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T Tanabe

Publications and source records attributed to T Tanabe.

At least 37 records · Page 2Linked to original sources

Intact LTP and fear memory but impaired spatial memory in mice lacking Ca(v)2.3 (alpha(IE)) channel.

To investigate the functional roles of the Ca(v)2.3 (alpha(1E)) channel in hippocampal CA1 pyramidal neurons, we studied in vitro synaptic properties and in vivo behaviors of the Ca(v)2.3 gene deficient mice. The Ca(v)2.3 channel mRNA was identified in the hippocampal formation of the wild-type mouse by in situ hybridization. The basic excitatory synaptic transmission and long-term potentiation by theta-burst stimulation were intact in CA1 region of Ca(v)2.3-/- mice. We performed two forms of behavioral tests to examine the hippocampus-dependent function, i.e., emotional and spatial learning tests. The Ca(v)2.3-/- mice were able to establish and maintain fear memories. Although general improvement in the performance of Morris water maze test was seen in Ca(v)2.3-/- mice, they displayed an obvious impairment in the probe test. These results suggest that the Ca(v)2.3 channel plays some role in formation of the accurate spatial memory but not of the fear memory.

Animals↗

Thiolated dermal bovine collagen as a novel support for bioactive substances--conjugation with lysozyme.

Thiol groups were introduced to dermal bovine collagen (DBC) by the reaction with gamma-thiobutyrolactone. Thiolated DBC reacted with 2-pyridyl disulfide group introduced to lysozyme to form DBC-lysozyme conjugate through disulfide bridge. The enzymatic activity of freshly prepared conjugate was almost unchanged during ten consecutive runs over one month. The DBC-lysozyme conjugate showed the maximum activity at pH 6.3, on the contrary, that of native lysozyme was pH 9.0. Thermal stability of lysozyme was enhanced by the conjugation with DBC. The present results showed that the conjugation using thiolated collagen could be one of the useful alternative approaches to modify collagen with bioactive molecules.

Animals↗

XANES analyses of silicon crystalline irradiated by nitrogen/oxygen ions.

X-ray absorption techniques have been applied to the characterization of 5 keV nitrogen / oxygen ions implanted silicon samples. The depth selective measurement of XANES by recording in PEY mode and the quantitative analysis by superposition of XANES spectra were carried out to elucidate the depth profile of implanted ions. It has been revealed that the silicon nitride phase were formed in silicon after prolonged N+ irradiation and it extended over the deep part of the damaged region from the surface. On the other hand, for the O+ irradiation, silicon dioxide phase were produced only in the shallow part of the damaged region, i.e., the silicon dioxide phase likely broke off during the irradiation.

Journal Article↗

Cyclooxygenase-2 stimulates production of amyloid beta-peptide in neuroblastoma x glioma hybrid NG108-15 cells.

Cyclooxygenase (COX) synthesizes bioactive prostaglandins from arachidonic acid, and there are COX-1 and COX-2 isoforms with distinct pathophysiological functions. Recent studies demonstrated that COX-2 expression was up-regulated in the brain of patients with Alzheimer's disease. We established mouse neuroblastoma x rat glioma hybrid NG108-15 cells stably expressing human COX-2. The COX-2-expressing cells showed 3- to 4-fold increases in both COX activity and prostaglandin E(2) production. The mRNA level of amyloid precursor protein (APP) was elevated by approximately 2-fold in the COX-2-expressing cells compared with mock-transfected cells. Amyloid beta-peptide and a secreted form of APP, both derived from APP by proteolysis was also increased. Interestingly, neurite outgrowth was stimulated in the COX-2-expressing cells with concomitant reduction of the cell proliferation rate. A selective COX-2 inhibitor (JTE-522) and a nonselective COX inhibitor (indomethacin) suppressed production of amyloid beta-peptide and a secreted form of APP by inhibition of APP mRNA level, suggesting that COX-2 plays important roles in the neurodegenerative processes of Alzheimer's disease.

Amyloid beta-Peptides↗

Glucocorticoid-regulated expression of exogenous human growth hormone gene in rats.

