of PCOS patients were R/Q; and 5% of controls and 6% of PCOS patients were Q/Q; chi(2) = 9.1; P = 0.011). Patients homozygous for R453 alleles presented with increased cortisol and 17-hydroxyprogesterone levels, compared with carriers of Q453 alleles, but these differences were not observed in controls. On the contrary, HSD11B1 83557insA genotypes were not associated with PCOS and did not influence any phenotypic variable. CONCLUSIONS: Digenic triallelic genotypes of the H6PD R453Q variant and HSD11B1 83557insA mutation do not always cause CRD. On the contrary, the H6PD R453Q variant is associated with PCOS and might influence its phenotype by influencing adrenal activity.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗

PubMed2006

Lack of Association of the 11beta-hydroxysteroid dehydrogenase type 1 gene 83,557insA and hexose-6-phosphate dehydrogenase gene R453Q polymorphisms with body composition, adrenal androgen production, blood pressure, glucose metabolism, and dementia.

CONTEXT: Recently, it was proposed that a combination of the 83,557insA polymorphism in the 11beta-hydroxysteroid dehydrogenase type 1 (HSD11B1) gene and the R453Q polymorphism in the hexose-6-phosphate dehydrogenase (H6PD) gene interacts to cause cortisone reductase deficiency (CRD) when at least three alleles are affected. OBJECTIVE: The aim was to study the separate and combined effects of these polymorphisms on body composition, adrenal androgen production, blood pressure, glucose metabolism, and the incidence of dementia in the healthy elderly population. DESIGN/SETTING/PARTICIPANTS: The Rotterdam study (n = 6105) and the Frail Old Men study (n = 347) are population-based cohort studies in the elderly. MAIN OUTCOME MEASURES: Genotype distributions and influences of (combined) genotypes on body mass index, adrenal androgen production, waist to hip ratio, systolic and diastolic blood pressure, fasting glucose levels, glucose tolerance test, and incidence of dementia were measured. RESULTS: No influence of the HSD11B1 83,557insA (allele frequencies 22.0 and 21.5%) and H6PD R453Q (allele frequencies 22.9 and 20.2%) variants was found for the different outcome measures that were investigated, either separately or when at least three alleles were affected. CONCLUSIONS: Two population-based studies among Caucasian elderly showed no evidence for (combined) effects of two polymorphisms in the HSD11B1 and H6PD genes on body composition, adrenal androgen production, blood pressure, glucose metabolism, and incidence of dementia. Moreover, the high frequencies observed for these two polymorphisms do not correspond to the low incidence of CRD observed in the general population. Altogether, it is unlikely that these polymorphisms cause CRD.

11-beta-Hydroxysteroid Dehydrogenases↗

PubMed2005

Hexose-6-phosphate dehydrogenase confers oxo-reductase activity upon 11 beta-hydroxysteroid dehydrogenase type 1.

Two isozymes of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) interconvert active cortisol and inactive cortisone. 11 beta-HSD2 (renal) acts only as a dehydrogenase, converting cortisol to cortisone. 11 beta-HSD1 (liver) is a bi-directional enzyme in cell homogenates, whereas in intact cells it typically displays oxo-reductase activity, generating cortisol from cortisone. We recently established that cortisone reductase deficiency is a digenic disease requiring mutations in both the gene encoding 11 beta-HSD1 and in the gene for a novel enzyme located within the lumen of the endoplasmic reticulum (ER), hexose-6-phosphate dehydrogenase (H6PDH). This latter enzyme generates NADPH, the co-factor required for oxo-reductase activity. Therefore, we hypothesized that H6PDH expression may be an important determinant of 11 beta-HSD1 oxo-reductase activity. Transient transfection of chinese hamster ovary (CHO) cells with 11 beta-HSD1 resulted in the appearance of both oxo-reductase and dehydrogenase activities in intact cells. Co-transfection of 11 beta-HSD1 with H6PDH increased oxo-reductase activity whilst virtually eliminating dehydrogenase activity. In contrast, H6PDH had no effect on reaction direction of 11 beta-HSD2, nor did the cytosolic enzyme, glucose-6-phosphate dehydrogenase (G6PD) affect 11 beta-HSD1 oxo-reductase activity. Conversely in HEK 293 cells stably transfected with 11 beta-HSD1 cDNA, transfection of an H6PDH siRNA reduced 11 beta-HSD1 oxo-reductase activity whilst simultaneously increasing 11 beta-HSD1 dehydrogenase activity. In human omental preadipocytes obtained from 15 females of variable body mass index (BMI), H6PDH mRNA levels positively correlated with 11 beta-HSD1 oxo-reductase activity, independent of 11 beta-HSD1 mRNA levels. H6PDH expression increased 5.3-fold across adipocyte differentiation (P < 0.05) and was associated with a switch from 11 beta-HSD1 dehydrogenase to oxo-reductase activity. In conclusion, H6PDH is a crucial determinant of 11 beta-HSD1 oxo-reductase activity in intact cells. Through its interaction with 11 beta-HSD1, H6PDH may represent a novel target in the pathogenesis and treatment of obesity.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗

PubMed1995

31P-nuclear magnetic resonance evidence of an activated hexose-monophosphate shunt in hyperglycemic rat lenses in vivo.

