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Biomedical subjects

L F Martin

Publications and source records attributed to L F Martin.

At least 55 records · Page 3Linked to original sources
PubMed1991

Intravascular plastic catheters. How they potentiate tumor necrosis factor release and exacerbate complications associated with sepsis.

We tested the hypothesis that long-term intravascular cannulation exacerbates the harmful effects of an infectious challenge. Four groups of rats were initially studied: rats without intravascular catheters or infection (group 1), rats without catheters with a polymicrobial infection (group 2), rats with catheters but no infection (group 3), and rats with catheters and infection (group 4). Infected animals had an increased mortality and generated a significantly increased tumor necrosis factor response compared with noninfected animals. Animals with catheters and infection generated far less cardiac output than animals from the other three groups. No histologic changes differentiated the four groups. Therefore, the presence of a sterile intravascular catheter significantly increases cardiac dysfunction and mortality rates in rats with chronic bacteremia. These results suggest that intravascular plastic catheters potentiate the destructive cascade of events produced by the host in response to bacteremia.

Abscess↗
PubMed1991

Preoperative insurance status influences postoperative complication rates for gastric bypass.

One hundred morbidly obese patients who had gastric bypass surgery were studied to determine how various demographic and medical variables affected complication rates, weight loss, and reduction in comorbidities associated with obesity. During the follow-up period (range: 12 to 59 months), 42 patients developed at least 1 complication. Twenty-three patients developed postoperative medical complications, 9 developed psychiatric complications, and 24 developed complications related to food ingestion. No significant relationships were observed between outcome and age, sex, age of obesity onset, or associated medical disorders. Striking differences in outcome were noted, however, when patients were contrasted according to their preoperative insurance status. Patients dependent on medical assistance, social security disability, or workman's compensation (publicly funded group) (n = 40) developed significantly more medical and psychiatric complications than did those (n = 60) who had private medical insurance (p less than 0.02). Despite the higher complication rate, both groups had the same average weight loss (44.9 +/- 15.3 kg for the publicly funded group versus 43.1 +/- 12.9 kg for those with private insurance) and similar reductions in percent excess weight (66.0 +/- 18.4% versus 75.7 +/- 23.0%) during the first postoperative year. All patients also had similar reductions in medication requirements for hypertension, diabetes, and degenerative joint disease. Additionally, 45% of the publicly funded insurance group who either received public welfare (n = 26) or disability benefits (n = 14) preoperatively were able to attain either full-time or part-time employment postoperatively which allowed them to decrease their level of support (58% and 21%, respectively). Forty-six percent of women in the private insurance group who were not working outside the home also began part-time or full-time employment postoperatively. All patients who were working preoperatively continued to work. These data suggest that although the risks associated with gastric bypass surgery are greater in patients dependent on public funding, these patients benefit significantly from the surgery.

Adolescent↗
PubMed1991

Sonication provides maximal recovery of staphylococcus epidermidis from slime-coated vascular prosthetics.

Staphylococcus epidermidis (S. epidermidis) prosthetic vascular graft infections are often difficult to detect. A reliable culture method is needed so that appropriate therapeutic decisions can be initiated in a timely fashion. Sonication of graft material has been proposed as a method of enhancing bacterial recovery. Theoretically, however, this could cause cell lysis and false-negative culture results. Several methods of obtaining bacterial cultures were compared to determine the best method of quantitative bacterial recovery from infected graft material. Polytetrafluoroetehylene (PTFE) and knitted Dacron graft segments (n = 192) were exposed to a slime-producing strain of S. epidermidis or Escherichia coli (E. coli) at four different bacterial concentrations. Recovery of bacteria from the segments was then compared using three different methods to obtain organisms. One-third of the segments were pressed directly onto the agar to transfer bacteria while the other two-thirds were placed in broth and then either sonicated or vortexed prior to plating onto agar. The direct technique was significantly less effective (P less than 0.01) at recovering bacteria than either sonicating or vortexing for both graft materials at bacterial concentrations of 10, 10(2), and 10(4) CFU/ml of S. epidermidis. Sonication was significantly better at recovery from either material at 10(2) and 10(4) CFU/ml of S. epidermidis than vortexing (P less than 0.05). E. coli graft adherence was poor, and significant recovery occurred only at 10(8) CFU/ml. Sonication is necessary to maximally recover S. epidermidis from infected prosthetic grafts.