The aim of this study was to control in vitro and in vivo expression of the growth hormone (GH) gene using a glucocorticoid-sensitive promoter, the mouse mammary tumor virus long terminal repeat (MMTV LTR). We inserted the cDNA encoding the 20-kDa form of human GH (20K-GH) downstream of the MMTV LTR of plasmid pMSG, and used lipofection to transfer it to 3Y1 cells together with plasmid pMX, which contains a puromycin-resistant element. The secretion of GH from the selected transformants was dose-dependently augmented by the application of hydrocortisone, corticosterone, or dexamethasone, among which dexamethasone was the most potent. Analysis of the time course showed that 20K-GH secretion began to increase within 2 hours after the addition of glucocorticoid and reached a maximal level of about threefold over the unstimulated control at 3 hours; secretion then gradually declined and returned to near basal levels at 19 hours. Repeated glucocorticoid application led to repeated increases in GH secretion. When GH-producing cells were microcapsulated and transplanted into the abdominal cavities of rats, 20K-GH was detected in the plasma under control conditions and increased about 3.3-fold after administration of dexamethasone. We suggest that GH expression driven by the MMTV LTR promoter may be under the control of an endogenous glucocorticoid in vivo.

Animals↗

A patient with type I CD36 deficiency whose myocardium accumulated 123I-BMIPP after 4 years.

A 73-year-old man with aortic regurgitation was examined by 123I-alpha-methyl-p-iodophenylpentadecanoic acid (BMIPP) myocardial single photon emission computed tomography (SPECT) in 1995. Myocardial accumulation was not evident on either the early or the delayed image obtained 15 minutes and 3 hours, respectively, after injecting 123I-BMIPP. Flow cytometric analysis of CD36 expression in monocytes and platelets identified a type I CD36 deficiency. The patient was hospitalized for severe heart failure in 1999. Upon admission, the cardiothoracic ratio on chest X-rays was 73%, and the left ventricular end-diastolic diameter on echocardiograms was enlarged to 77 mm. On the second day, we performed 123I-BMIPP myocardial SPECT. Myocardial accumulation was evident in the delayed, but not in the early image. We repeated 123I-BMIPP myocardial SPECT on the 10th day after admission. Myocardial accumulation was evident on both early and delayed images. 99mTc-tetrofosmin myocardial SPECT was immediately performed after 123I-BMIPP myocardial SPECT to distinguish myocardial from pooling images in the left ventricle, but, because the images from both 99Tc-tetrofosmin and 123I-BMIPP myocardial SPECT were idential, we considered that the 123I-BMIPP myocardial SPECT images reflected the actual myocardial condition. The CD36 molecule transports long-chain fatty acid (LCFA) on the myocardial membrane, but 123I-BMIPP scintigraphy does not show any myocardial accumulation in patients with type I CD36 deficiency, indicating that myocardial LCFA uptake occurs through CD36 on the human myocardial membrane. Even though our patient had type I CD36 deficiency, BMIPP was uptaken by the myocardium during heart failure, suggesting a variant pathway on the human myocardial membrane for LCFA uptake.

Aged↗

Assessment of ampulla (Takotsubo) cardiomyopathy with coronary angiography, two-dimensional echocardiography and 99mTc-tetrofosmin myocardial single photon emission computed tomography.

UNLABELLED: We studied the causative mechanism of ampulla (Takotsubo) cardiomyopathy. METHODS: We examined 7 patients with ampulla cardiomyopathy by means of coronary angiography, two-dimensional echocardiography and 99Tc-tetrofosmin myocardial SPECT at the time of emergency admission (acute phase), at 3 to 5 days after the attack (subacute phase) and at 1 month after the attack (chronic phase). The left ventricle was divided into 9 regions on two-dimensional echocardiograms and 99mTc-tetrofosmin myocardial SPECT images, then the degree of abnormalities in each region was scored in four grades from normal (0) to severely abnormal (3). We injected nicorandil into the coronary arteries and determined the elevation in the ST segment before and after administration. RESULTS: Coronary angiography did not show stenotic lesions in any patient. The acute, subacute and chronic phase myocardial perfusion scores on 99mTc-tetrofosmin myocardial SPECT were 11.2 +/- 3.4, 2.7 +/- 2.3 and 0.4 +/- 0.5, respectively, and wall motion scores on echocardiograms were 13.0 +/- 3.6, 4.4 +/- 2.2 and 0.6 +/- 0.6, respectively, indicating improvement in all scores during the subacute phase (p < 0.01). The elevation in the ST segment (mm) on the electrocardiogram was improved from 8.3 +/- 2.7 to 4.9 +/- 1.9 after the administration of nicorandil (p < 0.05). CONCLUSION: These findings indicated that coronary microvascular spasm is one causative mechanism of ampulla cardiomyopathy.