Using 31P-nuclear magnetic resonance spectroscopy, we have identified elevated concentrations of sedoheptulose-7-phosphate (S-7-P) in lenses from three animal models of hyperglycemia: streptozotocin-induced diabetic rats, galactose-fed rats, and xylose-fed rats. This observation provides a unique and independent confirmation of the activation of the hexose monophosphate shunt (HMPS) pathway in the hyperglycemic lens in vivo. While the elevation in concentration of S-7-P was very dramatic, the other HMPS metabolites in these tissues were below the threshold of detection, as expected for the HMPS pathway near equilibrium. In terms of nonenzymatic glycation, these results suggest that the only HMPS metabolite of importance in the hyperglycemic rat lens is S-7-P. Although in the diabetic lens its role appears to be relatively minor, in the galactosemic lens this compound may be an important contributor to the increased production of advanced glycosylation end products.

Animals↗

PubMed2001

Radiometric assessment of hexose monophosphate shunt capacity in erythrocytes of rhinoceroses.

OBJECTIVES: To measure metabolic rates of the hexose monophosphate shunt (HMPS) in erythrocytes of rhinoceroses, and to test the hypothesis that low concentrations of endogenous ATP in erythrocytes impair HMPS capacity, thereby increasing susceptibility to oxidant-induced hemolysis. ANIMALS: 13 black and 3 white rhinoceroses, free-ranging in several regions of southern Africa, and 1 Sumatran rhinoceros in US captivity. PROCEDURE: HMPS fluxes were measured in rhinoceros erythrocytes with carbon-labeled glucose in the presence and absence of known HMPS activators. RESULTS: Compared with values for human erythrocytes, mean basal state HMPS fluxes were appreciably lower (22 to 46%) in all 3 rhinoceros species studied. Shunt activators increased HMPS rates approximately 5-fold over basal rates in rhinoceros erythrocytes, compared with increases in humans of 10-fold with ascorbate and 15-fold with methylene blue. Stimulated HMPS rates in human erythrocytes were quantitatively 5- to 10-times greater than those observed in rhinoceros erythrocytes. Overall HMPS catabolic rates were completely independent of intracellular ATP concentrations. CONCLUSIONS AND CLINICAL RELEVANCE: HMPS glycolytic and recycling rates and responses to activators are inherently low in erythrocytes from 3 species of rhinoceros, likely contributing to (but not solely responsible for) the high susceptibility of black rhinoceroses to oxidant-induced hemolysis. Slow erythrocyte HMPS capacities were independent of intracellular ATP concentrations, invalidating a current hypothesis regarding the pathogenesis of hemolytic anemia in captive black rhinoceroses. Limitations in HMPS capacities emphasize the importance of protecting rhinoceroses from exposure to drugs, chemicals, toxins, foodstuffs, and other conditions known to increase production of oxidizing metabolites, reactive oxygen species, and free radicals.

Adenosine Triphosphate↗

PubMed1987

The role of glycolysis and hexose monophosphate pathway in the hypoxic toxicity of misonidazole.

The metabolic activation of misonidazole (MISO) and its effects on the hexose monophosphate pathway (HMP) and clonogenicity were studied in hypoxic EMT6/Ro, wildtype Chinese hamster ovary (CHO) and mutant CHO cells deficient in glucose-6-phosphate dehydrogenase. In all three cell lines metabolic activation of MISO, as indicated by the binding of 14C-MISO to the acid-insoluble fraction of these cells, was increased by the presence of glucose. In EMT6/Ro cells and wildtype CHO cells, MISO caused a significant stimulation of the activity of the HMP while in the mutant CHO cells no HMP activity was measurable, even in the presence of MISO. Loss of clonogenicity induced by MISO occurred markedly earlier in EMT6/Ro cells than in the CHO cells. In the latter cells, however, only a small difference was observed between the wildtype and mutant cell line. From these results it is concluded that not only the HMP but also glycolysis and other, glucose-independent, metabolic pathways are able to provide electrons for the reductive activation of MISO and hence contribute to the hypoxic toxicity of this compound.

