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Yangsoo Jang

Publications and source records attributed to Yangsoo Jang.

At least 91 records · Page 5Linked to original sources
PubMed2003

A paclitaxel-eluting stent for the prevention of coronary restenosis.

BACKGROUND: Intimal hyperplasia and resulting restenosis limit the efficacy of coronary stenting. We studied a coronary stent coated with the antiproliferative agent paclitaxel as a means of preventing restenosis. METHODS: We conducted a multicenter, randomized, controlled, triple-blind study to evaluate the ability of a paclitaxel-eluting stent to inhibit restenosis. At three centers, 177 patients with discrete coronary lesions (<15 mm in length, 2.25 to 3.5 mm in diameter) underwent implantation of paclitaxel-eluting stents (low dose, 1.3 microg per square millimeter, or high dose, 3.1 microg per square millimeter) or control stents. Antiplatelet therapies included aspirin with ticlopidine (120 patients), clopidogrel (18 patients), or cilostazol (37 patients). Clinical follow-up was performed at one month and four to six months, and angiographic follow-up at four to six months. RESULTS: Technical success was achieved in 99 percent of the patients (176 of 177). At follow-up, the high-dose group, as compared with the control group, had significantly better results for the degree of stenosis (mean [+/-SD], 14+/-21 percent vs. 39+/-27 percent; P<0.001), late loss of luminal diameter (0.29+/-0.72 mm vs. 1.04+/-0.83 mm, P<0.001), and restenosis of more than 50 percent (4 percent vs. 27 percent, P<0.001). Intravascular ultrasound analysis demonstrated a dose-dependent reduction in the volume of intimal hyperplasia (31, 18, and 13 mm3, in the high-dose, low-dose, and control groups, respectively). There was a higher rate of major cardiac events in patients receiving cilostazol than in those receiving ticlopidine or clopidogrel. Among patients receiving ticlopidine or clopidogrel, event-free survival was 98 percent and 100 percent in the high-dose and control groups, respectively, at one month, and 96 percent in both at four to six months. CONCLUSIONS: Paclitaxel-eluting stents used with conventional antiplatelet therapy effectively inhibit restenosis and neointimal hyperplasia, with a safety profile similar to that of standard stents.

Angiogenesis Inhibitors↗
PubMed2003

A novel uracil-DNA glycosylase family related to the helix-hairpin-helix DNA glycosylase superfamily.

Cytosine bases can be deaminated spontaneously to uracil, causing DNA damage. Uracil-DNA glycosylase (UDG), a ubiquitous uracil-excising enzyme found in bacteria and eukaryotes, is one of the enzymes that repair this kind of DNA damage. To date, no UDG-coding gene has been identified in Methanococcus jannaschii, although its entire genome was deciphered. Here, we have identified and characterized a novel UDG from M.jannaschii designated as MjUDG. It efficiently removed uracil from both single- and double-stranded DNA. MjUDG also catalyzes the excision of 8-oxoguanine from DNA. MjUDG has a helix-hairpin-helix motif and a [4Fe-4S]-binding cluster that is considered to be important for the DNA binding and catalytic activity. Although MjUDG shares these features with other structural families such as endonuclease III and mismatch-specific DNA glycosylase (MIG), unique conserved amino acids and substrate specificity distinguish MjUDG from other families. Also, a homologous member of MjUDG was identified in Aquifex aeolicus. We report that MjUDG belongs to a novel UDG family that has not been described to date.

Amino Acid Sequence↗
PubMed2003

Calreticulin inhibits the MEK1,2-ERK1,2 pathway in alpha 1-adrenergic receptor/Gh-stimulated hypertrophy of neonatal rat cardiomyocytes.