Bacteriological Techniques↗
PubMed1991

Evaluation of three techniques for documenting Staphylococcus epidermidis vascular prosthetic graft infections.

Staphylococcus epidermidis (S. epidermidis) vascular prosthetic graft infections are notoriously hard to detect. Three different techniques of determining whether vascular prosthetic grafts were infected using a dog model were evaluated. Aortic angiograms were compared with nuclear magnetic resonance (NMR) imaging and systemic norepinephrine (NE) kinetics to determine if either newer technique would be more reliable than standard angiograms. Twelve dogs were randomized to control (n = 6) or infected groups (n = 6). All dogs had a 5 cm section of their infrarenal aorta replaced with knitted Dacron vascular prosthetic graft. The grafts in the infected group were contaminated by soaking them in a broth containing S. epidermidis. NE production and clearance rates were calculated for all animals after an infusion of 3H-NE using the steady-state radionuclide tracer methodology. One week following graft insertion, dogs were reanesthetized, and the 3H-NE infusion and measurements were repeated. Standard angiograms and NMR imaging were also performed. Once all tests were performed, the prosthetic grafts were removed for cultures. Comparisons between the initial and final norepinephrine measurements for each group were made using the nonparametric Wilcoxon two-sample test, while comparisons between the groups were made by chi square or the Student's t test. Angiogram results were similar for control and infected animals. Angiograms missed disruption of the proximal anastomosis found in three of the six infected dogs at graft removal. None of the six control animals, while five of the six infected animals, had localized areas of high signal intensity on NMR imaging (P less than 0.01) suggesting abscess formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Metabolism of nicotine by hepatocytes.

The profile of nicotine metabolites produced by freshly isolated hepatocytes from rats, hamsters, guinea pigs, mice and humans was investigated after a 30-min exposure to nicotine ([2-14C]pyrrolidine). Large species differences occurred in the extent of nicotine metabolism; these ranged from 95% metabolism in guinea pig hepatocytes to only 30% metabolism in human and rat hepatocytes. The spectrum of metabolites formed also varied widely in different species. In hepatocytes from obese human subjects, nicotine was metabolized most extensively in smokers, least in nonsmokers, and to an intermediate degree in exsmokers, suggesting that cigarette smoking enhances the rate of nicotine metabolism. Pretreatment of all nonhuman species studied with phenobarbital and beta-naphthoflavone and with Aroclor in rats produced distinctive inductive patterns. Phenobarbital pretreatment of nonsmokers for 2 days prior to liver biopsy doubled the extent of nicotine conversion to cotinine by their hepatocytes. Rat and hamster hepatocytes exhibited sex and stereoselectivity differences in nicotine metabolism. Collectively, these studies indicate that hepatocytes offer some advantages over in vivo systems in investigating certain aspects of nicotine metabolism.

Animals↗
PubMed1990

A randomized clinical study of cefoperazone and sulbactam versus gentamicin and clindamycin in the treatment of intra-abdominal infections.

This report summarizes the experience of investigators in four medical centres who compared the combination of cefoperazone/sulbactam against gentamicin/clindamycin in the treatment of intra-abdominal infections. One hundred and fifty-two patients were enrolled in the study and all were evaluable for safety and tolerance, 110 were evaluable for efficacy. Of the 76 patients (49 male, 27 female) treated with cefoperazone/sulbactam 66 (86.8%) were cured, five (6.6%) improved and five (6.6%) failed to respond to treatment. Of 34 patients treated with gentamicin/clindamycin, 21 (61.8%) were cured, four (11.8%) improved and nine (26.4%) failed. Cure rates for patients receiving cefoperazone/sulbactam were significantly higher than those of patients receiving gentamicin/clindamycin (P less than 0.006). Failures in both groups were attributable in part to pseudomonal and enterococcal infection and abscess formation. The addition of sulbactam to cefoperazone rendered cefoperazone-resistant organisms susceptible to cefoperazone in 11 of the 76 cases (14.4%) and thus permitted treatment with this agent. The present study confirms the safety and clinical efficacy of cefoperazone/sulbactam and suggests that this combination is a viable alternative to an aminoglycoside plus clindamycin for intra-abdominal infections.