Acute Disease↗

A monoclonal antibody against the glutaraldehyde-conjugated polyamine, putrescine: application to immunocytochemistry.

We developed a mouse monoclonal antibody (mAb; APUT-32, IgG1 subisotype mAb) against putrescine (Put) conjugated to bovine serum albumin using a glutaraldehyde (GA)-sodium borohydride procedure, for applications in immunocytochemistry (ICC). The antibody specificity was evaluated by an ELISA binding test, simulating the ICC of tissue sections. APUT-32 mAb was highly specific to Put, and distinguished alterations in the chemical structure of other polyamine (PA) analogs, showing 3.8% crossreaction with cadaverine, 3.3% with spermidine (Spd), and 2.3% with 1,3-diaminopropane. Comparable results in immunoreactivity of APUT-32 mAb were obtained with the ELISA inhibition test. By the indirect immunoperoxidase method using the APUT-32 mAb, Put-like immunoreactivities were observed in the cytoplasm of HeLa and MCF-7 cell lines fixed with GA in combination with NaBH4 reduction, but almost no immunoreaction was seen in the cytoplasm of the human melanoma BD cell line. On the other hand, the same method but using a previously prepared ASPM-29 mAb, specific for spermine (Spm) and Spd, produced intense immunostaining in the cytoplasm of all the three cell types. The Put-like immunoreaction was completely abolished by absorption of the APUT-32 mAb with 10 microg/ml Put-human serum albumin conjugate prepared using GA and NaBH4. HPLC analysis was also performed for the levels of each of the PAs in the three types of cell, showing that the levels of Put detected were much lower than those of Spm and Spd, and were strikingly different in the three cell lines among which the human melanoma BD cell line contained the lowest levels of Put. These results strongly suggest that APUT-32 mAb reacts specifically with Put in the tumor cells and therefore has the potential as a new tool for elucidating the biological roles of Put in cells and tissues.

Animals↗

Immunoelectron-microscopic demonstration of histamine depletion in the gastric enterochromaffin-like cells of rats treated with alpha-fluoromethylhistidine.

We conducted an immunoelectron-microscopic study for histamine (HA) in the enterochromaffin-like (ECL) cells of normal rats and rats given alpha-fluoromethylhistidine (alpha-FMH, 3 mg/kg per hour) via osmotic minipumps over a period of 24 h. The indirect immunoperoxidase procedure utilized a mouse monoclonal antibody (mAb), AHA-2, which is produced against glutaraldehyde-conjugated HA. alpha-FMH is a potent and irreversible inhibitor of the HA-forming enzyme histidine decarboxylase and is known to reduce tissue HA concentrations in several tissues. The present study clearly demonstrated that HA immunoreactivity, which was found to a high degree in the cores of the granules and secretory vesicles and in the cytoplasm of ECL cells of control rats, was completely abolished from the corresponding compartments in the cells of alpha-FMH-treated rats. Furthermore, treatment with alpha-FMH drastically lowered the number of secretory vesicles and was associated with larger cores in the granules of the ECL cells. These results seem to support the idea of a HA-pathway mechanism, emphasizing that the granules in normal ECL cells take up HA from the cytosol during its transport from the Golgi zone to the more peripheral portion of the cell and condense it in their cores, thus forming mature secretory vesicles. However, the present study showed that not only the secretory vesicles but also almost all the granules seen in ECL cells were already loaded with HA in their cores, suggesting that the newborn granules very rapidly take up HA from the cytosol. Also suggested was the fact that HA depletion impairs the maturation of the granules into secretory vesicles.

Animals↗

Immunoblot detection and expression of enamel proteins at the apical portion of the forming root in porcine permanent incisor tooth germs.

