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PubMed2000

Relative risk of cancer in sonographically detected thyroid nodules with calcifications.

PURPOSE: The aim of this prospective study was to evaluate the significance of sonographically detected thyroid calcifications in the diagnosis of thyroid cancer. METHODS: One hundred eighty-eight patients with thyroid disease, including 37 with thyroid cancer, were included in the study. Each patient underwent preoperative, high-resolution sonography to evaluate the thyroid gland for the presence of calcifications. RESULTS: The highest incidence of calcification was found in thyroid cancer (54%), followed by multinodular goiter (40%), solitary nodular goiter (14%), and follicular adenomas (12%). The incidence of cancer was significantly higher in calcified nodules (29%) than in noncalcified nodules in the entire group (14%) (p = 0.019), with a relative risk of 2.5. In the group of solitary thyroid nodules, the incidence of cancer in the calcified nodules (55%) was higher than in the nodules without calcification (23%) (p = 0.016). Multiple noncalcified thyroid nodules harbored cancer in only 5% of cases. Compared with multiple noncalcified thyroid nodules, the solitary calcified nodules demonstrated a relative risk of 22.8. In both the solitary and multiple nodules, the relative risk in the presence of calcification was about the same, around 4. Patients younger than 40 years with calcified nodules constituted a high-risk group, with a relative risk of 3.8 versus 2.5 in patients older than 40 years with calcified nodules. CONCLUSIONS: The detection of thyroid calcifications by sonography is diagnostically valuable, especially in cases involving a solitary nodule or a young person. The presence of calcifications in these cases should raise the suspicion of malignancy. The low incidence of cancer in patients with multiple noncalcified thyroid nodules suggests that a more conservative approach may be appropriate in such cases.

Adult↗
PubMed2006

Phosphocitrate blocks calcification-induced articular joint degeneration in a guinea pig model.

OBJECTIVE: Calcium deposition occurs frequently in osteoarthritic (OA) joints. However, evidence for a causal role of calcification in cartilage degeneration is inferential. The present study was undertaken to examine the role of calcification in OA disease progression and to evaluate a formulation of phosphocitrate (PC) as a potential therapeutic agent. METHODS: We have identified a guinea pig OA model in which meniscal calcification appears to correlate with aging and disease progression. We synthesized a new formulation of PC, [CaNa(PC)2(H2O)](n) (CaNaPC), which is a potent antimineralization agent and a specific inhibitor of crystal-induced biologic effects. After weekly treatment of guinea pigs with experimental OA with CaNaPC for 3 months, we examined calcification in menisci and cartilage degeneration. As a control, we examined whether similar CaNaPC treatment had any therapeutic effect in a hemi-meniscectomy model in which there is no known crystal involvement. RESULTS: Meniscal calcification correlated with cartilage degeneration in this animal model. PC treatment led to significant reduction of calcium deposits and arrested OA disease progression. Similar treatment had no effect in the hemi-meniscectomy model. CONCLUSION: CaNaPC diminishes mineralization in a cutaneous calcergy model and a model of OA in which intraarticular mineralization is a prominent feature. In the OA guinea pig model, inhibition of calcification is accompanied by diminished cartilage degeneration. CaNaPC has no therapeutic effect in the hemi-meniscectomy model. We conclude that pathologic calcification may initiate or amplify processes leading to cartilage degeneration and that CaNaPC may interrupt such a pathway.

Animals↗
PubMed2002

Effect of elastin on the calcification rate of collagen-elastin matrix systems.