In cardiac myocytes, stimulation of alpha(1)-adrenoceptor (AR) leads to a hypertrophic phenotype. The G(h) protein (transglutaminase II, TGII) is tissue type transglutaminase and transmits the alpha(1B)-adrenoceptor signal with GTPase activity. Recently, it has been shown that the calreticulin (CRT) down-regulates both GTP binding and transglutaminase activities of TGII. To elucidate whether G(h) mediates norepinephrine-stimulated intracellular signal transductions leading to activation of extracellular signal-regulated kinases (ERKs) and neonatal rat cardiomyocyte hypertrophy, we examined the effects of G(h) on the activation of ERKs and inhibitory effects of CRT on alpha(1)-adrenoceptor/G(h) signaling. In neonatal rat cardiomyocytes, norepinephrine-induced ERKs activation was inhibited by an alpha(1)-adrenoceptor blocker (prazosin), but not by an beta-adrenoceptor blocker (propranolol). Overexpression of the G(h) protein stimulated norepinephrine-induced ERKs activation, which was inhibited by alpha-adrenoceptor blocker (prazosin). Co-overexpression of G(h) and CRT abolished norepinephrine-induced ERKs activation. Taken together, norepinephrine induces hypertrophy in neonatal rat cardiomyocytes through alpha(1)-AR stimulation and G(h) is partly involved in norepinephrine-induced MEK1,2/ERKs activation. Activation of G(h)-mediated MEK1,2/ERKs was completely inhibited by CRT.

Adrenergic alpha-Agonists↗
PubMed2003

Pulmonary venous flow in pure mitral stenosis and sinus rhythm--does pulmonary hypertension alter pulmonary venous flow velocity?

Pulmonary venous flow (PVF) is influenced by changes in left atrial (LA) pressure and function in various diseases. In mitral stenosis (MS), there is an alteration of LA hemodynamic due to the impaired ventricular filling caused by the stenotic valve and elevation of LA pressure. Although a variety of altered patterns of PVF have been described in MS, the potential influence of pulmonary hypertension, which is frequently associated with MS and has an adverse effect on the functional status and the prognosis of MS, on the PVF pattern is not clearly defined. The aim of this study is to determine the effects of pulmonary hypertension on PVF in patients with MS. Thirty-eight consecutive patients with pure MS and sinus rhythm (30 females, mean age 40 years old) underwent transthoracic and transesophageal echocardiography. Right heart and transseptal catheterization was also performed to measure pulmonary artery systolic pressure (PASP), pulmonary artery diastolic pressure (PADP), pulmonary capillary wedge pressure (PCWP), and left atrial pressure (LAP). The subjects were divided into two groups: group 1 (n = 25)included subjects with PASP < 50 mmHg, group 2(n = 13)included subjects with PASP 50 mmHg. LA size, mitral valve area (MVA), mean mitral gradient (MG), LAP, PASP, PADP, PCWP, and the peak velocity of PV systolic (PVFS), diastolic (PVFD) and atrial reversal flow (PVFAr) were also measured and compared between the two groups. There was no significant difference in age, heart rate, MVA, and LA size between the two groups. LAP, PASP, PADP, PCWP, and MG were significantly higher in group 2. However, PVFS and PVFAr were significantly lower in group2 (46.6 +/- 15.8 vs 29.9 +/- 12.8 cm/sec, P < 0.005; 22.1 +/- 6.8 vs 17.3 +/- 5.9 cm/sec, P < 0.05). There was no significant difference of PVFD between the two groups. PVFS had negative correlation to LAP, MG, PASP, PADP, and PCWP. PVFAr had negative correlation with PASP, PADP, and PCWP. There was no significant correlation between PVFAr and MVA. LA size and LAP. In conclusion, in patients with pure MS and sinus rhythm, PVF, especially PVFAr, is influenced by the presence of pulmonary hypertension.

Adult↗
PubMed2003

Endovascular therapy combined with immunosuppressive treatment for pseudoaneurysms in patients with Behçet's disease.

PURPOSE: To evaluate the feasibility, efficacy, and outcome of endovascular therapy combined with immunosuppression for the treatment of arterial pseudoaneurysms due to Behçet's disease. METHODS: Eleven pseudoaneurysms (3 in the abdominal aorta, 3 in the subclavian artery, and individual lesions in the brachiocephalic artery, renal artery, common iliac artery, common carotid artery, and the descending thoracic aorta) in 9 patients with Behçet's disease were treated with 10 stent-grafts and 1 self-expanding stent. All patients with elevated erythrocyte sedimentation rate (ESR) were treated with immunosuppressive agents (azathioprine, prednisolone) before and after the procedure. RESULTS: Endovascular treatment was successful in all cases, without major adverse events. The ESR was reduced from 42.7+/-18.0 mm/h initially to 18.6+/-12.6 mm/h after immunosuppressive therapy prior to endovascular repair. During follow-up (mean 24.1+/-14.0 months, range 6-43), 8 of 11 lesions showed complete resolution. One stent-graft to treat a postsurgical recurrent carotid artery pseudoaneurysm was occluded, and an abdominal aortic pseudoaneurysm recurred; both patients stopped their medications. ESR during follow-up was 7.9+/-4.5 mm/h. CONCLUSIONS: Endovascular treatment for pseudoaneurysms due to Behçet's disease is feasible and effective when disease activity is strictly controlled with immunosuppressive therapy.

