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At least 433 records · Page 24Linked to original sources
PubMed1992

Quantitation of in situ contact areas at the glenohumeral joint: a biomechanical study.

Glenohumeral arthritis may result from abnormal articular mechanics, and shoulder reconstructive procedures often rely implicitly on the belief that the restoration of normal articular mechanics is required to obtain satisfactory clinical results. Despite this, limited knowledge of normal or pathologic glenohumeral joint articular mechanics and contact is available. This study uses a stereophotogrammetry technique to determine contact areas in normal cadaver glenohumeral joints with intact ligaments and capsule through a large range of motion using simulated forces of the four rotator cuff muscles and three deltoid heads. All shoulders were first elevated to their maximum elevation in the scapular plane at an external rotation (starting rotation = 40 +/- 8 degrees), which allowed each shoulder to attain its maximal elevation in the scapular plane, and then repeated at 20 degrees internal to this rotation. Contact areas consistently increased with increasing elevation until 120 degrees to an average of 5.07 cm2 before decreasing with further increased elevation to an average of 2.59 cm2 at 180 degrees of total arm elevation. At 20 degrees internal to the starting rotation, contact areas reached high values 60 degrees earlier (averaged 4.56 cm2 at 60 degrees of total arm elevation) and then remained fairly constant through 120 degrees before decreasing with further increased elevation to 2.51 cm2 at 180 degrees total arm elevation. With increasing elevation in the external starting rotation, humeral head contact dramatically migrates from an inferior region to a superocentral-posterior region while glenoid contact shifts posteriorly. When the humeral shaft is positioned 20 degrees internal to the starting rotation, humeral head contact shifts from inferocentral-anterior to superocentral-posterior regions. Simultaneously, a similar posterior shift in glenoid contact is observed. Furthermore, whereas only a small portion of the humeral head surface area is in contact in any given position, contact on the glenoid surface is much more uniformly distributed over its entire articulating surface.

Aged↗
PubMed2001

Reed warbler orientation: initiation of nocturnal migratory flights in relation to visibility of celestial cues at dusk.

We used radiotelemetry to investigate the time of migratory flight initiation relative to available celestial orientation cues and departure direction of a nocturnal passerine migrant, the reed warbler, Acrocephalus scirpaceus, during autumn migration. The study was carried out at Falsterbo, a coastal site in southwest Sweden. The warblers initiated migration from times well after local sunset and well into the night, corresponding to sun elevations between -4 degrees and -35 degrees, coinciding with the occurrence of stars at night. They departed in the expected migratory direction towards south of southwest with a few initiating migration in reverse directions towards northeast to east. Flight directions under overcast conditions (7-8/8) were more scattered than under clear sky conditions (0-4/8). There were fewer clouds on departure nights than on nights when the birds did not initiate migration. For birds staying longer than one night at stopover the horizontal visibility was higher and precipitation was less likely on departure nights than on the previous night. The results show that the visibility of celestial cues, and stars in particular, are important for the decision to initiate migration in reed warblers. However, cloud cover, horizontal visibility and precipitation might be correlated with other weather variables (i.e. wind or air pressure) that are also likely to be important for the decision to migrate. Copyright 2001 The Association for the Study of Animal Behaviour.

Journal Article↗
PubMed2000

Expression of adhesion molecules and cytokines on saphenous veins in chronic venous insufficiency.

The objective of this study was to assess the relationship of signaling molecules to monocyte/ macrophages as a precursor to venous valve and venous wall dysfunction in patients with varicose veins. One of the hallmarks of venous dysfunction is destruction of venous valves with subsequent reflux and elevation of distal venous pressure. We recently observed that monocytes/macrophages migrate into the venous walls and valves of patients with venous insufficiency. There, they may play a role in the pathogenesis of primary venous insufficiency. If so, an important element in their performance would be the interaction between the monocytes and the endothelium as a precursor of damage to venous valves and the venous wall. To explore this interaction, immunohistochemistry was carried out to detect adhesion molecules and cytokines in surgical specimens removed during surgical therapy. Twenty-four surgical specimens consisting of proximal saphenous vein and subterminal valve were obtained using minimally traumatic technique in 6 males and 18 females who ranged in age from 31 to 79 years. Reflux was confirmed preoperatively by duplex technique, and severity was classified by the CEAP classification of the American Venous Forum. Ten patient limbs were class 2, eight were class 3, four were class 4, and two were class 6. The venous specimens were labeled using monoclonal antibody against ICAM-1, E-selectin, IL-1alpha, and TNF-alpha. CD68 was used for detection of monocytes/macrophages. Our results indicate that not only luminal venous endothelium but also endothelium in the vasa vasora of refluxing saphenous veins is activated, as indicated by the up-regulation of ICAM-1. However, IL-1alpha and TNF-alpha were increased in only selected specimens and are mainly detected in the vein wall. The factors that serve as trigger mechanisms to activate cells in the pathogenesis of primary venous dysfunction remain to be explored.

