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S K Durham

Publications and source records attributed to S K Durham.

At least 91 records · Page 5Linked to original sources
PubMed1990

Comparative endotoxin-induced hepatic injury in young and aged rats.

Recent studies have demonstrated that aged rats are more susceptible to the lethal effects of endotoxin (ET) than young rats. The early (15 min to 7 h) hepatic ultrastructural and biochemical changes induced by ET in young (6 months) and aged (24 months) rats were evaluated to elucidate cell populations and/or the mechanisms that may be responsible for the previously observed differential effects. Aged rats given ET had significantly increased numbers of neutrophils in hepatic sinusoids at 30 min and thereafter as compared with ET-treated young rats. Morphologic evidence of coagulation within hepatic sinusoids, including aggregates of fibrin enmeshed among polymorphonuclear leukocytes and platelet aggregates, was frequently observed in ET-treated aged rats but not in ET-treated young rats. In contrast, Kupffer cells of ET-treated young rats frequently contained phagocytized neutrophils and platelets, whereas this phenomenon was rarely observed in Kupffer cells of ET-treated aged rats. Hepatocellular morphologic injury was more pronounced and occurred at earlier time periods in ET-treated aged rats, and was accompanied by significant increase in hepatic transaminases. ET-treated aged rats had an earlier onset and greater severity of endothelial cell injury than did ET-treated young rats. The results of this study indicate a greater aggregation of blood elements in the hepatic sinusoids of aged rats following the intravenous administration of ET, which suggests that a greater diminution in microcirculation was induced in aged rats by ET. Additionally, the increased phagocytosis of inflammatory cells by Kupffer cells of young rats may be a mechanism which affords protection against endotoxin-induced lethality.

Aging↗
PubMed1990

Early and late effects of fractionated irradiation and the kinetics of repair in rat lung.

The thorax of WAG/Rij rats was irradiated with fractionated doses of X rays. Irradiation schedules were designed either to allow virtually complete repair of sublethal damage between subsequent fractions by fractionating at 6-h intervals, or to result in incomplete repair by allowing only 1-h intervals between subsequent fractions. Combination of the data from both experimental series permitted the calculation of alpha/beta ratios and values for the repair halftime T1/2. The animals were monitored by assessment of the breathing frequency and by recording deaths. At the end of the experiments, 18 months after treatment, the hydroxyproline content of the lung tissue was determined as a biochemical indicator of radiation-induced fibrosis, and an histopathological analysis was performed. Early endpoints, indicative of radiation-induced pneumonitis, resulted in an alpha/beta ratio of 3.5 Gy and a T1/2 value of 0.95 h. Late endpoints were presumed to be indicative of radiation-induced fibrosis. Based on the combined analysis of data from three different late endpoints, the mean alpha/beta ratio was 2.3 Gy, and the T1/2 value was 1.13 h. The difference in alpha/beta ratio and T1/2 value between early and late endpoints was not significant, since the 95% confidence limits were overlapping. For each individual early or late endpoint as well as for the two early or the three late endpoints combined, there was a trend for lower alpha/beta ratios and higher T1/2 values associated with low doses per fraction. However, widely overlapping confidence limits indicated that again the differences were not significant.

Animals↗
PubMed1990

Phospholipase A2-induced pulmonary and hemodynamic responses in the guinea pig. Effects of enzyme inhibitors and mediators antagonists.

The effect of phospholipase A2 (Naja naja) PLA2) on mean arterial blood pressure and intratracheal pressure was examined in anesthetized guinea pigs. Intracheally administered PLA2 (1 to 10 U) produced acute, dose-dependent increases in mean arterial blood pressure and intracheal pressure. However, Intravenously administered PLA2 (doses as large as 1,000 U) did not alter monitored variables. Acute PLA2-induced morphologic alterations were characterized by airway constriction, airway/alveolar cell damage, and pulmonary sequestration of both leukocytes and platelets. PLA2-induced increases in both mean arterial blood pressure and intratracheal pressure were attenuated to varying degrees by pretreating intravenously with indomethacin (10 mg/kg), a cyclooxygenase inhibitor, and WEB 2086 (0.1 mg/kg), a platelet-activating factor antagonist. Both ICI 198,615 (1 mg/kg), a leukotriene D4, receptor antagonist given intravenously, and dexamethasone (50 mg/kg), a steroidal anti-inflammatory agent given intraperitoneally as a 2-day pretreatment, reduced PLA2-induced increases in intratracheal pressure. Pyrilamine (2 mg/kg), a histamine1-receptor antagonist given intravenously, did not modify PLA2-induced pathophysiologic responses. Guinea pigs exposed to aerosolized PLA2 (100 U/ml) exhibited evidence of increased bronchoalveolar lavage macrophage, leukocyte, and lymphocyte accumulation at 24 h post-PLA2. These studies suggest that in vivo PLA2-induced pathophysiologic changes in the guinea pig involve alterations in resident airway cell populations as well as sequestration and infiltration of inflammatory cells. Both eicosanoids and platelet-activating factor appear to contribute to these PLA2-induced pathophysiologic effects.