Adult↗
PubMed2003

Inhibitory effect of salmosin, a Korean snake venom-derived disintegrin, on the integrin alphav-mediated proliferation of SK-Mel-2 human melanoma cells.

We have investigated the inhibitory effect of salmosin on integrin-mediated human tumour cell proliferation. SK-Mel-2 human melanoma cell adhesion to denatured collagen or vitronectin was found to be significantly and statistically inhibited by salmosin in a dose-dependent manner (P<0.05). Moreover, the binding of SK-Mel-2 cells to salmosin-coated plates was specifically disrupted by anti-integrin alphav monoclonal antibody at 8 microg mL(-1), but not by anti-integrin monoclonal antibody. These findings indicated that salmosin inhibited the adhesion of SK-Mel-2 cells to denatured collagen by specifically blocking integrin alphav. The proliferation of SK-Mel-2 cells on a denatured collagen-coated plate was statistically and significantly inhibited by salmosin induced apoptosis in a dose-dependent manner (P<0.05). Anti-integrin alphav monoclonal antibody, anti-integrin alphavbeta3 monoclonal antibody, and synthetic RGD peptide also suppressed SK-Mel-2 cell proliferation. Several lines of experimental evidence strongly suggested that the inhibition of SK-Mel-2 cell proliferation by salmosin was due to the induction of apoptosis via the blocking of integrin alphav-mediated cell survival.

Apoptosis↗
PubMed2002

Identification of the dITP- and XTP-hydrolyzing protein from Escherichia coli.

A hypothetical 21.0 kDa protein (ORF O197) from Escherichia coli K-12 was cloned, purified, and characterized. The protein sequence of ORF O197 (termed EcO197) shares a 33.5% identity with that of a novel NTPase from Methanococcus jannaschii. The EcO197 protein was purified using Ni-NTA affinity chromatography, protease digestion, and gel filtration column. It hydrolyzed nucleoside triphosphates with an O6 atom-containing purine base to nucleoside monophosphate and pyrophosphate. The EcO197 protein had a strong preference for deoxyinosine triphosphate (dITP) and xanthosine triphosphate (XTP), while it had little activity in the standard nucleoside triphosphates (dATP, dCTP, dGTP, and dTTP). These aberrant nucleotides can be produced by oxidative deamination from purine nucleotides in cells; they are potentially mutagenic. The mutation protection mechanisms are caused by the incorporation into DNA of unwelcome nucleotides that are formed spontaneously. The EcO197 protein may function to eliminate specifically damaged purine nucleotide that contains the 6-keto group. This protein appears to be the first eubacterial dITP- and XTPhydrolyzing enzyme that has been identified.

Acid Anhydride Hydrolases↗
PubMed2002

Deficiency of von Willebrand factor-cleaving protease activity in the plasma of malignant patients.

von Willebrand factor (vWF) multimeric pattern and von Willebrand factor-cleaving protease activity (vWF-cp) were studied using plasmas from patients with advanced stage- and limited stage-malignant tumors. Deficiency of highly polymeric forms of vWF was observed in plasmas from 7 of 11 patients tested. vWF-cp activity was deficient in plasma samples of six patients with advanced stage-malignant tumors (ranging from 6% to 30% activity of normal plasma), whereas an essentially normal vWF-cp activity was observed in samples taken from patients with limited stage-malignant tumors. Inhibitor of vWF-cp was not detected in any plasma samples tested. To further analyze the relevance of this enzymatic activity in metastatic diagnosis, a study of vWF-cp activity was conducted in 17 patients with colon cancer, and it was shown that deficiency of vWF-cp was associated with the progression of the disease.

ADAM Proteins↗
PubMed2002

Is prophylactic aortic valve replacement indicated during mitral valve surgery for mild to moderate aortic valve disease?