Abdomen↗
PubMed1990

Glutathione catabolism by the ischemic rat kidney.

The glutathione (GSH) content of rat kidney decreases after cessation of blood flow, falling to 40% of control levels 35 min after renal artery occlusion [R. C. Scaduto, Jr., V. H. Gattone II, L. W. Grotyohann, J. Wertz, and L. F. Martin. Am. J. Physiol. 255 (Renal Fluid Electrolyte Physiol. 24): F911-F921, 1988]. Renal GSH levels remained depressed for at least 2 h after resumption of blood flow. Because GSH functions in the removal of free radicals, and lipid peroxidation is a free radical-initiated process that occurs in the ischemic kidney, we investigated the fate of this GSH pool in the ischemic kidney. Using high-performance liquid chromatography to measure thiols, we found the loss of GSH to be associated with a stoichiometric accumulation of cysteine in the kidney. Moreover, preischemic labeling of the renal GSH pool with 35S led to accumulation of [35S]cysteine during ischemia that had the same specific activity as that of tissue GSH. Formation of cysteine during ischemia was suppressed in rats pretreated with acivicin, an inhibitor of gamma-glutamyltransferase (gamma-GT), although the degree of suppression was small in comparison to the extent of gamma-GT inhibition. During the initial 2 min of blood reflow after ischemia, tissue cysteine returned to control levels, and a transient increase in the cysteine content of renal venous blood was observed. After ischemia, renal GSH levels remained depressed, but postischemic GSH levels could be increased by administration of N-acetylcysteine during the ischemic period.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcysteine↗
PubMed1990

Winner of the 1988 NAASO Young Investigator Award. Regulation of fat cell adenylate cyclase in young Zucker (fa/fa) rats: alterations in GTP sensitivity of adenosine A1 mediated inhibition.

Lipolysis in rat adipocytes is controlled by the hormonally mediated stimulation and inhibition of adenylate cyclase. This dual regulation involves stimulatory (Gs) and inhibitory (Gi) GTP-binding proteins which control cAMP production in a GTP dependent manner. Adenosine, acting via the A1 receptor-Gi complex provides tonic regulation of adenylate cyclase and lipolysis in rat adipocytes. Adipocytes prepared from young obese Zucker (fa/fa) rats exhibit less stimulation (or greater inhibition) in response to adenosine deaminase, alone or in combination with lipolytic hormones, as compared with their lean littermates. Adenylate cyclase, measured in membranes prepared from obese adipocytes, showed decreased sensitivity to activation by low concentrations of GTP and was not inhibited by higher concentrations of the guanine nucleotide which, in lean control rats results in a biphasic activity curve. Adenosine A1 receptor binding, measured in these same membranes, demonstrated an increased sensitivity to activation by the GTP analogue, guanylyl imidodiphosphate. The presence of the analogue results in the dissociation of the receptor-Gi complex and conversion to the low affinity form in a greater proportion of receptors in the obese membranes. These results are consistent with an increased sensitivity to adenosine mediated inhibition of adenylate cyclase and lipolysis in the fat cells of the young obese (fa/fa) Zucker rat.

Adenosine↗
PubMed1990

Alterations in adipocyte adenylate cyclase activity in morbidly obese and formerly morbidly obese humans.

Studies examining animal models of genetic obesity have identified defects in adipocyte hormone-stimulated lipolysis that involve the adenylate cyclase transmembrane signaling system, specifically those components that decrease adenylate cyclase activity. To determine whether obese people demonstrate alterations in adenylate cyclase activity that could contribute to the maintenance of obesity by inhibiting lipolysis, we examined human adipocytes from patients who were lean, obese, or formerly obese. Fat samples were obtained from the lower abdomen of 14 women who were morbidly obese (obese group), from 10 women who were formerly morbidly obese and had lost weight after gastric stapling (postobese group), and from 10 similarly aged women of normal weight (controls). Adipocyte adenylate cyclase activity was determined under ligand-free (no stimulatory or inhibitory influences present), hormone-stimulated (isoproterenol, 10(-6) mmol/L), and maximal (cells stimulated with 10 mumol/L forskolin) conditions by measuring cyclic adenosine monophosphate (cAMP) levels by radioimmunoassay. The activity of adenylate cyclase was significantly different (p less than 0.01) in the three groups. Adipocytes from obese women had lower levels of cyclase activity under both ligand-free (5% vs 16% of maximal) and hormone-stimulated conditions (76% vs 100% of maximal) than adipocytes from normal women. Postobese women had levels of hormone-stimulated cAMP identical to those of normal women but still had abnormal ligand-free levels (under 5%). These results suggest the presence of an alteration in adipocyte adenylate cyclase regulation in morbidly obese women that is not entirely corrected when weight is lost after food intake is reduced by gastric stapling. This alteration in ligand-free cAMP activity may contribute to the development and maintenance of obesity.