Animals↗
PubMed1990

3,4,3',4'-Tetrachlorobiphenyl distribution and induced effects in the rat adrenal gland. Localization in the zona fasciculata.

The distribution of radiolabeled 3,4,3',4'-tetrachlorobiphenyl (TCB) and TCB-induced effects on serum and adrenal gland retinoid content, and adrenal gland morphology was studied by liquid scintillation counting, high performance liquid chromatography, light microscopic autoradiography, and transmission electron microscopy. Adult, female WAG/Rij rats received a single intraperitoneal injection of either vehicle (corn oil), 15 mg TCB/kg, or 200 mg TCB/kg body weight and were sacrificed (N = 3 per group) at 1, 3, 7, and 14 days after treatment. One rat of the high dose group that was sacrificed at each sampling time had received radiolabeled compound (containing 1.85 mCi of 3H-TCB). At day 1, the adrenal gland had the greatest concentration of radioactivity (dpm x 10(-6)/gm wet tissue) of any organ examined. There was a selective distribution of radiolabeled compound to the zona fasciculata accompanied by morphometric evidence of hypertrophy of the zona fasciculata. The vast majority of 3H-TCB present in the adrenal gland was parent compound at all time periods. Serum retinol content was significantly decreased in the high dose group by 61 and 54% at days 3 and 7, respectively. No significant decrease in adrenal gland retinoid content occurred at any time in this study, but in contrast, adrenal gland retinol and retinyl palmitate content was increased. Serum cortisol levels were transiently decreased in the high dose group. Ultrastructural alterations were only observed in cells of the zona fasciculata. Predominant changes included mitochondrial hypertrophy and concentric whorling lamellar arrays of the membranes of the outer mitochondrial compartment and mitochondrial cristae. The results of this study indicate that the rat adrenal gland is an early target organ after TCB intoxication, and that there is an early and selective distribution of TCB in the rat adrenal gland accompanied by morphologic alterations in the sites of compound localization. The results further suggest that the observed morphologic changes did not result from hypovitaminosis A.

Animals↗
PubMed1990

Phospholipase A2-induced pathophysiologic changes in the guinea pig lung.

The pathophysiology of lung injury induced by phospholipase A2 (PLA2), a lipolytic enzyme implicated in a variety of pulmonary diseases, was examined in the guinea pig. One hundred microliters of saline or 10 units of PLA2 suspended in saline was given as a bolus injection into either the trachea or jugular vein. Intratracheal pressure and mean arterial blood pressure were continuously monitored. The lungs were examined by light and transmission electron microscopy at 1, 10, and 30 minutes after administration. Pulmonary morphologic and physiologic changes were only observed in animals that received PLA2 via the trachea. Significant increases in peak intratracheal pressure occurred as early as 1 minute after intratracheal PLA2 administration. Morphologic evidence of airway constriction, accompanied by blebbing of the apical cytoplasm of airway epithelium, was also observed at this time. A transient increase in mean arterial blood pressure occurred 5 minutes after challenge. At 10 minutes after intratracheal PLA2, there was marked swelling of airway epithelial cells, pronounced blebbing of the apical cytoplasm, and a resultant decrease in size of the airway lumen. Morphologic changes in alveolar cell populations were initially observed 10 minutes after intratracheal PLA2. Interalveolar septa were hypercellular and multifocally thickened. There was prominent perivascular edema and alveolar spaces contained abundant proteinaceous material and occasional hemorrhage. Ultrastructurally, there was marked cell swelling and fragmentation of type I alveolar epithelium resulting in a denuded basal lamina. Sequestration of neutrophils and eosinophils, many of which lacked secretory granules, within alveolar capillaries was accompanied by aggregates of platelets and was observed in close proximity to injured endothelium. Morphologic changes indicative of cell injury were also observed in type II alveolar epithelium. Similar, but more frequent and severe, morphologic injury occurred 30 minutes after intratracheal PLA2. It is concluded that PLA2 induces pronounced morphologic and physiologic changes in the guinea pig and that the route of administration is important in the development of PLA2-induced lung injury.

