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At least 19 recordsLinked to original sources
PubMed1979

Plasma lipid distributions in selected North American populations: the Lipid Research Clinics Program Prevalence Study. The Lipid Research Clinics Program Epidemiology Committee.

Cross-sectional age- and sex-specific plasma lipid distributions (means, medians and selected percentiles) are given for 48,431 white participants in visit 1 of the Lipid Research Clinics (LRC) Prevalence Study. This study consisted of two visits in which 10 LRCs screened participants selected from well-defined North American target populations that included a broad range of sociodemographic subgroups. These data confirm findings from earlier studies in developed countries, showing age-related differences in plasma lipid levels. However, for overall distributions, the LRC data showed slightly lower cholesterol and markedly higher triglyceride values than those previously reported for North America. Some variation in plasma lipid values was evident among the clinic populations. The large number of participants within most subgroups permitted a variety of analytic and comparative studies. For example, data from the large pediatric population revealed a drop in plasma cholesterol levels in adolescent males and females. Males aged 20--50 years had higher cholesterol levels than females in the same age group, and higher triglyceride levels between ages 20--70 years. Numbers were also sufficient for meaningful comparisons between lipid distributions of females who were taking sex hormones and those who were not: In females taking sex hormones, cholesterol and triglyceride levels were higher for subjects younger than 45 years, but slightly lower after age 45, than lipid levels in females not taking hormones.

Adolescent↗
PubMed1979

Lipid protein interactions in mitochondria. VII. A comparison of the effects of lipid removal and lipid perturbation of the kinetic properties of mitochondrial ATPase.

We investigated the kinetics of mitochondrial ATPase in bovine heart mitochondria and submitochondrial particles upon treatment with phospholipase A2, or upon addition of n-butanol to perturb the lipid protein interactions. The changes observed are the following: (1) Lipid removal or perturbation with butanol is accompanied by loss of ATPase activity with decrease of both V and of the KM for ATP. (2) There are changes of activation energy of ATPase activity at temperatures above the discontinuity normally observed for membrane-bound enzymes in mitochondria. In particular, butanol abolishes the discontinuity, and induces a constant activation energy of about 32 kcal/mol in the range 8--37 degrees C. (3) Butanol modifies the pH dependence of ATPase shifting the pH optimum from around 10 to less alkaline values. The optimum for Mg2+ concentrations is increased by the solvent. (4) Treatment with phospholipase A2 results in a removal of oligomycin-sensitive ATPase, whereas butanol addition prevents oligomycin inhibition of ATPase. (5) In beef heart mitochondria, a spin-labelled analog of the inhibitor, dicyclohexyl carbodiimide, did not show any change in environment upon butanol addition, unlike that found in mitochondria from Saccharomyces cerevisiae.

Adenosine Triphosphatases↗
PubMed2026

Management of complex lipid disorders in a community lipid clinic setting: Implementing a multidisciplinary model.

BACKGROUND: Large treatment gaps exist in the management of lipid disorders, and many high-risk patients have factors that complicate management efforts. While lipid clinics exist within academic medical centers, most of these patients are cared for in community settings. OBJECTIVE: To report our experience and results managing challenging and complex lipid disorders in a community-based lipid clinic. METHODS: We established a specialized lipid clinic in a community medical setting, with a focus on patients with management challenges and/or suspicion of a genetic lipid disorder, employing a multidisciplinary approach to optimize patient outcomes, emphasizing appropriate medical therapies and lipid genetic testing in selected patients. Retrospective electronic health record data were collected to analyze patient characteristics, treatment patterns, and lipid results. RESULTS: Over the period 2022 through 2024, 183 patients were seen (mean 63 years, 62% female). The challenging nature of the patient population was highlighted by high rates of statin intolerance (50%), no lipid medical therapy at baseline (50%), and comorbidities (atherosclerotic cardiovascular disease [ASCVD], diabetes, and/or hypertension-61%). Despite this, over a mean follow-up of 9.4&#xa0;&#xb1;&#xa0;7.3 months, we observed a mean low-density lipoprotein cholesterol&#xa0;decrease of 49&#xa0;mg/dL (-24.5%, P&#xa0;<&#xa0;.001), along with significant decreases in total cholesterol and triglycerides. Pathogenic dyslipidemia genetic variants were discovered in 21 patients (of 105 tested). Significant lipid improvements in the whole cohort, as well as multiple subgroups, were associated with greater utilization of combination therapies. CONCLUSION: Patients with complex lipid disorders can be successfully managed within a specialized lipid clinic in community medical settings. Applying such a multidisciplinary model outside of traditional academic medical centers offers the potential to raise the level of lipid management and ASCVD prevention more broadly in larger populations.