Adenylyl Cyclases↗
PubMed1990

Cardiac dysfunction in a rat model of chronic bacteremia.

Cardiac function was examined in vivo and in vitro in rats to determine if cardiac dysfunction could be demonstrated in a nonlethal model of infection. Bacteremic rats (n = 6) had a subcutaneous polymicrobial abscess produced via repeated inoculations of an encapsulated foreign body with Escherichia coli, Bacteroides fragilis, and Staphylococcus aureus while control rats (n = 6) had the same subcutaneous, encapsulated foreign body (an inflammatory focus) but were not inoculated with bacteria. Cardiovascular function was assessed indirectly in vivo by measuring the maximal O2 uptake during a progressive exercise test in both groups before and 14 days after the initiation of inoculations. Cardiac function was also assessed in vitro in the same rats by measuring stroke volumes generated at six different preloads with constant heart rate and afterload. Bacteremic rats had a significantly different fever curve and leukocytotic response than control rats over the 14 day period. The majority of rats that received inoculations demonstrated bacteremias, while none of the control animals had positive cultures for the inoculated organisms. Although in vivo assessment of cardiovascular function showed no evidence of dysfunction, in vitro assessment demonstrated a significant rightward shift of the Starling curve in bacteremic rats. These data suggest that LV dysfunction occurs even during nonlethal infections but may be masked in vivo by compensatory mechanisms.

Animals↗
PubMed1990

Do trauma centers improve outcome over non-trauma centers: the evaluation of regional trauma care using discharge abstract data and patient management categories.

Development of regional medical care systems to treat patients who sustain major accidental injuries (trauma victims) has been based on autopsy studies which demonstrate that hospitals that meet certain accepted criteria of readiness (trauma centers) can prevent needless deaths of trauma victims. However, since only autopsy data have been available from non-trauma centers, it has not previously been possible to compare morbidity data between trauma centers and non-trauma hospitals. This study examines discharge abstract data and a new patient classification system called patient management categories (PMC) which are generated from this abstract data to evaluate length of stay (LOS), complications, and death to compare morbidity and mortality data from trauma centers and non-trauma centers. Discharge abstracts for 1,332 patients with the PMC of femoral shaft fracture with operation were obtained from all hospitals in Western Pennsylvania and Maryland for 1 year. Data from trauma centers were identified and compared to non-trauma centers using the following criteria: time to OR (less than or equal to 2 days vs. greater than 2 days), age (0-12, 13-55, greater than 55 years), associated injuries, and development of complications and death. Patients treated in trauma centers had significantly fewer complications (21% vs. 33%; p less than 0.001) and lower mortality rates (p less than 0.05) than those treated in non-trauma centers. Associated injuries, age, complications, and/or delay in time to OR significantly increased intensity and length of stay in both trauma and non-trauma centers. This significantly increased the cost of care provided to these patients in both types of centers.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Vitamin K1 reduction in human liver. Location of the coumarin-drug-insensitive enzyme.

The antidotal effect of vitamin K in overcoming poisoning by coumarin anticoagulant drugs is mediated by a vitamin K-reducing enzyme of the endoplasmic reticulum [Wallin & Martin (1987) Biochem. J. 241, 389-396]. With microsomes obtained from human liver biopsies, we have investigated the localization and the transverse orientation of this enzyme in the endoplasmic reticulum and compared its orientation to that of the other enzymes of the vitamin K-dependent carboxylation system. All enzymes were protected by the microsomal membrane and thus appear to have a luminal orientation in the endoplasmic reticulum, consistent with their role in the vitamin K-dependent modification of secretory glycoproteins. Separation of rough and smooth microsomes showed that vitamin K-dependent carboxylase activity was 6-fold higher in rough than in smooth microsomes. Vitamin K1 reduction by the coumarin-drug-sensitive (pathway I) and -insensitive (pathway II) enzymes of the vitamin K-dependent carboxylation system was the same in rough and smooth microsomes. The data suggest a close association between the pathway I and II enzymes in the endoplasmic reticulum. These pathways may be partial reactions of multienzyme complex which carries out the various activities associated with the vitamin K-dependent carboxylation system.