Animals↗
PubMed1989

Platelet participation in the increased severity of endotoxin-induced pulmonary injury in aged rats.

Recent studies have demonstrated that aged rats are more susceptible to the lethal effects of endotoxin as compared with young rats. The morphogenesis of early endotoxin-induced pulmonary injury in young (6 months) and aged (24 months) rats was examined by combined light and transmission electron microscopy to elucidate cell populations that may be responsible for these effects. Pulmonary endothelial cell injury was of greater severity and occurred at earlier time periods in aged rats as compared with young rats. Platelet sequestration and aggregation were observed only in aged rats in this study, and occurred in conjunction with the initial degenerative changes in the endothelium. Morphological evidence of granulocyte degranulation and fragmentation was also observed only in aged rats. These results suggest that pulmonary endothelial cells of aged rats are more susceptible to endotoxin-induced injury and that platelets may play an important role in the enhancement of initial endothelial damage. Furthermore, the extent of injury to the endothelial cell population may play an important role in accounting for differences in endotoxin-induced mortality between young and aged rats.

Aging↗
PubMed1989

A pneumotoxin, O,O,S-trimethyl phosphorothioate, induces hemorheological alteration in rats.

O,O,S-trimethyl phosphorothioate (OOS-TMP), an impurity present in widely used organophosphorus insecticides, has been shown to induce lung injury after oral administration. To date, very little is known about the hemorheological changes which may occur during the inflammation of lung caused by OOS-TMP. The present study has demonstrated that oral administration of OOS-TMP (10 mg/kg, 20 mg/kg) to rats produced an increase in whole blood apparent viscosity at 24, 48 and 72 h following the treatment in rats. Concomitantly, the plasma fibrinogen level and red blood cell (RBC) aggregation were increased at 24 and 48 h. There was no change in RBC filterability. Thus, OOS-TMP, a pneumotoxin, was capable of causing a systemic hemorheological alteration, probably via increase in fibrinogen content, an acute-phase protein, in rats.

Alkaline Phosphatase↗
PubMed1989

Long-term morphologic and biochemical changes induced by O,O,S-trimethyl phosphorothioate in the rat lung.

The long-term pulmonary morphologic and biochemical changes induced by a single, sublethal dose of O,O,S-trimethyl phosphorothioate (OOS-TMP), an impurity present in organophosphorus insecticides, was examined in female WAG/Rij rats. Animals received either corn oil or a corn oil solution of OOS-TMP at a dose of 40 mg/kg body weight by gavage and were studied at the following time intervals after treatment: 10 days, 30 days, 90 days, 6 months, and 1 year. No control or OOS-TMP-treated animal died spontaneously. Significant increases in wet and dry lung weights occurred at all times examined in OOS-TMP-treated rats compared to those in age-matched controls. No difference was observed in percentage lung water content between treated and control rats. OOS-TMP treatment resulted in hypertrophy and hyperplasia of type II alveolar epithelial cells having morphologic alterations in the size and number of osmiophilic lamellar bodies. Interstitial changes were characterized as increased numbers of fibroblasts accompanied by increased amounts of collagen fibrils and basement membrane alterations. There was also a significant increase in pulmonary hydroxyproline content in OOS-TMP-treated animals compared to that in controls at all time periods. Collagen deposition was predominantly associated with the interalveolar septa rather than being oriented around airways. The results of this study indicate that a single, sublethal dose of OOS-TMP induces long-term structural and biochemical changes in the rat lung.

Animals↗
PubMed1989

The influence of cisplatin and unilateral nephrectomy on the response of the rat kidney to irradiation.