Combination medical therapy↗
PubMed1977

Lipids of cultured hepatoma cells: VIII. Utilization of D-[1-14C] glucose for lipid biosynthesis.

Minimal deviation hepatoma 7288C cells (HTC) were incubated in serum-supplemented and serum-free Swim's 77 medium in the presence of D-[1-14C] glucose for 1, 2, 4, 8, 12 and 24 hr. Glucose oxidation to CO2, incorporation into total cell mass, and incorporation into cell and medium lipids were determined. The percentage distribution of total cell lipid radioactivity in individual neutral and polar lipid classes was followed as a function of time. Degradation studies of individual lipid classes were performed to ascertain the percentage of radioactivity in acyl and glycerol moieties. The percentage of D-[1-14C] glucose oxidized to 14CO2, incorporated into cell matter and cell lipids was elevated in cells incubated in serum-free medium as opposed to serum-supplemented medium. The percentage distribution of total cell lipid radioactivity into individual neutral lipid classes from both serum-free and serum-supplemented cultures was as follows: sterols greater than triglycerides greater than free fatty acids greater than sterol esters. The percentage distribution of total cell lipid radioactivity into individual polar lipid classes of serum-supplemented cultures was as follows: phosphatidylcholine greater than phosphatidylinositol greater than sphingomyelin greater than phosphatidylethanolamine greater than phosphatidylserine. The distribution of glucose radiolabel into individual polar lipid classes of serum-free HTC cells was different from their serum-supplemented counterparts: sphingomyelin greater than phosphatidylcholine greater than phosphatidylinositol greater than phosphatidylethanolamine greater than phosphatidylserine. Glycerol from glyceride classes contained a higher percentage of radioactivity than the acyl moieties, with this percentage significantly elevated in serum-free cultures. The data indicate that, although glucose is a substrate for HTC cell lipids, other precursors present in the culture system also contribute to the lipid constituency of this hepatoma cell line.

Blood↗
PubMed1978

Polymyxin binding to charged lipid membranes. An example of cooperative lipid-protein interaction.

The binding of polymyxin-B to lipid bilayer vesicles of synthetic phosphatidic acid was studied using fluorescence, ESR spectroscopy and electron microscopy. 1,6-Diphenylhexatriene (which exhibits polarized fluorescence) and pyrene decanoic acid (which forms excimers) were used as fluorescence probes to study the lipid phase transition. The polymyxin binds strongly to negatively charged lipid layers. As a result of lipid/polymyxin chain-chain interactions, the transition temperature of the lipid. This can be explained in terms of a slight expansion of the crystalline lipid lattice (Lindeman's rule). Upon addition of polymyxin to phosphatidic acid vesicles two rather sharp phase transitions (width deltaT = 5 degrees C) are observed. The upper transition (at Tu) is that of the pure lipid and the lower transition (at T1) concerns the lipid bound to the peptide. The sharpness of these transitions strongly indicates that the bilayer is characterized by a heterogeneous lateral distribution of free and bound lipid regions, one in the crystalline and the other in the fluid state. Such a domain structure was directly observed by electron microscopy (freeze etching technique). In (1 : 1) mixtures of dipalmitoyl phosphatidic acid and egg lecithin, polymyxin induces the formation of domains of charged lipid within the fluid regions of egg lecithin. With both fluorescence methods the fraction of lipid bound to polymyxin-B as a function of the peptide concentration was determined. S-shaped binding curves were obtained. The same type of binding curve is obtained for the interaction of Ca2+ with phosphatidic acid lamellae, while the binding of polylysine to such membranes is characterized by a linear or Langmuir type binding curve. The S-shaped binding curve can be explained in terms of a cooperative lipid-ligand (Ca2+, polymyxin) interaction. A model is proposed which explains the association of polymyxin within the membrane plane in terms of elastic forces caused by the elastic distortion of the (liquid crystalline) lipid layer by this highly asymmetric peptide.