Carbon-Carbon Ligases↗
PubMed1989

The effect of glutathione content on renal function following warm ischemia.

Reperfusion after ischemia produces tissue injury due to free radicals generated during the reflow period. Glutathione (GSH) mediates against this oxidant damage by scavenging free radicals and protecting cells against injury. In an attempt to reduce the injury caused by free radicals, rat kidneys were pretreated with GSH monoethyl ester to elevate renal GSH fivefold. Previous studies in a renal artery occlusion model showed that pretreated kidneys in comparison to untreated controls were functionally impaired as measured by glomerular filtration rate, urine flow rate, and histology. To eliminate systemic effects of the pretreatment, kidneys were subjected to a fixed period of warm ischemia but flushed of blood and transplanted into nonpretreated syngeneic recipients. As before, pretreated kidneys exhibited marked functional impairment. We conclude that (i) elevation of renal GSH with GSH monoethyl ester enhances rather than prevents renal dysfunction and (ii) the enhancement of renal ischemic injury following pretreatment is not due to nonspecific systemic effects of GSH monoethyl ester pretreatment.

Animals↗
PubMed1989

Vascular prosthetic infection with Staphylococcus epidermidis: experimental study of pathogenesis and therapy.

To determine whether a slime-producing strain of Staphylococcus epidermidis was capable of producing acute infection of a prosthetic vascular graft, 5 cm segments of knitted Dacron were implanted in the infrarenal aortic position of dogs in three groups of animals. These included a control group (no graft contamination), a contaminated group that received a graft soaked in an S. epidermidis solution (untreated group), and a contaminated group in which perioperative antibiotics (three doses of cefamandole, 100 mg/kg) were administered (prophylaxis group). In all the animals reexploration and graft removal were performed at 10 days, with replacement of the defect being achieved with a new uncontaminated graft. These animals underwent exploration a third time after an additional 10-day period. S. epidermidis was not grown from the control animals (n = 7) but was cultured in 44% of the prophylaxis group (n = 9) and 88% of the untreated group (n = 16) during at least one of the operative procedures (chi 2 = 15.859; p less than 0.001). The pathologic features of acute S. epidermidis infection were best seen in the untreated animals and included anastomotic disruption (56%), periaortic hematoma, and lymphadenopathy (94%). Microscopic examination of the aortic tissues revealed extensive infiltrates of leukocytes, macrophages, and foreign body giant cells with aortic necrosis. These features were less prominent in the prophylaxis animals. We conclude that S. epidermidis is capable of producing acute graft infection with perigraft inflammation and anastomotic disruption. The administration of perioperative antibiotics reduced but did not abolish these effects of bacterial contamination of prosthetic vascular grafts.

Animals↗
PubMed1989

A1-adenosine receptor-mediated inhibition of adipocyte adenylate cyclase and lipolysis in Zucker rats.

Hormone-stimulated lipolysis is reduced in genetically obese rodents and may contribute to the increased adiposity characteristic of the obese state. Endogenously released adenosine, acting via the A1 receptor coupled to the inhibitory guanosine 5'-triphosphate binding protein, Gi, provides a tonic inhibition of lipolysis in rat adipocytes. Removal of this inhibition by the addition of adenosine deaminase frequently results in maximal lipolytic activity. Adipocytes isolated from lean Zucker (Fa/?) rats responded normally to adenosine deaminase, where lipolysis in adipocytes from obese Zucker (fa/fa) rats remained approximately 50% inhibited. Adipocyte adenylate cyclase was equally responsive to activation by forskolin, but lipolytic hormones were significantly less effective in stimulating adenosine 3',5'-cyclic monophosphate (cAMP) production in the obese adipocytes. These cells also exhibited an increased sensitivity to inhibition by the adenosine agonist, N6-(L-2-phenylisopropyl)-adenosine, either in combination with forskolin or beta-adrenergic hormone stimulation. Treatment of isolated adipocytes with pertussis toxin, which uncouples receptor-mediated Gi function, had little effect in cells from lean rats but increased isoproterenol stimulated cAMP production of cells from obese rats to levels observed in the lean cells. In addition, the adenosine A1 antagonist, 8-phenyltheophylline, increased cAMP and lipolytic activity in the obese adipocytes while having little significant effect in the lean adipocytes. These results suggest that hormonal control of lipolysis is altered in the obese Zucker rat because of an alteration in A1-adenosine receptor-mediated inhibition of adenylate cyclase.