Adult↗
PubMed1995

Stimulation of avian respiratory phagocytes by Pasteurella multocida: effects of the route of exposure, bacterial dosage and strain, and the age of chickens.

The effects of the route of exposure (intratracheal [IT], drinking water [DW] and aerosolization [AS]), the age of chickens, and the dose of two vaccine strains of Pasteurella multocida (CU and M-9) on the number, phagocytic proportion and capacity of macrophages, granulocytes and lymphocytes (collectively avian respiratory phagocytes [ARPs]) were analyzed. Administration of P. multocida via the DW even at very high dose failed to stimulate ARPs. In contrast, administration of both strains of P. multocida either IT or by AS resulted in rapid and highly significant increases in the numbers of ARPs. 10 x 10(9) colony forming units (cfu) of aerosolized P. multocidaCU strain activated ARPs maximally in both young (3-6 weeks of age) and old (4-6 months of age) chickens. Old chickens responded in dose dependent manner to 20 x 10(9), 8 x 10(9), and 4 x 10(9) cfu of aerosolized P. multocida CU strain. Young chickens responded significantly only to 8 x 10(9) CU organisms. The M-9 and CU strains had limited differences in inducing migration of ARPs into the respiratory system of chickens or elevating phagocytic proportions and capacity of ARPs. The results indicate that the analyzed factors influence the response of ARPs to P. multocida to various degrees.

Age Factors↗
PubMed2004

Neuregulin-1 reduces ischemia-induced brain damage in rats.

Neuregulin-1 (NRG-1) is expressed throughout the immature and adult central nervous system and it has been demonstrated to influence the migration of a variety of cell types in developing brain. Elevated levels of NRG-1 transcript are found in the adult brain after injury, leading to the suggestion that NRG-1 is involved in the physiological response to neuronal injury. Here, we report our findings that rats pre-treated with NRG-1 protein, undergoing cerebral ischemia 30 min later, had increased motor performance and less cerebral infarction than untreated rats. In the cortex of NRG-1 treated rats, ischemia induced a decrease in caspase-3 immunoreactivity and a reduction in the density of cells positive for terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end-labeling. Improvement in behavioral assays was also found in animals treated with NRG-1. Pre-treatment with NRG-1 did not alter cerebral blood flow or other physiological parameters. NRG-1 reduced ischemia/reperfusion injury, indicating that it may act as an endogenous neuroprotective factor against stroke. Therefore, NRG-1 may represent a target for the development of new treatments for stroke.

Animals↗
PubMed2005

The over-expression of HAS2, Hyal-2 and CD44 is implicated in the invasiveness of breast cancer.

Within tumors there appears to be an intricate balance between hyaluronan (HA) synthesis and degradation where the invading edges display increased HA metabolism. The metabolism of HA has not been characterized in breast cancer cell lines; therefore, this study quantitatively identifies and characterizes the enzymes responsible for the synthesis and degradation of HA while correlating gene expression to cancer cell invasiveness and HA receptor status. In ten well-established breast cancer cell lines, the expression of the genes for each hyaluronan synthase (HAS) and hyaluronidase (Hyal) isoform was quantitated using real-time and reverse transcriptase polymerase chain reaction (PCR). The synthesis and degradation rates of hyaluronan were determined by ELISA, while quantitation of HA receptors, CD44 and RHAMM was performed by comparative Western blotting. The molecular weight of HA synthesized by each HAS isoform and the degradation products of each hyaluronidase were characterized by size exclusion chromatography. It was demonstrated that highly invasive cell lines preferentially expressed the HAS2 and Hyal-2 isoforms, while less invasive cells expressed HAS3 and Hyal-3. There was a correlation between elevated levels of HA synthesis, CD44 expression and cancer cell migration thereby highlighting the pivotal role that HA metabolism plays in the aggressive breast cancer phenotype.