BACKGROUND: Determining the need for surgical treatment of coexisting mild to moderate aortic valve disease in patients referred for mitral valve surgery is often difficult. The purpose of this study was to assess long-term clinical outcome and the need for subsequent aortic valve replacement in patients with mild to moderate rheumatic aortic valve disease at the time of mitral valve surgery. METHODS: A total of 275 patients (90 men and 185 women, mean age 43 years) with rheumatic disease who underwent mitral valve surgery were followed up for an average of 9 years. Patients were classified into two groups: those with coexisting mild to moderate aortic valve disease at the time of mitral valve surgery (141 patients, group A) and those without (134 patients, group B). Primary outcomes (death and subsequent aortic valve surgery) were compared between the two groups. RESULTS: At the time of mitral valve surgery, 104 patients (74%) in group A had mild aortic regurgitation, 37 (26%) had moderate aortic regurgitation, 5 had (4%) mild aortic stenosis, and 2 (1%) had moderate aortic stenosis. At the end of follow-up, no patient had severe aortic valve disease. In all, 12 patients (5%) in group A had primary events (eight deaths and four subsequent aortic valve replacements), and 12 patients (9%) in group B had such events (12 deaths). According to Kaplan-Meier analysis, neither the survival rate nor the event-free survival rate differed significantly over the follow-up period between the two groups. CONCLUSIONS: In most patients who have mild to moderate rheumatic aortic valve disease at the time of mitral valve surgery, the long-term outcome is comparable to that of subjects without aortic valve disease at the time of mitral valve surgery. Subsequent aortic valve replacement is rarely needed after a long follow-up period.

Adult↗
PubMed2002

Regulation of small dense LDL concentration in Korean and Scottish men and women.

Small dense LDL is now emerging as an important risk factor for coronary artery disease. The amount of the LDL III has been reported to differ between ethnic groups. To investigate differences in the distribution of LDL subfractions between Korean and Scottish populations, we measured the plasma concentration and percent distribution of three major LDL subfractions in age-and sex-matched, middle aged, healthy 124 Korean and Scottish subjects (32 Korean men vs. 32 Scottish men; 30 Korean women vs. 30 Scottish women). Body mass index and waist circumference did not differ between the two ethnic groups. Total cholesterol and LDL cholesterol concentrations were higher in Scottish men compared with Korean men (P<0.01), while plasma triglyceride concentration was higher in Korean men and women (P<0.01 in men, P<0.05 in women). HDL cholesterol concentrations in both Korean men and women were lower than that of their Scottish counterparts (P<0.05 in men; P<0.001 in women). Korean men had lower concentrations of total LDL (242+/-65 vs. 325+/-122 mg/dl, P<0.01), LDL I (24+/-18 vs. 60+/-36 mg/dl, P<0.001) and LDL II (110+/-56 vs. 196+/-78 mg/dl, P<0.001). In contrast, LDL III concentration was markedly higher in Korean men (108+/-75 vs. 70+/-65 mg/dl, P<0.05). Likewise, the percent of LDL I (10.0+/-7.3 vs. 19.1+/-10.1%, P<0.001) and LDL II (47.2+/-20.7 vs. 60.1+/-10.9%, P<0.01) were lower in Korean men, while that of LDL III was higher (42.8+/-24.9 vs. 20.8+/-15.0%, P<0.001). In the female population, there were no differences in total LDL and LDL I concentrations between Korean and Scottish. LDL II concentration was lower in Korean women (106+/-53 vs. 151+/-57 mg/dl, P<0.01). Korean women showed a higher percent of LDL III (24.8+/-24.7 vs. 14.2+/-5.9%, P<0.05) and a lower LDL II (47.8+/-19.1 vs. 61.0+/-10.0%, P<0.01). Multiple linear regression revealed that plasma triglyceride concentration was the most important determinant of the LDL III subfraction concentration in Korean men and women and in Scottish men. In Korean men, the LDL III concentration rose linearly through the whole range of plasma triglyceride concentration, whereas in Scottish men, there was a threshold at 108 mg/dl triglyceride above which there was a positive association. Korean women showed the same pattern as Scottish men. We suggest that LDL concentrations and LDL subfraction distributions are regulated differently in these two ethnic groups. The different relationships between triglyceride and LDL III subfraction in Koreans versus Scots suggest that other factors, such as hepatic lipase or cholesteryl ester transfer protein may additionally play a role determining the LDL subfraction profile.