Calcium↗
PubMed2026

The Lipid Interactome: an interactive and open access platform for exploring cellular lipid-protein interactions.

SUMMARY: Lipid-protein interactions play essential roles in cellular signaling and membrane dynamics, yet their systematic characterization has long been hindered by the inherent biochemical properties of lipids. Recent advances in functionalized lipid probes-equipped with photoactivatable crosslinkers, affinity handles, and photocleavable protecting groups-have enabled proteomics-based identification of lipid interacting proteins with unprecedented specificity and resolution. Despite the growing number of published lipid interactomes, there remains no centralized effort to harmonize, compare, or integrate these datasets. The Lipid Interactome addresses this gap by providing a structured, interactive web portal that adheres to FAIR data principles-ensuring that lipid interactome studies are Findable, Accessible, Interoperable, and Reusable. Through standardized data formatting, interactive visualizations, and direct cross-study comparisons, this resource enables researchers to systematically explore the protein-binding partners of diverse bioactive lipids. By consolidating and curating lipid interactome proteomics data from multiple studies, the Lipid Interactome database serves as a critical tool for deciphering the biological functions of lipids in cellularsystems. AVAILABILITY AND IMPLEMENTATION: This site can be viewed at LipidInteractome.org. All data are available for download. No user information is collected or necessary for data navigation, interaction, or download.

Proteins↗
PubMed1976

A possible correlation between lipid hydration and lipid activation of the C55-isoprenoid alcohol phosphokinase apoprotein.

1. A direct method for determining the binding of triated water to lipids is described. The experimental conditions were practically identical to those previously employed (1974) in the determination of the cofactor activities of a series of oleyl-lipids in reactivation of the C55-isoprenoid alcohol phosphokinase apoprotein. 2. Active cofactor lipids (dioleyl lecithin, sodium oleate, 1-monoolein, 1-monomyristin)bound between 2.3 and 5.3 nmol 3H2O per nmol lipid, whereas less than 0.14 nmol 3H2O were bound per nmol of the inactive lipids (1,2- and 1,3-diolein, triolein, oleyl alcohol, methyl oleate, cholesteryl oleate). 3. When exposed to 3H2O vapour, the active lipids adsorbed between 1 and 2 nmol 3H2O per nmol lipid, whereas the inactive lipids adsorbed less than 0.1 nmol 3H2O per nmol lipid. 4. The active lipid cofactor, egg lecithin, bound more than twice as much 3H2O as egg phosphatidylethanolamine which was devoid of cofactor activity in the absence of detergent. 5. Appropriately hydrated lipid polar groups are concluded to be required for an alignment with polar amino acid side chains of the enzyme apoprotein in the formation of a mixed micellar lipoprotein complex. The enzyme reaction might occur at the resulting lipoprotein/water interface.

Apoenzymes↗
PubMed1979

Lipid A and anti-lipid A.

Lipid A in free form, in crude antigen preparations, and on Formalin-treated Escherichia coli and Salmonella minnesota R595 was employed in studies of its antigenic composition, immunogenicity, and availability on gram-negative bacteria. Analyses with immunodiffusion and crossed immunoelectrophoresis of isolated lipid A preparations revealed three components. Inhibition experiments with enzyme-linked immunosorbent assay showed that the lipid A structure was not exposed on the tested smooth or rough E. coli strains or on S. minnesota R595. In crude O antigen preparations from some of the strains, however, lipid A was available for reaction with antibodies. The inaccessibility of lipid A on the bacterial surface may explain the poor protective capacity of anti-lipid A antibodies against bacterial infections. An enzyme-linked immunosorbent assay was more sensitive for measuring anti-lipid A antibody activity than indirect hemolysis or indirect hemagglutination. With an enzyme-linked immunosorbent assay it was shown that in rabbits the immunogenicity of lipid A was approximately the same when coated on erythrocytes or, as is more commonly done, when lipid A-coated hydrolyzed bacteria were used. Some antisera from rabbits immunized with E. coli of different serotypes showed activity against lipid A, with a higher frequency for antisera from rabbits immunized with R mutants.

Antibodies, Bacterial↗
PubMed1979

Effects of cerulenin upon the syntheses of lipid and protein and upon the formation of respiratory enzymes in adapting, lipid-limited Saccharomyces cerevisiae.