Breast Neoplasms↗
PubMed2002

Ecology of southern ocean pack ice.

Around Antarctica the annual five-fold growth and decay of sea ice is the most prominent physical process and has a profound impact on marine life there. In winter the pack ice canopy extends to cover almost 20 million square kilometres--some 8% of the southern hemisphere and an area larger than the Antarctic continent itself (13.2 million square kilometres)--and is one of the largest, most dynamic ecosystems on earth. Biological activity is associated with all physical components of the sea-ice system: the sea-ice surface; the internal sea-ice matrix and brine channel system; the underside of sea ice and the waters in the vicinity of sea ice that are modified by the presence of sea ice. Microbial and microalgal communities proliferate on and within sea ice and are grazed by a wide range of proto- and macrozooplankton that inhabit the sea ice in large concentrations. Grazing organisms also exploit biogenic material released from the sea ice at ice break-up or melt. Although rates of primary production in the underlying water column are often low because of shading by sea-ice cover, sea ice itself forms a substratum that provides standing stocks of bacteria, algae and grazers significantly higher than those in ice-free areas. Decay of sea ice in summer releases particulate and dissolved organic matter to the water column, playing a major role in biogeochemical cycling as well as seeding water column phytoplankton blooms. Numerous zooplankton species graze sea-ice algae, benefiting additionally because the overlying sea-ice ceiling provides a refuge from surface predators. Sea ice is an important nursery habitat for Antarctic krill, the pivotal species in the Southern Ocean marine ecosystem. Some deep-water fish migrate to shallow depths beneath sea ice to exploit the elevated concentrations of some zooplankton there. The increased secondary production associated with pack ice and the sea-ice edge is exploited by many higher predators, with seals, seabirds and whales aggregating there. As a result, much of the Southern Ocean pelagic whaling was concentrated at the edge of the marginal ice zone. The extent and duration of sea ice fluctuate periodically under the influence of global climatic phenomena including the El Niño Southern Oscillation. Life cycles of some associated species may reflect this periodicity. With evidence for climatic warming in some regions of Antarctica, there is concern that ecosystem change may be induced by changes in sea-ice extent. The relative abundance of krill and salps appears to change interannually with sea-ice extent, and in warm years, when salps proliferate, krill are scarce and dependent predators suffer severely. Further research on the Southern Ocean sea-ice system is required, not only to further our basic understanding of the ecology, but also to provide ecosystem managers with the information necessary for the development of strategies in response to short- and medium-term environmental changes in Antarctica. Technological advances are delivering new sampling platforms such as autonomous underwater vehicles that are improving vastly our ability to sample the Antarctic under sea-ice environment. Data from such platforms will enhance greatly our understanding of the globally important Southern Ocean sea-ice ecosystem.

Animals↗
PubMed2002

A restricted subset of dendritic cells captures airborne antigens and remains able to activate specific T cells long after antigen exposure.

Mice sensitized for a Th2 response to Leishmania LACK antigen developed allergic airway inflammation upon exposure to LACK aerosol. Using multimers of I-A(d) molecules bound to a LACK peptide as probes, we tracked the migration of LACK-specific Th2 cells to the airways. Elevated numbers of LACK-specific Th2 cells remained in the airways for 5 weeks after the last aerosol. Substantial numbers of DC presenting LACK peptides were found in the airways, but not in other compartments, for up to 8 weeks after antigen exposure. These LACK-presenting airway DC expressed CD11c and CD11b as well as high levels of surface molecules involved in uptake and costimulation. Taken together, our results may explain the chronic Th2 airway inflammation characteristic of allergic asthma.

Administration, Inhalation↗
PubMed2004

Epstein-Barr virus (EBV) LMP2A mediates B-lymphocyte survival through constitutive activation of the Ras/PI3K/Akt pathway.