Adult↗
PubMed2002

Characterization and cDNA cloning of halyxin, a heterogeneous three-chain anticoagulant protein from the venom of Agkistrodon halys brevicaudus.

We report upon the isolation, characterization, and cDNA cloning of an anticoagulant protein, halyxin from Agkistrodon halys brevicaudus venom. The protein exists as a 29kDa protein, and is separated into three chains on SDS-PAGE under reducing conditions. However, we cloned only two cDNAs encoding halyxin from the cDNA library of the snake venom gland, on the basis of the determined amino acid sequences. The complete amino acid sequences were deduced from their nucleotide sequences and named halyxin A (129 amino acid residues) and B chain (123 amino acid residues). The deduced amino acid sequence of halyxin A chain corresponds to the two smaller chains. Thus, it is considered that halyxin A chain could be synthesized as a single-chain protein that is subsequently cleaved to yield the mature two-chain protein. The amino acid sequence of halyxin is similar to that of other snake venom proteins of the C-type lectin superfamily, and prolongs plasma-clotting time. In the presence of Ca(2+) ions, halyxin binds to coagulation factors IX, X, IXa, and Xa, but not to other vitamin K-dependent coagulation factors. It also inhibits factor Xa in a non-competitive manner but does not affect other activated coagulation factors.

Agkistrodon↗
PubMed2002

Inhibition of MEK1,2/ERK mitogenic pathway by estrogen with antiproliferative properties in rat aortic smooth muscle cells.

Proliferation and migration of vascular smooth muscle cells (VSMCs) are believed to contribute significantly to intimal thickening in atheroscleosis, restenosis, and venous bypass graft disease. Estrogen inhibits proliferation and migration of VSMCs. However, antiproliferative mechanisms of estrogen were not well elucidated yet. In this study, we investigated the antiproliferative effect of estrogen to determine whether the transduction signals and protooncogenes were affected in rat aortic smooth muscle cells (RASMCs). Estrogen inhibited the proliferative response stimulated by 5% fetal bovine serum (FBS) dose-dependently in RASMCs (IC50: 40 nM). In 0.5% serum-treated RASMCs, estrogen dramatically inhibited the activity of extracellular signal-regulated kinases (ERK) followed by inhibition of MEK1,2 activity in dose-dependent manner without affecting the other mitogen-activating protein kinases (MAPKs), c-jun N-terminal kinases (JNK) and p38. Induction of Elk-1 mRNA was significantly reduced dose-dependently up to 100 nM of estrogen. These results indicate that the antiproliferative effects of estrogen in RASMCs involved ERK inhibition followed by the inactivation of MEK1,2 and downregulation of Elk-1 expression.

Animals↗
PubMed2002

Relation of vasodilator response of the brachial artery to inflammatory markers in patients with coronary artery disease.

Endothelial dysfunction of the coronary artery is closely related to elevated levels of systemic inflammatory markers and cardiovascular events in patients with coronary artery disease (CAD). We hypothesized that patients with CAD may have a higher risk of endothelial dysfunction of the peripheral artery than patients without evidence of CAD, and that endothelial dysfunction of the peripheral artery also may be related to elevated levels of inflammatory markers. Using high resolution ultrasound, we assessed the brachial vasodilator response to reactive hyperemia (endothelium-dependent) and sublingual nitroglycerin (endothelium-independent). As inflammatory markers, serum C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) levels, and lipid profiles were measured in patients with CAD (n = 30, 16 male and 14 female) and normal subjects without evidence of CAD (n = 45, 23 male and 22 female). Patients with CAD (Group II) showed a significantly reduced endothelium-dependent vasodilation as compared with normal subjects (Group I) (4.4 +/- 3.6 vs 7.4 +/- 6.1%, P < 0.05). However, endothelium-independent vasodilation was not significantly different between the two groups (7.7 +/- 7.1 vs 9.7 +/- 8.0%, P > 0.05). In Group II, CRP level was inversely related to endothelium-dependent vasodilation (r = -0.398, P = 0.029). In contrast, ESR level was not significantly associated to endothelium-dependent vasodilation (r = -0.113, P = 0.552). On multivariate analysis, CRP and low density lipoprotein cholesterol levels were significant independent predictors of a blunted endothelium-dependent vasodilation in Group II. Our study showed that elevated CRP level was associated with blunted endothelium-dependent vasodilation of the brachial artery in patients with CAD. Thus, identification of elevated CRP levels combined with demonstration of endothelial dysfunction of the brachial artery may have a possible clinical application for the detection of high risk CAD patients.