When bakers' yeast cells were grown anaerobically in a medium supplemented with Tween 80 and ergosterol, exposure during aeration to the fatty acid synthesis inhibitor, cerulenin, had little effect upon respiratory adaptation, the induction of enzymes of electron transport, or the in vivo incorporation of [(14)C]leucine into mitochondrial membranes. These lipid-supplemented cells were apparently able to undergo normal respiratory adaptation utilizing endogenous lipids alone. The level of cerulenin used (2 mug/ml) inhibited the in vivo incorporation of [(14)C]acetate into mitochondrial membrane lipids by 96%. If, however, the cells were deprived of exogenous lipid during anaerobic growth, subsequent exposure to cerulenin severely reduced their capacity to undergo respiratory adaptation, to form enzymes of electron transport, and to incorporate amino acid into both total cell and mitochondrial membrane proteins. This cerulenin-mediated inhibition of enzyme formation and of protein synthesis was nearly completely reversed by the addition of exogenous lipid during the aeration of the cells. In lipid-limited cells, chloramphenicol also had dramatic inhibitory effects, both alone (75%) and together with cerulenin (85%), upon total cell and mitochondrial membrane [(14)C]leucine incorporation. This marked chloramphenicol-mediated inhibition was also largely reversed by exogenous lipid. It is concluded that, in lipid-limited cells, either cerulenin or chloramphenicol may prevent the emergence of a pattern of lipids required for normal levels of protein synthetic activity. The effect of cerulenin upon the formation of mitochondrial inner membrane enzymes thus appears to reflect a nonspecific effect of this antilipogenic antibiotic upon total cell protein synthesis.

Antifungal Agents↗
PubMed1975

Chemically induced lipid phase separation in model membranes containing charged lipids: a spin label study.

The lipid distribution in binary mixed membranes containing charged and uncharged lipids and the effect of Ca2+ and polylysine on the lipid organization was studied by the spin label technique. Dipalmitoyl phosphatidic acid was the charged, and spin labelled dipalmitoyl lecithin was the uncharged (zwitterionic) component. The ESR spectra were analyzed in terms of the spin exchange frequency, Wex. By measuring Wex as a function of the molar percentage of labelled lecithin a distinction between a random and a heterogeneous lipid distribution could be made. It is established that mixed lecithin-phosphatidic acid membranes exhibit lipid segregation (or a miscibility gap) in the fluid state. Comparative experiments with bilayer and monolayer membranes strongly suggest a lateral lipid segregation. At low lecithin concentration, aggregates containing between 25% and 40% lecithin are formed in the fluid phosphatidic acid membrane. This phase separation in membranes containing charged lipids is understandable on the basis of the Gouy-Chapman theory of electric double layers. In dipalmitoyl lecithin and in dimyristoyl phosphatidylethanolamine membranes the labelled lecithin is randomly distributed above the phase transition and has a coefficient of lateral diffusion of D = 2.8-10(-8) cm2/s at 59 degrees C. Addition of Ca2+ dramatically increases the extent of phase separation in lecithin-phosphatidic acid membranes. This chemically (and isothermally) induced phase separation is caused by the formation of crystalline patches of the Ca2+-bound phosphatidic acid. Lecithin is squeezed out from these patches of rigid lipid. The observed dependence of Wex on the Ca2+ concentration could be interpreted quantitatively on the basis of a two-cluster model. At low lecithin and Ca2+ concentration clusters containing about 30 mol % lecithin are formed. At high lecithin or Ca2+ concentrations a second type of precipitation containing 100% lecithin starts to form in addition. A one-to-one binding of divalent ions and phosphatidic acid at pH 9 was assumed. Such a one-to-one binding at pH 9 was established for the case of Mn2+ using ESR spectroscopy. Polylysine leads to the same strong increase in the lecithin segregation as Ca2+. The transition of the phosphatidic acid bound by the polypeptide is shifted from Tt = 47.5 degrees to Tt = 62 degrees C. This finding suggests the possibility of cooperative conformational changes in the lipid matrix and in the surface proteins in biological membranes.

Calcium↗
PubMed1979

Lipid peroxidation of the microsomal fraction and extracted microsomal lipids from DAB-induced hepatomas.