Cisplatin was administered as a single i.p. dose of 5 mg/kg to WAG/Rij rats at intervals of 7 days or 0.5 h before, or 7 days after graded X-ray doses to the left kidney. The right kidney was surgically removed 4 weeks after irradiation. Renal function was determined by measuring total urine volume excreted in 24 h, urine osmolality and serum urea. The severity of alterations in the various anatomic compartments of the kidney induced by the various treatments were graded histologically. The administration of 2 or 5 mg/kg cisplatin alone did not alter any of the kidney function parameters. Isoeffective radiation doses calculated for each of the functional parameters continuously decreased with increasing time after treatment. Differences between the isoeffective doses for the three combined treatments and for treatment with irradiation alone were only observed for urine osmolality and urine volume which primarily are tubular-related functional parameters. The histopathological grading studies also indicated that enhancement by cisplatin of radiation-induced damage was almost entirely confined to the tubules. The results of this study indicate that the sequence and length of time between treatments is an important variable in the development of cisplatin plus radiation-induced renal injury, but that none of the tested combinations showed a more than additive toxicity.

Animals↗
PubMed1989

Pulmonary responses to phospholipase A2 in the perfused guinea pig lung.

We examined the effect of phospholipase A2 (PLA2; Naja naja) challenge on pulmonary hemodynamics, airway constriction, and fluid filtration in isolated Ringer-perfused guinea pig lungs. Intratracheal PLA2 (10-100 U) produced dose-dependent increases in pulmonary arterial pressure, intratracheal pressure, and lung weight, although intravenous PLA2 administration had no effect on monitored variables. Morphological features indicative of airway constriction and pulmonary edema were observed by light microscopy. PLA2-induced increases in intratracheal pressure and/or lung weight were attenuated to varying degrees by pretreatment with indomethacin (1 microM, a cyclooxygenase inhibitor), ICI-198,615 (1 microM, a leukotriene D4 receptor antagonist), and WEB 2086 (1 microM, a platelet-activating factor antagonist). PLA2-induced increases in pulmonary arterial pressure and intratracheal pressure were also reduced in lungs removed from animals pretreated with dexamethasone (50 mg/kg ip for 2 days; a steroidal antiinflammatory agent). Pyrilamine (1 microM, a histamine1-receptor antagonist) and Takeda AA861 (1 microM, a delta 5-lipoxygenase inhibitor) did not produce significant inhibitory effects on PLA2-induced pathophysiological changes. Intratracheal instillation of high-dose platelet-activating factor (50 micrograms) or lysophosphatidylcholine (100 micrograms) produced gradual increases in intratracheal pressure and lung weight, but these changes were not as large as those induced by PLA2. Thus these studies suggest that resident cell populations associated with airways may play an important role in PLA2-induced pathophysiological changes in the perfused guinea pig lung. These PLA2-induced effects are most likely partially mediated by generation of eicosanoids and platelet-activating factor.

Animals↗
PubMed1989

3,4,3',4'-tetrachlorobiphenyl-induced effects in the rat liver. I. Serum and hepatic retinoid reduction and morphologic changes.

The distribution of 3,4,3',4'-tetrachlorobiphenyl (TCB), its effects on serum and hepatic retinoid, content and liver morphology were investigated in adult female WAG/Rij rats. Animals received a single intraperitoneal injection of either a corn oil vehicle, 15 or 200 mg TCB/kg body weight and were killed at 1, 3, 7, and 14 days after treatment. One rat of the high-dose group that had received 200 mg TCB/kg containing 1.85 mCi of 3H-TCB was sacrificed at each sampling time. There was a significant increase in liver weight when expressed as a percentage of body weight in the high-dose group at day 3 (122% of controls), day 7 (116% of controls), and day 14 (110% of controls). There was a rapid rise in the amount of 3H-TCB present in the liver that peaked at day 7 followed by a rapid decline in the amount of radiolabelled material by day 14. Greater than 90% of the radiolabelled material in the liver was parent compound. TCB treatment induced a significant decrease in serum retinol content in the high-dose group at day 3 (39% of controls) and day 7 (46% of controls) following exposure. There was a significant decrease in hepatic retinol content in the high-dose group at day 3 (34% of controls), day 7 (25% of controls), and day 14 (42% of controls) following exposure. TCB treatment induced a significant decrease in hepatic retinyl palmitate content in the high-dose group at day 7 (56% of controls) following exposure. Ultrastructural alterations in hepatocytes included the proliferation and vesiculation of endoplasmic reticulum, and mitochondrial enlargement with paracrystalline inclusions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

3,4,3',4'-tetrachlorobiphenyl-induced effects in the rat liver. II. Electron microscopic autoradiographic localization of 3H-TCB.