Epstein-Barr virus (EBV) establishes a lifelong latent infection in host B cells and is associated with the development of a variety of malignancies. The viral LMP2A protein mediates viral latency by mimicking a constitutively activated B-cell receptor (BCR). In vivo LMP2A provides developmental and survival signals to BCR-negative B cells, allowing them to survive in peripheral lymphoid organs. In this study, we have demonstrated that Ras is constitutively active in peripheral, BCR-negative B cells from LMP2A transgenic mice. Furthermore, increased expression of activated Ras correlated with elevated levels of Bcl-xL expression and a slower migrating, band-shifted form of Bcl-2. B cells from LMP2A transgenic mice were sensitive to apoptosis induction in the presence of specific inhibitors of Ras, phosphatidylinositol 3-kinase (PI3K), and Akt, indicating that LMP2A activates the Ras/PI3K/Akt pathway to mediate B-cell survival. Increased B-cell apoptosis correlated with reduced expression of Bcl-xL, suggesting that this Bcl-2 family member may be involved in apoptosis inhibition mediated by LMP2A. The ability of LMP2A to activate constitutively the Ras pathway, a common event during tumorigenesis, suggests that this viral protein plays an active role in the development of EBV-associated malignancies.

Animals↗
PubMed2005

Rap1 GTPase inhibits leukocyte transmigration by promoting endothelial barrier function.

The passage of leukocytes out of the blood circulation and into tissues is necessary for the normal inflammatory response, but it also occurs inappropriately in many pathological situations. This process is limited by the barrier presented by the junctions between adjacent endothelial cells that line blood vessels. Here we show that activation of the Rap1 GTPase in endothelial cells accelerated de novo assembly of endothelial cell-cell junctions and increased the barrier function of endothelial monolayers. In contrast, depressing Rap1 activity by expressing Rap1GAP led to disassembly of these junctions and increased their permeability. We also demonstrate that endogenous Rap1 was rapidly activated at early stages of junctional assembly, confirming the involvement of Rap1 during junctional assembly. Intriguingly, elevating Rap1 activity selectively within endothelial cells decreased leukocyte transendothelial migration, whereas inhibiting Rap1 activity by expression of Rap1GAP increased leukocyte transendothelial migration, providing physiological relevance to our hypothesis that Rap1 augments barrier function of inter-endothelial cell junctions. Furthermore, these results suggest that Rap1 may be a novel therapeutic target for clinical conditions in which an inappropriate inflammatory response leads to disease.

Cell Movement↗
PubMed2002

The focal adhesion kinase--a regulator of cell migration and invasion.

Cell migration plays an important role in embryonic development, wound healing, immune responses, and in pathological phenomena such as tissue invasion and metastasis formation. In this review, we summarize recent reports that connect the focal adhesion kinase (FAK) to cell migration and invasion. FAK is a nonreceptor protein tyrosine kinase involved in signal transduction from integrin-enriched focal adhesion sites that mediate cell contact with the extracellular matrix. Multiple protein-protein interaction sites allow FAK to associate with adapter and structural proteins allowing for the modulation of mitogen-activated protein (MAP) kinases, stress-activated protein (SAP) kinases, and small GTPase activity. FAK-enhanced signals have been shown to mediate the survival of anchorage-dependent cells and are critical for efficient cell migration in response to growth factor receptor and integrin stimulation. Elevated expression of FAK in human tumors has been correlated with increased malignancy and invasiveness. Because recent findings show that FAK contributes to the secretion of matrix-metalloproteinases, FAK may represent an important checkpoint in coordinating the dynamic processes of cell motility and extracellular matrix remodeling during tumor cell invasion.

Cell Movement↗
PubMed1992

Severe type III hyperlipoproteinemia associated with unusual apolipoprotein E1 phenotype and epsilon 1/'null' genotype.