Animals↗

PubMed1999

Effects of hexose pentaacetates on electrical activity and cytosolic Ca2+ in mouse pancreatic islets.

Electrical activity of beta-cells and cytosolic Ca2+ concentration ([Ca2+]i) were monitored in mouse pancreatic islets exposed to the pentaacetate esters of alpha-D-glucose, beta-D-galactose and beta-L-glucose, all tested at 1.7 mM concentration. In the presence of 5 mM D-glucose, alpha-D-glucose pentaacetate induced electrical activity and increased [Ca2+]i, whilst beta-D-galactose pentaacetate failed to do so. The electrical and cationic response to the D-glucose ester occurred with a delay of between 5 and 10 min, the ester-induced increase in [Ca2+]i being suppressed in the absence of extracellular Ca2+. As a rule, beta-L-glucose pentaacetate also failed to evoke biophysical responses in the islets exposed to 5 mM D-glucose. However, in the presence of 10 mM L-leucine the L-glucose ester induced electrical activity. These findings, which parallel the insulinotropic action of the same esters in rat pancreatic islets reinforce the view that the positive insulinotropic action of selected hexose pentaacetates cannot be attributed to the catabolism of their acetate moiety but, instead, involves a dual mode of action linked to both the metabolism of their carbohydrate moiety and a direct effect of the ester itself upon a yet unidentified receptor system. Furthermore, this study provides the first evidence that the latter direct effect results in the induction of both electrical activity and [Ca2+]i oscillations.

Animals↗

PubMed2000

Suppressive effect of active hexose correlated compound (AHCC) on thymic apoptosis induced by dexamethasone in the rat.

OBJECTIVE: Mushroom extracts are known to have immunomodulating and antitumor effects in humans as well as in animals. In the present study Active Hexose Correlated Compound (AHCC), an extract obtained from several kinds of basidiomycetes was examined for its suppressive effect on thymocyte apoptosis induced by dexamethasone. METHOD: Thymic apoptosis was evaluated by gel electrophoresis and by flow cytometry at 3 h after injection of dexamethasone to rats. RESULTS: When given to rats at 4 % concentration in drinking water for more than 4 days, AHCC suppressed the internucleosomal DNA fragmentation in the thymus induced by dexamethasone. Flow cytometry also revealed that thymic apoptosis induced by dexamethasone was prevented by pretreatment with AHCC. Dexamethasone increased the caspase 3-like activity within 3 h after its treatment and AHCC pretreatment suppressed the increased enzyme activity only slightly. No apparent increase in serum levels of melatonin and interleukin 1beta was observed after AHCC treatment. CONCLUSIONS: These results suggest that AHCC exhibits immuno-modulating effects at least partially by regulating thymic apoptosis.

Adjuvants, Immunologic↗

PubMed2001

Neonatal screening for galactosemia by quantitative analysis of hexose monophosphates using tandem mass spectrometry: a retrospective study.

BACKGROUND: Classic galactosemia (OMIM 230400) is an inherited disorder in the metabolism of galactose caused by deficiency of the enzyme galactose 1-phosphate uridyl transferase (EC 2.7.7.12). Galactosemia leads to accumulation of galactose and galactose 1-phosphate (gal-1-P) in blood and tissues and, if untreated, produces neonatal death or severe mental retardation, cirrhosis of the liver, and cataracts. Hence, the disorder is included in many neonatal screening programs. METHODS: We retrospectively analyzed filter-paper blood samples obtained 4-8 days postpartum for routine neonatal screening from 12 galactosemia patients and 2055 random controls. Total hexose monophosphates (HMPs) were used as a marker of gal-1-P and were assayed by negative-ion mode electrospray tandem mass spectrometry (tandem MS) with settings biased toward gal-1-P detection. The predominant precursor/product ion pair m/z 259/79 was used to quantify total HMPs by external standardization. RESULTS: Linear calibration curves were obtained in the range 0-8 mmol/L gal-1-P. The detection limit was 0.1 mmol/L HMP, and total CVs ranged from 13% at the detection limit to <8% at >1 mmol/L HMP. The method was in agreement with an alkaline phosphatase-galactose dehydrogenase method. All samples from galactosemia patients contained increased HMP concentrations (range for patients, 2.6-5.2 mmol/L; range for reference group, <0.10-0.94 mmol/L). The diagnostic sensitivity and specificity were 100% at a cutoff of 1.2 mmol/L HMP. A Duarte/classic galactosemia compound heterozygous sample could be discriminated clearly from both patient and reference samples. CONCLUSION: Quantitative analysis of HMPs by tandem MS can be used in laboratory investigations of galactosemia.

Alkaline Phosphatase↗