Recent results (3) indicate that 200 mg 3,4,3',4'-tetrachlorobiphenyl induces hepatomegaly accompanied by significant decreases in serum and hepatic retinoid content and hepatocyte morphologic alterations of proliferated and vesiculated endoplasmic reticulum and megamitochondria with paracrystalline inclusions. There was also an associated change in the number, size, and distribution of lipid droplets in hepatocytes and fat-storing cells. Electron microscopic autoradiographic techniques were utilized to determine the cellular and subcellular distribution of 3H-3,4,3',4'-tetrachlorobiphenyl (3H-TCB) in the adult rat liver and determine if there is any relationship between subcellular morphologic change and radiolabel localization. Adult female WAG/Rij rats received a single intraperitoneal injection of 200 mg TCB/kg containing 1.85 mCi of 3H-TCB and were sacrificed at 1, 3, 7, and 14 days following exposure. The vast majority of 3H-TCB-derived radioactivity was located in the hepatocyte at all time points examined, ranging from 79-86% of the total number of autoradiographic grains counted over the liver cells. Sequential order of radiolabel localization per liver cell type at 1, 3, and 7 days was hepatocyte much greater than Kupffer cell greater than fat-storing cell greater than endothelial cell. At day 14, the sequential order of radiolabel localization per liver cell type was hepatocyte much greater than fat-storing cell greater than Kupffer cell greater than endothelial cell, which indicates that there was some shift movement of label over time. The lipid droplet, mitochondria, and endoplasmic reticulum were the subcellular structures or organelles of hepatocytes having the highest number of 3H-TCB-derived grains at all time periods examined.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Pulmonary endothelial and alveolar epithelial lesions induced by O,O,S-trimethyl phosphorothioate in rats.

The morphogenesis of pulmonary injury induced by an impurity present in a commercially important organophosphorus insecticide, O,O,S-trimethyl phosphorothioate (OOS-TMP), was studied by combined light and transmission electron microscopy. Weanling female WAG/Rij rats received OOS-TMP dissolved in corn oil by gavage and were studied at intervals from 6 to 168 h after treatment. Sequestration of neutrophils was initially observed at 12 h after treatment and was accompanied by interstitial oedema. Plasmalemma alterations in endothelium lining capillaries and small arteries and veins were observed from 12 to 120 h after treatment and were accompanied by endothelial cell detachment and separation from the basal lamina. Abundant aggregates of fibrin were sequentially observed in intravascular, interstitial, and alveolar spaces. Platelet aggregation and degranulation were occasionally observed in capillaries as early as 12 h after treatment, and frequently observed in capillaries and small vessels from 24 to 96 h after treatment. Significant increases in wet lung weight and lung water content occurred at the same time that morphologic changes were observed in pulmonary endothelium. Alterations in type I alveolar epithelial cells were initially observed at 24 h after treatment. Cell swelling, fragmentation, and necrosis were observed in both type I and type II cells and resulted in a bare basal lamina. Marked attenuation, hypertrophy, and proliferation of type II epithelial cells followed alveolar epithelial cell injury and loss. Minimal changes were observed in non-ciliated bronchiolar epithelial (Clara) cells; predominant changes included the loss of surface microvilli and apical cytoplasmic bulge. The results of this study indicate that the endothelium and alveolar epithelium are the predominant cell types in the rat lung injured following OOS-TMP administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Morphogenesis of O,O,S-trimethyl phosphorothioate-induced pulmonary injury in mice.