NADPH- and ascorbic acid-induced microsomal lipid peroxidation was almost absent in subcutaneously implanted DAB-induced hepatomas D23, D30 and D192A, and present at greatly reduced levels in DAB-induced primary hepatomas when compared with normal liver controls. Fatty acid analysis of the microsomal lipid from passaged tumours demonstrated adequate levels of substrate in the phospholipid fractions to support lipid peroxidation. Lipid extracted from hepatoma microsomal fractions was shown to undergo ascorbic acid-induced lipid peroxidation, but to a lesser extent that the corresponding liver extract. This may be partially explained by a decrease in the phospholipid content of hepatoma microsomal membranes. However, phospholipid extracted from microsomal fractions of hepatoma and liver supported lipid peroxidation to a similar extent. The possible role of the non-lipid component of the membrane in the process of lipid peroxidation is discussed.

Animals↗
PubMed1975

Replacement time for alveolar lipid removed by pulmonary lavage: effects of multiple lavage on lung lipids.

Daily washing in vivo of the lung with 0.15 M saline did not deplete the Beagle dog lung of surfactant lipids, but rather increased the quantity of surfactant lipid in the tissue. Replacement time for the lung lipids removed by the lavage was approximately 5 hours. This rate is one indication of the time required for movement of surfactant lipid from storage areas to the surface of the alveoli. The increase in tissue surfactant lipid following multiple lavage suggests that the rate of surfactant lipid synthesis is controlled in part by the level of surfactant lipid in the alveoli.

Animals↗
PubMed1975

A method for microdetermination of major neutral lipids and an application of the procedure to tissue lipids.

Cholesterol, cholesteryl esters, triglycerides and fatty acids as major neutral lipids and phospholipids were examined in quantitative analysis. The method consisted of three steps: (1) separation of lipids by one-dimensional thin-layer chromatography on silica gel plates; (2) elution of neutral lipids from scraped silica gel with chloroform-methanol (4:1); and (3) colorimetric determination of individual neutral lipids in eluates and phospholipids in silica gel. The conditions were modified for chromotropic acid reaction for determining triglycerides. Laurell's method for determining fatty acids was also modified to apply to quantitative thin-layer chromatography. The accuracy of the modified methods was well-defined as the absorbance values were on a linear curve. A quantitative study was made of the recovery of triglycerides and fatty acids after chromatography. Combining these modified methods and colorimetry for determination of cholesterol cholesteryl esters and phospholipids, the author established a micromethod for determining the major neutral lipids and phospholipids by thin-layer chromatography. Lipids from HeLa, S-3 cells were analyzed to examine the applicability of this method to tissues. The results indicated that the new method permitted a reliable estimation of the major neutral lipids and phospholipids from small amounts of tissues.

Cholesterol↗
PubMed1976

The binding of lipid to the lipid-free adenosine triphosphatase protein of sarcoplasmic reticulum.

Dinitrophenylated dipalmitoyl phosphatidylethanolamine and its lyso derivative have been shown to bind to the lipid-free ATPase protein derived from the sarcoplasmic reticulum. The binding of these lipids is accompained by the quenching of up to 95% of the tryptophyl fluorescence of the protein. This effect is reversed by 9-10 mM deoxycholate. The solubility of the lipid-free ATPase protein in the absence of deoxycholate and the solubility of submillimolar concentrations of the dinitrophenylated monopalmitoyl phosphatidylethanolamine anion in aqueous media allowed binding experiments using this lipid ligand to be carried out in a simple buffer system. It is shown that in the case of this lipid the initial phase of the binding process displays an apparent positive co-operatively. Data from the second phase in the saturation of the protein with this lipid is consistent with binding to independent, equivalent, non-interacting sites with a microscopic (intrinsic) association constant of 1.63 x 10(6) M-1, the fluorescence being quenched in the geometric fashion. Altogether a total of about 15 molecules of this lipid may be bound by the protein.

Adenosine Triphosphatases↗
PubMed2026

Remodeling of host lipid metabolism by Wolbachia strain wAlbB is associated with lipid accumulation and cardiolipin dysregulation in the Aedes aegypti fat body.