Adult↗
PubMed2002

Fate of collateral circulation after successful coronary angioplasty of total occlusion assessed by coronary angiography and myocardial contrast echocardiography.

A well-developed collateral circulation is frequently observed in patients with total coronary occlusion. However, the fate of the collateral circulation after successful percutaneous transluminal coronary angioplasty (PTCA) has not been fully characterized. The purpose of this study was to compare the efficacy of coronary angiography and myocardial contrast echocardiography (MCE) in the evaluation of the collateral circulation after PTCA and to assess the temporal changes of the collateral circulation after successful PTCA of a totally occluded artery by using these 2 diagnostic methods. The study group was comprised of 20 consecutive patients (16 male, mean age 54 years) who underwent elective PTCA for total coronary occlusion. Coronary angiography was performed before, immediately after, and 24 hours after PTCA. MCE was also performed before, immediately after, and 24 hours after PTCA, by the intracoronary injection of sonicated radiographic contrast medium. According to the angiographic findings, the collateral circulation was graded on a scale of 0 to 3 as follows: 0 = no visible filling; 1 = collateral filling of side branches; 2 = partial collateral filling of the epicardial artery; 3 = complete filling of the epicardial artery. By MCE, myocardial perfusion by the collateral circulation was assessed by scoring the contrast pattern of collateral-dependent myocardial segments as follows: 0 = none; 0.5 = patchy or epicardial; 1 = homogeneous. The left anterior descending artery was occluded in 12 patients and the right coronary artery in 8 patients. Coronary angiographic collateral grades before PTCA were grade 2 in 5 patients and grade 3 in 15. PTCA with stenting was successfully performed in all patients without significant residual stenosis. Coronary angiography showed collateral circulation disappeared after PTCA in all patients. However, residual collateral perfusion was observed in 7 patients by MCE, performed immediately after PTCA (score 1 in 3 patients; score 0.5 in 4 patients). This residual collateral perfusion could be demonstrated even 24 hours after PTCA by MCE in 3 patients (all patients were 0.5 in myocardial perfusion score). In conclusion, successful PTCA with stenting of a totally occluded coronary artery leads to a disappearance of collateral vessels by coronary angiography in most of the patients. However, although angiographically not visible, coronary collateral circulation may persist even 24 hours after successful PTCA of a totally occluded artery demonstrated by MCE.

Adult↗
PubMed2002

Epigallocatechin-3-gallate inhibits basic fibroblast growth factor-induced intracellular signaling transduction pathway in rat aortic smooth muscle cells.

Daily green tea drinking showed preventive effects on the progression of atherosclerosis. Although epigallocatechin-3-gallate [EGCG] has anti-proliferative effects on various cells, relatively little is known about the molecular mechanisms of the anti-proliferative effects of EGCG. To determine whether the transduction signals and protooncogene expression were affected by EGCG, this study investigated the molecular mechanism of the anti-proliferative effects in basic fibroblast growth factor (bFGF)-stimulated rat aortic smooth muscle cells (RAoSMCs). EGCG inhibited the proliferative response stimulated by 10% fetal bovine serum dose dependently in RAoSMCs (median inhibitory concentration [IC50]: 28.4 x 10(-6) M ). EGCG also inhibited the migration of bFGF-stimulated RAoSMCs in a dose-dependent manner, showing that 21.8 x 10(-6) M of EGCG significantly inhibited the migration by 75 +/- 5% in comparison with bFGF-stimulated migration. In RAoSMCs, EGCG dramatically inhibited Ras activation and c-jun N-terminal kinase (JNK) activity without affecting protein kinase C expression. Induction of c-jun mRNA stimulated by bFGF was significantly reduced dose dependently up to 87.3 x 10(-6) M of EGCG. These results indicate that the anti-proliferative effect of EGCG on RAoSMCs is partly Ras/JNK mediated, independent of protein kinase C, and is attributable to the downregulation of c-jun expression.

Animals↗