The purpose of this study was to establish and characterize an experimental model in mice that examined the pulmonary effects of O,O,S-trimethyl phosphorothioate (OOS-TMP), a contaminant present in commercially important organophosphorus insecticides. Characterization of the model will allow the delineation of comparative effects between species and its possible extrapolation to man, and provide an additional experimental animal species satisfactory for mechanistic-oriented studies on OOS-TMP and related compounds. The morphogenesis of pulmonary injury induced by OOS-TMP was studied in mice by light and transmission electron microscopy. Weanling female C57BL/Ka mice received OOS-TMP dissolved in corn oil by intraperitoneal injection and were studied at intervals from 6 to 168 hr after treatment. Morphologic changes were observed in Clara cells only at the initial time period examined. Injury of pulmonary parenchymal cell populations, including the endothelium and type I alveolar epithelium, occurred after morphologic changes indicative of severe cell injury and necrosis in Clara cells. Endothelial cell injury was accompanied by significant increases in wet lung weight and percentage lung water content. Type I alveolar epithelial cell injury and loss resulted in a bare basal lamina, followed by attenuation, hypertrophy, and hyperplasia of type II alveolar epithelial cells. The results of this study document the successful establishment of a mouse experimental model of OOS-TMP-induced pulmonary toxicity. It is concluded that the Clara cell was the initial and most severely affected pulmonary cell population in mice receiving OOS-TMP. The administration of OOS-TMP in mice also results in marked morphologic alterations in the pulmonary parenchyma that were accompanied by significant changes in lung weight and composition.

Animals↗
PubMed1988

Albumin elimination in female WAG/Rij rats with age: a longitudinal study.

A longitudinal study was performed to examine total albumin elimination and urinary albumin excretion in the female WAG/Rij rat. Complete necropsies were performed following the spontaneous death of the animals. The survival characteristics of this group was similar to that of survival cohorts. An increase in total albumin elimination, urinary protein excretion and urinary albumin excretion was observed with age. A proportional increase in the contribution of albumin to the urinary protein excretion was also observed. However, the observed increase in urinary albumin excretion could not totally account for the increase in total albumin elimination. The predominant kidney lesion was chronic progressive nephrosis. The histological severity of the renal lesions were closely correlated with the increase in urinary albumin and total protein loss. It is concluded that the increase in total albumin elimination in rats in this study was due to age-related changes and not to cohort effects.

Aging↗
PubMed1988

Successful treatment of EAE in rhesus monkeys with MHC class II specific monoclonal antibodies.

Experimental Allergic Encephalomyelitis (EAE) was induced in rhesus monkeys by subcutaneous immunization with calfbrain homogenate in complete Freunds adjuvant. Monkeys were treated with major histocompatibility complex (MHC) Class II specific monoclonal antibodies (MoAb) as soon as the first clinical EAE signs became apparent. Two different treatments were tested. One consisted of 10 daily injections of a mixture of two MHC Class II specific MoAb, reactive with a monomorphic structure of rhesus monkey Class II molecules. The other consisted of 10 daily injections of Genox3.53, specific for HLA-DQW1. This MoAb crossreacts well with monkeys and also detects a polymorphism in this species and is presumably reactive with the RhLA-DQW1 antigen. Both MoAb treatments could modify the clinical course of EAE favourably. Untreated animals invariably died within 3 d of the onset of clinical EAE signs. Only one of the three monkeys treated with the monomorphic MHC Class II MoAb preparation died within 3 d, and the other two survived significantly longer than untreated animals. Both animals treated with Genox3.53 survived significantly longer than untreated control animals. Although only a few animals were tested, these results clearly show the possible beneficial influence of MHC Class II specific MoAb on a T-cell mediated autoimmune disease.

Animals↗
PubMed1988

The role of proteases in 4-ipomeanol-induced enhancement of Sendai viral pneumonia in mice.

The ability of reconstituted, concentrated lyophilized lavage fluid to activate noninfectious Sendai virus (NISV) in vitro was examined. Lavage fluid was obtained from 4-ipomeanol (4-IP)-injured lungs at 1, 3, 5, 7, 9, and 13 days after treatment, and 1, 7, and 13 days after sham treatment (controls). Significantly higher viral titers were obtained using lavage fluid collected 1 day after 4-IP treatment. Higher protein concentrations were present in lavage fluid obtained at day 1 and 3 after 4-IP treatment. It is concluded that local viral-activating protease concentrations resulting from 4-IP-induced pulmonary injury is a likely microenvironmental modulator of paramyxoviral replication and can play an important role in paramyxoviral-induced lung injury.

Animals↗