There have been many immunohistochemical studies of enamel proteins during root formation. In the present article, the detection and expression of enamel proteins in tissue samples prepared from the apical portion of the forming root (APFR) in porcine permanent incisor tooth germs were studied. Amelogenin, enamelin, and sheathlin were detected by immunoblot analysis, but only in small amounts. The detection of their derivatives indicated their degradation. It is, at present, unclear as to which proteinases are involved in these degradations, because activity of enamel matrix serine proteinase 1 and enamelysin was not detected on gelatin and casein zymograms. The expression of enamel proteins was also proved in the APFR sample by the detection of polymerase chain reaction products of their cDNAs, and this may be related to cells of fragmentized Hertwig's epithelial root sheath. Amelogenin expression was not greater than that of enamelin and sheathlin. It was different from the expression pattern of secretory ameloblasts involved in enamel matrix formation. These results suggest that the amelogenins found in the APFR do not form a three-dimensional structure of amelogenin micelles, which has been proposed for the secretory enamel matrix structure. In this case, the enamel proteins could spread out easily following degradation into the matrix of future cementum. Some of their derivatives may play a role in the formation of the cementum.

Amelogenin↗

Calcium binding of enamel proteins and their derivatives with emphasis on the calcium-binding domain of porcine sheathlin.

Dental enamel is believed to form by the transfer of ions from solution, primarily calcium, phosphate, hydroxyl and carbonate, to the surface of solid-state mineral. Such precipitation phenomena can be controlled by regulating the degree of saturation of the solution with respect to the potential solid phases that can form. The concentration of free calcium is the factor that most affects the degree of saturation for calcium hydroxyapatite, and its buffering by calcium-binding proteins has been proposed as the mechanism that determines the enamel mineral structure. In this study, Stains-all staining was used to identify and isolate calcium-binding proteins from the enamel matrix, and determine their structures and association constants for calcium. Proteolytic cleavage fragments derived from the C-terminus of sheathlin, having apparent molecular weights of 13, 15, 27 and 29 kDa, were characterized by amino-terminal protein sequencing, amino acid analysis, and sugar, phosphate and sulphate determinations. Sheathlin C-terminal cleavage products were shown to have no N-linked glycosylations or phosphorylated amino acids, but Pro(350) was hydroxylated, and there was one sulphated O-linked glycosylation at Thr(386), containing galactose and N-acetylgalactosamine. The calcium-binding association constants for enamel proteins ranged from a high of 1.2 x 10(4) M(-1) to a low of 4.4x10(1) M(-1). The relative strengths of binding in order of decreasing affinity were: 13 and 15 kDa calcium-binding domain of sheathlin >27 and 29 kDa calcium-binding proteins >32 kDa enamelin >89 kDa enamelin >6.5 kDa, 25 kDa, 23 kDa, 20 kDa, 13 kDa, 5.3 kDa amelogenins. It is concluded that if enamel proteins have similar calcium-binding properties in vivo as have been measured in vitro, they would tend to buffer the free calcium ion concentration in enamel fluid.

Acetylgalactosamine↗

Films of collagen crosslinked by S-S bonds: preparation and characterization.

Collagen (type I from calf-skin) was chemically modified by 4-butyrothiolactone to obtain the mercapto group-bearing collagen (collagenSH), which possessed SH groups in 8-19 M% of a total amino acid residues. The triple helical strands of the collagen was not completely perturbed to exhibit the rotary dispersion [theta]221, which was as much as 70% of an original intensity of the collagen. In the presence of the oxygen dissolved in water, the collagenSH was cross-linked by disulfide bonds to afford the collagenSS. The collagenSS could preserve about 15 and 40% of an original helix structure at 55-70 degrees C and in 2mm sodium dodecyl sulfate, respectively. The film made of the collagenSS exhibited the tensile strength as high as 36 MPa and was insoluble in most organic solvents including water. The collagenSS film was more resistant to degradation by collagenase (type I) than the collagen film. The collagenSS film supported the growth of L929 fibroblast cell in a manner similar to a collagen film.

Animals↗

Pars plana vitrectomy for cystoid macular edema secondary to sarcoid uveitis.