The role of elastin in the aortic wall calcification and involved mechanisms were investigated. The major hypothesis of this work is that elastin is one of the major components to regulate calcification of bioprosthetic heart valve (BHV). The relationship between the elastin content and the calcification rate of the aortic wall was established using collagen-elastin matrices (CEM) made of varying ratios of collagen and elastin (90 and 10, 50 and 50, and 20 and 80). Biophysical characterization of CEM was performed by water content measurement and the tensile strength test. The conformational changes of the calcifiable matrix were evaluated as a function of elastin content using Fourier transform infrared (FTIR) spectroscopy. The calcium contents in CEM implanted in the rat subcutaneous model for 7 days were measured using atomic absorption (AA) spectroscopy. As the concentration of elastin in CEM increased from 10 to 80%, the total amount of calcium accumulated in CEM also increased. The calcium level in CEM containing the collagen and an elastin ratio of 20:80 was 20.16 +/- 0.70 microg/mg compared with 1.96 +/- 0.04 microg/mg in CEM containing the collagen and an elastin ratio of 90:10. The calcification rate of CEM pretreated with ethanol increased, as the elastin concentration in the CEM. However, the calcification rate of CEM pretreated with ethanol is significantly lower than that of the untreated control. The permeation rate of ethanol through CEM with the collagen and an elastin ratio of 20:80 (0.37 +/- 0.13 mmol/cm(2)/h) is significantly smaller than that through CEM with 90:10 (0.94 +/- 0.27 mmol/cm(2)/h). These results indicate that elastin has a significant role in tissue calcification and that elastin's resistance to ethanol penetration partially contributes less effectiveness of ethanol on aortic wall calcification.

Aorta↗
PubMed1992

Calcification of implanted vascular tissues associated with elastin in an experimental animal model.

We have previously studied the process of calcification in bioprosthetic porcine heart valves crosslinked with glutaraldehyde. Observations using light microscopy had indicated that calcification of elastic fibers occurs in implanted heart valves, in addition to calcification associated with collagen fibers. To determine the contribution of elastin to the process of calcification, small pieces of rabbit aorta were cross-linked with 0.2% glutaraldehyde, rinsed in buffer, and implanted subcutaneously in young adult male rats. Cross-linked jugular vein implants were included as controls. After an implantation period of 1 month or longer, we observed many areas of calcification in the aortic media associated with elastin and fewer such areas associated with collagen. The elastin-rich aortic tissues accumulated more calcium than venous tissues. Calcium deposits appeared similar in both allogenic and xenogeneic implants. Calcified areas viewed under the electron microscope included intercellular nonfibrous material. Calcified areas involved predominantly the outer layers of elastic fibers. Calcific deposits included needle-like crystals of hydroxyapatite but often consisted of an amorphous flocculant material surrounded by crystals. The close spatial relationship of hydroxyapatite crystals and elastic membranes seen in this study may be relevant to the initiation of dystrophic calcification in glutaraldehyde cross-linked aortic grafts.

Animals↗
PubMed1995

Role of glutaraldehyde in calcification of porcine heart valves: comparing cusp and wall.

Experiments were performed to better understand the relationship between glutaraldehyde and calcification of bioprosthetic heart valves, using both the cusps and the wall of porcine aortic roots. The results of the first experiment, for which 3H-labeled glutaraldehyde solutions were used, indicated that binding of glutaraldehyde in cusps and wall is concentration-dependent, that the wall contains significantly less glutaraldehyde than the cusp, and that glutaraldehyde, which penetrates in the wall at similar rates from the intima and the adventitia, is homogeneously distributed throughout the wall after 7 days of fixation, except for the intima side, where it is significantly lower. The results of the second experiment, for which cusps and 1-cm2 pieces of wall from glutaraldehyde-fixed porcine aortic roots were implanted subdermally in young rats, indicated that for both types of tissue, calcification appears to first initiate predominantly in the cell nuclei before extending to the other structures. After 8 weeks of implantation, whereas the cusps were completely calcified, calcification of the wall was limited to two longitudinal bands 150-300 microns thick, located below the adventitia and intima surfaces. The results of the third experiment indicated that cusp calcification, which decreased significantly after a 12-month storage period, was reset to high levels by reexposing the valves to glutaraldehyde at the end of the 12-month storage period. Wall calcification remained constant under all tested conditions. The results suggest that the mechanism(s) of calcification in the wall and the cusp may be different, and that calcification may be related to a particular molecular configuration resulting from exposure to glutaraldehyde.

Animals↗
PubMed2001

Arterial calcification: a review of mechanisms, animal models, and the prospects for therapy.