A 60-year-old white male (KH) was diagnosed to suffer from severe type III hyperlipoproteinemia (HLP) and premature cardiovascular disease. Biochemical analysis revealed an unusual apolipoprotein (apo) E phenotype and genotype. All clinical characteristics of type III HLP were present in the patient. His very low density lipoprotein (VLDL) cholesterol to plasma triglyceride (TG) ratio was elevated at 0.97 without therapy which is unusually high (normal ratio about 0.18). By contrast his plasma apo E level was only moderately elevated (6.8 mg dl-1). The patient's apo E migrated in the apo E1 position on isoelectric focusing gels. Chemical modification with cysteamine and treatment with neuraminidase confirmed the presence of two cysteine residues in the patient's apo E and a normal sialylation pattern. Pedigree analysis suggested that the patient was a compound heterozygote with one apo epsilon 1 allele and another allele whose product did not appear in the plasma compartment ('null' allele). Direct sequencing of polymerase chain reaction (PCR) amplified segments of the apo E gene as well as restriction fragment length polymorphism (RFLP) analysis with the endonuclease Taq I identified an adenosine for guanosine (G-->A) exchange in the second base of codon 127 that is predictive for an Asp for Gly substitution in the encoded apo E amino acid sequence. This mutation is the structural basis for the apo E1 isoform identified upon isoelectric focusing. Five other family members are also carriers of the mutant apo epsilon 1 allele. Two of those were hyperlipidemic and exhibited biochemical characteristics of type III HLP. A second mutation, a deletion of a G in codon 31, is predictive for a reading frameshift that encodes for a premature stop in codon 60. Our inability to identify the product of a second apo E allele in the plasma of the patient and two other members of the KH family corresponds with the heterozygous presence of this mutation in the affected individuals. Both relatives (like the index case) had an increased VLDL cholesterol to plasma TG ratio, which indicates the presence of cholesterol-enriched VLDL particles. We propose that the single base deletion in the apo E gene which is the cause of a non-functional 'null' allele in addition to a probably dominant apo E1 (Gly127-->Asp, Arg158-->Cys) variant of late or incomplete penetrance are the primary genetic defects in this kindred leading to severe dysbetalipoproteinemia.

Adolescent↗
PubMed1991

Biologic basis for a risk assessment model for cleft palate.

A biologic model for palatogenesis is presented, intended as a basis for risk assessment. It comprises a sequence of developmental stages: growth and migration of neural crest cells, downward growth of palatal buds, elevation of palatal shelves, and differentiation of the epithelium followed by shelf fusion. Several events representing these stages and amenable to mathematical translation may be measurable in the form of biomarkers such as DNA and protein synthesis, phospholipid metabolism, and signal transducing systems. Interrupting components of the model will result in cleft palate. Teratogens with known mechanisms of action are compared with the model. The quantitative risk of cleft palate is conceived as a sequence of mathematical probabilities that any stage of the model runs an abnormal course. Stage-specific probabilities are determined by a chemical's potency and dose, and by duration of exposure and gestational age. Species or strain sensitivity may be expressed as quantitative differences in model parameters. Although the model is designed for cleft palate, the risk model may also estimate a multiple response risk to the same exposures.

Animals↗
PubMed2026

High-fat diet-responsive DNM1 promotes hepatocellular carcinoma progression and predicts poor prognosis in viral-associated patients.

Hepatocellular carcinoma (HCC) arises from diverse etiologies, among which metabolic dysfunction-associated liver disease and chronic viral hepatitis are the two major drivers worldwide. However, the molecular mechanisms linking metabolic stress to HCC progression remain incompletely understood. Dynamin-1 (DNM1), primarily known for its role in vesicular trafficking, has emerged as a potential oncogene, yet its prognostic and functional significance in HCC remains largely unexplored. Here, we investigated the role of DNM1 in high-fat diet (HFD)-associated hepatocarcinogenesis. Transcriptomic profiling was conducted to identify differentially expressed genes between normal and high-fat diet murine models, with human orthologs mapped. Clinical relevance was validated using The Cancer Genome Atlas (TCGA-LIHC) dataset. Survival analysis, GSEA (Gene Set Enrichment Analysis), and subgroup stratifications based on viral hepatitis status were performed. In vitro, loss-of-function assays (shRNA knockdown) were executed in HepG2 and SK-Hep1 cell lines to assess cell viability and migration. DNM1 was significantly upregulated in high-fat diet models. In the TCGA-LIHC cohort, high DNM1 expression was an independent risk factor for poor overall survival (HR=1.44, P=0.039) and correlated with advanced tumor stages (Stage III+IV, P=0.010). In vitro knockdown of DNM1 profoundly impaired cell proliferation and migration in HCC cell lines. Strikingly, DNM1 expression was further elevated in patients with concurrent viral hepatitis (P=0.009). GSEA revealed that high DNM1 expression was positively associated with viral infection pathways and negatively correlated with critical immune responses, including interferon-alpha/gamma responses and host immune cytolysis. Survival analysis stratified by four subgroups demonstrated that patients with both viral infection and high DNM1 expression exhibited the worst prognosis (Overall Log-rank P < 0.001). Our findings identify DNM1 as a high-fat diet-responsive regulator that links metabolic stress to hepatocellular carcinoma progression. Elevated DNM1 expression promotes malignant phenotypes in HCC and identifies a subgroup of viral-associated patients with particularly poor prognosis, highlighting DNM1 as a potential prognostic biomarker and therapeutic target.