OBJECTIVE: To examine the results of pars plana vitrectomy for cystoid macular edema secondary to sarcoid uveitis resistant to medical treatment. DESIGN: Retrospective, interventional, noncomparative case series. SUBJECTS: Fourteen consecutive subjects (18 eyes) with cystoid macular edema associated with sarcoid uveitis resistant to medical treatment. INTERVENTION: All eyes underwent pars plana vitrectomy. Nine eyes also underwent peeling of the epiretinal membrane or removal of the posterior vitreous cortex. MAIN OUTCOME MEASURES: Status of macular edema, visual acuity, and complications. RESULTS: Ten eyes (56%) improved 2 or more lines of Snellen visual acuity within 12 months. Six eyes (33%) remained unchanged, within a line of preoperative Snellen visual acuity, and two eyes (11%) worsened by 2 or more lines of Snellen visual acuity. Slit-lamp biomicroscopy showed that cystoid macular edema had resolved in 14 eyes (78%) within 9 months postoperatively. One eye (6%) had minimal edema, whereas three eyes (17%) remained unchanged biomicroscopically at the final visit. Postoperative complications included cataract formation, glaucoma, optic nerve atrophy, epiretinal membrane formation, and tractional retinal detachment. No severe postoperative inflammation was noted. CONCLUSIONS: Pars plana vitrectomy seems to have a beneficial effect on cystoid macular edema caused by sarcoidosis resistant to medical treatment.

Adult↗

Allosterically controllable maxizyme-mediated suppression of progression of leukemia in mice.

Chronic myelogenous leukemia (CML) is a hematopoietic malignant disease associated with expression of a chimeric BCR-ABL gene. We recently succeeded in designing a novel allosterically controllable ribozyme, the maxizyme (Tanabe et al. Biomacromolecules 2000, 1, 108-117; Kuwabara et al. Biomacromolecules 2001, 2, 788-799), that not only specifically cleaves BCR-ABL mRNA and induces apoptosis in cultured CML cells but also shows significant inhibition against the growth of an established BV173 cell line in a mouse model (Tanabe et al. Nature 2000, 406, 473-474). As an extension of our studies, we tested the maxizyme against primary CML cells in the same mouse model. The maxizyme under the control of a tRNA(Val) promoter showed significant inhibition against the growth of the primary bone marrow cells from a Japanese patient with CML. Specifically, to examine the applicability of the maxizyme in the treatment of CML, we assessed the antitumor effect of the maxizyme in murine models of CML. Fourteen weeks after the injection of primary CML cells into a NOD-SCID mouse, the bone marrow of the mouse was filled with primary CML cells as a result of diffuse leukemia. In marked contrast, when maxizyme-expressing primary CML cells were injected, the mouse remained disease-free. These results further strengthen our earlier suggestion that the maxizyme technology might provide a useful approach to the treatment of CML.

Allosteric Regulation↗

Haematopoietic progenitor cells from the common marmoset as targets of gene transduction by retroviral and adenoviral vectors.

To establish a new non-human primate model for human cytokine and gene therapy, we characterized lymphocytes and haematopoietic progenitor cells of the small New World monkey, the common marmoset. We first assessed the reactions of marmoset bone marrow (BM) and peripheral blood (PB) cells to mouse anti-human monoclonal antibodies (mAbs) for the purpose of isolating marmoset lymphocytes and haematopoietic progenitor cells. Both cell fractions stained with CD4 and CD8 mAbs were identified as lymphocytes by cell proliferation assay and morphological examination. Myeloid-specific mAbs such as CD14 and CD33 did not react with marmoset BM and PB cells. No available CD34 and c-kit mAbs could be used to purify the marmoset haematopoietic progenitor cells. Furthermore, we studied the in vitro transduction of the bacterial beta-galactosidase (LacZ) gene into CFU-GM derived from marmoset BM using retroviral and adenoviral vectors. The transduction efficiency was increased by using a mixed culture system consisting of marmoset BM stromal cells and retroviral producer cells. It was also possible to transduce LacZ gene into marmoset haematopoietic progenitor cells with adenoviral vectors as well as retroviral vectors. The percentage of adenovirally transduced LacZ-positive clusters was 15% at day 4 (multiplicity of infection=200), but only 1-2% at day 14. The differential use of viral vector systems is to be recommended in targeting different diseases. Our results suggested that marmoset BM progenitor cells were available to examine the transduction efficiency of various viral vectors in vitro.

Adenoviridae↗

Cerebrospinal fluid and serum neuron-specific enolase levels after febrile seizures.