The causes of arterial calcification are beginning to be elucidated. Macrophages, mast cells, and smooth muscle cells are the primary cells implicated in this process. The roles of a variety of bone-related proteins including bone morphogenetic protein-2 (BMP-2), matrix Gla protein (MGP), osteoprotegerin (OPG), osteopontin, and osteonectin in regulating arterial calcification are reviewed. Animals lacking MGP, OPG, smad6, carbonic anhydrase isoenzyme II, fibrillin-1, and klotho gene product develop varying extents of arterial calcification. Hyperlipidemia, vitamin D, nicotine, and warfarin, alone or in various combinations, produce arterial calcification in animal models. MGP has recently been discovered to be an inhibitor of bone morphogenetic protein-2, the principal osteogenic growth factor. Many of the forces that induce arterial calcification may act by disrupting the essential post-translational modification of MGP, allowing BMP-2 to induce mineralization. MGP requires gamma-carboxylation before it is functional, and this process uses vitamin K as an essential cofactor. Vitamin K deficiency, drugs that act as vitamin K antagonists, and oxidant stress are forces that could prevent the formation of GLA residues on MGP. The potential role of arterial apoptosis in calcification is discussed. Potential therapeutic options to limit the rate of arterial calcification are summarized.

Animals↗
PubMed2002

Increased incidence of radial artery calcification in patients with diabetes mellitus.

BACKGROUND: The radial artery (RA) has become a popular conduit for coronary artery bypass (CAB). Preoperative RA evaluation in CAB patients has focused on ulnar collateral circulation to the hand and not on the conduit itself, yet the RA is prone to atherosclerosis and perhaps calcification, particularly in patients with diabetes mellitus (DM). We sought to determine the incidence of RA calcific disease in diabetic vs nondiabetic patients using ultrasonography to establish its role in preoperative evaluation of CAB patients. METHODS: Ultrasound images of the RA were obtained in 102 men (49 with DM) referred to a vascular laboratory. For each patient, a RA calcification index (CI; 0-4) was derived from separate scores accounting for calcification density, longitudinal vessel involvement, and bilaterality. Differences between diabetic and nondiabetic patients were determined by unpaired t test. RESULTS: Mean (+/-SEM) CI was greater in diabetic patients vs nondiabetics (2.32 +/- 0.21 vs 1.17 +/- 0.20; P < 0.0001), due mainly to an increase in dense calcification, which was observed in 17 (34%) diabetics vs 5 (9.6%) nondiabetics (P = 0.007). Calcifications were completely absent in 27 (52%) nondiabetics vs 9 (18%) diabetics (P = 0.000). CONCLUSIONS: These data indicate that both the incidence and the severity of RA calcific disease are increased by DM. Preoperative imaging of the RA should be considered in diabetic CAB candidates and perhaps in nondiabetics with multiple risk factors to avoid unnecessary forearm exploration or inadvertent use of a diseased conduit.

Aged↗
PubMed1977

The mode of calcification in atherosclerotic lesions.

In serveral arterial provinces, atherosclerosis and atherosclerotic calcifications are preceded by primary calcifications which develop in a seemingly unchanged arterial wall and often show regular gross patterns. In contrast, secondary calcifications which appear in the atherosclerotic lesions are irregularly distributed along the thickened atherosclerotic intima. At the predilection sites of atherosclerotic lesions, pronounced primary calcifications often precede the fatty streaking representing an independent pathological process. The deformation of the arterial wall resulting from calcific plaques may favor the activation of intimal mesenchyme and contribute to increased accumulation of lipid above and around calcific deposits. The exact nature of structural and biochemical changes which precede and result in primary and secondary arterial calcification still remains obscure.

Arteries↗
PubMed1985

Prevalences of CT-detected calcification in the basal ganglia in idiopathic hypoparathyroidism and pseudohypoparathyroidism.

Sixteen patients with idiopathic hypoparathyroidism (IHP) and eight patients with pseudohypoparathyroidism (PHP) were examined by CT scan of the brain. Calcification in the basal ganglia was observed in 11 patients with IHP (69%) and in all eight patients with PHP. Of the 19 patients with basal ganglia calcification, nine had calcification in the cerebral cortex (47%), and four had calcification in the cerebellum (21%). Observation of basal ganglia calcification on CT gave rise to suspicion of IHP or PHP in three patients (12%). The remaining patients were examined at varying time after diagnosis. Since arrest in growth of calcification after institution of treatment has never been proven, the reported prevalences of calcification may not be valid to the situation at the time of diagnosis.

Adolescent↗
PubMed1993

Medial arterial calcification in the feet of diabetic patients and matched non-diabetic control subjects.