Adenosine↗
PubMed1988

Early processing of prothrombin and factor X by the vitamin K-dependent carboxylase.

Binding interactions between the membrane-associated vitamin K-dependent carboxylase and its prothrombin and factor X substrates have been investigated in liver microsomes. Both substrates are firmly attached to microsomal membrane fragments which also harbor the carboxylase. In vitro 14CO2 gamma-carboxylation of these substrates, triggered by reduced vitamin K1H2, resulted in release of 14C-labeled prothrombin precursors from the membrane fragments, but no release of 14C-labeled factor X precursors could be demonstrated, which suggested a difference in early processing of these substrates by the carboxylase. Warfarin treatment of rats resulted in a 3-fold increase in the membrane concentration of factor X antigens and a 20-fold increase in 14C gamma-carboxylation of the membrane pool of factor X carboxylase substrates. There was a dose-response relationship between the amount of drug administered to the rats and 14C labeling of the membrane pool of factor X carboxylase substrates. On the other hand, the membrane concentration of prothrombin antigens did not increase in response to the drug, and 14CO2 gamma-carboxylation of the membrane pool of prothrombin carboxylase substrates was the same in warfarin and saline-treated rats. The results demonstrate significant differences in the interaction between the carboxylase and its prothrombin and factor X substrates. It appears that the different interactions result from binding of the prothrombin and the factor X precursors to separate microsomal membrane proteins that are involved in the gamma-carboxylation reaction. Warfarin appears to induce the factor X precursor-specific but not the prothrombin precursor-specific binding proteins, which suggests a new mechanism for the action of warfarin. These binding proteins may be under different genetic control. Treatment of the prothrombin and the factor X carboxylase substrates with endonuclease H showed that the rat prothrombin and the human factor X carboxylase substrates are high mannose glycoproteins. The human prothrombin and the rat factor X carboxylase substrates did not, on the other hand, change their migration in sodium dodecyl sulfate-polyacrylamide gel electrophoresis gels after endonuclease H treatment. The data demonstrate differences in the glycoprotein nature of the rat and the human carboxylase substrates.

Animals↗
PubMed1988

No evidence for vitamin K-dependent carboxylation of canine surfactant apoproteins, 28-36 kDa.

Recent research has shown that rat surfactant apoproteins (26-38 kDa) are vitamin K-dependent [Rannels, Gallaher, Wallin & Rannels (1987) Proc. Natl. Acad. Sci. U.S.A. 84, 5952-5956]. We have investigated the effect of the vitamin K antagonist warfarin on this family of apoproteins in surfactant from dog lung. Our data suggest that warfarin does not interfere with synthesis and secretion of these proteins into dog lung surfactant. Abnormal surfactant apoproteins, produced in response to warfarin treatment of the dog, were also not found in lung surfactant. 4-Carboxyglutamic acid analysis of purified dog apoproteins also failed to detect the vitamin K-modification. When vitamin K-dependent 14C labelling of precursors of vitamin K-dependent proteins was carried out, fluorography of these precursors, when electrophoresed into SDS/polyacrylamide gels, revealed 14C-labelled proteins of apparent molecular mass 74, 46, 42, 34, 31 and 23 kDa. Antibodies produced against purified dog surfactant apoproteins recognized precursors of the surfactant apoproteins in lung microsomes but did not recognize any 14C-labelled carboxylase substrates. These precursors appeared on immunoblots with apparent molecular mass 29, 32, 33 and 50 kDa. Our data suggest that there are significant differences between this class of surfactant apoproteins in the rat and the dog.

Animals↗