Hepatocellular carcinoma (HCC)↗
PubMed2005

[Expressions and role of endogenetic matrix metalloproteinases-9 and transforming growth factor-beta during wound healing of blast injury].

OBJECTIVE: To investigate the expression of endogenetic matrix metalloproteinases-9 (MMP-9) and transforming growth factor-beta(TGF-beta) and their role in the wound healing of blast injury. METHODS: Rat models of blast injury under a humid and hot environment were established and the effusion from the wound surface was collected at 4, 24, 48 h and 5, 7, 14, 21 and 28 days after injury, respectively. The contents of MMP-9 and TGF-beta in the effusion of the wound were measured by zymography and enzyme-linked immunosorbent assay (ELISA), respectively. RESULTS: During the wound healing of blast injury, MMP-9 and TGF-beta exhibited changes that followed a regular pattern, both reaching the peak value at 48 h after the injury. TGF-beta content reached the another peak on day 7. TGF-beta value and MMP-9 contents decreased in the second week after injury and their reduction was no longer parallel. Administration of tissue inhibitor of metalloproteinase (TIMP) in the early phase of injury showed no obvious effect, but during the 2 weeks after the injury, its administration caused decrease in MMP-9 content and increase in TGF-beta content in the effusion. CONCLUSIONS: In the early phase of wound healing, the elevation of MMP-9 and TGF-beta accelerated cell migration to promote the clearance of the inflammatory necrosis tissues, which might be one of the wound healing mechanisms. But overexpression of MMP-9 in the wound may hinder wound healing, and appropriate use of TIMP can accelerate the delayed wound healing.

Animals↗
PubMed2002

Complexities in ETS-domain transcription factor function and regulation: lessons from the TCF (ternary complex factor) subfamily. The Colworth Medal Lecture.

The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.

Amino Acid Sequence↗
PubMedDate not supplied

Cellular defense of the avian respiratory system: dose-response relationship and duration of response in intratracheal stimulation of avian respiratory phagocytes by a Pasteurella multocida bacterin.

In experiments analyzing dose-response, intratracheal inoculation of chickens with 10(8) and 10(9) avirulent Pasteurella multocida organisms induced the migration within 24 hr of large numbers of respiratory lavage cells (RLC) with increased phagocytic proportions and phagocytic capacity. Doses from 10(4) to 10(7) organisms per bird resulted in elevated numbers of RLCs that were not significantly higher (P > 0.05) than values of uninoculated or mock-inoculated control chickens. When analyzing the duration of response, we found that inoculation with 10(9) organisms resulted in significantly higher (P < 0.05) numbers of RLCs for 63 to 89 hr without significant elevation in phagocytic proportion and capacity. The numbers of RLCs were elevated, although not significantly (P > 0.05), up to 11 days after inoculation. These results indicate that RLCs migrate to the respiratory tract only in response to a relatively high number of stimulating bacterial organisms and that the duration of response is relatively short. Although there were elevated numbers of RLCs beyond 89 hours after stimulation, the question remains as to whether these cells would enhance nonspecific defense of the respiratory system of chickens.

Animals↗