The prevalence and distribution of medial arterial calcification was assessed in the feet of four subject groups; 54 neuropathic diabetic patients with previous foot ulceration (U), median age 60.5 (50.5-67 interquartile range) years, duration of diabetes 19.5 (9.9-29.9) years; 40 neuropathic diabetic patients without a foot ulcer history (N), age 68 (62-73) years, duration of diabetes 14.0 (8.0-28.0) years; 43 non-neuropathic diabetic patients (NN), age 60.5 (52-68.5) years, duration of diabetes 14.0 (8.0-28.0) years and 50 non-diabetic control subjects, age 62.5 (53.7-70) years. A single radiologist graded medial arterial calcification as absent, mild or severe, at the ankle, hind-foot, mid-foot, metatarsals and toes on standardised plain lateral and antero-posterior foot radiographs taken by a single radiographer. Diabetes history, vibration perception threshold, ankle systolic pressure and serum creatinine were also assessed. Medial arterial calcification was significantly greater (total score 18 [3-31]) in neuropathic diabetic patients with previous ulceration (U vs N p < 0.01, U vs NN p < 0.001). Non-neuropathic diabetic patients did not have significantly higher arterial calcification scores than age-matched non-diabetic control subjects. Medial arterial calcification correlated with vibration perception threshold (r = 0.35), duration of diabetes (r = 0.32) and serum creatinine (r = 0.41), (all p < 0.01). Logistic regression models showed vibration perception and duration of diabetes to predict the probability of any calcification. Serum creatinine level was added to predict severe calcification.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1975

Renal calcification in genito-urinary tuberculosis a clinical study.

1. Calcification in renal tuberculosis is not warranting a healing process, but may be a clinical manifestation of the disease. 2. Calcification presenting at least one year after the start of treatment should be considered differently from calcification first seen on presentation, and s,ould be treated in the same way as renal calculi. In view of the high incidence of associated active renal tuberculosis, calcification present when first seen should be removed, preferably with partial excision if the lesion is amenable to this form of treatment, but if it is not removed, patients should be followed up indefinitely, as complications can occur at any time. 3. Extra-renal calcification is more common in patients suffering from genito-urinary tuberculosis who present with renal calcification. 4. The incidence of renal calcification in patients suffering from renal tuberculosis is increasing. This could either be due to the host, the pathogenic organism, or possibly the treatment. As the host and treatment have not changed, it would suggest some alteration in the character of the organism.

Calcinosis↗
PubMed2001

Bone loss and the progression of abdominal aortic calcification over a 25 year period: the Framingham Heart Study.

Vascular calcification and osteoporosis are common age-related processes that are prominently displayed on routine lateral lumbar spine radiographs as dense calcium mineral deposits of the aorta that lie adjacent to osteopenic vertebrae. Using a population-based cohort of older men and women, we tested the hypothesis that the progression of vascular calcification of the abdominal aorta should be greatest in those individuals with the greatest amount of bone loss. From the original population-based Framingham Heart Study cohort, 364 women and 190 men had lateral lumbar spine and hand radiographs performed between 1966 and 1970 and repeated between 1992 and 1993. The lateral lumbar films were read for the presence of aortic calcification using a semiquantitative method, and the hand films were read for second metacarpal relative cortical area (MCA). Using multivariate regression techniques, the 25-year progression of the abdominal aortic calcification index was examined in relation to the change in the MCA, while adjusting for recognized risk factors for atherosclerotic cardiovascular disease. During the 25 years of follow-up, the MCA decreased by 22.4% in women (from 79.6 +/- 7.8 (SD) to 61.8 +/- 10.3) and by 13.3% in men (from 80.6 +/- 6.9 to 69.9 +/- 8.3). The aortic calcification score increased over eightfold in women (from 1.2 +/- 2.7 (SD) to 9.9 +/- 6.7) and sixfold in men (from 1.6 +/- 2.8 to 9.6 +/- 6.3). There was a significant association between percent change in MCA and change in aortic calcification index (P = 0.01) in women after controlling for all potential confounders. No association was observed in men (P = 0.50), including the 50% of men with the greatest bone loss. This is the first longitudinal study to show that women with the greatest magnitude of bone loss also demonstrate the most severe progression of abdominal aortic calcification, suggesting that the two processes may be related.

Absorptiometry, Photon↗
PubMed2001

Transforming growth factor-betas and CD105 expression in calcification and bone formation in human atherosclerotic lesions.