PURPOSE: Neuron-specific enolase (NSE) has been established as a reliable marker of neuronal damage in various neurologic disorders. The aim of this study was to evaluate whether febrile seizures (FS) cause brain damage, based on the serum and cerebrospinal fluid (CSF) levels of NSE. METHODS: Fifty-three patients aged from 6 months to 7 years were enrolled. Among them, 36 patients had generalized seizures, and 17 had partial seizures. The maximal seizure duration was 90 min. Blood and CSF samples for measurement of NSE were obtained immediately after the seizure. NSE was measured using an enzyme immunoassay (EIA). RESULTS: Serum and CSF levels of NSE ranged up to 10 ng/mL, but very high levels were not observed. In patients with partial seizures, the NSE level in the CSF and the ratio of the CSF to serum NSE levels showed a strong correlation with seizure duration. Conversely, there were no correlations between NSE levels and seizure duration in the patients with generalized seizures. CONCLUSIONS: These results indicate that FS seldom cause severe neurologic damage, but prolonged partial seizures may cause slight neuronal injury.

Biomarkers↗

Longer longitudinal atrial dimension in patients with idiopathic paroxysmal atrial fibrillation: A possible cause of atrial fibrillation.

BACKGROUND: The ostium of the superior pulmonary veins or superior vena cava has been reported to be an important source of the ectopic beats that initiate paroxysmal atrial fibrillation (PAF). The structural details of the atria in patients with idiopathic PAF, however, remain unknown. METHODS: We studied 113 patients (92 men and 21 women) with idiopathic PAF and 128 normal control subjects (100 men and 28 women). None of the subjects in either group were found to have any evidence of structural cardiac disease. The echocardiographic measurements were performed in the apical 4-chamber view during end-systole of sinus rhythm. RESULTS: The longitudinal dimension of the left and right atria was longer in patients with PAF who were not administered any drugs (non-drug-taking patients) than in the control subjects (P <.001 and P <.01, respectively). However, there were no significant differences in the transverse dimension of either atrium between such patients and control subjects. The longitudinal and transverse dimensions and volume determinations of atria were greater in the patients with idiopathic PAF who were administered class 1 antiarrhythmic drugs than in non-drug-taking patients (P <.05 to.001). In non-drug-taking patients, prolongation of the atrial longitudinal dimension did not depend on either age, the total frequency of PAF, or the interval from the first episode of PAF. The longitudinal dimension of the left and right atria was longer even in the patients with a short history of PAF (<1 month) as compared with control subjects (P <.001 and.05, respectively). CONCLUSIONS: These observations suggest that there is prolongation of the longitudinal dimension in patients with idiopathic PAF independent of PAF frequency and age (and that PAF is probably a consequence of the prolongation).

Adult↗

Feline immunodeficiency virus lacks sensitivity to the antiviral activity of feline IFN-gamma.

The antiviral activity of recombinant feline interferon-gamma (rFeIFN-gamma) against feline immunodeficiency virus (FIV) was investigated. A persistently FIV(Bang)-infected feline T cell line (FeT-J/Bang) was treated with either rFeIFN-omega, rFeIFN-gamma, or recombinant human IFN-alpha2 (rHuIFN-alpha2), and the culture fluids were tested for antiviral activity by reverse transcriptase (RT) assay. FeT-J/Bang cell cultures treated with rFeIFN-omega showed dose-dependent inhibition of RT activity. In contrast, rFeIFN-gamma treatment had no antiviral effect on FIV replication but instead caused a statistically significant enhancement on day 9 of culture. Antiviral activity of rFeIFN-gamma was also tested on feline peripheral blood mononuclear cells (PBMC). PBMC cultures were inoculated with FIV(Bang) and simultaneously treated with either rFeIFN-omega, rFeIFN-gamma, or rHuIFN-alpha2. FeIFN-gamma had no effect on FIV replication, unlike the rFeIFN-omega and rHuIFN-alpha2, which had strong anti-FIV effects. In another study, rFeIFN-gamma treatment was initiated 3 days before FIV(Bang) infection, the day of FIV(Bang) infection, or 3 days post-FIV(Bang) infection and then tested for antiviral activity. The time of initiating rFeIFN-gamma treatment had no effect on the antiviral activity. Hence, these results suggest that unlike rHuIFN-alpha2 and rFeIFN-omega, rFeIFN-gamma has no inhibitory effect on FIV replication in PBMC but causes a slight enhancement in a feline T cell line.

Animals↗