BACKGROUND: The intracellular symbiont Wolbachia, particularly the wAlbB strain, is a promising biocontrol agent against mosquito-borne diseases. Although Wolbachia infection is known to perturb host metabolism, the underlying mechanisms, especially those related to lipid metabolism, remain poorly understood. METHODS: We performed an integrated multi-level analysis of the Aedes aegypti fat body in uninfected and wAlbB-infected mosquitoes, combining histology, biochemistry, untargeted liquid chromatography-mass spectrometry (LC-MS) lipidomics, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways enrichment analysis, reverse transcription quantitative PCR of key metabolic genes, and quantification of acetyl-coenzyme A (acetyl-CoA) and reduced nicotinamide adenine dinucleotide (NADH) levels. RESULTS: wAlbB infection increased fat body wet weight and thickness, accompanied by accumulation of triglyceride and of lipid droplets. Lipidomic analysis further revealed extensive lipidome remodeling, with elevated free fatty acid, diglyceride, and triglyceride, but broad depletion of glycerophospholipids, particularly cardiolipin. These changes were supported by transcriptional alterations: upregulation of fatty acid synthase 1 and glycerol-3-phosphate acyltransferase 1, and downregulation of adipose triglyceride lipase and carnitine palmitoyltransferase 1. Cardiolipin depletion correlated with downregulation of genes involved in its synthesis and remodeling, including phosphatidylglycerophosphate synthase and calcium-independent phospholipase A2&#x3b3;. These lipid changes were also associated with accumulation of acetyl-CoA and NADH. CONCLUSIONS: Our findings suggest that wAlbB infection is associated with extensive lipid metabolic remodeling in the Aedes aegypti fat body, characterized by accumulation of neutral lipids and cardiolipin depletion, accompanied by transcriptional remodeling of key metabolic enzymes. This study establishes the fat body as a primary tissue-level hub for Wolbachia-associated lipid remodeling and provides a foundational framework for future mechanistic investigations into host-symbiont metabolic interactions.

Animals↗
PubMed1979

Lipid-protein interactions in membranes: effect of lipid composition on mobility of spin-labeled cysteine residues in yeast plasma membrane.

In order to gain direct evidence for lipid-dependent protein conformation in membrane, effects of modification of lipid composition on mobility of spin-labeled cysteine residues were investigated in the plasma membrane of the yeast Saccharomyces cerevisiae. Conversion of the bulk of phospholipids to diglycerides by treatment of the membrane with phospholipase C substantially enhanced spectral anisotropy. However, alterations of the viscosity of the lipid-bilayer by enriching the membrane with palmitelaidic or oleic acid had no effect on mobility of spin-labeled cysteine residues. These observations indicate that while the spin-labeled residues are not in direct contact with the lipid core of the membrane, there are lipid-protein interactions to the extent that removal of the polar portion of the bulk of phospholipids induces conformational changes in proteins, which in turn restrict mobility of these residues. It is concluded that conformation of membrane proteins on lipid structure and that phospholipids have a role in preserving the native conformation of proteins.

Adenosine Triphosphatases↗
PubMed1977

Lipid chemotaxins isolated from culture filtrates of Escherichia coli and from oxidized lipids.

Lipid extracts of sterile culture filtrates of Escherichia coli were shown to contain approximately 75% of the chemotactic activity for human polymorphonuclear leukocytes and rabbit alveolar macrophages. Fractionation and purification of these lipids revealed the presence of many unknown lipids of widely different properties, but all were anionic and at very low concentrations, chemotactic. The only one of active molecules that could be identified was an unsaturated ultraviolet-absorbing hydroxy fatty acid, which, following catalytic reduction with hydrogen, was found to be hydroxyeicosanoic acid. This fatty acid's chromatographic behavior was very similar to that of 12-hydroxy-5,8,10,14-eicosatetraenoic acid (HETE), which is a potent chemotaxin for polymorphonuclear leukocytes and macrophages. Unknown chemotaxins could be generated by the oxidation of known unsaturated lipids. Prostaglandins A2 and E2 produced potent chemotaxins upon aerobic oxidation. Malonaldehyde, a peroxidation product of unsaturated lipids, when reacted with phosphatidylethanolamine in aerobic conditions, also produced strong chemotactic agents. The chemotactic activity of these products could be destroyed by catalytic reduction with hydrogen and by methylation with dry methanolic HCl. These data indicate that the nonenzymatic oxidation of unsaturated lipids generates some products that are potent chemotaxins for mammalian inflammatory cells.

Animals↗