OBJECTIVES: To investigate the expression and localisation of transforming growth factor betas (TGF beta s) and their receptor CD105 (endoglin) in relation to calcification and bone formation in atherosclerotic lesions of human carotid arteries. BACKGROUND: The TGF beta family regulates cellular growth, differentiation and angiogenesis and plays a key role in enchondral bone formation. CD105 is part of the TGF beta receptor complex preferentially expressed on endothelial cells (EC). METHODS: Immunohistochemical methods were used to determine the localisation of TGF beta isoforms 1, 2 and 3 and their spatial expression patterns in relation to calcification and bone formation in atherosclerotic lesions. Cellular sources of TGF beta s and CD105 were assessed using cell-type specific antibodies. RESULTS: There was marked variability in TGF beta expression in different cell types associated with calcification. Smooth muscle cells (SMC) in the atheroma cap showed higher levels of TGF beta 3 and 2 than 1, but in the deep musculoelastic intima there were higher levels of TGF beta 1 and alpha-actin. All three TGF beta isoforms were expressed in monocyte-macro-phages. Giant cells associated with calcifications showed intense staining for TGF beta 2. TGF beta 1 was most strongly expressed on matrix and cells associated with bone formation. CD105 expression on SMCs and monocyte-macrophages was lower on cells in close association with calcification. SMCs associated with bone formation expressed high levels of CD105. CONCLUSIONS: The different TGF beta isoforms exhibit distinct but overlapping patterns of expression, and support the hypothesis that they are involved in the process of calcification and bone formation in human atherosclerotic lesions. Lower expression of CD105 on cells associated with calcification may represent their state of lower responsiveness to TGF beta s.

Antigens, CD↗
PubMed2004

[Diabetes mellitus type 2: coronary calcifications as a predictor of coronary artery disease].

BACKGROUND AND PURPOSE: Patients with diabetes mellitus have an increased risk of developing cardiovascular disease. Therefore, coronary artery disease (CAD) is the most common cause of mortality in these patients. The early and reliable diagnosis of coronary atherosclerosis is crucial for an effective treatment. Determination of coronary calcifications with multislice computed tomography offers the possibility to detect coronary calcifications as a sign of early coronary atherosclerosis. The present study examined the possibility to predict CAD in patients with diabetes mellitus by determination of coronary calcifications. PATIENTS AND METHODS: 632 patients (417 men, 215 women, age 54.6 +/- 17.3 years) with diabetes mellitus and suspected CAD were examined. All patients underwent coronary angiography. Coronary stenoses with lumen narrowing > 50% were regarded as significant CAD. Within 3 days coronary multislice computed tomography (Sensation 4, Siemens Medical Solutions, Forchheim, Germany) was performed and coronary calcifications were quantified using the volume score. Sensitivity, specificity, negative and positive predictive value for prediction of CAD were determined for different cutpoints. RESULTS: 440 patients showed a significant CAD, 315 patients underwent coronary transluminal angioplasty and 57 patients coronary artery bypass surgery. Mean volume score was 421 +/- 461. Volume score increased from 2 +/- 6 for patients < 40 years to 751 +/- 801 for patients > 70 years. Women showed a significantly lower score in all age groups. The mean volume score was significantly higher in patients with CAD compared to those without CAD (587 +/- 642 compared to 40 +/- 53; p < 0.01). In all patients without coronary calcifications, CAD could be ruled out angiographically. Using score 0, 10, 100 as cutoff points for the prediction of CAD, a sensitivity of 100%, 97%, and 87% at a specificity of 25%, 69%, and 82% was calculated. Best results were achieved using the 75th percentile as cutoff point with a sensitivity of 91% and a specificity of 84%. In total, CAD could be diagnosed correctly by quantification of coronary calcifications in 94% of all patients. CONCLUSION: Determination of coronary calcifications by multislice computed tomography could be used in patients with diabetes mellitus to detect coronary atherosclerosis and allows the early and exact diagnosis of CAD.

Calcinosis↗
PubMed2006

[Prevalence and pathogenesis of aortic valve calcifications].

BACKGROUND: Calcific aortic valve disease is present in more than 25% of patients > 65 years of age and is associated with a 50% increased risk of cardiovascular events. The clinical significance of aortic valve calcification detected incidentally by radiologic examinations, especially on CT scans of the chest, was unknown. Concerning the multifactorial pathogenesis of aortic valve calcification, recent data indicate that, besides other factors, also the regulators of calcification play a key role in the disease process. PURPOSE: This study aims to give an overview of the prevalence and clinical significance of incidentally detected aortic valve calcifications. Moreover, the role calcification inhibitors in the pathogenesis of aortic valve calcification is discussed.

Adult↗
PubMed2001

Calcification of the alar ligament of the cervical spine: imaging findings and clinical course.

Ligamentous calcification of the cervical spine has been reported in the yellow ligament, anterior and posterior longitudinal ligaments and interspinous ligament. Calcification in the upper cervical spine is rare, although some cases with calcification of the transverse ligament of the atlas have been reported. Two patients with calcification of the alar ligament with an unusual clinical presentation and course are described. Examination by tomography and computed tomography (CT) showed calcification of the alar ligament and the transverse ligament of the atlas. CT documented decreased calcification as symptoms resolved. There may be a role for CT in the search for calcifications in the upper cervical spine in patients presenting with neck pain and pharyngodynia if radiographs are normal.

Adult↗
PubMed2006

MR arthrography in calcific tendinitis of the shoulder: diagnostic performance and pitfalls.

The purpose was to assess the diagnostic performance of MR arthrography to diagnose calcific tendinitis of the shoulder and to assess the reasons for diagnostic errors. Standard MR arthrograms of 22 patients with calcific tendinitis and 61 controls were retrospectively analyzed by two independent and blinded radiologists. All cases were consecutively collected from a database. Conventional radiographs were available in all cases serving as gold standard. The supraspinatus was involved in 16, the infraspinatus in four and the subscapularis in two patients. All diagnostic errors were analyzed by two additional readers. Reader 1 correctly detected 12 of the 22 shoulders with and 42 of the 61 shoulders without calcific tendinitis (sensitivity 0.55, specificity 0.66). The corresponding values for reader 2 were 13 of 22 and 40 of 61 cases (sensitivity 0.59, specificity 0.69). Inter-rater agreement (kappa-value) was 0.42. Small size of the calcific deposits and isointensity compared to the surrounding tissue were the most important reasons for false negative results. Normal hypointense areas within the supraspinatus tendon substance and attachment were the main reason for false positive results. In conclusion, MR arthrography is insufficient in the diagnosis of calcific tendinitis. Normal hypointense parts of the rotator cuff may mimic calcific deposits and calcifications may not be detected when they are isointense compared to the rotator cuff. Therefore, MR imaging should not be interpreted without corresponding radiographs.

Adult↗
PubMed2004

Taurine prevents beta-glycerophosphate-induced calcification in cultured rat vascular smooth muscle cells.

Vascular calcification is an ectopic calcification that commonly occurs in atherosclerosis. Because taurine was previously shown to protect against cardiovascular diseases, the effect of taurine on vascular calcification was evaluated in calcified vascular smooth muscle cells (VSMCs) of rat in vitro in the present study. Osteoblastic differentiation, calcification, and proliferation in VSMCs were detected in the presence and absence of taurine. Alkaline phosphatase (ALP), cellular calcium content, and (45)Ca accumulation were measured as the indicators of osteoblastic differentiation and calcification. Incubation of VSMCs with Beta-glycerophosphate for 10 days induced an osteoblast-like morphological change. The activity of ALP was enhanced. Calcium content and (45)Ca uptake were increased in these cells. Calcification of these VSMCs was demonstrated with Beta-glycerophosphate treatment. In association with these alterations, cell proliferation, detected by cell counting, [(3)H]thymidine ([(3)H]TdR), and [(3)H]leucine ([(3)H]Leu) incorporation, was also increased in these calcified VSMCs. Taurine at 20 mmol/l decreased calcium content, (45)Ca(2+) uptake, and ALP activity both after early and late treatment, in which a reduction of the cell count, [(3)H"]TdR, and [(3)H]Leu incorporation of calcified VSMCs was also noted. Compared with the calcified group, morphological changes in the VSMCs of the early-treated group were deferred. These results demonstrated that calcification of VSMCs could be alleviated by taurine. Taurine treatment appeared to be more beneficial when the treatment was started earlier.

Animals↗